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"Heart attack" redirects here. For other uses, see Heart attack (disambiguation).
| Myocardial infarction Classification & external resources | |
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| 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 | I21.-I22. |
| ICD-9 | 410 |
| DiseasesDB | 8664 |
| MedlinePlus | 000195 |
| eMedicine | med/1567 emerg/327 ped/2520 |
Acute myocardial infarction (AMI or MI), more commonly known as a heart attack, is a medical condition that occurs when the blood supply to a part of the heart is interrupted, most commonly due to rupture of a vulnerable plaque. The resulting ischemia or oxygen shortage causes damage and potential death of heart tissue. It is a medical emergency, and the leading cause of death for both men and women all over the world. (2004) The World Health Report 2004 - Changing History (PDF), World Health Organization, 120-4. ISBN 92-4-156265-X. Important risk factors are a history of vascular disease such as atherosclerotic coronary heart disease and/or angina, a previous heart attack or stroke, any previous episodes of abnormal heart rhythms or syncope, older age—especially men over 40 and women over 50, smoking, excessive alcohol consumption, the abuse of certain drugs, high triglyceride levels, high LDL (low-density lipoprotein, "bad cholesterol") and low HDL (high density lipoprotein, "good cholesterol"), diabetes, high blood pressure, obesity, and chronically high levels of stress. Chronic kidney diseaseBax L, Algra A, Mali WP, Edlinger M, Beutler JJ, van der Graaf Y (2008). "Renal function as a risk indicator for cardiovascular events in 3216 patients with manifest arterial disease". Atherosclerosis. doi:10.1016/j.atherosclerosis.2007.12.006. PMID 18241872. and a history of heart failurePearte CA, Furberg CD, O\'Meara ES, et al (2006). "Characteristics and baseline clinical predictors of future fatal versus nonfatal coronary heart disease events in older adults: the Cardiovascular Health Study". Circulation 113 (18): 2177–85. doi:10.1161/CIRCULATIONAHA.105.610352. PMID 16651468. are also significant risk factors which may also predict fatality from MI.
The term myocardial infarction is derived from myocardium (the heart muscle) and infarction (tissue death due to oxygen starvation). 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.
Classical symptoms of acute myocardial infarction include 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). Patients frequently feel suddenly ill. Women often experience different symptoms from men. The most common symptoms of MI in women include shortness of breath, weakness, and fatigue. Approximately one third of all myocardial infarctions are silent, without chest pain or other symptoms. A history of diabetes should heighten the index of suspicion, particularly if the patient has diabetic neuropathy (diabetes-related nerve damage).
Immediate treatment for suspected acute myocardial infarction includes oxygen, aspirin, and sublingual glyceryl trinitrate (colloquially referred to as nitroglycerin and abbreviated as NTG). Pain relief is also often given, classically morphine sulfate.Erhardt L, Herlitz J, Bossaert L, et al (2002). "Task force on the management of chest pain" (PDF). Eur. Heart J. 23 (15): 1153–76. doi:10.1053/euhj.2002.3194. PMID 12206127.
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 the creatine kinase-MB (CK-MB) fraction or in troponin I (TnI) or troponin T (TnT) levels (these are chemical markers specific to the myocardium and are often referred to as cardiac markers). 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 performed by a cardiothoracic surgeon is an option. Once admitted to hospital, the patient is observed on a coronary care unit, as the incidence of sustained ventricular tachycardia or ventricular fibrillation in the case of MI is high. In cases where the patient is unstable, more intensive nursing care may be warranted.
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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. Ischemic heart disease is the leading cause of death in developed countries, but third to AIDS and lower respiratory infections in developing countries.Cause of Death - UC Atlas of Global Inequality. Center for Global, International and Regional Studies (CGIRS) at the University of California Santa Cruz. Retrieved on December 7, 2006.
