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The dataset generation failed because of a cast error
Error code: DatasetGenerationCastError
Exception: DatasetGenerationCastError
Message: An error occurred while generating the dataset
All the data files must have the same columns, but at some point there are 4 new columns ({'doc_id', 'relevance', 'subtopic_id', 'query_id'}) and 2 missing columns ({'contents', 'id'}).
This happened while the json dataset builder was generating data using
hf://datasets/algoprog/TREC-ICAT/qrels.jsonl (at revision e0f48abe14d5667ff814f35021bd9dca75464c75)
Please either edit the data files to have matching columns, or separate them into different configurations (see docs at https://hf.co/docs/hub/datasets-manual-configuration#multiple-configurations)
Traceback: Traceback (most recent call last):
File "/src/services/worker/.venv/lib/python3.9/site-packages/datasets/builder.py", line 1870, in _prepare_split_single
writer.write_table(table)
File "/src/services/worker/.venv/lib/python3.9/site-packages/datasets/arrow_writer.py", line 622, in write_table
pa_table = table_cast(pa_table, self._schema)
File "/src/services/worker/.venv/lib/python3.9/site-packages/datasets/table.py", line 2292, in table_cast
return cast_table_to_schema(table, schema)
File "/src/services/worker/.venv/lib/python3.9/site-packages/datasets/table.py", line 2240, in cast_table_to_schema
raise CastError(
datasets.table.CastError: Couldn't cast
query_id: string
doc_id: string
relevance: int64
subtopic_id: string
to
{'id': Value(dtype='string', id=None), 'contents': Value(dtype='string', id=None)}
because column names don't match
During handling of the above exception, another exception occurred:
Traceback (most recent call last):
File "/src/services/worker/src/worker/job_runners/config/parquet_and_info.py", line 1420, in compute_config_parquet_and_info_response
parquet_operations = convert_to_parquet(builder)
File "/src/services/worker/src/worker/job_runners/config/parquet_and_info.py", line 1052, in convert_to_parquet
builder.download_and_prepare(
File "/src/services/worker/.venv/lib/python3.9/site-packages/datasets/builder.py", line 924, in download_and_prepare
self._download_and_prepare(
File "/src/services/worker/.venv/lib/python3.9/site-packages/datasets/builder.py", line 1000, in _download_and_prepare
self._prepare_split(split_generator, **prepare_split_kwargs)
File "/src/services/worker/.venv/lib/python3.9/site-packages/datasets/builder.py", line 1741, in _prepare_split
for job_id, done, content in self._prepare_split_single(
File "/src/services/worker/.venv/lib/python3.9/site-packages/datasets/builder.py", line 1872, in _prepare_split_single
raise DatasetGenerationCastError.from_cast_error(
datasets.exceptions.DatasetGenerationCastError: An error occurred while generating the dataset
All the data files must have the same columns, but at some point there are 4 new columns ({'doc_id', 'relevance', 'subtopic_id', 'query_id'}) and 2 missing columns ({'contents', 'id'}).
This happened while the json dataset builder was generating data using
hf://datasets/algoprog/TREC-ICAT/qrels.jsonl (at revision e0f48abe14d5667ff814f35021bd9dca75464c75)
Please either edit the data files to have matching columns, or separate them into different configurations (see docs at https://hf.co/docs/hub/datasets-manual-configuration#multiple-configurations)Need help to make the dataset viewer work? Make sure to review how to configure the dataset viewer, and open a discussion for direct support.
id
string | contents
string |
|---|---|
clueweb09-enwp01-01-19098 | Hyperlipidemia - Wikipedia, the free encyclopedia Hyperlipidemia From Wikipedia, the free encyclopedia (Redirected from B��rger-Gr��tz syndrome ) Jump to: navigation , search Hyperlipidemia Classification and external resources ICD - 10 E 78. ICD - 9 272.0 - 272.4 DiseasesDB 6255 MeSH D006949 Hyperlipidemia , hyperlipoproteinemia or dyslipidemia is the presence of raised or abnormal levels of lipids and/or lipoproteins in the blood . Lipids (fatty molecules) are transported in a protein capsule, and the density of the lipids and type of protein determines the fate of the particle and its influence on metabolism . Lipid and lipoprotein abnormalities are extremely common in the general population, and are regarded as a highly modifiable risk factor for cardiovascular disease due to the influence of cholesterol , one of the most clinically relevant lipid substances, on atherosclerosis . In addition, some forms may predispose to acute pancreatitis . Contents 1 Classification 1.1 Hyperlipoproteinemia type I 1.2 Hyperlipoproteinemia type II 1.2.1 Type IIa 1.2.2 Type IIb 1.2.3 Treatment 1.3 Hyperlipoproteinemia type III 1.4 Hyperlipoproteinemia type IV (type 4 = familial) 1.5 Hyperlipoproteinemia type V (type 5 = endogenous) 2 Unclassified forms 3 References 4 External links [ edit ] Classification Hyperlipidemias are classified according to the Fredrickson classification which is based on the pattern of lipoproteins on electrophoresis or ultracentrifugation . [ 1 ] It was later adopted by the World Health Organization (WHO). It does not directly account for HDL , and it does not distinguish among the different genes that may be partially responsible for some of these conditions. It remains a popular system of classification, but is considered dated by many. Fredrickson classification of Hyperlipidemias Hyperlipoproteinemia Synonyms Problems Increased lipoprotein Treatment Serum appearnace Type I (rare) Buerger-Gruetz syndrome , Primary hyperlipoproteinaemia , or Familial hyperchylomicronemia Decreased lipoprotein lipase (LPL) or altered ApoC2 Chylomicrons Diet Control Creamy top layer Type IIa Polygenic hypercholesterolaemia or Familial hypercholesterolemia LDL receptor deficiency LDL Bile Acid Sequestrants , Statins , Niacin Clear Type IIb Combined hyperlipidemia Decreased LDL receptor and Increased ApoB LDL and VLDL Statins , Niacin , Fibrate Clear Type III (rare) Familial Dysbetalipoproteinemia Defect in Apo E 2 synthesis IDL Drug of choice: Fibrate Turbid Type IV Familial Hyperlipemia Increased VLDL production and Decreased elimination VLDL Drug of choice: Fibrate , Niacin Turbid Type V (rare) Endogenous Hypertriglyceridemia Increased VLDL production and Decreased LPL VLDL and Chylomicrons Niacin , Fibrate Creamy top layer & turbid bottom [ edit ] Hyperlipoproteinemia type I This very rare form (also known as Buerger-Gruetz syndrome , primary hyperlipoproteinaemia , or familial hyperchylomicronemia ) is due to a deficiency of lipoprotein lipase (LPL) or altered apolipoprotein C2 , resulting in elevated chylomicrons , the particles that transfer fatty acids from the digestive tract to the liver . Lipoprotein lipase is also responsible for the initial breakdown of endogenously made triacylglycerides in the form of very low density lipoprotein (VLDL). As such, one would expect a defect in LPL to also result in elevated VLDL. Its prevalence is 0.1% of the population. [ edit ] Hyperlipoproteinemia type II Hyperlipoproteinemia type II, by far the most common form, is further classified into type IIa and type IIb, depending mainly on whether there is elevation in the triglyceride level in addition to LDL cholesterol. [ edit ] Type IIa Main article: Familial hypercholesterolemia This may be sporadic (due to dietary factors), polygenic, or truly familial as a result of a mutation either in the LDL receptor gene on chromosome 19 (0.2% of the population) or the ApoB gene (0.2%). The familial form is characterized by tendon xanthoma , xanthelasma and premature cardiovascular disease. The incidence of this disease is about 1 in 500 for heterozygotes, and 1 in 1,000,000 for homozygotes. [ edit ] Type IIb The high VLDL levels are due to overproduction of substrates, including triglycerides, acetyl CoA, and an increase in B-100 synthesis. They may also be caused by the decreased clearance of LDL. Prevalence in the population is 10%. Familial combined hyperlipoproteinemia (FCH) Secondary combined hyperlipoproteinemia (usually in the context of metabolic syndrome , for which it is a diagnostic criterion) [ edit ] Treatment While dietary modification is the initial approach, many patients require treatment with statins (HMG-CoA reductase inhibitors) to reduce cardiovascular risk. If the triglyceride level is markedly raised, fibrates may be preferable due to their beneficial effects. Combination treatment of statins and fibrates, while highly effective, causes a markedly increased risk of myopathy and rhabdomyolysis and is therefore only done under close supervision. Other agents commonly added to statins are ezetimibe , niacin and bile acid sequestrants . There is some evidence for benefit of plant sterol-containing products and �� 3 -fatty acids [ 2 ] [ edit ] Hyperlipoproteinemia type III This form is due to high chylomicrons and IDL (intermediate density lipoprotein). Also known as broad beta disease or dysbetalipoproteinemia , the most common cause for this form is the presence of ApoE E2/E2 genotype. It is due to cholesterol-rich VLDL (��-VLDL). Prevalence is 0.02% of the population. [ edit ] Hyperlipoproteinemia type IV (type 4 = familial) This form is due to high triglycerides . It is also known as hypertriglyceridemia (or pure hypertriglyceridemia ). According to the NCEP-ATPIII definition of high triglycerides (>200 mg/dl), prevalence is about 16% of adult population. [ 3 ] [ edit ] Hyperlipoproteinemia type V (type 5 = endogenous) This type is very similar to type I, but with high VLDL in addition to chylomicrons. It is also associated with glucose intolerance and hyperuricemia [ edit ] Unclassified forms Non-classified forms are extremely rare: Hypo-alpha lipoproteinemia Hypo-beta lipoproteinemia (prevalence 0.01-0.1%) [ edit ] References ^ Frederickson DS, Lee RS. A system for phenotyping hyperlipidemia. Circulation 1965;31:321-7. PMID 14262568 . ^ Thompson GR. Management of dyslipidaemia. Heart 2004;90:949-55. PMID 15253984 . ^ Third Report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III) Final Report. Circulation 2002; 106; page 3240 [ edit ] External links The Fredrickson papers (with photos from early lipoprotein research) 745209914 at GPnotebook Hyperlipoproteinemia OMIM GPnotebook WebMD Others Type I Online 'Mendelian Inheritance in Man' (OMIM) 238600 -1389035478 at GPnotebook . MeritCare Type IIa Online 'Mendelian Inheritance in Man' (OMIM) 144400 -1664090094 at GPnotebook . Merck Type IIb -1375338454 at GPnotebook . Type III . 630849560 at GPnotebook WebMD Yahoo Type IV Online 'Mendelian Inheritance in Man' (OMIM) 144600 -1362100182 at GPnotebook WebMD Yahoo Type V Online 'Mendelian Inheritance in Man' (OMIM) 144600 -1355481046 at GPnotebook . . v ��� d ��� e Lipid metabolism disorders / Inborn error of lipid metabolism - dyslipidemia ( E78 and E71.3 , 272 ) Hyperlipidemia Hypercholesterolemia / Hypertriglyceridemia ( Familial hypercholesterolemia , Combined hyperlipidemia ) - Xanthoma Hypolipoproteinemia Hypoalphalipoproteinemia/HDL ( Lecithin cholesterol acyltransferase deficiency , Tangier disease ) Hypobetalipoproteinemia/LDL ( Abetalipoproteinemia , Apolipoprotein B deficiency ) Lipodystrophy Barraquer-Simons syndrome Fatty acid metabolism deficiency transport: Carnitine ( Primary , I , II , -acylcarnitine ) - Adrenoleukodystrophy beta oxidation : Acyl CoA dehydrogenase ( Short-chain , Medium-chain , Long-chain 3-hydroxy , Very long-chain ) - Mitochondrial trifunctional protein deficiency to acetyl-CoA: Malonic aciduria Cholesterol synthesis Smith-Lemli-Opitz syndrome Other Sj��gren-Larsson syndrome - Lipomatosis - Adiposis dolorosa - Lipoid proteinosis see also lipid metabolism enzymes , lipoprotein metabolism Retrieved from " http://en.wikipedia.org/wiki/Hyperlipidemia " Categories : Metabolic disorders | Cardiology | Lipid disorders Views Article Discussion Edit this page History Personal tools Log in / create account Navigation Main page Contents Featured content Current events Random article Search Interaction About Wikipedia Community portal Recent changes Contact Wikipedia Donate to Wikipedia Help Toolbox What links here Related changes Upload file Special pages Printable version Permanent link Cite this page Languages Deutsch Fran��ais ���������� �������������� Svenska This page was last modified on 24 February 2009, at 07:01. All text is available under the terms of the GNU Free Documentation License . (See Copyrights for details.) Wikipedia® is a registered trademark of the Wikimedia Foundation, Inc. , a U.S. registered 501(c)(3) tax-deductible nonprofit charity . Privacy policy About Wikipedia Disclaimers |
clueweb09-enwp00-22-22167 | Myocardial infarction - Wikipedia, the free encyclopedia Myocardial infarction From Wikipedia, the free encyclopedia (Redirected from Cardial infarction ) Jump to: navigation , search "Heart attack" redirects here. For other uses, see Heart attack (disambiguation) . Myocardial infarction Classification and external resources Diagram of a myocardial infarction (2) of the tip of the anterior wall of the heart (an apical infarct ) after occlusion (1) of a branch of the left coronary artery (LCA, right coronary artery = RCA). ICD - 10 I 21. - I 22. ICD - 9 410 DiseasesDB 8664 MedlinePlus 000195 eMedicine med/1567 emerg/327 ped/2520 MeSH D009203 Myocardial infarction ( MI or AMI for acute myocardial infarction ), commonly known as a heart attack , occurs when the blood supply to part of the heart is interrupted. This is most commonly due to occlusion (blockage) of a coronary artery following the rupture of a vulnerable atherosclerotic plaque , which is an unstable collection of lipids (like cholesterol ) and white blood cells (especially macrophages ) in the wall of an artery . The resulting ischemia (restriction in blood supply) and oxygen shortage , if left untreated for a sufficient period, can cause damage and/or death ( infarction ) of heart muscle tissue ( myocardium ). Classical symptoms of acute myocardial infarction include sudden chest pain (typically radiating to the left arm or left side of the neck), shortness of breath , nausea , vomiting , palpitations , sweating , and anxiety (often described as a sense of impending doom). Women may experience fewer typical symptoms than men, most commonly shortness of breath, weakness, a feeling of indigestion, and fatigue . [ 1 ] Approximately one quarter of all myocardial infarctions are silent, without chest pain or other symptoms. A heart attack is a medical emergency , and people experiencing chest pain are advised to alert their emergency medical services , because prompt treatment is beneficial. Heart attacks are the leading cause of death for both men and women all over the world. [ 2 ] Important risk factors are previous cardiovascular disease (such as angina , a previous heart attack or stroke ), older age (especially men over 40 and women over 50), tobacco smoking , high blood levels of certain lipids ( triglycerides , low-density lipoprotein or "bad cholesterol") and low levels of high density lipoprotein (HDL, "good cholesterol"), diabetes , high blood pressure , obesity , chronic kidney disease , heart failure , excessive alcohol consumption , the abuse of certain drugs (such as cocaine ), and chronic high stress levels. [ 3 ] [ 4 ] Immediate treatment for suspected acute myocardial infarction includes oxygen , aspirin , and sublingual glyceryl trinitrate (colloquially