According to Widipedia Encyclopedia:
What causes a heart attack? When an artery supplying blood to the heart becomes completely obstructed, portions of the heart deprived of oxygen die. The result is a heart attack. Heart disease is the gradual building-up of plaque. Plaque is “pus-filled pimple” that grows within the walls of arteries. If one “lesion” pops open, a blood clot forms over the spot to seal it & the clot blocks the artery & that what causes a heart attack.
How do you stop a “Heart Attack” from happening? We must take preventive measures: 1- Keep your weight down; 2-physical exercise activity daily; 3- No cigarette smoking; 4-Keep blood pressure & cholesterol under control; 5-Take medications if necessary.
25%-of Americans over 50 have at least 2 risk factors: blood pressure or cholesterol levels or an elevated blood-sugar.
10% of Americans have every risk factor under control.
When a person has a heart attack at least 2 or 3 risk factors could have been avoided. And if that person has just 1 risk factor his chances for having a heart attack sours to 50%.
Approximately, 1.1 million people will have a heart attack this year.
A Must To Do Follow List:
1-Keep your cholesterol in check-LDL-60 to 130; should be no higher than 70. If you have diabetes your level should be below 100.
2-Exercise regularly-30 min. daily preferred.
3-Lower your blood pressure-Know Your # s high blood pressure: 140/90 mmHg higher prehypertension(hbp); 120/80 to 139/89 mmHg normal blood pressure(nbp) 119/79 mmHg or lower blood pressure(lbp)
4-Control your weight-loose weight to not be at risk
5-Stop smoking-to reduce risk of heart attack
6-Control your blood sugar-safe level 70 to 130 milligrams per deciliter of blood
For other uses, see Heart attack (disambiguation). Myocardial infarction (MI) or acute myocardial infarction (AMI), commonly known as a heart attack, is the interruption of blood supply to a part of the heart, causing heart cells to 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 lipids (fatty acids) 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 of time, can cause damage or death (infarction) of heart muscle tissue (myocardium).
Classical symptoms of acute myocardial infarction include sudden chest pain (typically radiating to left arm or left side of neck), shortness of breath, nausea, vomiting, palpitations, sweating, & 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. Approximately one quarter of all myocardial infarctions are “silent”, without chest pain or other symptoms.
Among diagnostic tests available to detect heart muscle damage are “electro-cardiogram” (ECG), echocardiography, & various blood tests. Most often used markers are “creatine kinase”-MB (CK-MB) fraction & “troponin” levels. Immediate treatment for suspected acute myocardial infarction include: oxygen, aspirin, & sublingual nitroglycerin.
Most cases of STEMI (ST elevation MI) are treated with “thrombolysis” or “percutaneous coronary intervention” (PCI). NSTEMI (non-ST elevation MI) should be managed with medication, although PCI is often performed during hospital admission. In people who have multiple blockages & who are relatively stable, or in a few emergency cases, bypass surgery may be an option.
Heart attacks are the leading cause of death for both men & women worldwide. Important risk factors: previous cardiovascular disease, older age, tobacco smoking, high blood levels of certain lipids (triglycerides, low-density lipoprotein) & low levels of high density lipoprotein (HDL), diabetes, high blood pressure, obesity, chronic kidney disease, heart failure, excessive alcohol consumption, abuse of certain drugs:(cocaine & methamphetamine), & chronic high stress levels.
Classification: There’re two basic types of acute myocardial infarction:
Transmural: associated with atherosclerosis involving major coronary artery. It can be subclassified into anterior, posterior, or inferior. Transmural infarcts extend through the whole thickness of the heart muscle & are usually a result of complete occlusion of area’s blood supply.
Subendocardial: involving a small area in the subendocardial wall of the left ventricle, ventricular septum, or papillary muscles. Subendocardial infarcts are thought to be a result of locally decreased blood supply, possibly from a narrowing of the coronary arteries. The subendocardial area is farthest from the heart’s blood supply and is more susceptible to this type of pathology.
Clinically, 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 result of acute myocardial infarction. A heart attack is different from, but can be the cause of cardiac arrest, which is stopping of heartbeat, & cardiac arrhythmia, an abnormal heartbeat. It’s distinct from heart failure, in which pumping action of heart is impaired; severe myocardial infarction may lead to heart failure, but not necessarily.