In the United States, diseases of the heart are the leading cause of death, causing a higher mortality than cancer (malignant neoplasms).Deaths and percentage of total death for the 10 leading causes of death: United States, 2002-2003 (PDF). National Center of Health Statistics. Retrieved on April 17, 2007. 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.Heart Attack and Angina Statistics. American Heart Association (2003). Retrieved on December 7, 2006. 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.Mukherjee AK. (1995). "Prediction of coronary heart disease using risk factor categories.". J Indian Med Assoc. PMID 8713248. 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.Ghaffar A, Reddy KS and Singhi M (2004). "Burden of non-communicable diseases in South Asia." (PDF). BMJ 328: 807-810. 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.Rastogi T, Vaz M, Spiegelman D, Reddy KS, Bharathi AV, Stampfer MJ, Willett WC and Ascherio1 A (2004). "Physical activity and risk of coronary heart disease in India." (PDF). Int. J. Epidemiol 33: 1-9. Gupta R. (2007). "Escalating Coronary Heart Disease and Risk Factors in South Asians." (PDF). Indian Heart Journal: 214-17. 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.Gupta R, Misra A, Pais P, Rastogi P and Gupta VP. (2006). "Correlation of regional cardiovascular disease mortality in India with lifestyle and nutritional factors." (PDF). International Journal of Cardiology 108 (3): 291-300. doi:10.1016/j.ijcard.2005.05.044. 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).Rastogi T, Vaz M, Spiegelman D, Reddy KS, Bharathi AV, Stampfer MJ, Willett WC and Ascherio1 A (2004). "Physical activity and risk of coronary heart disease in India." (PDF). Int. J. Epidemiol 33: 1-9. CVD also affects Indians at a younger age (in their 30s and 40s) than is typical in other countries.
Risk factors for atherosclerosis are generally risk factors for myocardial infarction:
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.Jensen G, Nyboe J, Appleyard M, Schnohr P. (1991). "Risk factors for acute myocardial infarction in Copenhagen, II: Smoking, alcohol intake, physical activity, obesity, oral contraception, diabetes, lipids, and blood pressure.". Eur Heart J 12 (3): 298-308. PMID 2040311. 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.
Socioeconomic factors such as a shorter education and lower income (particularly in women), and living with a partner may also contribute to the risk of MI.Nyboe J, Jensen G, Appleyard M, Schnohr P. (1989). "Risk factors for acute myocardial infarction in Copenhagen. I: Hereditary, educational and socioeconomic factors. Copenhagen City Heart Study.". Eur Heart J 10 (10): 910-6. PMID 2598948. 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.
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.Khader YS, Rice J, John L, Abueita O. (2003). "Oral contraceptives use and the risk of myocardial infarction: a meta-analysis.". Contraception 68 (1): 11-7. PMID 12878281.
Inflammation is known to be an important step in the process of atherosclerotic plaque formation.Wilson AM, Ryan MC, Boyle AJ. (2006). "The novel role of C-reactive protein in cardiovascular disease: risk marker or pathogen.". Int J Cardiol 106 (3): 291-7. PMID 16337036. 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.Pearson TA, Mensah GA, Alexander RW, Anderson JL, Cannon RO 3rd, Criqui M, Fadl YY, Fortmann SP, Hong Y, Myers GL, Rifai N, Smith SC Jr, Taubert K, Tracy RP, Vinicor F; Centers for Disease Control and Prevention; American Heart Association. (2003). "Markers of inflammation and cardiovascular disease: application to clinical and public health practice: A statement for healthcare professionals from the Centers for Disease Control and Prevention and the American Heart Association." (PDF). Circulation 107 (3): 499-511. PMID 12551878. Whether CRP plays a direct role in atherosclerosis remains uncertain.