referred to as nitroglycerin and abbreviated as NTG or GTN). Pain relief is also often given, classically morphine sulfate . [ 5 ] The patient will receive a number of diagnostic tests, such as an electrocardiogram (ECG, EKG), a chest X-ray and blood tests to detect elevations in cardiac markers (blood tests to detect heart muscle damage). The most often used markers are the creatine kinase -MB (CK-MB) fraction and the troponin I (TnI) or troponin T (TnT) levels. On the basis of the ECG, a distinction is made between ST elevation MI (STEMI) or non-ST elevation MI (NSTEMI). Most cases of STEMI are treated with thrombolysis or if possible with percutaneous coronary intervention (PCI, angioplasty and stent insertion), provided the hospital has facilities for coronary angiography . NSTEMI is managed with medication, although PCI is often performed during hospital admission. In patients who have multiple blockages and who are relatively stable, or in a few extraordinary emergency cases, bypass surgery of the blocked coronary artery is an option. The phrase "heart attack" is sometimes used incorrectly to describe sudden cardiac death , which may or may not be the result of acute myocardial infarction. A heart attack is different from, but can be the cause of cardiac arrest , which is the stopping of the heartbeat, and cardiac arrhythmia , an abnormal heartbeat. It is also distinct from heart failure , in which the pumping action of the heart is impaired; severe myocardial infarction may lead to heart failure, but not necessarily. Contents 1 Signs and symptoms 2 Causes 3 Pathophysiology 4 Diagnosis 4.1 Diagnostic criteria 4.2 Physical examination 4.3 Electrocardiogram 4.4 Cardiac markers 4.5 Angiography 4.6 Histopathology 5 Epidemiology 5.1 Risk factors 6 First aid 6.1 Immediate care 6.2 Automatic external defibrillation (AED) 6.3 Emergency services 6.4 Wilderness first aid 6.5 Air travel 7 Treatment 7.1 First line 7.2 Reperfusion 7.2.1 Thrombolytic therapy 7.2.2 Percutaneous coronary intervention 7.2.3 Coronary artery bypass surgery 7.3 Monitoring for arrhythmias 7.4 Rehabilitation 7.5 Secondary prevention 7.6 New therapies under investigation 8 Complications 8.1 Congestive heart failure 8.2 Myocardial rupture 8.3 Life-threatening arrhythmia 8.4 Pericarditis 8.5 Cardiogenic shock 9 Prognosis 10 Legal implications 11 See also 12 References 13 External links [ edit ] Signs and symptoms Rough diagram of pain zones in myocardial infarction (dark red = most typical area, light red = other possible areas, view of the chest). Back view. The onset of symptoms in myocardial infarction (MI) is usually gradual, over several minutes, and rarely instantaneous. [ 6 ] Chest pain is the most common symptom of acute myocardial infarction and is often described as a sensation of tightness, pressure, or squeezing. Chest pain due to ischemia (a lack of blood and hence oxygen supply) of the heart muscle is termed angina pectoris . Pain radiates most often to the left arm , but may also radiate to the lower jaw , neck , right arm, back , and epigastrium , where it may mimic heartburn . Levine's sign , in which the patient localizes the chest pain by clenching their fist over the sternum , has classically been thought to be predictive of cardiac chest pain, although a prospective observational study showed that it had a poor positive predictive value. [ 7 ] Shortness of breath ( dyspnea ) occurs when the damage to the heart limits the output of the left ventricle , causing left ventricular failure and consequent pulmonary edema . Other symptoms include diaphoresis (an excessive form of sweating ), weakness, light-headedness , nausea , vomiting , and palpitations . These symptoms are likely induced by a massive surge of catecholamines from the sympathetic nervous system [ 8 ] which occurs in response to pain and the hemodynamic abnormalities that result from cardiac dysfunction. Loss of consciousness (due to inadequate cerebral perfusion and cardiogenic shock) and even sudden death (frequently due to the development of ventricular fibrillation) can occur in myocardial infarctions. Women and older patients experience atypical symptoms more frequently than their male and younger counterparts. [ 9 ] Women also have more symptoms compared to men (2.6 on average vs 1.8 symptoms in men). [ 9 ] The most common symptoms of MI in women include dyspnea , weakness, and fatigue . Fatigue, sleep disturbances, and dyspnea have been reported as frequently occurring symptoms which may manifest as long as one month before the actual clinically manifested ischemic event. In women, chest pain may be less predictive of coronary ischemia than in men. [ 10 ] Approximately half of all MI patients have experienced warning symptoms such as chest pain prior to the infarction. [ 11 ] Approximately one fourth of all myocardial infarctions are silent, without chest pain or other symptoms. [ 12 ] These cases can be discovered later on electrocardiograms or at autopsy without a prior history of related complaints. A silent course is more common in the elderly , in patients with diabetes mellitus [ 13 ] and after heart transplantation , probably because the donor heart is not connected to nerves of the host. [ 14 ] In diabetics, differences in pain threshold , autonomic neuropathy , and psychological factors have been cited as possible explanations for the lack of symptoms. [ 13 ] Any group of symptoms compatible with a sudden interruption of the blood flow to the heart are called an acute coronary syndrome . [ 15 ] The differential diagnosis includes other catastrophic causes of chest pain, such as pulmonary embolism , aortic dissection , pericardial effusion causing cardiac tamponade , tension pneumothorax , and esophageal rupture . [ 16 ] [ edit ] Causes Heart attack rates are higher in association with intense exertion, be it psychological stress or physical exertion, especially if the exertion is more intense than the individual usually performs. [ 17 ] Quantitatively, the period of intense exercise and subsequent recovery is associated with about a 6-fold higher myocardial infarction rate (compared with other more relaxed time frames) for people who are physically very fit. [ 17 ] For those in poor physical condition, the rate differential is over 35-fold higher. [ 17 ] One observed mechanism for this phenomenon is the increased arterial pulse pressure stretching and relaxation of arteries with each heart beat which, as has been observed with intravascular ultrasound , increases mechanical "shear stress" on atheromas and the likelihood of plaque rupture. [ 17 ] Acute severe infection, such as pneumonia , can trigger myocardial infarction. A more controversial link is that between Chlamydophila pneumoniae infection and atherosclerosis. [ 18 ] While this intracellular organism has been demonstrated in atherosclerotic plaques, evidence is inconclusive as to whether it can be considered a causative factor. [ 18 ] Treatment with antibiotics in patients with proven atherosclerosis has not demonstrated a decreased risk of heart attacks or other coronary vascular diseases. [ 19 ] There is an association of an increased incidence of a heart attack in the morning hours, more specifically around 9 a.m. [ 20 ] [ 21 ] [ 22 ] . Some investigators have noticed that the ability of platelets to aggregate varies according to a circadian rhythm, although they have not proven causation. [ 23 ] Some investigators theorize that this increased incidence may be related to the circadian variation in cortisol production affecting the concentrations of various cytokines and other mediators of inflammation. [ 24 ] [ edit ] Pathophysiology A myocardial infarction occurs when an atherosclerotic plaque slowly builds up in the inner lining of a coronary artery and then suddenly ruptures, totally occluding the artery and preventing blood flow downstream. Main article: Acute coronary syndrome Acute myocardial infarction refers to two subtypes of acute coronary syndrome , namely non-ST-elevated myocardial infarction and ST-elevated myocardial infarction , which are most frequently (but not always) a manifestation of coronary artery disease . The most common triggering event is the disruption of an atherosclerotic plaque in an epicardial coronary artery, which leads to a clotting cascade, sometimes resulting in total occlusion of the artery. Atherosclerosis is the gradual buildup of cholesterol and fibrous tissue in plaques in the wall of arteries (in this case, the coronary arteries ), typically over decades. Blood stream column irregularities visible on angiography reflect artery lumen narrowing as a result of decades of advancing atherosclerosis. Plaques can become unstable, rupture, and additionally promote a thrombus (blood clot) that occludes the artery; this can occur in minutes. When a severe enough plaque rupture occurs in the coronary vasculature, it leads to myocardial infarction (necrosis of downstream myocardium). If impaired blood flow to the heart lasts long enough, it triggers a process called the ischemic cascade ; the heart cells die (chiefly through necrosis ) and do not grow back. A collagen scar forms in its place. Recent studies indicate that another form of cell death called apoptosis also plays a role in the process of tissue damage subsequent to myocardial infarction. [ 25 ] As a result, the patient's heart will be permanently damaged. This scar tissue also puts the patient at risk for potentially life threatening arrhythmias, and may result in the formation of a ventricular aneurysm that can rupture with catastrophic consequences. Injured heart tissue conducts electrical impulses more slowly than normal heart tissue. The difference in conduction velocity between injured and uninjured tissue can trigger re-entry or a feedback loop that is believed to be the cause of many lethal arrhythmias. The most serious of these arrhythmias is ventricular fibrillation ( V-Fib /VF), an extremely fast and chaotic heart rhythm that is the leading cause of sudden cardiac death. Another life threatening arrhythmia is ventricular tachycardia ( V-Tach /VT), which may or may not cause sudden cardiac death. However, ventricular tachycardia usually results in rapid heart rates that prevent the heart from pumping blood effectively. Cardiac output and blood pressure may fall to dangerous levels, which can lead to further coronary ischemia and extension of the infarct. The cardiac defibrillator is a device that was specifically designed to terminate these potentially fatal arrhythmias. The device works by delivering an electrical shock to the patient in order to depolarize a critical mass of the heart muscle, in effect " rebooting " the heart. This therapy is time dependent, and the odds of successful defibrillation decline rapidly after the onset of cardiopulmonary arrest. [ edit ] Diagnosis The diagnosis of myocardial infarction is made by integrating the history of the presenting illness and physical examination with electrocardiogram findings and cardiac markers ( blood tests for heart muscle cell damage). [ 26 ] A coronary angiogram allows visualization of narrowings or obstructions on the heart vessels, and therapeutic measures can follow immediately. At autopsy , a pathologist can diagnose a myocardial infarction based on anatomopathological findings. A chest radiograph and routine blood tests may indicate complications or precipitating causes and are often performed upon arrival to an emergency department . New regional wall motion abnormalities on an echocardiogram are also suggestive of a myocardial infarction. Echo may be performed in equivocal cases by the on-call cardiologist. [ 27 ] In stable patients whose symptoms have resolved by the time of evaluation, technetium-99m 2-methoxyisobutylisonitrile (Tc99m MIBI) or thallium-201 chloride can be used in nuclear medicine to visualize areas of reduced blood flow in conjunction with physiologic or pharmocologic stress. [ 27 ] [ 28 ] Thallium may also be used to determine viability of tissue, distinguishing whether non-functional myocardium is actually dead or merely in a state of hibernation or of being stunned. [ 29 ] [ edit ] Diagnostic criteria WHO criteria [ 30 ] have classically been used to diagnose MI; a patient is diagnosed with myocardial infarction if two (probable) or three (definite) of the following criteria are satisfied: Clinical history of ischaemic type chest pain lasting for more than 20 minutes Changes in serial ECG tracings Rise and fall of serum cardiac biomarkers such as creatine kinase -MB fraction and troponin The WHO criteria were refined in 2000 to give more prominence to cardiac biomarkers. [ 31 ] According to the new guidelines, a cardiac troponin rise accompanied by either typical symptoms, pathological Q waves, ST elevation or depression or coronary intervention are diagnostic of MI. [ edit ] Physical examination The general appearance of patients may vary according to the experienced symptoms; the patient may be comfortable, or restless and in severe distress with an increased respiratory rate . A cool and pale skin is common and points to vasoconstriction . Some patients have low-grade fever (38���39 ��C). Blood pressure may be elevated or decreased, and the pulse can be become irregular . [ 32 ] [ 33 ] If heart failure ensues, elevated jugular venous pressure and hepatojugular reflux , or swelling of the legs due to peripheral edema may be found on inspection. Rarely, a cardiac bulge with a pace different from the pulse rhythm can be felt on precordial examination . Various abnormalities can be found on auscultation , such as a third and fourth heart sound , systolic murmurs , paradoxical splitting of the second heart sound, a pericardial friction rub and rales over the lung. [ 32 ] [ 34 ] [ edit ] Electrocardiogram Main article: Electrocardiogram 12-lead electrocardiogram showing ST-segment elevation (orange) in I, aVL and V1-V5 with reciprocal changes (blue) in the inferior leads, indicative of an anterior wall myocardial infarction. The primary purpose of the electrocardiogram is to detect ischemia or acute coronary injury in broad, symptomatic emergency department populations. However, the standard 12 lead ECG has several limitations. An ECG represents a brief sample in time. Because unstable ischemic syndromes have rapidly changing supply versus demand characteristics, a single ECG may not accurately represent the entire picture. [ 35 ] It is therefore desirable to obtain serial 12 lead ECGs, particularly if the first ECG is obtained during a pain-free episode. Alternatively, many emergency departments and chest pain centers use computers capable of continuous ST segment monitoring. [ 36 ] The standard 12 lead ECG also does not directly examine the right ventricle , and is relatively poor at examining the posterior basal and lateral walls of the left ventricle . In particular, acute myocardial infarction in the distribution of the circumflex artery is likely to produce a nondiagnostic ECG. [ 35 ] The use of additional ECG leads like right-sided leads V3R and V4R and posterior leads V7, V8, and V9 may improve sensitivity for right ventricular and posterior myocardial infarction. In spite of these limitations, the 12 lead ECG stands at the center of risk stratification for the patient with suspected acute myocardial infarction. Mistakes in interpretation are relatively common, and the failure to identify high risk features