Myocardial Infarction 

  • Author: A Maziar Zafari, MD, PhD; Chief Editor: Eric H Yang, MD   more...
 
Updated: Jan 9, 2012
 

Background

Myocardial infarction, commonly known as a heart attack, is the irreversible necrosis of heart muscle secondary to prolonged ischemia. This usually results from an imbalance in oxygen supply and demand, which is most often caused by plaque rupture with thrombus formation in a coronary vessel, resulting in an acute reduction of blood supply to a portion of the myocardium. The electrocardiographic result of an acute myocardial infarction is seen below. (See Etiology.)

The electrocardiogram shows lateral ST-segment eleThe electrocardiogram shows lateral ST-segment elevation that is consistent with a lateral wall acute myocardial infarction.

Although the clinical presentation of a patient is a key component in the overall evaluation of the patient with myocardial infarction, many events are either "silent" or are clinically unrecognized, evidencing that patients, families, and health care providers often do not recognize symptoms of a myocardial infarction. (See Clinical Presentation.) The appearance of cardiac markers in the circulation generally indicates myocardial necrosis and is a useful adjunct to diagnosis. (See Workup.)

Myocardial infarction is considered part of a spectrum referred to as acute coronary syndrome (ACS). The ACS continuum representing ongoing myocardial ischemia or injury consists of unstable angina, non–ST-segment elevation myocardial infarction (NSTEMI), and ST-segment elevation myocardial infarction (STEMI). Patients with ischemic discomfort may or may not have ST-segment or T-wave changes denoted on the electrocardiogram (ECG). ST elevations seen on the ECG reflect active and ongoing transmural myocardial injury. Without immediate reperfusion therapy, most persons with STEMI develop Q waves, reflecting a dead zone of myocardium that has undergone irreversible damage and death. Those without ST elevations are diagnosed either with unstable angina or NSTEMI―differentiated by the presence of cardiac enzymes. Both these conditions may or may not have changes on the surface ECG, including ST-segment depression or T-wave morphological changes.

Myocardial infarction may lead to impairment of systolic or diastolic function and to increased predisposition to arrhythmias and other long-term complications.

Coronary thrombolysis and mechanical revascularization have revolutionized the primary treatment of acute myocardial infarction, largely because they allow salvage of the myocardium when implemented early after the onset of ischemia. (See Treatment Strategies and Management.) The modest prognostic benefit of an opened infarct-related artery may be realized even when recanalization is induced only 6 hours or more after the onset of symptoms, that is, when the salvaging of substantial amounts of jeopardized ischemic myocardium is no longer likely. The opening of an infarct-related artery may improve ventricular function, collateral blood flow, and ventricular remodeling, and it may decrease infarct expansion, ventricular aneurysm formation, left ventricular dilatation, late arrhythmia associated with ventricular aneurysms, and mortality.[1, 2, 3, 4, 5]

Evidence suggests a benefit from the use of beta-blockers, angiotensin-converting enzyme (ACE) inhibitors, angiotensin II receptor blockers, and statins.

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Anatomy

The right and left coronary arteries most often arise independently from individual ostia in association with the right and left aortic valve cusps.

The left anterior descending (LAD) and left circumflex (LCX) coronary arteries arise at the left main coronary artery bifurcation; they supply the anterior LV, the bulk of the interventricular septum (anterior two thirds), the apex, and the lateral and posterior LV walls. The right coronary artery (RCA) generally supplies the right ventricle (RV), the posterior third of the interventricular septum, the inferior wall (diaphragmatic surface) of the left ventricle (LV), and a portion of the posterior wall of the LV (by means of the posterior descending branch).

When the posterior descending coronary artery (PDA), which supplies the posterior interventricular septum, arises from the LCX artery, the circulation is called left dominant. Most often, the PDA arises from the RCA; this anatomy is called right-dominant circulation.

In two thirds of patients, the first branch of the RCA is the conus artery, which supplies the conus arteriosus (RV outflow tract); occasionally the conus arteriosus arises from a separate orifice.

In 60% of patients, the sinus node artery arises from the proximal RCA, and in 40% of patients, it arises from the LCX artery. The anterior branches supply the free wall of the RV, and the acute marginal branches supply the RV. When the RCA extends to the crux (the origin of the PDA), it supplies the atrioventricular (AV) node (90%); otherwise, the AV node is supplied by the LCX.