Inflammation in periodontal disease may be linked coronary heart disease, and since periodontitis is very common, this could have great consequences for public health.Janket SJ, Baird AE, Chuang SK, Jones JA. (2003). "Meta-analysis of periodontal disease and risk of coronary heart disease and stroke.". Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 95 (5): 559-69. PMID 12738947. Serological studies measuring antibody levels against typical periodontitis-causing bacteria found that such antibodies were more present in subjects with coronary heart disease.Pihlstrom BL, Michalowicz BS, Johnson NW. (2005). "Periodontal diseases.". Lancet 366 (9499): 1809-20. PMID 16298220. Periodontitis tends to increase blood levels of CRP, fibrinogen and cytokines;Scannapieco FA, Bush RB, Paju S. (2003). "Associations between periodontal disease and risk for atherosclerosis, cardiovascular disease, and stroke. A systematic review.". Ann Periodontol 8 (1): 38-53. PMID 14971247. thus, periodontitis may mediate its effect on MI risk via other risk factors.D\'Aiuto F, Parkar M, Nibali L, Suvan J, Lessem J, Tonetti MS. (2006). "Periodontal infections cause changes in traditional and novel cardiovascular risk factors: results from a randomized controlled clinical trial.". Am Heart J 151 (5): 977-84. PMID 16644317. Preclinical research suggests that periodontal bacteria can promote aggregation of platelets and promote the formation of foam cells.Lourbakos A, Yuan YP, Jenkins AL, Travis J, Andrade-Gordon P, Santulli R, Potempa J, Pike RN. (2001). "Activation of protease-activated receptors by gingipains from Porphyromonas gingivalis leads to platelet aggregation: a new trait in microbial pathogenicity." (PDF). Blood 97 (12): 3790-7. PMID 11389018. Qi M, Miyakawa H, Kuramitsu HK. (2003). "Porphyromonas gingivalis induces murine macrophage foam cell formation.". Microb Pathog 35 (6): 259-67. PMID 14580389. A role for specific periodontal bacteria has been suggested but remains to be established.Spahr A, Klein E, Khuseyinova N, Boeckh C, Muche R, Kunze M, Rothenbacher D, Pezeshki G, Hoffmeister A, Koenig W. (2006). "Periodontal infections and coronary heart disease: role of periodontal bacteria and importance of total pathogen burden in the Coronary Event and Periodontal Disease (CORODONT) study.". Arch Intern Med 166 (5): 554-9. PMID 16534043.
Baldness, hair greying, a diagonal earlobe creaseLichstein E, Chadda KD, Naik D, Gupta PK. (1974). "Diagonal ear-lobe crease: prevalence and implications as a coronary risk factor.". N Engl J Med 290 (11): 615-6. PMID 4812503. and possibly other skin features are independent risk factors for MI. Their role remains controversial; a common denominator of these signs and the risk of MI is supposed, possibly genetic.Miric D, Fabijanic D, Giunio L, Eterovic D, Culic V, Bozic I, Hozo I. (1998). "Dermatological indicators of coronary risk: a case-control study.". Int J Cardiol 67 (3): 251-5. PMID 9894707.
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.
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.Krijnen PA, Nijmeijer R, Meijer CJ, Visser CA, Hack CE, Niessen HW. (2002). "Apoptosis in myocardial ischaemia and infarction.". J Clin Pathol 55 (11): 801-11. PMID 12401816. 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.