has a negative effect on the quality of patient care. [ 37 ] The 12 lead ECG is used to classify patients into one of three groups: [ 38 ] those with ST segment elevation or new bundle branch block (suspicious for acute injury and a possible candidate for acute reperfusion therapy with thrombolytics or primary PCI ), those with ST segment depression or T wave inversion (suspicious for ischemia), and those with a so-called non-diagnostic or normal ECG. A normal ECG does not rule out acute myocardial infarction. Sometimes the earliest presentation of acute myocardial infarction is the hyperacute T wave, which is treated the same as ST segment elevation. [ 39 ] In practice this is rarely seen, because it only exists for 2-30 minutes after the onset of infarction. [ 40 ] Hyperacute T waves need to be distinguished from the peaked T waves associated with hyperkalemia . [ 41 ] The current guidelines for the ECG diagnosis of acute myocardial infarction require at least 1 mm (0.1 mV) of ST segment elevation in the limb leads, and at least 2 mm elevation in the precordial leads. These elevations must be present in anatomically contiguous leads. [ 38 ] (I, aVL, V5, V6 correspond to the lateral wall; V1-V4 correspond to the anterior wall; II, III, aVF correspond to the inferior wall.) This criterion is problematic, however, as acute myocardial infarction is not the most common cause of ST segment elevation in chest pain patients. [ 42 ] Over 90% of healthy men have at least 1 mm (0.1 mV) of ST segment elevation in at least one precordial lead. [ 43 ] The clinician must therefore be well versed in recognizing the so-called ECG mimics of acute myocardial infarction, which include left ventricular hypertrophy , left bundle branch block , paced rhythm , early repolarization , pericarditis , hyperkalemia , and ventricular aneurysm . [ 44 ] [ 45 ] [ 43 ] [ edit ] Cardiac markers Main article: Cardiac marker Cardiac markers or cardiac enzymes are proteins from cardiac tissue found in the blood. These proteins are released into the bloodstream when damage to the heart occurs, as in the case of a myocardial infarction. Until the 1980s, the enzymes SGOT and LDH were used to assess cardiac injury. Then it was found that disproportional elevation of the MB subtype of the enzyme creatine kinase (CK) was very specific for myocardial injury. Current guidelines are generally in favor of troponin sub-units I or T, which are very specific for the heart muscle and are thought to rise before permanent injury develops. [ 46 ] Elevated troponins in the setting of chest pain may accurately predict a high likelihood of a myocardial infarction in the near future. [ 47 ] New markers such as glycogen phosphorylase isoenzyme BB are under investigation. [ 48 ] The diagnosis of myocardial infarction requires two out of three components (history, ECG, and enzymes). When damage to the heart occurs, levels of cardiac markers rise over time, which is why blood tests for them are taken over a 24-hour period. Because these enzyme levels are not elevated immediately following a heart attack, patients presenting with chest pain are generally treated with the assumption that a myocardial infarction has occurred and then evaluated for a more precise diagnosis. [ 49 ] [ edit ] Angiography Angiogram of the coronary arteries. Main article: Coronary catheterization In difficult cases or in situations where intervention to restore blood flow is appropriate, coronary angiography can be performed. A catheter is inserted into an artery (usually the femoral artery ) and pushed to the vessels supplying the heart. A radio-opaque dye is administered through the catheter and a sequence of x-rays (fluoroscopy) is performed. Obstructed or narrowed arteries can be identified, and angioplasty applied as a therapeutic measure (see below). Angioplasty requires extensive skill, especially in emergency settings. It is performed by a physician trained in interventional cardiology . [ edit ] Histopathology Further information: Timeline of myocardial infarction pathology Microscopy image (magn. ca 100x, H&E stain ) from autopsy specimen of myocardial infarct (7 days post-infarction). Histopathological examination of the heart may reveal infarction at autopsy. Under the microscope, myocardial infarction presents as a circumscribed area of ischemic, coagulative necrosis (cell death). On gross examination, the infarct is not identifiable within the first 12 hours. [ 50 ] Although earlier changes can be discerned using electron microscopy , one of the earliest changes under a normal microscope are so-called wavy fibers . [ 51 ] Subsequently, the myocyte cytoplasm becomes more eosinophilic (pink) and the cells lose their transversal striations, with typical changes and eventually loss of the cell nucleus . [ 52 ] The interstitium at the margin of the infarcted area is initially infiltrated with neutrophils , then with lymphocytes and macrophages , who phagocytose ("eat") the myocyte debris. The necrotic area is surrounded and progressively invaded by granulation tissue , which will replace the infarct with a fibrous ( collagenous ) scar (which are typical steps in wound healing ). The interstitial space (the space between cells outside of blood vessels) may be infiltrated with red blood cells . [ 50 ] These features can be recognized in cases where the perfusion was not restored; reperfused infarcts can have other hallmarks, such as contraction band necrosis. [ 53 ] [ edit ] Epidemiology Myocardial infarction is a common presentation of ischemic heart disease . The WHO estimated that in 2002, 12.6 percent of deaths worldwide were from ischemic heart disease. [ 2 ] Ischemic heart disease is the leading cause of death in developed countries, but third to AIDS and lower respiratory infections in developing countries. [ 54 ] In the United States , diseases of the heart are the leading cause of death , causing a higher mortality than cancer ( malignant neoplasms ). [ 55 ] Coronary heart disease is responsible for 1 in 5 deaths in the U.S.. Some 7,200,000 men and 6,000,000 women are living with some form of coronary heart disease. 1,200,000 people suffer a (new or recurrent) coronary attack every year, and about 40% of them die as a result of the attack. [ 56 ] This means that roughly every 65 seconds, an American dies of a coronary event. In India , cardiovascular disease (CVD) is the leading cause of death. [ 57 ] The deaths due to CVD in India were 32% of all deaths in 2007 and are expected to rise from 1.17 million in 1990 and 1.59 million in 2000 to 2.03 million in 2010. [ 58 ] Although a relatively new epidemic in India, it has quickly become a major health issue with deaths due to CVD expected to double during 1985-2015. [ 59 ] [ 60 ] Mortality estimates due to CVD vary widely by state, ranging from 10% in Meghalaya to 49% in Punjab (percentage of all deaths). Punjab (49%), Goa (42%), Tamil Nadu (36%) and Andhra Pradesh (31%) have the highest CVD related mortality estimates. [ 61 ] State-wise differences are correlated with prevalence of specific dietary risk factors in the states. Moderate physical exercise is associated with reduced incidence of CVD in India (those who exercise have less than half the risk of those who don't). [ 59 ] CVD also affects Indians at a younger age (in their 30s and 40s) than is typical in other countries. [ edit ] Risk factors Risk factors for atherosclerosis are generally risk factors for myocardial infarction: Older age Male sex [ 17 ] Tobacco smoking Hypercholesterolemia (more accurately hyperlipoproteinemia , especially high low density lipoprotein and low high density lipoprotein ) Hyperhomocysteinemia (high homocysteine , a toxic blood amino acid that is elevated when intakes of vitamins B2, B6, B12 and folic acid are insufficient) Diabetes (with or without insulin resistance ) High blood pressure Obesity [ 62 ] (defined by a body mass index of more than 30 kg/m��, or alternatively by waist circumference or waist-hip ratio ). Stress Occupations with high stress index are known to have susceptibility for atherosclerosis . Many of these risk factors are modifiable, so many heart attacks can be prevented by maintaining a healthier lifestyle. Physical activity, for example, is associated with a lower risk profile. [ 63 ] Non-modifiable risk factors include age, sex, and family history of an early heart attack (before the age of 60), which is thought of as reflecting a genetic predisposition . [ 17 ] Socioeconomic factors such as a shorter education and lower income (particularly in women), and unmarried cohabitation may also contribute to the risk of MI. [ 64 ] To understand epidemiological study results, it's important to note that many factors associated with MI mediate their risk via other factors. For example, the effect of education is partially based on its effect on income and marital status . [ 64 ] Women who use combined oral contraceptive pills have a modestly increased risk of myocardial infarction, especially in the presence of other risk factors, such as smoking. [ 65 ] Inflammation is known to be an important step in the process of atherosclerotic plaque formation. [ 66 ] C-reactive protein (CRP) is a sensitive but non-specific marker for inflammation . Elevated CRP blood levels, especially measured with high sensitivity assays, can predict the risk of MI, as well as stroke and development of diabetes. [ 66 ] Moreover, some drugs for MI might also reduce CRP levels. [ 66 ] The use of high sensitivity CRP assays as a means of screening the general population is advised against, but it may be used optionally at the physician's discretion, in patients who already present with other risk factors or known coronary artery disease . [ 67 ] Whether CRP plays a direct role in atherosclerosis remains uncertain. [ 66 ] Inflammation in periodontal disease may be linked coronary heart disease, and since periodontitis is very common, this could have great consequences for public health . [ 68 ] Serological studies measuring antibody levels against typical periodontitis-causing bacteria found that such antibodies were more present in subjects with coronary heart disease. [ 69 ] Periodontitis tends to increase blood levels of CRP, fibrinogen and cytokines ; [ 70 ] thus, periodontitis may mediate its effect on MI risk via other risk factors. [ 71 ] Preclinical research suggests that periodontal bacteria can promote aggregation of platelets and promote the formation of foam cells . [ 72 ] [ 73 ] A role for specific periodontal bacteria has been suggested but remains to be established. [ 74 ] Baldness , hair greying , a diagonal earlobe crease ( Frank's sign [ 75 ] ) and possibly other skin features have been suggested as independent risk factors for MI. [ 76 ] Their role remains controversial; a common denominator of these signs and the risk of MI is supposed, possibly genetic. [ 77 ] Calcium deposition is another part of atherosclerotic plaque formation. Calcium deposits in the coronary arteries can be detected with CT scans . Several studies have shown that coronary calcium can provide predictive information beyond that of classical risk factors. [ 78 ] [ 79 ] [ 80 ] [ edit ] First aid As myocardial infarction is a common medical emergency, the signs are often part of first aid courses. The emergency action principles also apply in the case of myocardial infarction. [ edit ] Immediate care When symptoms of myocardial infarction occur, people wait an average of three hours, instead of doing what is recommended: calling for help immediately. [ 81 ] [ 82 ] Acting immediately by calling the emergency services can prevent sustained damage to the heart ("time is muscle"). [ 83 ] Certain positions allow the patient to rest in a position which minimizes breathing difficulties. A half-sitting position with knees bent is often recommended. Access to more oxygen can be given by opening the window and widening the collar for easier breathing. Aspirin can be given quickly (if the patient is not allergic to aspirin); but taking aspirin before calling the emergency medical services may be associated with unwanted delay. [ 84 ] Aspirin has an antiplatelet effect which inhibits formation of further thrombi (blood clots) that clog arteries. Chewing is the preferred method of administration, so that the Aspirin can be absorbed quickly. Dissolved soluble preparations or sublingual administration can also be used. U.S. guidelines recommend a dose of 162���325 mg. [ 85 ] Australian guidelines recommend a dose of 150���300 mg. [ 86 ] Glyceryl trinitrate (nitroglycerin) sublingually (under the tongue) can be given if available. If an automated external defibrillator (AED) is available the rescuer should immediately bring the AED to the patient's side and be prepared to follow its instructions, especially should the victim lose consciousness. If possible the rescuer should obtain basic information from the victim, in case the patient is unable to answer questions once emergency medical technicians arrive. The victim's name and any information regarding the nature of the victim's pain will be useful to health care providers. The exact time that these symptoms started may be critical for determining what interventions can be safely attempted once the victim reaches the medical center. Other useful pieces of information include what the patient was doing at the onset of symptoms, and anything else that might give clues to the pathology of the chest pain. It is also very important to relay any actions that have been taken, such as the number or dose of aspirin or nitroglycerin given, to the EMS personnel. Other general first aid principles include monitoring pulse, breathing, level of consciousness and, if possible, the blood pressure of the patient. In case of cardiac arrest , cardiopulmonary resuscitation (CPR) can be administered. [ edit ] Automatic external defibrillation (AED) Since the publication of data showing that the availability of automated external defibrillators (AEDs) in public places may significantly increase chances of survival, many of these have been installed in public buildings, public transport facilities, and in non-ambulance emergency vehicles (e.g. police cars and fire engines ). AEDs analyze the heart's rhythm and determine whether the rhythm is amenable to defibrillation ("shockable"), as in ventricular tachycardia and ventricular fibrillation . [ edit ] Emergency services Emergency Medical Services (EMS) Systems vary considerably in their ability to evaluate and treat patients with suspected acute myocardial infarction. Some provide as little as first aid and early defibrillation. Others employ highly trained paramedics with sophisticated technology and advanced protocols. [ 87 ] Early access to EMS is promoted by a 9-1-1 system currently available to 90% of the population in the United States. [ 87 ] Most are capable of providing oxygen , IV access, sublingual nitroglycerine , morphine , and aspirin . Some are capable of providing thrombolytic therapy in the prehospital setting. [ 88 ] [ 89 ] With primary PCI emerging as the preferred therapy for ST segment elevation myocardial infarction, EMS can play a key role in reducing door to balloon intervals (the time from presentation to a hospital ER to the restoration of coronary artery blood flow) by performing a 12 lead ECG in the field and using this information to triage the patient to the most appropriate medical