Therefore, obstruction of the RCA commonly affects the sinus node and the AV node, resulting in bradycardia, with or without heart block. Not surprisingly, RCA occlusion frequently manifests with sinus bradycardia, AV block, RV myocardial infarction, and/or inferoposterior myocardial infarction (of the LV). (See Etiology.)

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Pathophysiology

The spectrum of myocardial injury depends not only on the intensity of impaired myocardial perfusion but also on the duration and the level of metabolic demand at the time of the event. The damage in the myocardium is essentially the result of a tissue response that includes apoptosis (cell death) and inflammatory changes. Therefore, the hearts of patients who suddenly die from an acute coronary event may show little or no evidence of damage response to the myocardium at autopsy.

The typical myocardial infarction initially manifests as coagulation necrosis that is ultimately followed by myocardial fibrosis. Contraction-band necrosis is also seen in many patients with ischemia. This is followed by reperfusion, or it is accompanied by massive adrenergic stimulation, often with concomitant myocytolysis.

The left coronary artery system covers more territory than does the right system; therefore, a myocardial infarction in this system is most likely to produce extensive injury, with impairment of function, pulmonary congestion, and low output. Occlusion of the left coronary artery may also cause a left anterior hemiblock or a left posterosuperior hemiblock conduction abnormality; these effects are evidenced by a change of frontal axis on the electrocardiogram (ECG). (See Electrocardiogram.)

Inferior-wall myocardial infarction and right ventricular myocardial infarction

In severe cases of acute inferior-wall myocardial infarction with RV involvement, the forward delivery of blood from the RV to the LV may be insufficient to fill the LV, resulting in low blood pressure even if the LV is intact. (See Physical Examination.)

Chemoreceptor activation in the myocardium actuates vagal (parasympathetic) efferent discharge, known as the Bezold-Jarisch reflex, which causes bradycardia and vessel dilation that may further lower blood pressure. Adenosine may accumulate in the infarct zone secondary to a local inhibition of adenosine deaminase, for which aminophylline may act pharmacologically as an antagonist. The hemodynamic changes resemble many of those seen with pericardial constriction or tamponade. Patients with this condition respond well to an infusion of normal sodium chloride solution. Improvement with such infusion compensates for failure of the pumping action of the RV; it reduces vagal tone, and it deactivates the pressure sensors that were sending a hormonal signal to the kidneys to retain salt.

Arrhythmogenesis

In addition to the direct effects of ischemia and tissue hypoxia, decreased removal of noxious metabolites, including potassium, calcium, amphophilic lipids, and oxygen-centered free radicals, also impair ventricular performance. These abnormalities promote potentially lethal arrhythmias.

Pericarditis

Epicardial inflammation may initiate pericarditis, which is seen in more than 20% of patients presenting with Q-wave infarctions.

Reduced systolic function

Lack of adequate oxygen and insufficient metabolite delivery to the myocardium diminish the force of muscular contraction and decrease systolic wall motion in the affected territory.

Abnormal regional wall motion

Even brief deprivation of oxygen and the requisite metabolites to the myocardium diminishes diastolic relaxation and causes abnormal regional systolic contractile function, wall thickening, and abnormal wall motion. If the area affected is extensive, diminished stroke volume and cardiac output may result.

Hypokinesis and akinesis

In general, regions of hypokinesis and akinesis of the ventricular myocardium reflect the location and extent of myocardial injury. Evidence of hypokinesis is seen on the echocardiogram below.

Hypokinesis of the anteroseptal wall observed duriHypokinesis of the anteroseptal wall observed during echocardiography in a patient presenting with an acute anteroseptal myocardial infarction.

Myocardial infarction expansion

In general, expansion of infarcted myocardium and resultant ventricular dilatation (ie, ventricular remodeling) ensues within a few hours after the onset of a myocardial infarction. An expanding myocardial infarction leads to thinning of the infarct zone and realignment of layers of tissue in and adjacent to it, causing ventricular dilatation.

