heart stroke

心発作

関

cardiac attack、heart attack

WordNet

1. treat gingerly or carefully; "You have to stroke the boss"
2. a sudden loss of consciousness resulting when the rupture or occlusion of a blood vessel leads to oxygen lack in the brain (同)apoplexy, cerebrovascular_accident, CVA
3. (golf) the unit of scoring in golf is the act of hitting the ball with a club; "Nicklaus won by three strokes"
4. (sports) the act of swinging or striking at a ball with a club or racket or bat or cue or hand; "it took two strokes to get out of the bunker"; "a good shot requires good balance and tempo"; "he left me an almost impossible shot" (同)shot
5. a light touch with the hands (同)stroking
6. a single complete movement
7. any one of the repeated movements of the limbs and body used for locomotion in swimming or rowing
8. a light touch
9. a mark made on a surface by a pen, pencil, or paintbrush; "she applied the paint in careful strokes"
10. the oarsman nearest the stern of the shell who sets the pace for the rest of the crew
11. row at a particular rate
12. strike a ball with a smooth blow
13. touch lightly and repeatedly, as with brushing motions; "He stroked his long beard"
14. a plane figure with rounded sides curving inward at the top and intersecting at the bottom; conventionally used on playing cards and valentines; "he drew a heart and called it a valentine"
15. the courage to carry on; "he kept fighting on pure spunk"; "you havent got the heart for baseball" (同)mettle, nerve, spunk
16. an inclination or tendency of a certain kind; "he had a change of heart" (同)spirit
17. a playing card in the major suit that has one or more red hearts on it; "he led the queen of hearts"; "hearts were trumps"
18. the locus of feelings and intuitions; "in your heart you know it is true"; "her story would melt your bosom" (同)bosom
19. the hollow muscular organ located behind the sternum and between the lungs; its rhythmic contractions move the blood through the body; "he stood still, his heart thumping wildly" (同)pump, ticker
20. a firm rather dry variety meat (usually beef or veal); "a five-pound beef heart will serve six"
21. able to perceive sound
22. an opportunity to state your case and be heard; "they condemned him without a hearing"; "he saw that he had lost his audience" (同)audience
23. (law) a proceeding (usually by a court) where evidence is taken for the purpose of determining an issue of fact and reaching a decision based on that evidence
24. the ability to hear; the auditory faculty; "his hearing was impaired" (同)audition, auditory sense, sense of hearing, auditory modality
25. a session (of a committee or grand jury) in which witnesses are called and testimony is taken; "the investigative committee will hold hearings in Chicago"
26. receive a communication from someone; "We heard nothing from our son for five years"
27. examine or hear (evidence or a case) by judicial process; "The jury had heard all the evidence"; "The case will be tried in California" (同)try
28. perceive (sound) via the auditory sense
29. a form of whist in which players avoid winning tricks containing hearts or the queen of spades (同)Black_Maria