facility. [ 90 ] [ 91 ] [ 92 ] [ 93 ] In addition, the 12 lead ECG can be transmitted to the receiving hospital, which enables time saving decisions to be made prior to the patient's arrival. This may include a "cardiac alert" or "STEMI alert" that calls in off duty personnel in areas where the cardiac cath lab is not staffed 24 hours a day. [ 94 ] Even in the absence of a formal alerting program, prehospital 12 lead ECGs are independently associated with reduced door to treatment intervals in the emergency department. [ 95 ] [ edit ] Wilderness first aid In wilderness first aid , a possible heart attack justifies evacuation by the fastest available means, including MEDEVAC , even in the earliest or precursor stages. The patient will rapidly be incapable of further exertion and have to be carried out. [ edit ] Air travel Certified personnel traveling by commercial aircraft may be able to assist an MI patient by using the on-board first aid kit , which may contain some cardiac drugs (such as glyceryl trinitrate spray, aspirin , or opioid painkillers), an AED, [ 96 ] and oxygen . Pilots may divert the flight to land at a nearby airport. Cardiac monitors are being introduced by some airlines, and they can be used by both on-board and ground-based physicians. [ 97 ] [ edit ] Treatment A heart attack is a medical emergency which demands both immediate attention and activation of the emergency medical services . The ultimate goal of the management in the acute phase of the disease is to salvage as much myocardium as possible and prevent further complications. As time passes, the risk of damage to the heart muscle increases; hence the phrase that in myocardial infarction, "time is muscle," and time wasted is muscle lost. [ 83 ] The treatments itself may have complications. If attempts to restore the blood flow are initiated after a critical period of only a few hours, the result is reperfusion injury instead of amelioration. [ 98 ] Other treatment modalities may also cause complications; the use of antithrombotics for example carries an increased risk of bleeding . [ edit ] First line Oxygen , aspirin , glyceryl trinitrate (nitroglycerin) and analgesia (usually morphine , although experts often argue this point), hence the popular mnemonic MONA , morphine, oxygen, nitro, aspirin ) are administered as soon as possible. In many areas, first responders can be trained to administer these prior to arrival at the hospital. Morphine is classically the preferred pain relief drug due to its ability to dilate blood vessels, which aids in blood flow to the heart as well as its pain relief properties. However, morphine can also cause hypotension (usually in the setting of hypovolemia), and should be avoided in the case of right ventricular infarction. Moreover, the CRUSADE trial also demonstrated an increase in mortality with administering morphine in the setting of NSTEMI. [ 99 ] Of the first line agents, only aspirin has been proven to decrease mortality . [ 100 ] Once the diagnosis of myocardial infarction is confirmed, other pharmacologic agents are often given. These include beta blockers , [ 101 ] [ 102 ] anticoagulation (typically with heparin ), [ 85 ] and possibly additional antiplatelet agents such as clopidogrel . [ 85 ] These agents are typically not started until the patient is evaluated by an emergency room physician or under the direction of a cardiologist. These agents can be used regardless of the reperfusion strategy that is to be employed. While these agents can decrease mortality in the setting of an acute myocardial infarction, they can lead to complications and potentially death if used in the wrong setting. Cocaine associated myocardial infarction should be managed in a manner similar to other patients with acute coronary syndrome except beta blockers should not be used and benzodiazepines should be administered early. [ 103 ] [ edit ] Reperfusion The concept of reperfusion has become so central to the modern treatment of acute myocardial infarction, that we are said to be in the reperfusion era. [ 104 ] [ 105 ] Patients who present with suspected acute myocardial infarction and ST segment elevation (STEMI) or new bundle branch block on the 12 lead ECG are presumed to have an occlusive thrombosis in an epicardial coronary artery. They are therefore candidates for immediate reperfusion, either with thrombolytic therapy , percutaneous coronary intervention (PCI) or when these therapies are unsuccessful, bypass surgery . Individuals without ST segment elevation are presumed to be experiencing either unstable angina (UA) or non-ST segment elevation myocardial infarction (NSTEMI). They receive many of the same initial therapies and are often stabilized with antiplatelet drugs and anticoagulated . If their condition remains ( hemodynamically ) stable, they can be offered either late coronary angiography with subsequent restoration of blood flow (revascularization), or non-invasive stress testing to determine if there is significant ischemia that would benefit from revascularization. If hemodynamic instability develops in individuals with NSTEMIs, they may undergo urgent coronary angiography and subsequent revascularization. The use of thrombolytic agents is contraindicated in this patient subset, however. [ 106 ] The basis for this distinction in treatment regimens is that ST segment elevations on an ECG are typically due to complete occlusion of a coronary artery. On the other hand, in NSTEMIs there is typically a sudden narrowing of a coronary artery with preserved (but diminished) flow to the distal myocardium. Anticoagulation and antiplatelet agents are given to prevent the narrowed artery from occluding. At least 10% of patients with STEMI don't develop myocardial necrosis (as evidenced by a rise in cardiac markers) and subsequent Q waves on EKG after reperfusion therapy. Such a successful restoration of flow to the infarct-related artery during an acute myocardial infarction is known as "aborting" the myocardial infarction. If treated within the hour, about 25% of STEMIs can be aborted. [ 107 ] [ edit ] Thrombolytic therapy Main article: Thrombolysis Thrombolytic therapy is indicated for the treatment of STEMI if the drug can be administered within 12 hours of the onset of symptoms, the patient is eligible based on exclusion criteria, and primary PCI is not immediately available. [ 85 ] The effectiveness of thrombolytic therapy is highest in the first 2 hours. After 12 hours, the risk associated with thrombolytic therapy outweighs any benefit. [ 106 ] [ 108 ] Because irreversible injury occurs within 2���4 hours of the infarction, there is a limited window of time available for reperfusion to work. Thrombolytic drugs are contraindicated for the treatment of unstable angina and NSTEMI [ 106 ] [ 109 ] and for the treatment of individuals with evidence of cardiogenic shock . [ 110 ] Although no perfect thrombolytic agent exists, an ideal thrombolytic drug would lead to rapid reperfusion, have a high sustained patency rate, be specific for recent thrombi, be easily and rapidly administered, create a low risk for intra-cerebral and systemic bleeding, have no antigenicity, adverse hemodynamic effects, or clinically significant drug interactions, and be cost effective. [ 111 ] Currently available thrombolytic agents include streptokinase , urokinase , and alteplase (recombinant tissue plasminogen activator , rtPA). More recently, thrombolytic agents similar in structure to rtPA such as reteplase and tenecteplase have been used. These newer agents boast efficacy at least as good as rtPA with significantly easier administration. The thrombolytic agent used in a particular individual is based on institution preference and the age of the patient. Depending on the thrombolytic agent being used, adjuvant anticoagulation with heparin or low molecular weight heparin may be of benefit. [ 112 ] [ 113 ] With TPa and related agents (reteplase and tenecteplase), heparin is needed to maintain coronary artery patency. Because of the anticoagulant effect of fibrinogen depletion with streptokinase [ 114 ] and urokinase [ 115 ] [ 116 ] [ 117 ] treatment, it is less necessary there. [ 112 ] Intracranial bleeding (ICB) and subsequent cerebrovascular accident (CVA) is a serious side effect of thrombolytic use. The risk of ICB is dependent on a number of factors, including a previous episode of intracranial bleed, age of the individual, and the thrombolytic regimen that is being used. In general, the risk of ICB due to thrombolytic use for the treatment of an acute myocardial infarction is between 0.5 and 1 percent. [ 112 ] Thrombolytic therapy to abort a myocardial infarction is not always effective. The degree of effectiveness of a thrombolytic agent is dependent on the time since the myocardial infarction began, with the best results occurring if the thrombolytic agent is used within two hours of the onset of symptoms. [ 118 ] [ 89 ] If the individual presents more than 12 hours after symptoms commenced, the risk of intracranial bleed are considered higher than the benefits of the thrombolytic agent. [ 119 ] Failure rates of thrombolytics can be as high as 20% or higher. [ 120 ] In cases of failure of the thrombolytic agent to open the infarct-related coronary artery, the patient is then either treated conservatively with anticoagulants and allowed to "complete the infarction" or percutaneous coronary intervention (PCI, see below) is then performed. Percutaneous coronary intervention in this setting is known as "rescue PCI" or "salvage PCI". Complications, particularly bleeding, are significantly higher with rescue PCI than with primary PCI due to the action of the thrombolytic agent. [ edit ] Percutaneous coronary intervention Main article: Percutaneous coronary intervention Thrombus material (in a cup, upper left corner) removed from a coronary artery during a percutaneous coronary intervention to abort a myocardial infarction. Five pieces of thrombus are shown (arrow heads). The benefit of prompt, expertly performed primary percutaneous coronary intervention over thrombolytic therapy for acute ST elevation myocardial infarction is now well established. [ 121 ] [ 122 ] [ 123 ] When performed rapidly by an experienced team, primary PCI restores flow in the culprit artery in more than 95% of patients compared with the spontaneous recanalization rate of about 65%. [ 121 ] Logistic and economic obstacles seem to hinder a more widespread application of percutaneous coronary intervention (PCI) via cardiac catheterization , [ 124 ] although the feasibility of regionalized PCI for STEMI is currently being explored in the United States. [ 125 ] The use of percutaneous coronary intervention as a therapy to abort a myocardial infarction is known as primary PCI. The goal of primary PCI is to open the artery as soon as possible, and preferably within 90 minutes of the patient presenting to the emergency room. This time is referred to as the door-to-balloon time. Few hospitals can provide PCI within the 90 minute interval, [ 126 ] which prompted the American College of Cardiology (ACC) to launch a national Door to Balloon (D2B) Initiative in November 2006. Over 800 hospitals have joined the D2B Alliance as of March 16, 2007. [ 127 ] One particularly successful implementation of a primary PCI protocol is in the Calgary Health Region under the auspices of the Libin Cardiovascular Institute of Alberta . Under this model, EMS teams responding to an emergency electronically transmit the ECG directly to a digital archiving system that allows emergency room physicians and/or cardiologists to immediately confirm the diagnosis. This in turn allows for redirection of the EMS teams to facilities prepped to conduct time-critical angioplasty, based on the ECG analysis. In an article published in the Canadian Medical Association Journal in June 2007, the Calgary implementation resulted in a median time to treatment of 62 minutes. [ 128 ] The current guidelines in the United States restrict primary PCI to hospitals with available emergency bypass surgery as a backup, [ 85 ] but this is not the case in other parts of the world. [ 129 ] Primary PCI involves performing a coronary angiogram to determine the anatomical location of the infarcting vessel, followed by balloon angioplasty (and frequently deployment of an intracoronary stent) of the thrombosed arterial segment. In some settings, an extraction catheter may be used to attempt to aspirate (remove) the thrombus prior to balloon angioplasty. While the use of intracoronary stents do not improve the short term outcomes in primary PCI, the use of stents is widespread because of the decreased rates of procedures to treat restenosis compared to balloon angioplasty. [ 130 ] Adjuvant therapy during primary PCI include intravenous heparin , aspirin , and clopidogrel . The use of glycoprotein IIb/IIIa inhibitors are often used in the setting of primary PCI to reduce the risk of ischemic complications during the procedure. [ 131 ] [ 132 ] Due to the number of antiplatelet agents and anticoagulants used during primary PCI, the risk of bleeding associated with the procedure are higher than during an elective PCI. [ 133 ] [ edit ] Coronary artery bypass surgery Main article: Coronary artery bypass graft surgery Coronary artery bypass surgery during mobilization (freeing) of the right coronary artery from its surrounding tissue, adipose tissue (yellow). The tube visible at the bottom is the aortic cannula (returns blood from the HLM ). The tube above it (obscured by the surgeon on the right) is the venous cannula (receives blood from the body). The patient's heart is stopped and the aorta is cross-clamped. The patient's head (not seen) is at the bottom. Despite the guidelines, emergency bypass surgery for the treatment of an acute myocardial infarction (MI) is less common than PCI or medical management. In an analysis of patients in the U.S. National Registry of Myocardial Infarction (NRMI) from January 1995 to May 2004, the percentage of patients with cardiogenic shock treated with primary PCI rose from 27.4% to 54.4%, while the increase in CABG treatment was only from 2.1% to 3.2%. [ 134 ] Emergency coronary artery bypass graft surgery (CABG) is usually undertaken to simultaneously treat a mechanical complication, such as a ruptured papillary muscle, or a ventricular septal defect, with ensueing cardiogenic shock. [ 135 ] In uncomplicated MI, the mortality rate can be high when the surgery is performed immediately following the infarction. [ 136 ] If this option is entertained, the patient should be stabilized prior to surgery, with supportive interventions such as the use of an intra-aortic balloon pump . [ 137 ] In patients developing cardiogenic shock after a myocardial infarction, both PCI and CABG are satisfactory treatment options, with similar survival rates. [ 138 ] [ 139 ] Coronary artery bypass surgery involves an artery or vein from the patient being implanted to bypass narrowings or occlusions on the coronary arteries. Several arteries and veins can be used, however internal mammary artery grafts have demonstrated significantly better long-term patency rates than great saphenous vein grafts. [ 140 ] In patients with two or more coronary arteries affected, bypass surgery is associated with higher long-term survival rates compared to percutaneous interventions. [ 141 ] In patients with single vessel disease, surgery is