Myocardial rupture

Myocardial rupture was seen in as many as 10% of fatal myocardial infarctions before the era of thrombolytics, but it is now encountered much less often. When rupture occurs, it may be associated with large infarctions; indications include cardiogenic shock or hemodynamically significant arrhythmia. Patients may have a history of hypertension with ventricular hypertrophy.

Ventricular aneurysm

A ventricular aneurysm is an outward bulging of a noncontracting segment. In the early days of cardiac imaging, ventricular aneurysms were seen in as many as 20% of patients with Q-wave myocardial infarction, but now it is seen in less than 8%.

Cardiogenic shock

In patients with extensive myocardial injury, coronary blood flow diminishes as cardiac output declines and heart rate accelerates. Because coronary artery disease is usually generalized or diffuse, ischemia that occurs at a distance from the infracted segment may result in a vicious cycle in which a stuttering and expanding myocardial infarction ultimately leads to profound LV failure, hypotension, and cardiogenic shock.

Effect on diastolic function

Immediately after the onset of myocardial infarction, the ability of ischemic myocardium to relax declines. Relaxation is an active process that uses ATP. Impaired relaxation increases LV end-diastolic volume (LVEDV) and LV end-diastolic pressure (LVEDP).

The increased LVEDP results in ventricular dilation, increased pulmonary venous pressure, decreased pulmonary compliance, and interstitial and (ultimately) alveolar pulmonary edema. These effects lead to increased hypoxemia, which may worsen ischemic injury to the myocardium.

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Etiology

Atherosclerosis is the disease primarily responsible for most acute coronary syndrome (ACS) cases. Approximately 90% of myocardial infarctions result from an acute thrombus that obstructs an atherosclerotic coronary artery. Plaque rupture and erosion are considered to be the major triggers for coronary thrombosis. Following plaque erosion or rupture, platelet activation and aggregation, coagulation pathway activation, and endothelial vasoconstriction occur, leading to coronary thrombosis and occlusion.

Within the coronary vasculature, flow dynamics and endothelial shear stress are implicated in the pathogenesis of vulnerable plaque formation.[6] Evidence indicates that in numerous cases, culprit lesions are stenoses of less than 70% and are located proximally within the coronary tree.[7, 8] Coronary atherosclerosis is especially prominent near branching points of vessels.[9] Culprit lesions that are particularly prone to rupture are atheromas containing abundant macrophages, a large lipid-rich core surrounded by a thinned fibrous cap.

Nonmodifiable risk factors for atherosclerosis include the following:

  • Age
  • Sex
  • Family history of premature coronary heart disease
  • Male-pattern baldness
  • Modifiable risk factors for atherosclerosis include the following:
  • Smoking or other tobacco use
  • Diabetes mellitus
  • Hypertension
  • Hypercholesterolemia and hypertriglyceridemia, including inherited lipoprotein disorders
  • Dyslipidemia
  • Obesity
  • Sedentary lifestyle and/or lack of exercise
  • Psychosocial stress
  • Poor oral hygiene
  • Type A personality

Elevated homocysteine levels and the presence of peripheral vascular disease are also risk factors for atherosclerosis.

Intramural thrombus development

Inflammation of the endocardial surfaces and stasis of blood flow associated with regional akinesis (no wall motion) or dyskinesis (abnormal, passively reversed wall motion) may lead to the formation of ventricular mural thrombi, which have the potential to embolize.

Patients with acute myocardial infarction are prone to cerebrovascular injury as a result of emboli from ventricular mural thrombi; the rate is approximately 1%.

Causes of myocardial infarction other than atherosclerosis

Nonatherosclerotic causes of myocardial infarction include the following:

  • Coronary occlusion secondary to vasculitis
  • Ventricular hypertrophy (eg, left ventricular hypertrophy, idiopathic hypertrophic subaortic stenosis [IHSS], underlying valve disease)
  • Coronary artery emboli, secondary to cholesterol, air, or the products of sepsis
  • Congenital coronary anomalies
  • Coronary trauma
  • Primary coronary vasospasm (variant angina)
  • Drug use (eg, cocaine, amphetamines, ephedrine)
  • Arteritis
  • Coronary anomalies, including aneurysms of coronary arteries
  • Factors that increase oxygen requirement, such as heavy exertion, fever, or hyperthyroidism
  • Factors that decrease oxygen delivery, such as hypoxemia of severe anemia
  • Aortic dissection, with retrograde involvement of the coronary arteries
  • Infected cardiac valve through a patent foramen ovale (PFO)
  • Significant gastrointestinal bleed

In addition, myocardial infarction can result from hypoxia due to carbon monoxide poisoning or acute pulmonary disorders. Infarcts due to pulmonary disease usually occur when demand on the myocardium dramatically increases relative to the available blood supply.