PrepTutorEJDIC

1. (こぶし・武器・金づちなどの)『一打ち』,一撃,打告《+of+名》 / 《単数形で》(運の)巡り合わせ《+of+名》 / 《単数形で》(…の)ひと仕事,ひと働き;みごとな成果《+of+名》 / (鐘・時計などの)『打つ音』《+of+名》 / (時計などが打って示す)時刻 / (繰り返される動作・運動の)『一動作』,一行程 / (ペン・鉛筆・筆などの)ひと筆,ひとなで;筆の運び,筆致 / 卒中 / (ゴルフ・テニスなどの)一打ち,ストローク / (心臓などの)一打ち,鼓動,脈搏 / (ボートの)整調[手] / 〈ボート〉‘の'整調をこぐ / 《副詞[句]を伴って》〈ボール〉‘を'打つ
2. 〈髪・動物など〉‘を'なでる,さする / 〈人〉‘を'なだめる《+名+down, down+名》 / 一なで,一さすり
3. 〈C〉『心臓』;胸 / 〈C〉(感情の中心をなす)『心』,気持ち / 〈U〉愛情,同情 / 〈U〉『勇気』,元気,熱意 / 《the ~》『中心』,内部,(物事の)本質,核心 / 〈C〉ハート形の物;(カードの)ハートの札
4. 〈U〉『聴力』,聴覚〈U〉〈C〉(…を)『聞くこと』,(…の)聞き取り《+『of』+『名』》・〈C〉聞いてもらう機会,聞いてやること・聴取・聴聞会〈C〉(法廷などでの)尋問,審問,;(刑罰の減免を求める)釈明,意見陳述 / 〈U〉聞こえる距離(範囲)
5. 〈音〉‘が'『聞こえる』,‘を'聞く(進行形にできない) / 〈人の言うこと〉‘に'『耳を傾ける』,‘を'注意深く聞く(listen);(裁判官などが)…の申し立てを聞く / 〈うわさ・ニュースなど〉‘を'『耳にしている』,聞いている / 『耳が聞こえる』 / 《しばしば命令形で》耳を傾ける,注意を向ける / 『うわさ』(『消息』)『を聞く』

Wikipedia preview

出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2013/07/21 11:58:23」(JST)

wiki en

[Wiki en表示]

"Heart attack" redirects here. For other uses, see Heart attack (disambiguation).

Not to be confused with Cardiac arrest.

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). In the diagram, RCA is the right coronary artery.
ICD-10	I21-I22
ICD-9	410
DiseasesDB	8664
MedlinePlus	000195
eMedicine	med/1567 emerg/327 ped/2520
MeSH	D009203

Myocardial infarction (MI) or acute myocardial infarction (AMI), commonly known as a heart attack, results from the partial interruption of blood supply to a part of the heart muscle, causing the heart cells to be damaged or die. 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 cholesterol and fatty acids and white blood cells in the wall of an artery. The resulting ischemia (restriction in blood supply) and ensuing oxygen shortage, if left untreated for a sufficient period of time, can cause damage or death (infarction) of heart muscle tissue (myocardium).

Typical symptoms of acute myocardial infarction include sudden retrosternal 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. A sizeable proportion of myocardial infarctions (22–64%) are "silent", that is without chest pain or other symptoms.

A number of diagnostic tests are available to detect heart muscle damage including, an electrocardiogram (ECG), echocardiography, cardiac MRI and various blood tests. The most often used blood markers are the creatine kinase-MB (CK-MB) fraction and the troponin levels. Immediate treatment for suspected acute myocardial infarction includes oxygen, aspirin, and sublingual nitroglycerin.

Most cases of myocardial infarction with ST elevation on ECG (STEMI) are treated with reperfusion therapy, such as percutaneous coronary intervention (PCI) or thrombolysis. Non-ST elevation myocardial infarction (NSTEMI) may be managed with medication, although PCI may be required if the patient's risk warrants it. People who have multiple blockages of their coronary arteries, particularly if they also have diabetes mellitus, may benefit from bypass surgery (CABG). The European Society of Cardiology guidelines in 2011 proposed treating the blockage causing the myocardial infarction by PCI and performing CABG later when the patient is more stable. Rarely CABG may be preferred in the acute phase of myocardial infarction, for example when PCI has failed or is contraindicated.

Ischemic heart disease (which includes myocardial infarction, angina pectoris and heart failure when preceded by myocardial infarction) was the leading cause of death for both men and women worldwide in 2004. Important risk factors are previous cardiovascular disease, older age, tobacco smoking, high blood levels of certain lipids (low-density lipoprotein cholesterol, triglycerides) and low levels of high density lipoprotein (HDL) cholesterol, diabetes, high blood pressure, lack of physical activity and obesity, chronic kidney disease, excessive alcohol consumption, the use of illicit drugs (such as cocaine and amphetamines), and chronic high stress levels.