comparably safe and effective, and may be a treatment option in selected cases. [ 142 ] Bypass surgery has higher costs initially, but becomes cost-effective in the long term. [ 143 ] A surgical bypass graft is more invasive initially but bears less risk of recurrent procedures (but these may be again minimally invasive ). [ 142 ] [ edit ] Monitoring for arrhythmias Additional objectives are to prevent life-threatening arrhythmias or conduction disturbances. This requires monitoring in a coronary care unit and protocolised administration of antiarrhythmic agents . Antiarrhythmic agents are typically only given to individuals with life-threatening arrhythmias after a myocardial infarction and not to suppress the ventricular ectopy that is often seen after a myocardial infarction. [ 144 ] [ 145 ] [ 146 ] [ edit ] Rehabilitation Cardiac rehabilitation aims to optimize function and quality of life in those afflicted with a heart disease. This can be with the help of a physician, or in the form of a cardiac rehabilitation program. [ 147 ] Physical exercise is an important part of rehabilitation after a myocardial infarction, with beneficial effects on cholesterol levels, blood pressure, weight, stress and mood . [ 147 ] Some patients become afraid of exercising because it might trigger another infarct. [ 148 ] Patients are stimulated to exercise, and should only avoid certain exerting activities such as shovelling. Local authorities may place limitations on driving motorised vehicles . [ 149 ] Some people are afraid to have sex after a heart attack. Most people can resume sexual activities after 3 to 4 weeks. The amount of activity needs to be dosed to the patient's possibilities. [ 150 ] [ edit ] Secondary prevention The risk of a recurrent myocardial infarction decreases with strict blood pressure management and lifestyle changes, chiefly smoking cessation , regular exercise , a sensible diet for patients with heart disease , and limitation of alcohol intake . Patients are usually commenced on several long-term medications post-MI, with the aim of preventing secondary cardiovascular events such as further myocardial infarctions, congestive heart failure or cerebrovascular accident (CVA). Unless contraindicated, such medications may include: [ 151 ] [ 86 ] Antiplatelet drug therapy such as aspirin and/or clopidogrel should be continued to reduce the risk of plaque rupture and recurrent myocardial infarction. Aspirin is first-line, owing to its low cost and comparable efficacy, with clopidogrel reserved for patients intolerant of aspirin. The combination of clopidogrel and aspirin may further reduce risk of cardiovascular events, however the risk of hemorrhage is increased. [ 152 ] Beta blocker therapy such as metoprolol or carvedilol should be commenced. [ 153 ] These have been particularly beneficial in high-risk patients such as those with left ventricular dysfunction and/or continuing cardiac ischaemia . [ 154 ] ��-Blockers decrease mortality and morbidity. They also improve symptoms of cardiac ischemia in NSTEMI. ACE inhibitor therapy should be commenced 24���48 hours post-MI in hemodynamically-stable patients, particularly in patients with a history of MI, diabetes mellitus , hypertension , anterior location of infarct (as assessed by ECG), and/or evidence of left ventricular dysfunction. ACE inhibitors reduce mortality, the development of heart failure , and decrease ventricular remodelling post-MI. [ 155 ] Statin therapy has been shown to reduce mortality and morbidity post-MI. [ 156 ] [ 157 ] The effects of statins may be more than their LDL lowering effects. The general consensus is that statins have plaque stabilization and multiple other ("pleiotropic") effects that may prevent myocardial infarction in addition to their effects on blood lipids. [ 158 ] The aldosterone antagonist agent eplerenone has been shown to further reduce risk of cardiovascular death post-MI in patients with heart failure and left ventricular dysfunction, when used in conjunction with standard therapies above. [ 159 ] Omega-3 fatty acids , commonly found in fish, have been shown to reduce mortality post-MI. [ 160 ] While the mechanism by which these fatty acids decrease mortality is unknown, it has been postulated that the survival benefit is due to electrical stabilization and the prevention of ventricular fibrillation . [ 161 ] However, further studies in a high-risk subset have not shown a clear-cut decrease in potentially fatal arrhythmias due to omega-3 fatty acids. [ 162 ] [ 163 ] [ edit ] New therapies under investigation Patients who receive stem cell treatment by coronary artery injections of stem cells derived from their own bone marrow after a myocardial infarction (MI) show improvements in left ventricular ejection fraction and end-diastolic volume not seen with placebo . The larger the initial infarct size, the greater the effect of the infusion. Clinical trials of progenitor cell infusion as a treatment approach to ST elevation MI are proceeding. [ 164 ] There are currently 3 biomaterial and tissue engineering approaches for the treatment of MI, but these are in an even earlier stage of medical research , so many questions and issues need to be addressed before they can be applied to patients. The first involves polymeric left ventricular restraints in the prevention of heart failure . The second utilizes in vitro engineered cardiac tissue, which is subsequently implanted in vivo . The final approach entails injecting cells and/or a scaffold into the myocardium to create in situ engineered cardiac tissue. [ 165 ] [ edit ] Complications Complications may occur immediately following the heart attack (in the acute phase), or may need time to develop (a chronic problem). After an infarction, an obvious complication is a second infarction, which may occur in the domain of another atherosclerotic coronary artery, or in the same zone if there are any live cells left in the infarct. [ edit ] Congestive heart failure Main article: Congestive heart failure A myocardial infarction may compromise the function of the heart as a pump for the circulation , a state called heart failure . There are different types of heart failure; left- or right-sided (or bilateral) heart failure may occur depending on the affected part of the heart, and it is a low-output type of failure. If one of the heart valves is affected, this may cause dysfunction, such as mitral regurgitation in the case of left-sided coronary occlusion that disrupts the blood supply of the papillary muscles. The incidence of heart failure is particularly high in patients with diabetes and requires special management strategies. [ 166 ] [ edit ] Myocardial rupture Main article: Myocardial rupture Myocardial rupture is most common three to five days after myocardial infarction, commonly of small degree, but may occur one day to three weeks later. In the modern era of early revascularization and intensive pharmacotherapy as treatment for MI, the incidence of myocardial rupture is about 1% of all MIs. [ 167 ] This may occur in the free walls of the ventricles , the septum between them, the papillary muscles , or less commonly the atria . Rupture occurs because of increased pressure against the weakened walls of the heart chambers due to heart muscle that cannot pump blood out effectively. The weakness may also lead to ventricular aneurysm , a localized dilation or ballooning of the heart chamber. Risk factors for myocardial rupture include completion of infarction (no revascularization performed), female sex, advanced age, and a lack of a previous history of myocardial infarction. [ 167 ] In addition, the risk of rupture is higher in individuals who are revascularized with a thrombolytic agent than with PCI. [ 168 ] [ 169 ] The shear stress between the infarcted segment and the surrounding normal myocardium (which may be hypercontractile in the post-infarction period) makes it a nidus for rupture. [ 170 ] Rupture is usually a catastrophic event that may result a life-threatening process known as cardiac tamponade , in which blood accumulates within the pericardium or heart sac, and compresses the heart to the point where it cannot pump effectively. Rupture of the intraventricular septum (the muscle separating the left and right ventricles) causes a ventricular septal defect with shunting of blood through the defect from the left side of the heart to the right side of the heart, which can lead to right ventricular failure as well as pulmonary overcirculation. Rupture of the papillary muscle may also lead to acute mitral regurgitation and subsequent pulmonary edema and possibly even cardiogenic shock . [ edit ] Life-threatening arrhythmia A 12 lead electrocardiogram showing ventricular tachycardia. Since the electrical characteristics of the infarcted tissue change (see pathophysiology section ), arrhythmias are a frequent complication. [ 171 ] The re-entry phenomenon may cause rapid heart rates ( ventricular tachycardia and even ventricular fibrillation ), and ischemia in the electrical conduction system of the heart may cause a complete heart block (when the impulse from the sinoatrial node , the normal cardiac pacemaker, does not reach the heart chambers). [ 172 ] [ 173 ] [ edit ] Pericarditis Main article: Pericarditis As a reaction to the damage of the heart muscle, inflammatory cells are attracted. The inflammation may reach out and affect the heart sac. This is called pericarditis . In Dressler's syndrome , this occurs several weeks after the initial event. [ edit ] Cardiogenic shock A complication that may occur in the acute setting soon after a myocardial infarction or in the weeks following it is cardiogenic shock . Cardiogenic shock is defined as a hemodynamic state in which the heart cannot produce enough of a cardiac output to supply an adequate amount of oxygenated blood to the tissues of the body. While the data on performing interventions on individuals with cardiogenic shock is sparse, trial data suggests a long-term mortality benefit in undergoing revascularization if the individual is less than 75 years old and if the onset of the acute myocardial infarction is less than 36 hours and the onset of cardiogenic shock is less than 18 hours. [ 110 ] If the patient with cardiogenic shock is not going to be revascularized, aggressive hemodynamic support is warranted, with insertion of an intra-aortic balloon pump if not contraindicated. [ 110 ] If diagnostic coronary angiography does not reveal a culprit blockage that is the cause of the cardiogenic shock, the prognosis is poor. [ 110 ] [ edit ] Prognosis The prognosis for patients with myocardial infarction varies greatly, depending on the patient, the condition itself and the given treatment. Using simple variables which are immediately available in the emergency room , patients with a higher risk of adverse outcome can be identified. For example, one study found that 0.4% of patients with a low risk profile had died after 90 days, whereas the mortality rate in high risk patients was 21.1%. [ 174 ] Although studies differ in the identified variables, some of the more reproduced risk stratifiers include age, hemodynamic parameters (such as heart failure , cardiac arrest on admission, systolic blood pressure , or Killip class of two or greater), ST-segment deviation, diabetes , serum creatinine concentration, peripheral vascular disease and elevation of cardiac markers. [ 174 ] [ 175 ] [ 176 ] Assessment of left ventricular ejection fraction may increase the predictive power of some risk stratification models. [ 177 ] The prognostic importance of Q-waves is debated. [ 178 ] Prognosis is significantly worsened if a mechanical complication ( papillary muscle rupture, myocardial free wall rupture, and so on) were to occur. [ 168 ] There is evidence that case fatality of myocardial infarction has been improving over the years in all ethnicities. [ 179 ] [ edit ] Legal implications At common law , a myocardial infarction is generally a disease , but may sometimes be an injury . This has implications for no-fault insurance schemes such as workers' compensation . A heart attack is generally not covered; [ 180 ] however, it may be a work-related injury if it results, for example, from unusual emotional stress or unusual exertion. [ 181 ] Additionally, in some jurisdictions, heart attacks suffered by persons in particular occupations such as police officers may be classified as line-of-duty injuries by statute or policy. In some countries or states, a person who has suffered from a myocardial infarction may be prevented from participating in activity that puts other people's lives at risk, for example driving a car, taxi or airplane. [ 149 ] [ edit ] See also Acute coronary syndrome Angina Cardiac arrest Coronary thrombosis Hibernating myocardium Stunned myocardium Ventricular remodeling [ edit ] References ^ Kosuge, M; Kimura K, Ishikawa T et al. (March 2006). 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Circulation 79 (3): 528���36. PMID 2645061 . ^ Liew R, Sulfi S, Ranjadayalan K, Cooper J, Timmis AD. (2006). "Declining case fatality rates for acute myocardial infarction in South Asian and white patients in the past 15 years". Heart 92 (8): 1030���4. doi : 10.1136/hrt.2005.078634 . PMID 16387823 . ^ Workers' Compensation FAQ . Prairie View A&M University . Retrieved November 22, 2006. ^ SIGNIFICANT DECISIONS Subject Index . Board of Industrial Insurance Appeals. Retrieved November 22, 2006. [ edit ] External links Website of Image Analysis Inc. a software developer specializing in Coronary Calcium Scoring products. Find more about Myocardial infarction on Wikipedia's sister projects : Definitions from Wiktionary Textbooks from Wikibooks Quotations from Wikiquote Source texts from Wikisource Images and media from Commons News stories from Wikinews Learning resources from Wikiversity PROCAM Risk Calculator estimating your risk of a heart attack (myocardial infarction) within the next 10 years based on data of the PROCAM study, provided by the International Task Force for Prevention of Coronary Heart Disease Risk Assessment Tool for Estimating 10-year Risk of Having a Heart Attack - based on information of the Framingham Heart Study , from the United States National Heart, Lung and Blood Institute Heart Attack - overview of resources from MedlinePlus . American Heart Association's Heart Attack web site - Information and resources for preventing, recognizing and treating heart attack. v ��� d ��� e Cardiovascular disease : heart disease �� Circulatory system pathology ( I00-I52 , 390-429 ) Ischaemic CD/CHD CAD �� Coronary thrombosis �� Coronary vasospasm �� Coronary artery aneurysm Active ischemia Angina pectoris ( Prinzmetal's angina , Stable angina ) �� Acute coronary ( Unstable angina , Myocardial infarction / heart attack ) Sequelae Myocardial stunning �� Myocardial rupture �� Dressler's syndrome Layers Pericardium Pericarditis ( Acute , Chronic / Constrictive ) �� Pericardial effusion ( Hemopericardium , Cardiac tamponade ) Myocardium Myocarditis ( Chagas disease ) Cardiomyopathy : Dilated ( Alcoholic ) �� Hypertrophic �� Restrictive ( Loeffler endocarditis , Cardiac amyloidosis , Endocardial fibroelastosis ) Arrhythmogenic right ventricular dysplasia Endocardium / valves Endocarditis Infective endocarditis ( Subacute bacterial endocarditis ) �� noninfective endocarditis ( Nonbacterial thrombotic endocarditis , Libman-Sacks