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.Wilson PW, D\'Agostino RB, Levy D, Belanger AM, Silbershatz H, Kannel WB. "Prediction of coronary heart disease using risk factor categories". Circulation 1998; 97(18): 1837-47. PMID 9603539 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.Wilson PW, D\'Agostino RB, Levy D, Belanger AM, Silbershatz H, Kannel WB. "Prediction of coronary heart disease using risk factor categories". Circulation 1998; 97(18): 1837-47. PMID 9603539 For those in poor physical condition, the rate differential is over 35-fold higher.Wilson PW, D\'Agostino RB, Levy D, Belanger AM, Silbershatz H, Kannel WB. "Prediction of coronary heart disease using risk factor categories". Circulation 1998; 97(18): 1837-47. PMID 9603539 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.Wilson PW, D\'Agostino RB, Levy D, Belanger AM, Silbershatz H, Kannel WB. "Prediction of coronary heart disease using risk factor categories". Circulation 1998; 97(18): 1837-47. PMID 9603539
Acute severe infection, such as pneumonia, can trigger myocardial infarction. A more controversial link is that between Chlamydophila pneumoniae infection and atherosclerosis.Saikku P, Leinonen M, Tenkanen L, Linnanmaki E, Ekman MR, Manninen V, Manttari M, Frick MH, Huttunen JK. (1992). "Chronic Chlamydia pneumoniae infection as a risk factor for coronary heart disease in the Helsinki Heart Study.". Ann Intern Med 116 (4): 273-8. PMID 1733381. While this intracellular organism has been demonstrated in atherosclerotic plaques, evidence is inconclusive as to whether it can be considered a causative factor.Saikku P, Leinonen M, Tenkanen L, Linnanmaki E, Ekman MR, Manninen V, Manttari M, Frick MH, Huttunen JK. (1992). "Chronic Chlamydia pneumoniae infection as a risk factor for coronary heart disease in the Helsinki Heart Study.". Ann Intern Med 116 (4): 273-8. PMID 1733381. Treatment with antibiotics in patients with proven atherosclerosis has not demonstrated a decreased risk of heart attacks or other coronary vascular diseases.Andraws R, Berger JS, Brown DL. (2005). "Effects of antibiotic therapy on outcomes of patients with coronary artery disease: a meta-analysis of randomized controlled trials.". JAMA 293 (21): 2641-7. PMID 15928286.
There is an association of an increased incidence of MI in the morning hoursMuller JE, Stone PH, Turi ZG, et al (1985). "Circadian variation in the frequency of onset of acute myocardial infarction". N. Engl. J. Med. 313 (21): 1315–22. PMID 2865677. Beamer AD, Lee TH, Cook EF, et al (1987). "Diagnostic implications for myocardial ischemia of the circadian variation of the onset of chest pain". Am. J. Cardiol. 60 (13): 998–1002. PMID 3673917. Cannon CP, McCabe CH, Stone PH, et al (1997). "Circadian variation in the onset of unstable angina and non-Q-wave acute myocardial infarction (the TIMI III Registry and TIMI IIIB)". Am. J. Cardiol. 79 (3): 253–8. PMID 9036740. . Some investigators have noticed that the ability of platelets to aggregate varies according to a circadian rhythm, although they have not proven causation.Tofler GH, Brezinski D, Schafer AI, et al (1987). "Concurrent morning increase in platelet aggregability and the risk of myocardial infarction and sudden cardiac death". N. Engl. J. Med. 316 (24): 1514–8. PMID 3587281. 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.Fantidis P, Perez De Prada T, Fernandez-Ortiz A, et al (2002). "Morning cortisol production in coronary heart disease patients". Eur. J. Clin. Invest. 32 (5): 304–8. PMID 12027868.
Classification of acute coronary syndromes.Alpert JS, Thygesen K, Antman E, Bassand JP. (2000). "Myocardial infarction redefined--a consensus document of The Joint European Society of Cardiology/American College of Cardiology Committee for the redefinition of myocardial infarction.". J Am Coll Cardiol 36 (3): 959-69. PMID 10987628.
Acute myocardial infarction is a type of acute coronary syndrome, which is most frequently (but not always) a manifestation of coronary artery disease. The acute coronary syndromes include ST segment elevation myocardial infarction (STEMI), non-ST segment elevation myocardial infarction (NSTEMI), and unstable angina (UA).