A 2007 consensus document classifies myocardial infarction into five main types:
Type 1 ‘” Spontaneous myocardial infarction related to ischaemia due to a primary coronary event: plaque erosion &/or rupture, fissuring, or dissection
Type 2 ‘” Myocardial infarction secondary to ischaemia 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 presumably new ST elevation, or new LBBB, or evidence of fresh thrombus in a coronary artery by angiography &/or at autopsy, but death occurring before blood samples could be obtained, or at a time before appearance of cardiac biomarkers in 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 & symptoms
Onset of symptoms in myocardial infarction (MI) is usually gradual, over several minutes, & rarely instantaneous. Chest pain is most common symptom of acute myocardial infarction & is often described as a sensation of tightness, pressure, or squeezing. Chest pain due to ischemia (a lack of blood & hence oxygen supply) of heart muscle is “angina pectoris”. Pain radiates most often to left arm, but may radiate to lower jaw, neck, right arm, back, & epigastrium, where it may mimic heartburn. Levine’s sign, where patient localizes chest pain by clenching their fist over 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.
Symptoms include: Shortness of breath(dyspnea)(occurs when damage to heart limits out put of left ventricle, causing left ventricular failure & consequent pulmonary edema); diaphoresis (an excessive form of sweating), weakness, light-headedness, nausea, vomiting, & palpitations. These symptoms are likely induced by massive surge of catecholamines from sympathetic nervous system which occurs in response to pain & hemodynamic abnormalities resulting from cardiac dysfunction. Loss of consciousness (due to inadequate cerebral perfusion & cardiogenic shock) & sudden death (frequently due to development of ventricular fibrillation) can occur in myocardial infarctions.
Women & older patients report atypical symptoms more frequently than their male & younger counterparts. Women report more numerous symptoms compared with men (2.6 on average vs 1.8 symptoms in men). Most common symptoms of MI in women include dyspnea (shortness of breath), weakness, & fatigue. Fatigue, sleep disturbances, and dyspnea have been reported as frequently occurring symptoms & may manifest as long as one month before actual clinically manifested ischemic event. In women, chest pain may be less predictive of coronary ischemia than in men.
Approximately 1/4th of all myocardial infarctions are silent, with no chest pain or symptoms. This is evident on electrocardiograms, using blood enzyme tests or at autopsy without prior history of related complaints. Silent course is more common in elderly patients with diabetes mellitus & after heart transplantation, because the donor heart is not fully innervated by the nervous system of the recipient. In diabetics, differences in pain threshold, autonomic neuropathy, & psychological factors have been cited as possible explanations for lack of symptoms.
Any group of symptoms compatible with a sudden interruption of blood flow to heart are called an acute coronary syndrome.
Differential diagnosis includes other catastrophic causes of chest pain: pulmonary embolism, aortic dissection, pericardial effusion causing cardiac tamponade, tension pneumothorax, & esophageal rupture. Other non-catastrophic differentials include gastroesophageal reflux & Tietze’s syndrome.
Causes: Heart attack rates are higher in association with intense exertion, be it psychological stress or physical exertion, especially if exertion is more intense than individual usually performs. Quantitatively, period of intense exercise & 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. For those in poor physical condition, the rate differential is over 35-fold higher. One observed mechanism for this phenomenon is increased arterial pulse pressure stretching & relaxation of arteries with each heart beat which, as has been observed with intravascular ultrasound, increases mechanical “shear stress” on atheromas & likelihood of plaque rupture.
Acute severe infection: pneumonia, can trigger myocardial infarction.More controversial link is that between Chlamydophila pneumoniae infection & 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.
Increased incidence of a heart attack in morning hours, around 9 a.m. are frquent. Some investigators have noticed the ability of platelets to aggregate varies according to circadian rhythm, although they’ve not proven causation.
Risk factors:For atherosclerosis are basicly same risk factors for myocardial infarction:
Diabetes:single most important risk factor for ischaemic heart disease(IHD)(with or without insulin resistance)
Hyper-cholesterolemia: especially high low density lipoprotein & low high density lipoprotein)(hyper-lipoproteinemia,
High blood pressure
*Family history of ischaemic heart disease(IHD)
*Obesity(defined by a body mass index of more than 30 kg/m², or alternatively by waist circumference or waist-hip ratio).