Although rare, pediatric coronary artery disease may be seen with Marfan syndrome, Kawasaki disease, Takayasu arteritis, progeria, and cystic medial necrosis.

Imaging studies, such as contrast chest CT scans or transesophageal echocardiograms, should be used to differentiate myocardial infarction from aortic dissection in patients in whom the diagnosis is in doubt. Stanford type A aortic dissections may dissect in a retrograde fashion causing coronary blockage and dissection, which may result in myocardial infarction. In one study, 8% of patients with Stanford type A dissections had ST elevation on ECG. (See Echocardiography.)

Myocardial infarction induced by chest trauma has also been reported, usually following severe chest trauma such as motor vehicle accidents and sports injuries.

Acute myocardial infarction in childhood

Acute myocardial infarction is rare in childhood and adolescence (See Epidemiology). Although adults acquire coronary artery disease from lifelong deposition of atheroma and plaque, which causes coronary artery spasm and thrombosis, children with acute myocardial infarction usually have either an acute inflammatory condition of the coronary arteries or an anomalous origin of the left coronary artery. Intrauterine myocardial infarction also does occur, often in association with coronary artery stenosis.[10]

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Epidemiology

United States statistics – Incidence and mortality rate

Cardiovascular disease is the leading cause of death in the United States; approximately 500,000-700,000 deaths related to the coronary artery occur each year.

Approximately 1.5 million cases of myocardial infarction occur annually in the United States; the yearly incidence rate is approximately 600 cases per 100,000 people. The proportion of patients diagnosed with NSTEMI compared with STEMI has progressively increased. Despite an impressive decline in age-adjusted death rates attributable to acute myocardial infarction since the mid-1970s, the total number of myocardial infarction-related deaths in the United States has not declined. This may in part be the result of population growth.

Cardiovascular disease is the leading cause of morbidity and mortality among black, Hispanic, and white populations in the United States.

Cardiovascular disease in industrialized and developing nations

Ischemic heart disease is the leading cause of death worldwide.

Cardiovascular diseases cause 12 million deaths throughout the world each year, according to the third monitoring report of the World Health Organization, 1991-93. They cause half of all deaths in several industrialized countries and are one of the main causes of death in many developing countries; they are the major cause of death in adults everywhere. Of particular concern are projections from the World Heart Federation that the burden of atherosclerotic cardiovascular disease in developing countries will increasingly become commensurate with that seen in industrialized countries. With a decline in infectious disease-related deaths, in conjunction with accelerated economic development and life-style changes that promote atherosclerosis, rates of ischemic heart disease and myocardial infarction are expected to sharply increase in developing countries, especially such countries in Eastern Europe, Asia, and parts of Latin America.

Sex predilection in cardiovascular disease

A male predominance in the incidence of cardiovascular disease exists up to approximately age 70 years, when the sexes converge to equal incidence. Premenopausal women appear to be somewhat protected from atherosclerosis, possibly owing to the effects of estrogen.

Age predilection in cardiovascular disease

The incidence of cardiovascular disease increases with age, with acute myocardial infarction being rare in childhood and adolescence. Most patients who develop an acute myocardial infarction are older than 60 years. Elderly people also tend to have higher rates of morbidity and mortality from their infarcts. Age (≥75 y) is the strongest predictor of 90-day mortality in patients with STEMI undergoing percutaneous coronary intervention.[11] A continued focus on improving outcomes for these high-risk patients is needed.

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Prognosis

One third of patients who experience STEMI die within 24 hours of the onset of ischemia, and many of the survivors experience significant morbidity. However, a steady decline has occurred in the mortality rate from STEMI over the last several decades.