Classification

There are two basic types of acute myocardial infarction based on pathology:

• Transmural: associated with atherosclerosis involving a major coronary artery. It can be subclassified into anterior, posterior, inferior, lateral or septal. Transmural infarcts extend through the whole thickness of the heart muscle and are usually a result of complete occlusion of the area's blood supply. In addition, on ECG, ST elevation and Q waves are seen.
• Subendocardial: involving a small area in the subendocardial wall of the left ventricle, ventricular septum, or papillary muscles. The subendocardial area is particularly susceptible to ischemia. In addition, ST depression is seen on ECG.

In the clinical context, a myocardial infarction can be further subclassified into a ST elevation MI (STEMI) versus a non-ST elevation MI (non-STEMI) based on ECG changes. 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; however severe myocardial infarction may lead to heart failure. A 2007 consensus document classifies myocardial infarction into five main types:

• Type 1 – Spontaneous myocardial infarction related to ischemia due to a primary coronary event such as plaque erosion and/or rupture, fissuring, or dissection
• Type 2 – Myocardial infarction secondary to ischemia due to either increased oxygen demand or decreased supply, e.g. coronary artery spasm, coronary embolism, anaemia, arrhythmias, hypertension, or hypotension
• Type 3 – Sudden unexpected cardiac death, including cardiac arrest, often with symptoms suggestive of myocardial ischaemia, accompanied by new ST elevation, or new LBBB, or evidence of fresh thrombus in a coronary artery by angiography and/or at autopsy, but death occurring before blood samples could be obtained, or at a time before the appearance of cardiac biomarkers in the blood
• Type 4 – Associated with coronary angioplasty or stents:
  • Type 4a – Myocardial infarction associated with PCI
  • Type 4b – Myocardial infarction associated with stent thrombosis as documented by angiography or at autopsy
• Type 5 – Myocardial infarction associated with CABG

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. 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.

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 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 sudden death (frequently due to the development of ventricular fibrillation) can occur in myocardial infarctions.

Female, elderly, and diabetic patients report atypical symptoms more frequently than their male and younger counterparts. Women also report more numerous symptoms compared with men (2.6 on average vs 1.8 symptoms in men). The most common symptoms of MI in women include dyspnea (shortness of breath), weakness, and fatigue. Fatigue, sleep disturbances, and dyspnea have been reported as frequently occurring symptoms that 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.

At least one-fourth of all myocardial infarctions are silent, without chest pain or other symptoms. These cases can be discovered later on electrocardiograms, using blood enzyme tests or at autopsy without a prior history of related complaints. Estimates of the prevalence of silent myocardial infarctions vary between 22 and 64%. A silent course is more common in the elderly, in patients with diabetes mellitus and after heart transplantation, probably because the donor heart is not fully innervated by the nervous system of the recipient. In people with diabetes, differences in pain threshold, autonomic neuropathy, and psychological factors have been cited as possible explanations for the lack of symptoms.

Any group of symptoms compatible with a sudden interruption of the blood flow to the heart are called an acute coronary syndrome.

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. Other non-catastrophic differentials include gastroesophageal reflux and Tietze's syndrome.

Causes

 

The animation shows how plaque buildup or a coronary artery spasm can lead to a heart attack and how blocked blood flow in a coronary artery can lead to a heart attack.

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.^{[citation needed]} 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 very physically fit.^{[citation needed]} For those in poor physical condition, the rate differential is over 35-fold higher.^{[citation needed]} One observed mechanism for this phenomenon is increased pulse pressure, which increases stretching of the arterial walls.^{[citation needed]} This stretching results in significant shear stress on atheromas, which results in debris breaking loose from these deposits.^{[citation needed]} This debris floats through the blood vessels, eventually clogging the major coronary arteries.^{[citation needed]}

Acute severe infection, such as pneumonia, can trigger myocardial infarction. A more controversial link is that between Chlamydophila pneumoniae infection and atherosclerosis. While this intracellular organism has been demonstrated in atherosclerotic plaques, evidence is inconclusive as to whether it can be considered a causative factor. Treatment with antibiotics in patients with proven atherosclerosis has not demonstrated a decreased risk of heart attacks or other coronary vascular diseases.