*Age-Men acquire an independent risk factor at age 45, Women acquire an *independent risk factor at age 55; in addition individuals acquire another independent risk factor if they have a *first-degree male relative (brother, father) who suffered coronary vascular event at or before age 55. Another independent risk factor is acquired if one has a *first-degree female relative (mother, sister) who suffered a coronary vascular event at age 65 or younger.
Hyperhomocysteinemia (high homocysteine, *toxic blood amino acid is elevated when intakes of vitamins B2, B6, B12 and folic acid are insufficient)
*Stress-Occupations with high stress index are known to have susceptibility for atherosclerosis)
*Alcohol-Studies show prolonged exposure to high quantities of alcohol increase risk of heart attack
Males are at more risk than females
Risk factors of heart attacks can be prevented or modified by maintaining healthier lifestyle. Example: Physical activity is associated with lower risk profile. Non-modifiable risk factors: age, sex, family history of early heart attack (before age 60), (reflecting a genetic predisposition.
Factors: Socioeconomic, shorter education, lower income(women), unmarried cohabitation, contribute to risk of MI. To understand epidemiological study results, it’s important to note many factors associated with MI mediate their risk via other factors. Example, effect of education is based on effect on income & marital status.
Other risk factors: Women who use combined oral contraceptive pills & smoking has modestly increased risk of myocardial infarction.
Inflammation is an important step in 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 risk of MI, stroke & development of diabetes. Moreover, some drugs for MI might reduce CRP levels. The use of high sensitivity CRP assays as a means of screening 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, & since periodontitis is very common, it could have great consequences for public health. Serological studies measuring antibody levels against typical periodontitis-causing bacteria found antibodies were more present in subjects with coronary heart disease. Periodontitis tends to increase blood levels of CRP, fibrinogen & cytokines; periodontitis may mediate its effect on MI risk via other risk factors. Preclinical research suggests periodontal bacteria can promote aggregation of platelets & promote formation of foam cells. A role for specific periodontal bacteria has been suggested but remains to be established. There’s some evidence influenza may trigger an acute myocardial infarction.
Baldness, hair greying, diagonal ear lobe crease & possibly other skin features have been suggested as independent risk factors for MI. Their role remains controversial; common denominator of these signs & risk of MI may be, genetic.
Calcium deposition is part of atherosclerotic plaque formation. Calcium deposits in coronary arteries can be detected with CT scans. Several studies have shown coronary calcium provide predictive information beyond of classical risk factors.
European Society of Cardiology & European Association for Cardiovascular Prevention & Rehabilitation have developed an interactive tool for prediction & managing risk of heart attack & stroke in Europe. HeartScore is aimed at supporting clinicians in optimising individual cardiovascular risk reduction. The Heartscore Programme is available in 12 languages & offers web based or PC version.
Acute myocardial infarction refers to two subtypes of acute coronary syndrome, namely non-ST-elevated myocardial infarction & ST-elevated myocardial infarction, are manifestation of coronary artery disease. Most common triggering event is disruption of an atherosclerotic plaque in an epicardial coronary artery, which leads to clotting cascade, sometimes resulting in total occlusion of artery. Atherosclerosis is gradual buildup of cholesterol & fibrous tissue in plaques in 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, & additionally promote a thrombus (blood clot) that occludes the artery; this can occur in minutes. When severe enough plaque rupture occurs in coronary vasculature, it leads to myocardial infarction (necrosis of downstream myocardium).
If impaired blood flow to heart lasts long enough, it triggers process called ischemic cascade; heart cells in territory of occluded coronary artery die (chiefly through necrosis) & don’t grow back. A collagen scar forms in its place. Recent studies indicate another form of cell death called apoptosis & plays a role in process of tissue damage subsequent to myocardial infarction. As a result, patient’s heart will be permanently damaged. Myocardial scarring puts patient at risk for potentially life threatening arrhythmias, & may result in formation of a ventricular aneurysm & can rupture with catastrophic consequences.
Injured heart tissue conducts electrical impulses more slowly than normal heart tissue. Difference in conduction velocity between injured & uninjured tissue can trigger re-entry or a feedback loop that’s believed to be cause of lethal arrhythmias. Most serious of these arrhythmias is ventricular fibrillation (V-Fib/VF), a very fast & chaotic heart rhythm that is 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. Ventricular tachycardia usually results in rapid heart rates that prevent heart from pumping blood effectively. Cardiac output & blood pressure may fall to dangerous levels, can lead to further coronary ischemia & extension of 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.