Depending on the location of the obstruction in the coronary circulation, different zones of the heart can become injured. Using the anatomical terms of location corresponding to areas perfused by major coronary arteries, one can describe anterior, inferior, lateral, apical, septal, posterior, and right-ventricular infarctions (and combinations, such as anteroinferior, anterolateral, and so on).Dorland\'s Illustrated Medical Dictionary. WB Saunders, an Elsevier imprint. Retrieved on November 25, 2006. For example, an occlusion of the left anterior descending coronary artery(LAD) will result in an anterior wall myocardial infarct. (2001) Rubin\'s Pathology - Clinicopathological Foundations of Medicine. Maryland: Lippincott Williams & Wilkins, 525. ISBN 0-7817-4733-3. Infarcts of the lateral wall are caused by occlusion of the left circumflex coronary artery(LCx) or its oblique marginal branches (or even large diagonal branches from the LAD.) Both inferior wall and posterior wall infarctions may be caused by occlusion of either the right coronary artery or the left circumflex artery, depending on which feeds the posterior descending artery. Right ventricular wall infarcts are also caused by right coronary artery occlusion.
Another distinction is whether a MI is subendocardial, affecting only the inner third to one half of the heart muscle, or transmural, damaging (almost) the entire wall of the heart. (2001) Rubin\'s Pathology - Clinicopathological Foundations of Medicine. Maryland: Lippincott Williams & Wilkins, p. 545. ISBN 0-7817-4733-3. The inner part of the heart muscle is more vulnerable to oxygen shortage, because the coronary arteries run inward from the epicardium to the endocardium, and because the blood flow through the heart muscle is hindered by the heart contraction.
The phrases transmural and subendocardial infarction were previously considered synonymous with Q-wave and non-Q-wave myocardial infarction respectively, based on the presence or absence of Q waves on the ECG. It has since been shown that there is no clear correlation between the presence of Q waves with a transmural infarction and the absence of Q waves with a subendocardial infarction,Moon JC, De Arenaza DP, Elkington AG, Taneja AK, John AS, Wang D, Janardhanan R, Senior R, Lahiri A, Poole-Wilson PA, Pennell DJ. (2004). "The pathologic basis of Q-wave and non-Q-wave myocardial infarction: a cardiovascular magnetic resonance study.". J Am Coll Cardiol 44 (3): 554-60. PMID 15358019. but Q waves are associated with larger infarctions, while the lack of Q waves is associated with smaller infarctions. The presence or absence of Q-waves also has clinical importance,Yang H, Pu M, Rodriguez D, Underwood D, Griffin BP, Kalahasti V, Thomas JD, Brunken RC (2004). "Ischemic and viable myocardium in patients with non-Q-wave or Q-wave myocardial infarction and left ventricular dysfunction: a clinical study using positron emission tomography, echocardiography, and electrocardiography.". J Am Coll Cardiol 43 (4): 592-8. PMID 14975469. with improved outcomes associated with a lack of Q waves.Goodman SG, Langer A, Ross AM, Wildermann NM, Barbagelata A, Sgarbossa EB, Wagner GS, Granger CB, Califf RM, Topol EJ, Simoons ML, Armstrong PW. (1998). "Non-Q-wave versus Q-wave myocardial infarction after thrombolytic therapy: angiographic and prognostic insights from the global utilization of streptokinase and tissue plasminogen activator for occluded coronary arteries-I angiographic substudy. GUSTO-I Angiographic Investigators.". Circulation 97 (5): 444-50. PMID 9490238.
The phrase "massive attack" is not a recognized medical term.
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.National Heart, Lung and Blood Institute. Heart Attack Warning Signs. Retrieved November 22, 2006. 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 his chest pain by clenching his 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.Marcus GM, Cohen J, Varosy PD, et al (2007). "The utility of gestures in patients with chest discomfort". Am. J. Med. 120 (1): 83–9. doi:10.1016/j.amjmed.2006.05.045. PMID 17208083.