Acute myocardial infarction is associated with a 30% mortality rate; half of the deaths occur prior to arrival at the hospital. An additional 5-10% of survivors die within the first year after their myocardial infarction. Approximately half of all patients with a myocardial infarction are rehospitalized within 1 year of their index event.

In a study that assessed the impact of prehospital time on STEMI outcome, Chughatai et al suggest that "total time to treatment" should be used as a core measure instead of "door-to-balloon time."[12] This is because on-scene time was the biggest fraction of "prehospital time." The study compared groups with total time to treatment of more than 120 minutes compared with 120 minutes or less and found mortalities were 4 compared with 0 and transfers to a tertiary care facility were 3 compared with 1, respectively.

Overall, prognosis is highly variable and depends largely on the extent of the infarct, the residual left ventricular function, and whether the patient underwent revascularization.

Better prognosis is associated with the following factors:

  • Successful early reperfusion (STEMI goals: patient arrival to fibrinolysis infusion within 30 minutes OR patient arrival to percutaneous coronary intervention within 90 minutes)
  • Preserved left ventricular function
  • Short-term and long-term treatment with beta-blockers, aspirin, and ACE inhibitors

Poorer prognosis is associated with the following factors:

  • Increasing age
  • Diabetes
  • Previous vascular disease (ie, cerebrovascular disease or peripheral vascular disease)
  • Elevated Thrombolysis in Myocardial Infarction (TIMI) risk score for unstable angina/NSTEMI (7 factors: Age ≥65 y, ≥3 risk factors for cardiac disease, previous coronary disease, ST segment deviation ≥0.5 mm, ≥2 episodes of angina in last 24 h, aspirin use within prior wk, and elevated cardiac enzyme levels)[13]
  • Delayed or unsuccessful reperfusion
  • Poorly preserved left ventricular function (the strongest predictor of outcome)
  • Evidence of congestive heart failure (Killip classification ≥II)[14] or frank pulmonary edema (Killip classification ≥III)[15]
  • Elevated B-type natriuretic peptide (BNP) levels[16, 17, 18]
  • Elevated high sensitive C-reactive protein (hs-CRP), a nonspecific inflammatory marker[19]

Blood glucose

Beck et al found that elevated blood glucose level on admission is associated with increased short-term mortality in nondiabetic patients presenting with a first acute myocardial infarction. Analysis of data from a German myocardial infarction registry database showed that among 1,631 nondiabetic acute myocardial infarction patients with admission glucose level more than 152 mg/dL (top quartile), the risk of death within 28 days was higher than among patients in the bottom quartile (odds ratio, 2.82; 95% confidence interval, 1.30-6.12). However, in 659 registry patients with type 2 diabetes, admission glucose levels did not correlate significantly with short-term mortality. Beck et al concluded that nondiabetic acute myocardial infarction patients with elevated glucose levels constitute a high-risk group that requires aggressive intervention.[20]

Psychological depression

The combination of acute myocardial infarction and psychological depression appears to worsen the patient's prognosis. Acute myocardial infarction may precipitate reactive depression whether or not beta-adrenergic blocking agents or other CNS-active agents are administered.

Myocardial hibernation and stunning

After the occurrence of 1 or more ischemic insults, impaired wall motion is often transient (myocardial stunning) or prolonged (myocardial hibernation). These phenomena occur because of the loss of essential metabolites such as adenosine, which is needed for adenosine triphosphate (ATP)–dependent contraction. Hibernation, a persisting wall-motion abnormality that is curable with revascularization, must be differentiated from permanent, irreversible damage or completed infarct.

Scar tissue and prognosis

Scars involving less than one third of the thickness of the wall, as shown on contrast-enhanced MRI, likely correspond to a recovery of myocardial function, whereas with scars measuring more than one third the thickness of the wall, the potential for recovery with therapy is limited (except in cases involving research cell therapies or surgical scar revision). Other findings associated with recovery are activity on 2-[Fluorine 18]-fluoro-2-deoxy-D-glucose (FDG) positron emission tomography (PET) scanning and a monophasic or biphasic contractile response to dobutamine infusion, caused by the induction of ischemia. Cardiac scar tissue is seen in the image below.