endocarditis ) Valves mitral ( regurgitation , prolapse , stenosis ) �� aortic ( stenosis , insufficiency ) �� tricuspid ( stenosis , insufficiency ) �� pulmonary ( stenosis , insufficiency ) Conduction / arrhythmia Bradycardia Sinus bradycardia �� Sick sinus syndrome Heart block : Sinoatrial �� AV ( 1�� , 2�� , 3�� ) �� Intraventricular ( Bundle branch / Right / Left , Left anterior fascicular / Left posterior fascicular , Bifascicular / Trifascicular ) �� Adams-Stokes syndrome Tachycardia ( paroxysmal and sinus ) Supraventricular Atrial ( Multifocal ) �� Junctional ( AV nodal reentrant , Junctional ectopic ) Ventricular Torsades de pointes �� Catecholaminergic polymorphic �� Accelerated idioventricular rhythm Premature contraction Atrial �� Ventricular Pre-excitation syndrome Wolff-Parkinson-White �� Lown-Ganong-Levine Flutter/ fibrillation Atrial flutter �� Ventricular flutter �� Atrial fibrillation ( Familial ) �� Ventricular fibrillation Pacemaker Wandering pacemaker �� Ectopic pacemaker / Ectopic beat �� Parasystole �� Multifocal atrial tachycardia Long QT syndrome Romano-Ward syndrome �� Andersen-Tawil syndrome �� Jervell and Lange-Nielsen syndrome Cardiac arrest Sudden cardiac death �� Asystole �� Pulseless electrical activity Other/ungrouped Right axis deviation �� Short QT syndrome �� Sinoatrial arrest �� T wave alternans Other Cardiac fibrosis �� Cardiomegaly �� Ventricular hypertrophy ( Left , Right / Cor pulmonale ) Heart failure ( Cardiac asthma ) �� Rheumatic fever See also congenital , neoplasia Retrieved from " http://en.wikipedia.org/wiki/Myocardial_infarction " Categories : Aging-associated diseases | Cardiovascular diseases | Causes of death | Ischemic heart diseases | Medical emergencies Hidden categories: Pages with DOIs broken since 2008 | Wikipedia indefinitely move-protected pages Views Article Discussion Edit this page History Personal tools Log in / create account Navigation Main page Contents Featured content Current events Random article Search Interaction About Wikipedia Community portal Recent changes Contact Wikipedia Donate to Wikipedia Help Toolbox What links here Related changes Upload file Special pages Printable version Permanent link Cite this page Languages �������������� Bosanski ������������������ Catal�� Cebuano ��esky Dansk Deutsch Eesti ���������������� Espa��ol Esperanto Euskara ���������� Fran��ais ��������� Hrvatski Bahasa Indonesia ��slenska Italiano ���������� Kurd�� / ���������� Latina Lietuvi�� Magyar �������������������� ������������������ Nederlands ��������� ���Norsk (bokm��l)��� ���Norsk (nynorsk)��� Polski Portugu��s Runa Simi �������������� Shqip Simple English ������������ / Srpski Suomi Svenska ��������������� ��������� Ti���ng Vi���t T��rk��e �������������������� �������� ������������ ������ This page was last modified on 22 February 2009, at 23:43. 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clueweb09-enwp01-10-03579 | Historic Jamestowne - Wikipedia, the free encyclopedia Historic Jamestowne From Wikipedia, the free encyclopedia (Redirected from Jamestown National Historic Site ) Jump to: navigation , search Jamestown National Historic Site IUCN Category V (Protected Landscape/Seascape) Location James City County, Virginia , USA Nearest city Jamestown, Virginia Coordinates 37��12���35���N 76��46���44���W ��� / ��� 37.20972��N 76.77889��W ��� / 37.20972; -76.77889 Coordinates : 37��12���35���N 76��46���44���W ��� / ��� 37.20972��N 76.77889��W ��� / 37.20972; -76.77889 Area 20.63 acres (83,490 m��) Established December 18 , 1940 Governing body APVA Preservation Virginia (in partnership with NPS ) Historic Jamestowne is the official name used for promotional purposes for the original site of the 1607 James Fort and the later 17th century city of Jamestown, located on the James River at Jamestown, Virginia , an attraction operated by the U.S. National Park Service . Contents 1 History 2 Preservation 3 Gallery 4 See also 5 External links [ edit ] History Jamestown, first established in May 1607, was the site of the first permanent British colony in North America . Jamestown was the capital of the Virginia Colony , and saw Bacon's Rebellion in 1676, when the statehouse was burned. After a second burning in 1698, the capital was relocated to higher ground at Middle Plantation in 1699, which was then renamed Williamsburg . In the 19th century, Jamestown Island reverted to little-used farmland, and became the site of Confederate earthworks during the American Civil War intended to provide rivers defenses against Union gunboats. The Ambler Farm was burned by escaped slaves , who found the desolate island to be a haven. [ edit ] Preservation By 1893 the site of Jamestown was owned by Mr and Mrs Edward Barney, who donated 22�� acres of land, including the 1639 tower of the Jamestown Church , to the Association for the Preservation of Virginia Antiquities (now APVA Preservation Virginia). By this time, erosion from the river had eaten away the island's western shore; visitors began to conclude that the site of James Fort lay completely underwater. With federal assistance, a sea wall was constructed in 1900 to protect the area from further erosion. The archaeological remains of the original 1607 fort, which had been protected by the seawall, were discovered in 1994. The APVA property was designated Jamestown National Historic Site on December 18 , 1940 , and listed on the National Register of Historic Places on October 15 , 1966 . In 1934 , Colonial National Historical Park obtained the remaining 1500 acre (6.1 km��) island and partnered with the APVA to preserve the area and present it to visitors in an educational manner. In 2006, many preparations were underway for the Jamestown 2007 event celebrating the 400th anniversary of the settlement. Queen Elizabeth II visited Historic Jamestowne on May 4 2007 ��� she had previously visited the park in October 1957. [ edit ] Gallery Reconstruction of the barracks at James Fort Graves of settlers who died in 1607 Seawall along the James River Boardwalk and visitors' center at Jamestown National Historic Site Swampland at Jamestown Archaearium and memorial to those buried beneath it Reconstruction of Jamestown Fort, hidden by trees Yeardley House, home to the Jamestown Reconstruction project's offices Historic Jamestowne seen from the James River Ferry Jamestowne Tercentennial Monument near the historic settlement [ edit ] See also Colonial Parkway Colonial Williamsburg Jamestown Settlement Wikimedia Commons has media related to: Historic Jamestowne v ��� d ��� e Protected Areas of Virginia Units of the National Park Service and affiliated areas Appalachian Trail �� Appomattox Court House NHP �� Arlington House �� Assateague Island NS �� Blue Ridge Parkway �� Booker T. Washington NM �� Captain John Smith Chesapeake NHT �� Cedar Creek and Belle Grove NHP �� Chesapeake Bay Gateways Network �� Claude Moore Colonial Farm �� Colonial NHP �� Cumberland Gap NHP �� Fredericksburg and Spotsylvania NMP �� George Washington Memorial Parkway �� George Washington Birthplace NM �� Great Falls Park �� Green Spring District �� Lyndon Baines Johnson Memorial Grove on the Potomac �� Maggie L. Walker NHS �� Manassas NBP �� Overmountain Victory NHT �� Petersburg NB �� Potomac Heritage Trail �� Prince William Forest Park �� Richmond NBP �� Shenandoah NP �� Star-Spangled Banner NHT �� Wolf Trap National cemeteries Alexandria �� Arlington �� Balls Bluff �� City Point �� Cold Harbor �� Culpeper �� Danville �� Fort Harrison �� Fredericksburg �� Glendale �� Hampton �� Hampton VA �� Poplar Grove �� Quantico �� Richmond �� Seven Pines �� Staunton �� Winchester �� Yorktown National Wildlife Refuges Back Bay �� Chincoteague �� Eastern Shore of Virginia �� Mason Neck �� Featherstone �� Fisherman Island �� Great Dismal Swamp �� James River �� Nansemond �� Occoquan Bay �� Plum Tree Island �� Presquile �� Rappahannock River Valley �� Wallops Island National Forests and affiliated areas George Washington �� Jefferson �� Mount Rogers National Recreation Area �� Mountain Lake Wilderness State parks Bear Creek Lake �� Belle Isle �� Breaks Interstate �� Caledon Natural Area �� Chippokes Plantation �� Claytor Lake �� Douthat �� Fairy Stone �� False Cape �� First Landing �� Grayson Highlands �� High Bridge Trail �� Holliday Lake �� Hungry Mother �� James River �� Kiptopeke �� Lake Anna �� Leesylvania �� Mason Neck �� Natural Tunnel �� New River Trail �� Occoneechee �� Pocahontas �� Sailor's Creek Battlefield �� Shot Tower �� Shenandoah River �� Sky Meadows �� Smith Mountain Lake �� Southwest Virginia Museum �� Staunton River �� Staunton River Battlefield �� Tabb Monument �� Twin Lakes �� Westmoreland �� Wilderness Road �� York River State forests Appomattox-Buckingham �� Bourassa �� Browne �� Channels �� Chilton Woods �� Conway-Robinson �� Crawfords �� Cumberland �� Devil's Backbone �� Dragon Run �� Hawks �� Lesesne �� Matthews �� Niday Place �� Paul �� Prince Edward-Gallion �� Sandy Point �� Whitney �� Zoar Natural area preserves Antioch Pines �� Bethel Beach �� Big Spring Bog �� Blackwater �� Buffalo Mountain �� Bull Run Mountains �� Bush Mill Stream �� Camp Branch Wetlands �� Cape Charles Coastal Habitat �� The Cedars �� The Channels �� Cherry Orchard Bog �� Chestnut Creek Wetlands �� Chestnut Ridge �� Chotank Creek �� Chub Sandhill �� Cleveland Barrens �� Clover Hollow �� Cowbane Prairie �� Crow's Nest �� Cumberland Marsh �� Dameron Marsh �� Deep Run Ponds �� Dendron Swamp �� Difficult Creek �� Elklick Woodlands �� False Cape �� Folly Mills Creek Fen �� Goshen Pass �� Grafton Ponds �� Grassy Hill �� Grayson Glades �� Hickory Hollow �� Hughlett Point �� Johnsons Creek �� Magothy Bay �� Mark's and Jack's Island �� Mount Joy Pond �� Mutton Hunk Fen �� Naked Mountain �� New Point Comfort �� New Landing River �� Northwest River �� Ogdens Cave �� Parkers Marsh �� Parramore Island �� Pedlars Hill �� Pinnacle �� Poor Mountain �� Red Rock Mountain �� Savage Neck Dunes �� Unthanks Cave �� William B. Trower Bayshore �� Wreck Island Wildlife management areas Amelia �� Big Survey �� Briery Creek �� Chester F. Phelps �� Cavalier �� Chickahominy �� Clinch Mountain �� Crooked Creek �� Dick Cross �� Fairystone Farms �� Featherfin �� G. Richard Thompson �� Game Farm Marsh �� Goshen and Little North Mountain �� Hardware River �� Havens �� Hidden Valley �� Highland �� Hog Island �� Horsepen Lake �� James River �� Land's End �� Mockhorn Island �� Pettigrew �� Powhatan �� Princess Anne �� Ragged Island �� Rapidan �� Saxis �� Stewarts Creek �� T. M. Gathright �� Turkeycock �� Weston �� White Oak Mountain Registered Historic Places in Virginia Counties A���B �� C �� D���G �� H���M �� N���R �� S���Z �� Bridges �� National Historic Landmarks Virginia Department of Conservation and Recreation �� Virginia Department of Forestry �� Virginia Department of Game and Inland Fisheries �� Virginia Landmarks Register v ��� d ��� e U.S. National Register of Historic Places Keeper of the Register �� History of the National Register of Historic Places �� Property types �� Historic district �� Contributing property List of entries National Park Service �� National Historic Landmarks �� National Battlefields �� National Historic Sites �� National Historical Parks �� National Memorials �� National Monuments [ edit ] External links Historic Jamestowne official website NPS Historic Jamestowne official website Jamestown 2007 website APVA.org: History of Jamestown APVA.org: Satehouse Site and Early Burial Ground National Geographic Magazine Jamestown Interactive Retrieved from " http://en.wikipedia.org/wiki/Historic_Jamestowne " Categories : IUCN Category V | 1607 establishments | 1940 establishments | Archaeological sites in Virginia | Cities on the James River | Colonial Virginia | James City County, Virginia | James River (Virginia) | Lost cities and towns | National Historic Sites in Virginia | Settlements in colonial Virginia Views Article Discussion Edit this page History Personal tools Log in / create account Navigation Main page Contents Featured content Current events Random article Search Interaction About Wikipedia Community portal Recent changes Contact Wikipedia Donate to Wikipedia Help Toolbox What links here Related changes Upload file Special pages Printable version Permanent link Cite this page This page was last modified on 9 January 2009, at 20:39. 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clueweb09-en0001-51-15358 | Events - Joomla! Documentation Events From Joomla! Documentation Jump to: navigation , search This page covers events involving the Joomla! Documentation Working Group only. Contents 1 Forthcoming Events 2 Past Events 2.1 Pizza Bugs and Fun 2 2.2 Joomla! Doc Camp 2 2.3 Google Highly Open Participation Contest 2.4 Joomla! Doc Camp Forthcoming Events Joomla Day UK 2009 - 13/14 March 2009 Chris Davenport, Documentation Working Group Coordinator will be there, together with other members of the Core Team, OSM and the wider community. Past Events Pizza Bugs and Fun 2 Something for everyone at the Joomla! Bazaar: coding, documentation, testing and other fun stuff. This event took place on two consecutive weekends, 21/22 and 28/29 June 2008. For more information see Pizza Bugs and Fun 2 . Joomla! Doc Camp 2 Doc Camp 2 morphed into one of the "stalls" in the Joomla! Bazaar. See Pizza Bugs and Fun 2 . Google Highly Open Participation Contest The Google Highly Open Participation Contest for pre-university students (high school and secondary school students) took place between November 2007 and February 2008 and was aimed at encouraging young people to participate in open source projects. Joomla! is proud to have been invited to join with nine other open source organisations for this pilot program. Tomasz DobrzyDski was unanimously selected as Joomla!'s 2008 Grand Prize Winner of the Google Highly Open Participation Contest. Tomasz completed seven tasks during the competition. Translate part of the Installation Manual to a non-English Language - output - forum thread Create a Blog Entry Date Calendar Icon Plugin for Joomla! v 1.5 - output - forum thread Create a Joomla! v 1.5 Plugin to update Twitter status with article title when published - output - forum thread Carry out GHOP unit test on the Joomla1 1.5 Test Package for the Front Page Manager - output - forum thread Carry out GHOP unit test on the Joomla1 1.5 Test Package: Template Manager - output - forum thread Carry out GHOP unit test on the Joomla1 1.5 Test Package: Menu Manager - output - forum thread Implement Avatar/Gravatars for Joomla! v 1.5 - output - forum thread Selecting a winner was difficult because there were many deserving contestants. In review, it was obvious that GHOP was more than a contest for Tomasz. He demonstrated what contributing to a free software community should be like. He discovered that learning is fun, he expressed joy in sharing what he produced with others, he was proud to contribute his gifts, and he was honoured to be a part of the Joomla! community. As is true with many other contestants, Tomasz inspired those of us who worked with the program and reminded us why we also contribute. We congratulate Tomasz DobrzyDski on this well deserved honor and we thank him, and each of the others, who contributed to the Joomla! community. All completed contest tasks are available for review and download. See also: Google official contest website Google blog post announcing the Grand Prize Winners About the Joomla! GHOP students Contest announcement on www.joomla.org Joomla! contest pages on code.google.com Joomla! contest discussion forum Official Joomla! blog posts about the contest Fun at the Googleplex Grand Prize winners visit the Googleplex Joomla! Doc Camp The first Joomla! Doc Camp event took place over the weekend of 19 January 2008. Although most of the activity took place online, we were joined by physical locations in Vancouver, Canada and Brussels, Belgium. A huge "thank you" to all who contributed during the event. Your efforts are very much appreciated. Please read the Joomla! Doc Camp Report . You can see the results (and continue to work on the documentation) here: Joomla! Doc Camp . See also:- Full announcement Forum discussion thread Forum thread for Doc Camp topic suggestions Retrieved from " http://docs.joomla.org/Events " Views Page Discussion View source History Personal tools Log in / create account Navigation Main Page Recent changes Current events Random page Browse categories Help Joomla! Sites Main Community Help Forum Extensions Shop Developers API Search Toolbox What links here Related changes Upload file Special pages Printable version Permanent link This page was last modified on 4 January 2009, at 23:33. Content is available under Joomla! EDL . Privacy policy About Joomla! Documentation Disclaimers |