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 systemLittle RA, Frayn KN, Randall PE, et al (1986). "Plasma catecholamines in the acute phase of the response to myocardial infarction". Arch Emerg Med 3 (1): 20–7. PMID 3524599. 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 often experience markedly different symptoms than men. 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.McSweeney JC, Cody M, O\'Sullivan P, Elberson K, Moser DK, Garvin BJ (2003). "Women\'s early warning symptoms of acute myocardial infarction". Circulation 108 (21): 2619-23. PMID 14597589.
Approximately half of all MI patients have experienced warning symptoms such as chest pain prior to the infarction.D Lee, D Kulick, J Marks. Heart Attack (Myocardial Infarction) by MedicineNet.com . Retrieved November 28, 2006.
Approximately one fourth of all myocardial infarctions are silent, without chest pain or other symptoms.Kannel WB. (1986). "Silent myocardial ischemia and infarction: insights from the Framingham Study.". Cardiol Clin 4 (4): 583-91. PMID 3779719. 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 mellitusDavis TM, Fortun P, Mulder J, Davis WA, Bruce DG (2004). "Silent myocardial infarction and its prognosis in a community-based cohort of Type 2 diabetic patients: the Fremantle Diabetes Study". Diabetologia 47 (3): 395-9. PMID 14963648. and after heart transplantation, probably because the donor heart is not connected to nerves of the host. (2001) Rubin\'s Pathology - Clinicopathological Foundations of Medicine. Maryland: Lippincott Williams & Wilkins, p. 549. ISBN 0-7817-4733-3. In diabetics, 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.Acute Coronary Syndrome. American Heart Association. Retrieved November 25, 2006.
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.Boie ET (2005). "Initial evaluation of chest pain". Emerg. Med. Clin. North Am. 23 (4): 937–57. doi:10.1016/j.emc.2005.07.007. PMID 16199332.
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).Myocardial infarction: diagnosis and investigations - GPnotebook, retrieved November 27, 2006. 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.DE Fenton et al. Myocardial infarction - eMedicine, retrieved November 27, 2006. 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.HEART SCAN - Patient information from University College London. Retrieved November 27, 2006. 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.Skoufis E, McGhie AI (1998). "Radionuclide techniques for the assessment of myocardial viability". Tex Heart Inst J 25 (4): 272–9. PMID 9885104.
WHO criteriaGillum RF, Fortmann SP, Prineas RJ, Kottke TE. International diagnostic criteria for acute myocardial infarction and acute stroke. Am Heart J 1984;108:150-8. PMID 6731265 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:
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.
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.S. Garas et al.. Myocardial Infarction. eMedicine. Retrieved November 22, 2006.Kasper DL, Braunwald E, Fauci AS, Hauser SL, Longo DL, Jameson JL. Harrison\'s Principles of Internal Medicine. p. 1444. New York: McGraw-Hill, 2005. ISBN 0-07-139140-1.
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.Kasper DL, et al. Harrison\'s Principles of Internal Medicine. p. 1450.
12-lead electrocardiogram (ECG) showing acute inferior ST segment elevation MI (STEMI). Note the ST segment elevation in leads II, III, and aVF along with reciprocal ST segment depression in leads I and aVL.