There is an association of an increased incidence of a heart attack in the morning hours, more specifically around 9 a.m. Some investigators have noticed that the ability of platelets to aggregate varies according to a circadian rhythm, although they have not proven causation.

Risk factors

Myocardial infarction results from atherosclerosis. Smoking appears to be the cause of about 36% of coronary artery disease and obesity 20%. Lack of exercise has been linked to 7-12% of cases. Job stress appear to play a minor role accounting for about 3% of cases.

Risk factors for myocardial infarction include:

• Age
• Gender: At any given age men are more at risk than women, particularly before menopause, but because in general women live longer than men ischemic heart disease causes slightly more total deaths in women.
• Diabetes mellitus (type 1 or 2)
• High blood pressure
• Dyslipidemia/hypercholesterolemia (abnormal levels of lipoproteins in the blood), particularly high low-density lipoprotein, low high-density lipoprotein and high triglycerides
• Tobacco smoking, including secondhand smoke
• Short term exposure to air pollution including: carbon monoxide, nitrogen dioxide, and sulfur dioxide but not ozone.
• Family history of ischaemic heart disease or myocardial infarction particularly if one has a first-degree relative (father, brother, mother, sister) who suffered a 'premature' myocardial infarction (defined as occurring at or younger than age 55 years (men) or 65 (women).
• Obesity (defined by a body mass index of more than 30 kg/m², or alternatively by waist circumference or waist-hip ratio).
• Lack of physical activity.
• Psychosocial factors including, low socio-economic status, social isolation, negative emotions and stress increase the risk of myocardial infarction and are associated with worse outcomes after myocardial infarction. Socioeconomic factors such as a shorter education and lower income (particularly in women), and unmarried cohabitation are also correlated with a higher risk of MI.
• Alcohol — Studies show that prolonged exposure to high quantities of alcohol can increase the risk of heart attack.
• Oral contraceptive pill – 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.
• Hyperhomocysteinemia (high homocysteine) in homocysteinuria is associated with premature atherosclerosis, whether elevated homocysteine in the normal range is causal is contentious.

Inflammation is known to be an important step in the process of atherosclerotic plaque formation. 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. Moreover, some drugs for MI might also reduce CRP levels. 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. Whether CRP plays a direct role in atherosclerosis remains uncertain. Inflammation in periodontal disease may be linked to coronary heart disease, and, since periodontitis is very common, this could have great consequences for public health. Serological studies measuring antibody levels against typical periodontitis-causing bacteria found that such antibodies were more present in subjects with coronary heart disease. Periodontitis tends to increase blood levels of CRP, fibrinogen and cytokines; thus, periodontitis may mediate its effect on MI risk via other risk factors. Preclinical research suggests that periodontal bacteria can promote aggregation of platelets and promote the formation of foam cells. A role for specific periodontal bacteria has been suggested but remains to be established. There is some evidence that influenza may trigger an acute myocardial infarction.

Baldness, hair greying, a diagonal earlobe crease (Frank's sign) and possibly other skin features have been suggested as independent risk factors for MI. Their role remains controversial; a common denominator of these signs and the risk of MI is supposed, possibly genetic.

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.

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. Non-modifiable risk factors include age, sex, and family history of an early heart attack, which is thought of as reflecting a genetic predisposition.^{[citation needed]} To understand epidemiological study results, it is 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.

Pathophysiology

See also: Acute coronary syndrome

A myocardial infarction occurs when an atherosclerotic plaque slowly builds up in the inner lining of a coronary artery and then suddenly ruptures, causing catastrophic thrombus formation, totally occluding the artery and preventing blood flow downstream.

Drawing of the heart showing anterior left ventricle wall infarction

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 in the territory of the occluded coronary artery 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. As a result, the patient's heart will be permanently damaged. This myocardial scarring 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.