DiagnosisMain article: Myocardial infarction diagnosis
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 heart vessels. At autopsy, a pathologist can diagnose a myocardial infarction based on anatomopathological findings.
A chest radiograph & routine blood tests may indicate complications or precipitating causes & are often performed upon arrival to an emergency department. New regional wall motion abnormalities on an echocardiogram are suggestive of a myocardial infarction. Echo may be performed in equivocal cases by on-call cardiologist. In stable patients whose symptoms have resolved by 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 pharmocologic stress. Thallium may 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 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 & 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 are diagnostic of MI.
Prevention:Risk of recurrent myocardial infarction decreases with strict blood pressure management & 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 aim of preventing secondary cardiovascular events; 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 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), &/or evidence of left ventricular dysfunction. ACE inhibitors reduce mortality, development of heart failure, & decrease ventricular remodelling post-MI.
Statin therapy has been shown to reduce mortality & morbidity post-MI. 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.
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 consumption of polyunsaturated fats instead of saturated fats as measure of decreasing coronary heart disease. Omega-3 fatty acids, commonly found in fish, have been shown to reduce mortality post-MI. While mechanism by which these fatty acids decrease mortality is unknown, it has been postulated that survival benefit is due to electrical stabilization & prevention of ventricular fibrillation. However, further studies in high-risk subset haven’t shown clear-cut decrease in potentially fatal arrhythmias due to omega-3 fatty acids.
Blood donation may reduce risk of heart disease for men, but link hasn’t been firmly established.
A Cochrane review found that giving heparin to people who have heart conditions like unstable angina & some forms of heart attacks reduces risk of having another heart attack. Heparin increases the chance of suffering from minor bleeding.
ManagementMain article: Myocardial Infarction Management
An MI is a medical emergency which requires immediate medical attention. Treatment attempts to salvage as much myocardium as possible & to prevent further complications, thus the phrase “time is muscle”. Oxygen, aspirin, & nitroglycerin may be administered. Morphine was classically used if nitroglycerin wasn’t effective. It may increase mortality in setting of NSTEMI. A 2009 & 2010 review of high flow oxygen in myocardial infarction found increased mortality & infarct size, calling into question recommendation about its routine use. Other analgesics nitrous oxide are of unknown benefit. Percutaneous coronary intervention (PCI) or fibrinolysis are recommended in those with an STEMI.
Prognosis: Prognosis post myocardial infarction varies greatly, depending on a person’s health, extent of heart damage & treatment given. For period 2005′”2008 in US 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 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%.
The more reproduced risk stratifying factors include: age, hemodynamic parameters 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 & 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 occur. Morbidity and mortality from myocardial infarction has improved over the years due to better treatment.
ComplicationsMain article: Myocardial infarction complications
Complications may occur immediately following the heart attack (in the acute phase), or may need time to develop (a chronicproblem). Acute complications may include heart failure if damaged heart is no longer able to adequately pump blood around body; aneurysm or rupture of myocardium; mitral regurgitation, particularly if infarction causes dysfunction of papillary muscle; & arrhythmias: ventricular fibrillation, ventricular tachycardia, atrial fibrillation & heart block. Longer-term complications include heart failure, atrial fibrillation, & increased risk of second myocardial infarction.
EpidemiologyMyocardial infarction is a common presentation of ischemic heart disease. The WHO estimated in 2002, that 12.6 percent of worldwide deaths were from ischemic heart disease with it the leading cause of death in developed countries, and third to AIDS & lower respiratory infections in developing countries. Worldwide more than 3 million people have STEMIs and 4 million have NSTEMIs a year.
Coronary heart disease is responsible for 1 in 5 deaths in US. It’s becoming more common in developing world: India, cardiovascular disease (CVD) is leading cause of death. The deaths due to CVD in India were 32% of all deaths in 2007 & are expected to rise from 1.17 million in 1990 and 1.59 million in 2000 to 2.03 million in 2010. 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. 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. 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).
Legal implicationsAt 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; however, it may be a work-related injury if it results, for example, from unusual emotional stress or unusual exertion. In some jurisdictions, heart attacks suffered by persons in particular occupations: 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 or flying an airplane.