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.Cannon CP at al. Management of Acute Coronary Syndromes. p. 175. New Jersey: Humana Press, 1999. ISBN 0-89603-552-2. 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.Selker HP, Zalenski RJ, Antman EM, et al. "An evaluation of technologies for identifying acute cardiac ischemia in the emergency department: executive summary of a National Heart Attack Alert Program Working Group Report." Ann Emerg Med 1997; 29(1): 25-28. PMID 8998085 It should also be appreciated that the standard 12 lead ECG does not directly examine the right ventricle, and does a relatively poor job of 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. 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.Masoudi FA, Magid DJ, Vinson DR et al."Implications of the Failure to Identify High-Risk Electrocardiogram Findings for the Quality of Care of Patients With Acute Myocardial Infarction." Circulation 2006; 114: 1565-1571. The 12 lead ECG is used to classify patients into one of three groups:
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.Somers MP, Brady WJ, Perron AD, Mattu A. "The prominent T wave: electrocardiographic differential diagnosis." Am J Emerg Med 2002; 20(3): 243-51. PMID 11992348 In practice this is rarely seen, because it only exists for 2-30 minutes after the onset of infarction.Smith SW, Whitwam W. "Acute Coronary Syndromes." Emerg Med Clin N Am 2006; 24(1): 53-89. PMID 16308113 Hyperacute T waves need to be distinguished from the peaked T waves associated with hyperkalemia."The clinical value of the ECG in noncardiac conditions." Chest 2004; 125(4): 1561-76. PMID 15078775 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. (I, aVL, V5, V6 correspond to the lateral wall; V1-V4 correspond to the anterior wall; II, III, aVF corrrespond 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.Brady WJ, Perron AD, Martin ML, Beagle C, Aufderheide TP. "Cause of ST segment abnormality in ED chest pain patients." Am J Emerg Med 2001; 19(1): 25-8. PMID 11146012 Over 90% of healthy men have at least 1 mm (0.1 mV) of ST segment elevation in at least one precordial lead.Wang K, Asinger RW, Marriott HJ. "ST-segment elevation in conditions other than acute myocardial infarction." New Engl J Med 2003; 349(22): 2128-35. PMID 14645641 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, benign early repolarization, pericarditis, hyperkalemia, and ventricular aneurysm.Brady WJ, Chan TC, Pollack M. "Electrocardiographic manifestations: patterns that confound the EKG diagnosis of acute myocardial infarction-left bundle branch block, ventricular paced rhythm, and left ventricular hypertrophy." J Emerg Med 2000; 18(1): 71-8. PMID 10645842"Electrocardiographic ST-segment elevation: correct identification of acute myocardial infarction (AMI) and non-AMI syndromes by emergency physicians." Acad Emerg Med 2001; 8(4): 349-60. PMID 11282670"ST-segment elevation in conditions other than acute myocardial infarction." New Engl J Med 2003; 349(22): 2128-35. PMID 14645641
Left bundle branch block and pacing interferes with the electrocardiographic diagnosis of acute myocadial infarction by making the ST segment uninterpretable. The GUSTO investigators Sgarbossa et al. developed a set of criteria for identifying acute myocardial infarction in the presence of left bundle branch block and paced rhythm. They include concordant ST segment elevation > 1 mm (0.1 mV), discordant ST segment elevation > 5 mm (0.5 mV), and concordant ST segment depression in the left precordial leads.Sgarbossa EB, Pinski SL, Barbagelata A, Underwood DA, Gates KB, Topol EJ, Califf RM, Wagner GS. "Electrocardiographic diagnosis of evolving acute myocardial infarction in the presence of left bundle branch block." N Engl J Med 1996; 334 (8): 481-7. PMID 8559200 The presence of reciprocal changes on the 12 lead ECG may help distinguish true acute myocardial infarction from the mimics of acute myocardial infarction. The contour of the ST segment may also be helpful, with a straight or upwardly convex (non-concave) ST segment favoring the diagnosis of acute myocardial infarction."Electrocardiographic ST-segment elevation: the diagnosis of acute myocardial infarction by morphologic analysis of the ST segment." Acad Emerg Med 2001; 8(10): 961-7. PMID 11581081
The constellation of leads with ST segment elevation enables the clinician to identify what area of the heart is injured, which in turn helps predict the so-called culprit artery.
| Wall Affected | Leads Showing ST Segment Elevation | Leads Showing Reciprocal ST Segment Depression | Suspected Culprit Artery |
|---|---|---|---|
| Septal | V1, V2 | None | Left Anterior Descending (LAD) |
| Anterior | V3, V4 | None | Left Anterior Descending (LAD) |
| Anteroseptal | V1, V2, V3 |