Diagnosis

Main article: Myocardial infarction diagnosis

Medical societies recommend that the physician confirm that a patient is at high risk for myocardial infarction before conducting imaging tests to make a diagnosis. Patients who have a normal ECG and who are able to exercise, for example, do not merit routine imaging. Imaging tests such as stress radionuclide myocardial perfusion imaging or stress echocardiography can confirm a diagnosis when a patient's history, physical exam, ECG and cardiac biomarkers suggest the likelihood of a problem.

The diagnosis of myocardial infarction can be made after assessing patient's complaints and physical status. ECG changes, coronary angiogram and levels of cardiac markers help to confirm the diagnosis. ECG gives valuable clues to identify the site of myocardial damage while coronary angiogram allows visualization of narrowing or obstructions in the heart vessels. 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. In stable patients whose symptoms have resolved by the time of evaluation, Technetium (99mTc) sestamibi (i.e. a "MIBI scan") or thallium-201 chloride can be used in nuclear medicine to visualize areas of reduced blood flow in conjunction with physiologic or pharmacologic stress. 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.

WHO criteria formulated in 1979 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:

1. Clinical history of ischaemic type chest pain lasting for more than 20 minutes
2. Changes in serial ECG tracings
3. 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. According to the new guidelines, a cardiac troponin rise accompanied by either typical symptoms, pathological Q waves, ST elevation or depression, or coronary intervention is diagnostic of MI.

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 those with heart disease, and limitation of alcohol intake. People 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:

• 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.
• Beta blocker therapy such as metoprolol or carvedilol should be commenced. These have been particularly beneficial in high-risk patients such as those with left ventricular dysfunction and/or continuing cardiac ischaemia. β-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.
• Statin therapy has been shown to reduce mortality and morbidity post-MI. 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.
• 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. Spironolactone is another option that is sometimes preferable to eplerenone due to cost.
• Evidence supports the consumption of polyunsaturated fats instead of saturated fats as a measure of decreasing coronary heart disease. In high-risk people there is no clear-cut decrease in potentially fatal arrhythmias due to omega-3 fatty acids. And they may increase risk in some groups.
• Giving heparin to people with heart conditions like unstable angina and some forms of heart attacks reduces the risk of having another heart attack. However, heparin also increases the chance of minor bleeding.

Management

Main article: Myocardial infarction management

An MI requires immediate medical attention. Treatment attempts to salvage as much myocardium as possible and to prevent further complications, hence the phrase "time is muscle". Oxygen, aspirin, and nitroglycerin may be administered. Morphine was classically used if nitroglycerin was not effective; however, it may increase mortality in the setting of NSTEMI. Reviews of high flow oxygen in myocardial infarction found increased mortality and infarct size, calling into question the recommendation about its routine use. Other analgesics such as nitrous oxide are of unknown benefit.

STEMI

Percutaneous coronary intervention (PCI) is the treatment of choice for STEMI if it can be performed in a timely manner. If PCI cannot be performed within 90 to 120 minutes then fibrinolysis, preferably within 30 minutes, is recommended. If after fibrinolysis there is significant cardiogenic shock, continued severe chest pain, or less than a 50% improvement in ST elevation after 90 minutes then rescue PCI is indicated emergently. After PCI people are generally placed on dual antiplatelet therapy for at least a year (which is generally aspirin and clopidogrel).

Prognosis

The prognosis post myocardial infarction varies greatly, depending on a person's health, the extent of the heart damage and the treatment given. For the period 2005–2008 in the United States, the median mortality at 30 days was 16.6% with a range from 10.9% to 24.9% depending on the hospital. Using variables available in the emergency room, people with a higher risk of adverse outcome can be identified. One study found that 0.4% of patients with a low-risk profile died after 90 days, whereas in high-risk people it was 21.1%.

Some of the more reproduced risk-stratifying factors 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, peripheral vascular disease and elevation of cardiac markers. Assessment of left ventricular ejection fraction may increase the predictive power. The prognostic importance of Q-waves is debated. Prognosis is significantly worsened if a mechanical complication such as papillary muscle or myocardial free wall rupture occurs. Morbidity and mortality from myocardial infarction has improved over the years due to better treatment.