clueweb09-en0009-02-05429 | Music Composition Studio Music
Composition Studio Home Magic Hands-o-Music Are you looking for the Magic Hands-o-Music (also known as the hands-o-pitches )
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clueweb09-enwp00-89-19972 | Hyperlipidemia - Wikipedia, the free encyclopedia Hyperlipidemia From Wikipedia, the free encyclopedia (Redirected from Hyperlipoproteinemia type V ) Jump to: navigation , search Hyperlipidemia Classification and external resources ICD - 10 E 78. ICD - 9 272.0 - 272.4 DiseasesDB 6255 MeSH D006949 Hyperlipidemia , hyperlipoproteinemia or dyslipidemia is the presence of raised or abnormal levels of lipids and/or lipoproteins in the blood . Lipids (fatty molecules) are transported in a protein capsule, and the density of the lipids and type of protein determines the fate of the particle and its influence on metabolism . Lipid and lipoprotein abnormalities are extremely common in the general population, and are regarded as a highly modifiable risk factor for cardiovascular disease due to the influence of cholesterol , one of the most clinically relevant lipid substances, on atherosclerosis . In addition, some forms may predispose to acute pancreatitis . Contents 1 Classification 1.1 Hyperlipoproteinemia type I 1.2 Hyperlipoproteinemia type II 1.2.1 Type IIa 1.2.2 Type IIb 1.2.3 Treatment 1.3 Hyperlipoproteinemia type III 1.4 Hyperlipoproteinemia type IV (type 4 = familial) 1.5 Hyperlipoproteinemia type V (type 5 = endogenous) 2 Unclassified forms 3 References 4 External links [ edit ] Classification Hyperlipidemias are classified according to the Fredrickson classification which is based on the pattern of lipoproteins on electrophoresis or ultracentrifugation . [ 1 ] It was later adopted by the World Health Organization (WHO). It does not directly account for HDL , and it does not distinguish among the different genes that may be partially responsible for some of these conditions. It remains a popular system of classification, but is considered dated by many. Fredrickson classification of Hyperlipidemias Hyperlipoproteinemia Synonyms Problems Increased lipoprotein Treatment Serum appearnace Type I (rare) Buerger-Gruetz syndrome , Primary hyperlipoproteinaemia , or Familial hyperchylomicronemia Decreased lipoprotein lipase (LPL) or altered ApoC2 Chylomicrons Diet Control Creamy top layer Type IIa Polygenic hypercholesterolaemia or Familial hypercholesterolemia LDL receptor deficiency LDL Bile Acid Sequestrants , Statins , Niacin Clear Type IIb Combined hyperlipidemia Decreased LDL receptor and Increased ApoB LDL and VLDL Statins , Niacin , Fibrate Clear Type III (rare) Familial Dysbetalipoproteinemia Defect in Apo E 2 synthesis IDL Drug of choice: Fibrate Turbid Type IV Familial Hyperlipemia Increased VLDL production and Decreased elimination VLDL Drug of choice: Fibrate , Niacin Turbid Type V (rare) Endogenous Hypertriglyceridemia Increased VLDL production and Decreased LPL VLDL and Chylomicrons Niacin , Fibrate Creamy top layer & turbid bottom [ edit ] Hyperlipoproteinemia type I This very rare form (also known as Buerger-Gruetz syndrome , primary hyperlipoproteinaemia , or familial hyperchylomicronemia ) is due to a deficiency of lipoprotein lipase (LPL) or altered apolipoprotein C2 , resulting in elevated chylomicrons , the particles that transfer fatty acids from the digestive tract to the liver . Lipoprotein lipase is also responsible for the initial breakdown of endogenously made triacylglycerides in the form of very low density lipoprotein (VLDL). As such, one would expect a defect in LPL to also result in elevated VLDL. Its prevalence is 0.1% of the population. [ edit ] Hyperlipoproteinemia type II Hyperlipoproteinemia type II, by far the most common form, is further classified into type IIa and type IIb, depending mainly on whether there is elevation in the triglyceride level in addition to LDL cholesterol. [ edit ] Type IIa Main article: Familial hypercholesterolemia This may be sporadic (due to dietary factors), polygenic, or truly familial as a result of a mutation either in the LDL receptor gene on chromosome 19 (0.2% of the population) or the ApoB gene (0.2%). The familial form is characterized by tendon xanthoma , xanthelasma and premature cardiovascular disease. The incidence of this disease is about 1 in 500 for heterozygotes, and 1 in 1,000,000 for homozygotes. [ edit ] Type IIb The high VLDL levels are due to overproduction of substrates, including triglycerides, acetyl CoA, and an increase in B-100 synthesis. They may also be caused by the decreased clearance of LDL. Prevalence in the population is 10%. Familial combined hyperlipoproteinemia (FCH) Secondary combined hyperlipoproteinemia (usually in the context of metabolic syndrome , for which it is a diagnostic criterion) [ edit ] Treatment While dietary modification is the initial approach, many patients require treatment with statins (HMG-CoA reductase inhibitors) to reduce cardiovascular risk. If the triglyceride level is markedly raised, fibrates may be preferable due to their beneficial effects. Combination treatment of statins and fibrates, while highly effective, causes a markedly increased risk of myopathy and rhabdomyolysis and is therefore only done under close supervision. Other agents commonly added to statins are ezetimibe , niacin and bile acid sequestrants . There is some evidence for benefit of plant sterol-containing products and �� 3 -fatty acids [ 2 ] [ edit ] Hyperlipoproteinemia type III This form is due to high chylomicrons and IDL (intermediate density lipoprotein). Also known as broad beta disease or dysbetalipoproteinemia , the most common cause for this form is the presence of ApoE E2/E2 genotype. It is due to cholesterol-rich VLDL (��-VLDL). Prevalence is 0.02% of the population. [ edit ] Hyperlipoproteinemia type IV (type 4 = familial) This form is due to high triglycerides . It is also known as hypertriglyceridemia (or pure hypertriglyceridemia ). According to the NCEP-ATPIII definition of high triglycerides (>200 mg/dl), prevalence is about 16% of adult population. [ 3 ] [ edit ] Hyperlipoproteinemia type V (type 5 = endogenous) This type is very similar to type I, but with high VLDL in addition to chylomicrons. It is also associated with glucose intolerance and hyperuricemia [ edit ] Unclassified forms Non-classified forms are extremely rare: Hypo-alpha lipoproteinemia Hypo-beta lipoproteinemia (prevalence 0.01-0.1%) [ edit ] References ^ Frederickson DS, Lee RS. A system for phenotyping hyperlipidemia. Circulation 1965;31:321-7. PMID 14262568 . ^ Thompson GR. Management of dyslipidaemia. Heart 2004;90:949-55. PMID 15253984 . ^ Third Report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III) Final Report. Circulation 2002; 106; page 3240 [ edit ] External links The Fredrickson papers (with photos from early lipoprotein research) 745209914 at GPnotebook Hyperlipoproteinemia OMIM GPnotebook WebMD Others Type I Online 'Mendelian Inheritance in Man' (OMIM) 238600 -1389035478 at GPnotebook . MeritCare Type IIa Online 'Mendelian Inheritance in Man' (OMIM) 144400 -1664090094 at GPnotebook . Merck Type IIb -1375338454 at GPnotebook . Type III . 630849560 at GPnotebook WebMD Yahoo Type IV Online 'Mendelian Inheritance in Man' (OMIM) 144600 -1362100182 at GPnotebook WebMD Yahoo Type V Online 'Mendelian Inheritance in Man' (OMIM) 144600 -1355481046 at GPnotebook . . v ��� d ��� e Lipid metabolism disorders / Inborn error of lipid metabolism - dyslipidemia ( E78 and E71.3 , 272 ) Hyperlipidemia Hypercholesterolemia / Hypertriglyceridemia ( Familial hypercholesterolemia , Combined hyperlipidemia ) - Xanthoma Hypolipoproteinemia Hypoalphalipoproteinemia/HDL ( Lecithin cholesterol acyltransferase deficiency , Tangier disease ) Hypobetalipoproteinemia/LDL ( Abetalipoproteinemia , Apolipoprotein B deficiency ) Lipodystrophy Barraquer-Simons syndrome Fatty acid metabolism deficiency transport: Carnitine ( Primary , I , II , -acylcarnitine ) - Adrenoleukodystrophy beta oxidation : Acyl CoA dehydrogenase ( Short-chain , Medium-chain , Long-chain 3-hydroxy , Very long-chain ) - Mitochondrial trifunctional protein deficiency to acetyl-CoA: Malonic aciduria Cholesterol synthesis Smith-Lemli-Opitz syndrome Other Sj��gren-Larsson syndrome - Lipomatosis - Adiposis dolorosa - Lipoid proteinosis see also lipid metabolism enzymes , lipoprotein metabolism Retrieved from " http://en.wikipedia.org/wiki/Hyperlipidemia " Categories : Metabolic disorders | Cardiology | Lipid disorders Views Article Discussion Edit this page History Personal tools Log in / create account Navigation Main page Contents Featured content Current events Random article Search Interaction About Wikipedia Community portal Recent changes Contact Wikipedia Donate to Wikipedia Help Toolbox What links here Related changes Upload file Special pages Printable version Permanent link Cite this page Languages Deutsch Fran��ais ���������� �������������� Svenska This page was last modified on 24 February 2009, at 07:01. 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clueweb09-en0005-18-30601 | MODPlug Central Directory MODPLUG CENTRAL HOME Search: search the entire directory search this category only Top : Society : History : By_Region : North_America : United_States : Civil_Rights_Movement : Sound Clips Coldplay Tickets 15th Amendment @ (0) 24th Amendment @ (2) Douglass, Frederick @ (21) Jackson, Jesse @ (2) King, Martin Luther, Jr. @ (35) Lewis, John @ (13) Malcolm X @ (13) Marshall, Thurgood @ (5) Parks, Rosa @ (11) Rustin, Bayard @ (3) Truth, Sojourner @ (6) See also: Kids and Teens: People and Society: Biography: Civil Rights Leaders (105) Reference: Museums: Cultural: Ethnic: African American (48) Society: Ethnicity: African: African-American: History (136) Society: Issues: Race-Ethnic-Religious Relations (455) » A. Philip Randolph Pullman Porter Museum - Did you know...A. Philip Randolph first planned a March on Washington in 1941 to protest against governmental hiring practices that excluded African Americans from federal employment and federal contracts? » African American History: Welcome - This project documents a selection of important events in African American history. Currently it begins with the 1857 Dred Scott case and continues through Plessy v. Ferguson, the civil rights movement from 1955-1965, and school integration. It may be expanded in the future to contain information on other topics as well. » American Women in the Civil Rights Movement - A course by the Yale-New Haven Teachers Institute featuring six women in the Civil Rights Movement based on the literature of Eloise Greenfield. » The 1963 Birmingham Church Bombing - Information and history of the Birmingham Church bombing of 1963. » Civil Rights - A high-school level overview of the civil rights struggle, from Reconstruction through Dr. King. » Civil Rights Author Discusses Birmingham, Alabama Revolution - Diane McWhorter, Pulitzer Prize winning author of Carry Me Home, discusses the revoltion that led to the passing of the Civil Rights Act of 1964 in an interview with Jerry Jazz Musician. » Civil Rights Events, Strategies, and Forces - Captures several milestones, personalities, and influences that helped civil rights in America. » Civil Rights History Guide - The History Beat - The Search Beat covers a variety of topics, including a Civil Rights History Guide with top Civil Rights history, timelines of the Civil Rights struggle, and resources. Well organized by time periods; includes civil rights photography. » Civil Rights in Mississippi Digital Archive - The Civil Rights in Mississippi Digital Archive is an Internet-accessible, fully searchable database of digitized versions of rare and unique library and archival resources on race relations sponsored by The University of Southern Mississippi Libraries.Mississippi was a focal point in the struggle for civil rights in America, and Hattiesburg, where USM is located, had the largest and most successful Freedom Summer project in 1964. The original sources collected in the state represent local collections with truly national significance. Digitization provides an opportunity to make indigenous resources of this type available to a worldwide audience. » Civil Rights Movement: March on Washington 1963 - A short history leading to and following the March 18, 1963 March on Washington D.C. for Jobs and Freedom. » Civil Rights Oral History - A bibliography of interviews about the civil rights movement in Mississippi. » Click2History - Jim Crow Laws - Cites infamous "Jim Crow" laws against African Americans, with embedded links from national archives » Facing History and Ourselves - Educational organization. Video clips of individuals who involved the civil rights movement during the 1950s and 60s. Also describes educational and professional development programs and resources, lists regional offices, and provides news and event calendar. » Freetown Villiage - A Living History Museum - Freetown Village is a living history museum which depicts the lives and lifestyles of free African Americans in the year 1870. This symbolic community represents many of the predominantly African American settlements scattered throughout Indiana during the post-Civil War years. The residents of Freetown Village are composite characters of the approximately 3,000 men, women and children identified on the 1870 Indianapolis census. » Greensboro, North Carolina Sit-Ins - The Greensboro News and Record and Public Library chronicle the 1960 sit-in movement with a timeline, photos, and voices of the participants. » Harry T. Moore Homesite - Mims, Florida - Harry T. Moore Homesite site commemorates lives of two pioneering American Black civil rights workers, murdered in 1951. Organized first Brevard Co. Chapter NAACP in 1934, and led Florida fight for equality and justice. First killing of prominent civil rights leaders, historical spark helped ignite American civil rights movement. » Historic Places in the Civil Rights Movements - The National Parks Services' story of the Civil Rights