Complications

Main article: Myocardial infarction complications

Complications may occur immediately following the heart attack (in the acute phase), or may need time to develop (a chronic problem). Acute complications may include heart failure if the damaged heart is no longer able to adequately pump blood around the body; aneurysm or rupture of the myocardium; mitral regurgitation, in particular if the infarction causes dysfunction of the papillary muscle; and arrhythmias, such as ventricular fibrillation, ventricular tachycardia, atrial fibrillation and heart block. Longer-term complications include heart failure, atrial fibrillation, and the increased risk of a second myocardial infarction.

Epidemiology

Myocardial infarction is a common presentation of ischemic heart disease/coronary artery disease. The World Health Organization estimated in 2004, that 12.2% of worldwide deaths were from ischemic heart disease; with it being the leading cause of death in high or middle income countries and second only to lower respiratory infections in lower income countries. Worldwide more than 3 million people have STEMIs and 4 million have NSTEMIs a year.

Rates of death from ischemic heart disease have slowed or declined in most high income countries, although cardiovascular disease still accounted for 1 in 3 of all deaths in the USA in 2008. In contrast, ischemic heart disease is becoming a more common cause of death in the developing world. For example in India, ischemic heart disease had become the leading cause of death by 2004 accounting for 1.46 million deaths (14% of total deaths) and deaths due to ischemic heart disease were expected to double during 1985–2015. Globally it is predicted that disability adjusted life years (DALYs) lost to ischemic heart disease will account for 5.5% of total DALYs in 2030, making it the second most important cause of disability (after unipolar depressive disorder), as well as the leading cause of death by this date.

Legal implications

At common law, in general a myocardial infarction is a disease, but may sometimes be an injury. This can create coverage issues in administration of no-fault insurance schemes such as workers' compensation. In general, a heart attack is not covered; however, it may be a work-related injury if it results, for example, from unusual emotional stress or unusual exertion. In addition, 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 having 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 or flying an airplane.

Research

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.

There are currently three biomaterial and tissue engineering approaches for the treatment of post-MI conditions, but these are in an even earlier stage of medical research. Many questions and issues must 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.

References

External links

• Cardiac disorders - Open Directory Project
• American Heart Association's Heart Attack web site — Information and resources for preventing, recognizing and treating heart attack.

UpToDate Contents

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• 1. 冠動脈疾患および脳卒中の一次予防の概要 overview of primary prevention of coronary heart disease and stroke
• 2. 脳卒中評価の概要 overview of the evaluation of stroke
• 3. 虚血性脳卒中の二次予防の概要 overview of secondary prevention of ischemic stroke
• 4. 脳卒中の二次予防のための抗血小板療法 antiplatelet therapy for secondary prevention of stroke
• 5. 急性虚血性脳卒中および一過性脳虚血発作に対する抗血栓治療 antithrombotic treatment of acute ischemic stroke and transient ischemic attack

English Journal

• Relationship and factor structure in multisystem neurodegeneration in Parkinson's disease.

• Hattori T1, Orimo S, Hallett M, Wu T, Inaba A, Azuma R, Mizusawa H.
• Acta neurologica Scandinavica.Acta Neurol Scand.2014 Dec;130(6):347-53. doi: 10.1111/ane.12273. Epub 2014 Sep 11.
• OBJECTIVES: Parkinson's disease (PD) is a multisystem neurodegenerative disease. We aimed to identify the relationship and factor structure among its different features.MATERIALS & METHODS: Motor, olfactory and cognitive function, and cardiac sympathetic denervation were evaluated in 125 patient
• PMID 25209841

• The association between ambient air quality and cardiac rate and rhythm in ambulatory subjects.

• Cakmak S1, Kauri L2, Shutt R3, Liu L4, Green MS5, Mulholland M6, Stieb D7, Dales R8.
• Environment international.Environ Int.2014 Dec;73:365-71. doi: 10.1016/j.envint.2014.08.015. Epub 2014 Sep 16.
• BACKGROUND: Acute increases in ambient air pollution have been associated with increased hospitalization for cardiac diseases and stroke. Triggering of cardiac arrhythmia by changes in air quality could theoretically predispose individuals to cardiac arrest or heart failure, or stroke through precip
• PMID 25226341

• The impact of global budgeting on treatment intensity and outcomes.

• Kan K1, Li SF, Tsai WD.
• International journal of health care finance and economics.Int J Health Care Finance Econ.2014 Dec;14(4):311-37. doi: 10.1007/s10754-014-9150-0. Epub 2014 Jul 11.
• This paper investigates the effects of global budgets on the amount of resources devoted to cardio-cerebrovascular disease patients by hospitals of different ownership types and these patients' outcomes. Theoretical models predict that hospitals have financial incentives to increase the quantity of
• PMID 25012589

Japanese Journal

• 肝動脈塞栓症による肝梗塞を剖検で確認できた心原性脳塞栓症の1例

• 鈴木 由希子,米田 行宏,中島 直樹,鷹巣 晃昌,熊原 加奈,市川 桂二,影山 恭史
• 脳卒中 37(1), 12-16, 2015
• 要旨：糖尿病性腎症により維持透析を受けていた72 歳男性が，右内頸動脈領域に広範な脳梗塞を発症した．脳MRA では責任血管は再開通しており，心房細動を認めたことから心原性脳塞栓症と診断した．第8 病日に，突然，重篤な肝機能障害が出現し，腹部CT では肝右葉が淡い低吸収を呈していた．左上肢の透析シャント閉塞，両下肢の末梢動脈塞栓症も併発し，第11 病日に死亡した．剖検にて，急性および陳旧性心筋梗塞と …
• NAID 130004873645

• アルテプラーゼ投与後の心破裂

• 橋本 憲一郎,松田 信二,赤荻 悠一,小島 一歩,本間 甲一,藤川 厚,石毛 聡,町田 利生,小野 純一
• 脳卒中 37(1), 26-30, 2015
• 要旨：88 歳の女性．日常生活動作は自立しており降圧薬内服中．ショートステイ中に倒れているところを発見され当院に救急搬送された．来院時，右共同偏視と左片麻痺を認めNIHSS スコア12点．心電図で心房細動を，頭部CT およびMRI で右中大脳動脈領域の新鮮梗塞像を認めた．超急性期心原性脳塞栓症と診断し，最終未発症確認時刻から3 時間58 分でアルテプラーゼ静注療法を開始しエダラボンを併用した．アル …
• NAID 130004873636

• Need for Better Blood Pressure Measurement in Developing Countries to Improve Prevention of Cardiovascular Disease

• , ,
• Journal of Epidemiology 25(2), 91-98, 2015
• … Implementation of global prevention efforts urgently needs to be accelerated because of the increasing incidence of haemorrhagic stroke, renal failure, and hypertensive heart disease in developing countries. …
• NAID 130004851884

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Related Pictures

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★リンクテーブル★

リンク元	「心発作」「cardiac attack」
関連記事	「hearing」「stroke」「hear」「heart」

「心発作」

　　[★]

英

heart attack、cardiac attack、heart stroke

関

心臓発作

「cardiac attack」

　　[★]

心発作

関

heart attack、heart stroke

「hearing」

　　[★]

• n。

• 聴力、聴覚。聞くこと、聴取。聞こえる距離/範囲。聞いてやること、傾聴。聞いてもらうこと、発言の機会。(委員会などの)聴聞会、ヒアリング。(法)審問、尋問。

　 　 　 　 　 　

「stroke」

　　[★] 脳卒中 　 　 　 　 　 　 　 　 　 　 　 　 　 　 　

「hear」

　　[★]

• v.

• 聞く、聞こえる

　 　 　 　

「heart」

　　[★] 心臓