Movement centered around places listed in the National Register of Historic Places. » The History of Jim Crow - An educator's site that presents teachers with historical resources and teaching ideas on one of the most shameful periods in American history. » Ideas of Black Civil Rights Leaders - A short essay comparing the ideas of Civil Rights and African nationalism leaders. » Integrating Ole Miss - The Kennedy Presidential Library's account of James Meredith, the African-American student whose attempt to register at the University of Mississippi in 1962 provoked violent confrontation. Time lines, biographical profiles, and primary sources. » Jim Crow Online - The official home of the PBS documentary, The Rise and Fall of Jim Crow. » Juneteenth Worldwide Celebration - Website brings together the spirit of Juneteenth, the oldest known celebration of the ending of slavery. From its Galveston, Texas origin in 1865, the observance of June 19th as the African American Emancipation Day has spread across the United States and beyond. Juneteenth commemorates African American freedom and emphasizes education and achievement. It is a day, a week, and in some areas a month marked with celebrations, guest speakers, picnics and family gatherings. » Little Rock Central High 40th Anniversary - Background and history of events during the integration of Central High in 1957. Photos, articles, and news releases are published. Museum and visitor's center information is provided. » Men and Women in Struggle - In memory of the men and women who helped in the struggle to achieve mankind's greatest victories. » Milliken's Bend - Black Soldiers Defeat Confederates - Black soldiers vindicated President Abraham Lincoln by defeating Confederate soldiers at Milliken's Bend, in the critical battle for Vicksburg in the Civil War. As a result, most barriers to the enlistment and effective deployment of Colored recruits were eliminated in pursuit of the ultimate Union victory. Most of the Colored infantry had minimal training, were outnumbered and ill-equipped. Nevertheless, in close hand-to-hand combat, they routed the "Rebs" and won respect previously denied by both sides of the conflagration. Site features maps, links, historical articles, discussion group. » Mississippi Civil Rights Documentation Project - Funded by the Mississippi state legislature, presentation includes oral history bibliography, oral history transcripts, and civil rights timeline. » A Modern History of Blacks in Mathematics - A contemporary history of Blacks in Mathematics,featuring the first African Americans in the Mathematical Sciences and related events in the past 300 years. Links are presented in a timeline and include such information as first African American to obtain Ph.D. in math, first black math professors and related links. » The Montgomery Bus Boycott - Describes the incident which started on December 1, 1955, when Mrs. Rosa Parks refused to give up her seat, and move to the back of the bus. » A Photographic History of The Civil Rights Movement - Photos and text from The Civil Rights Movement. » Reporting Civil Rights - Features reporters and journalism of the American Civil Rights Movement. » Sojourn to the Past - Offers students, educators and parents the chance to travel for ten days through the South visiting the most dramatic sites and hearing the speakers that first witnessed and created the civil rights movement » The Story of the Montgomery Bus Boycott - Review of 1955-1956 landmark events from the Montgomery Advertiser. Features newspaper front pages, article archives, biographies of key pioneers, timeline of events, video clips. » Three Victims of the Freedom Summer 1964 Civil Rights Movement - A sculptural portrayal of James Earl Chaney, Andrew Goodman and Michael Schwerner, slain in the struggle for civil rights that they lived for, and that we all have. » Veterans of the Civil Rights Movement - Personal testimony and contact information from veterans of the Southern Freedom Movement. » Viola Liuzzo - Civil Rights Activist (1925-1965) - Viola Liuzzo, a white housewife who was killed while fighting for the rights of whites and nonwhites alike. » Voices of Civil Rights - The Voices of Civil Rights, a joint effort of AARP, the Leadership Conference on Civil Rights (LCCR), and the Library of Congress collects and preserves untold accounts of the Civil Rights Movement. » W.E.B. Du Bois, The Fight for Equality and the American Century, 1919-1963 - Randy Sydnor's audio interview of Dr. Daniel Levering Lewis, Du Bois biographer, on the show, Oxford Review. » National Center for Public Policy Research: Brown v. Board of Education - An unofficial text of the Supreme Court's landmark civil rights case. (May 17, 1954) Help build the largest human-edited
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clueweb09-enwp00-89-19971 | Hyperlipidemia - Wikipedia, the free encyclopedia Hyperlipidemia From Wikipedia, the free encyclopedia (Redirected from Hyperlipemia ) Jump to: navigation , search Hyperlipidemia Classification and external resources ICD - 10 E 78. ICD - 9 272.0 - 272.4 DiseasesDB 6255 MeSH D006949 Hyperlipidemia , hyperlipoproteinemia or dyslipidemia is the presence of raised or abnormal levels of lipids and/or lipoproteins in the blood . Lipids (fatty molecules) are transported in a protein capsule, and the density of the lipids and type of protein determines the fate of the particle and its influence on metabolism . Lipid and lipoprotein abnormalities are extremely common in the general population, and are regarded as a highly modifiable risk factor for cardiovascular disease due to the influence of cholesterol , one of the most clinically relevant lipid substances, on atherosclerosis . In addition, some forms may predispose to acute pancreatitis . Contents 1 Classification 1.1 Hyperlipoproteinemia type I 1.2 Hyperlipoproteinemia type II 1.2.1 Type IIa 1.2.2 Type IIb 1.2.3 Treatment 1.3 Hyperlipoproteinemia type III 1.4 Hyperlipoproteinemia type IV (type 4 = familial) 1.5 Hyperlipoproteinemia type V (type 5 = endogenous) 2 Unclassified forms 3 References 4 External links [ edit ] Classification Hyperlipidemias are classified according to the Fredrickson classification which is based on the pattern of lipoproteins on electrophoresis or ultracentrifugation . [ 1 ] It was later adopted by the World Health Organization (WHO). It does not directly account for HDL , and it does not distinguish among the different genes that may be partially responsible for some of these conditions. It remains a popular system of classification, but is considered dated by many. Fredrickson classification of Hyperlipidemias Hyperlipoproteinemia Synonyms Problems Increased lipoprotein Treatment Serum appearnace Type I (rare) Buerger-Gruetz syndrome , Primary hyperlipoproteinaemia , or Familial hyperchylomicronemia Decreased lipoprotein lipase (LPL) or altered ApoC2 Chylomicrons Diet Control Creamy top layer Type IIa Polygenic hypercholesterolaemia or Familial hypercholesterolemia LDL receptor deficiency LDL Bile Acid Sequestrants , Statins , Niacin Clear Type IIb Combined hyperlipidemia Decreased LDL receptor and Increased ApoB LDL and VLDL Statins , Niacin , Fibrate Clear Type III (rare) Familial Dysbetalipoproteinemia Defect in Apo E 2 synthesis IDL Drug of choice: Fibrate Turbid Type IV Familial Hyperlipemia Increased VLDL production and Decreased elimination VLDL Drug of choice: Fibrate , Niacin Turbid Type V (rare) Endogenous Hypertriglyceridemia Increased VLDL production and Decreased LPL VLDL and Chylomicrons Niacin , Fibrate Creamy top layer & turbid bottom [ edit ] Hyperlipoproteinemia type I This very rare form (also known as Buerger-Gruetz syndrome , primary hyperlipoproteinaemia , or familial hyperchylomicronemia ) is due to a deficiency of lipoprotein lipase (LPL) or altered apolipoprotein C2 , resulting in elevated chylomicrons , the particles that transfer fatty acids from the digestive tract to the liver . Lipoprotein lipase is also responsible for the initial breakdown of endogenously made triacylglycerides in the form of very low density lipoprotein (VLDL). As such, one would expect a defect in LPL to also result in elevated VLDL. Its prevalence is 0.1% of the population. [ edit ] Hyperlipoproteinemia type II Hyperlipoproteinemia type II, by far the most common form, is further classified into type IIa and type IIb, depending mainly on whether there is elevation in the triglyceride level in addition to LDL cholesterol. [ edit ] Type IIa Main article: Familial hypercholesterolemia This may be sporadic (due to dietary factors), polygenic, or truly familial as a result of a mutation either in the LDL receptor gene on chromosome 19 (0.2% of the population) or the ApoB gene (0.2%). The familial form is characterized by tendon xanthoma , xanthelasma and premature cardiovascular disease. The incidence of this disease is about 1 in 500 for heterozygotes, and 1 in 1,000,000 for homozygotes. [ edit ] Type IIb The high VLDL levels are due to overproduction of substrates, including triglycerides, acetyl CoA, and an increase in B-100 synthesis. They may also be caused by the decreased clearance of LDL. Prevalence in the population is 10%. Familial combined hyperlipoproteinemia (FCH) Secondary combined hyperlipoproteinemia (usually in the context of metabolic syndrome , for which it is a diagnostic criterion) [ edit ] Treatment While dietary modification is the initial approach, many patients require treatment with statins (HMG-CoA reductase inhibitors) to reduce cardiovascular risk. If the triglyceride level is markedly raised, fibrates may be preferable due to their beneficial effects. Combination treatment of statins and fibrates, while highly effective, causes a markedly increased risk of myopathy and rhabdomyolysis and is therefore only done under close supervision. Other agents commonly added to statins are ezetimibe , niacin and bile acid sequestrants . There is some evidence for benefit of plant sterol-containing products and �� 3 -fatty acids [ 2 ] [ edit ] Hyperlipoproteinemia type III This form is due to high chylomicrons and IDL (intermediate density lipoprotein). Also known as broad beta disease or dysbetalipoproteinemia , the most common cause for this form is the presence of ApoE E2/E2 genotype. It is due to cholesterol-rich VLDL (��-VLDL). Prevalence is 0.02% of the population. [ edit ] Hyperlipoproteinemia type IV (type 4 = familial) This form is due to high triglycerides . It is also known as hypertriglyceridemia (or pure hypertriglyceridemia ). According to the NCEP-ATPIII definition of high triglycerides (>200 mg/dl), prevalence is about 16% of adult population. [ 3 ] [ edit ] Hyperlipoproteinemia type V (type 5 = endogenous) This type is very similar to type I, but with high VLDL in addition to chylomicrons. It is also associated with glucose intolerance and hyperuricemia [ edit ] Unclassified forms Non-classified forms are extremely rare: Hypo-alpha lipoproteinemia Hypo-beta lipoproteinemia (prevalence 0.01-0.1%) [ edit ] References ^ Frederickson DS, Lee RS. A system for phenotyping hyperlipidemia. Circulation 1965;31:321-7. PMID 14262568 . ^ Thompson GR. Management of dyslipidaemia. Heart 2004;90:949-55. PMID 15253984 . ^ Third Report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III) Final Report. Circulation 2002; 106; page 3240 [ edit ] External links The Fredrickson papers (with photos from early lipoprotein research) 745209914 at GPnotebook Hyperlipoproteinemia OMIM GPnotebook WebMD Others Type I Online 'Mendelian Inheritance in Man' (OMIM) 238600 -1389035478 at GPnotebook . MeritCare Type IIa Online 'Mendelian Inheritance in Man' (OMIM) 144400 -1664090094 at GPnotebook . Merck Type IIb -1375338454 at GPnotebook . Type III . 630849560 at GPnotebook WebMD Yahoo Type IV Online 'Mendelian Inheritance in Man' (OMIM) 144600 -1362100182 at GPnotebook WebMD Yahoo Type V Online 'Mendelian Inheritance in Man' (OMIM) 144600 -1355481046 at GPnotebook . . v ��� d ��� e Lipid metabolism disorders / Inborn error of lipid metabolism - dyslipidemia ( E78 and E71.3 , 272 ) Hyperlipidemia Hypercholesterolemia / Hypertriglyceridemia ( Familial hypercholesterolemia , Combined hyperlipidemia ) - Xanthoma Hypolipoproteinemia Hypoalphalipoproteinemia/HDL ( Lecithin cholesterol acyltransferase deficiency , Tangier disease ) Hypobetalipoproteinemia/LDL ( Abetalipoproteinemia , Apolipoprotein B deficiency ) Lipodystrophy Barraquer-Simons syndrome Fatty acid metabolism deficiency transport: Carnitine ( Primary , I , II , -acylcarnitine ) - Adrenoleukodystrophy beta oxidation : Acyl CoA dehydrogenase ( Short-chain , Medium-chain , Long-chain 3-hydroxy , Very long-chain ) - Mitochondrial trifunctional protein deficiency to acetyl-CoA: Malonic aciduria Cholesterol synthesis Smith-Lemli-Opitz syndrome Other Sj��gren-Larsson syndrome - Lipomatosis - Adiposis dolorosa - Lipoid proteinosis see also lipid metabolism enzymes , lipoprotein metabolism Retrieved from " http://en.wikipedia.org/wiki/Hyperlipidemia " Categories : Metabolic disorders | Cardiology | Lipid disorders Views Article Discussion Edit this page History Personal tools Log in / create account Navigation Main page Contents Featured content Current events Random article Search Interaction About Wikipedia Community portal Recent changes Contact Wikipedia Donate to Wikipedia Help Toolbox What links here Related changes Upload file Special pages Printable version Permanent link Cite this page Languages Deutsch Fran��ais ���������� �������������� Svenska This page was last modified on 24 February 2009, at 07:01. All text is available under the terms of the GNU Free Documentation License . (See Copyrights for details.) Wikipedia® is a registered trademark of the Wikimedia Foundation, Inc. , a U.S. registered 501(c)(3) tax-deductible nonprofit charity . Privacy policy About Wikipedia Disclaimers |
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sublimation printing and digital printing. Exclusive
Sports - Negatives: Another original concept
of Clipart deSIGN is graphics specially prepared for screen printing on dark t-shirts or other dark
surfaces . This images are also excellent for vinyl
cutting, embroidery designs, engraving, sublimation
printing and digital printing. Great effect and idea! Bunny
Sports: This is rich collection of sport
images for kids featuring a bunny character. They
are great sport designs for kids, both for vinyl application,
t-shirt printing, embroidery designs, engraving, sublimation
printing and digital printing. Colored in Pantone
colors! Enjoy shopping with the
peace-of-mind of knowing that you are protected
from online fraud, by purchasing from 2CO Certified
Vendors. We accept all major credit cards listed
below. 2Checkout.com ,
Inc.(2CO) is an authorized retailer of goods
and services provided by Clipart deSIGN. IMPORTANT NOTE: absolutely NO credit card information
will be revealed to Clipart deSIGN owners upon
purchase , all transactions are on 2CO's
secure server and are subject to review by professional
fraud analysts. For more information visit 2CheckOut's
web site . HOME | CLIP ART | FLAMES | SPORTS |
VECTORIZATION | FREE
CLIPART | FEEDBACK | LINKS | ABOUT US | CONTACT | RESELL | SITE MAP Copyright (c) 2002 - 2006 Clipart deSIGN. All rights Reserved.
Web site optimized for 1024x768 and higher.Last update June 25,
2006. |
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