Image shows a scar in the anterior wall. Image shows a scar in the anterior wall.
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Patient Education

As recommended by the most recent American College of Cardiology/American Heart Association (ACC/AHA) guidelines for the management of unstable angina/NSTEMI, last updated in 2007, patients with symptoms that suggest an acute coronary syndrome should be referred to a facility where a physician can evaluate these symptoms in person and where a 12-lead ECG and cardiac biomarker testing is available (eg, emergency department, acute care facility).

Patients with active symptoms of ACS should be instructed to call emergency services (eg, 911 in the United State) and should be brought in by emergency medical services personnel, not by themselves, family, or friends. Patients should be instructed to come to the emergency department immediately if the suspected ACS symptoms last longer than 20 minutes at rest or are associated with near syncope/syncope or hemodynamic instability.

If nitroglycerin is prescribed to a patient with suspected ACS, the patient should be instructed to take a dose if symptoms arise. If no relief is experienced 5 minutes after the first dose, the patient should contact emergency services. If relief is experienced within 5 minutes of the first nitroglycerin dose, repeated doses can be given every 5 minutes for a maximum of 3 doses total. If by then the symptoms have not yet fully resolved, the patient, a family member, or caregiver should contact emergency services.[21]

Diet plays an important role in the development of coronary artery disease. Educate post–myocardial infarction patients about the role of a low-cholesterol and low-salt diet. Educate patients about the American Heart Association (AHA) dietary guidelines, including a low-fat, low-cholesterol diet. A dietitian should see and evaluate all patients post myocardial infarction prior to their discharge. Additionally, emphasis on exercise training should be made because current evidence demonstrates that cardiac rehabilitation post myocardial infarction results in lower rates of recurrent cardiovascular events.[22]

Following myocardial infarction, educate all patients regarding the critical role of smoking in the development of coronary artery disease. Smoking cessation classes should be offered to help patients avoid smoking after their myocardial infarction.

For excellent patient education resources, visit eMedicine's Cholesterol Center. Also, see eMedicine's patient education articles High Cholesterol, Understanding Your Cholesterol level, Lifestyle Cholesterol Management, Understanding Cholesterol-Lowering Medications, Chest Pain, Coronary Heart Disease, and Heart Attack.

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Contributor Information and Disclosures
Author

A Maziar Zafari, MD, PhD  Professor, Department of Medicine, Emory University School of Medicine; Chief, Section of Cardiology, Atlanta Veterans Affairs Medical Center

A Maziar Zafari, MD, PhD is a member of the following medical societies: American Association for the Advancement of Science, American College of Cardiology, American Heart Association, American Society of Echocardiography, and Association of Professors of Medicine

Disclosure: Nothing to disclose.

Coauthor(s)

Luis C Afonso, MD  Assistant Professor, Department of Internal Medicine-Cardiology, Program Director of Cardiology Fellowship Program, Wayne State University; Director of Echocardiography Laboratory, Harper University Hospital

Luis C Afonso, MD is a member of the following medical societies: American College of Cardiology, American College of Physicians, American Medical Association, and American Society of Echocardiography

Disclosure: Nothing to disclose.

Kul Aggarwal, MD, FACC  Professor of Clinical Medicine, Department of Internal Medicine, Division of Cardiology, University of Missouri-Columbia School of Medicine; Chief, Cardiology Section, Harry S Truman Veterans Hospital

Kul Aggarwal, MD, FACC is a member of the following medical societies: American College of Cardiology and American College of Physicians

Disclosure: Nothing to disclose.

Edward Bessman, MD  Chairman, Department of Emergency Medicine, John Hopkins Bayview Medical Center; Assistant Professor, Department of Emergency Medicine, Johns Hopkins University School of Medicine

Edward Bessman, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

David L Coven, MD, PhD  Assistant Professor of Medicine, Columbia University College of Physicians and Surgeons; Attending Physician in Interventional Cardiology, St Luke's-Roosevelt Hospital Center

David L Coven, MD, PhD is a member of the following medical societies: American College of Physicians, American Medical Association, and Massachusetts Medical Society

Disclosure: Nothing to disclose.

Kenneth B Desser, MD  Clinical Professor, Director of Cardiology Fellowship, Banner Good Samaritan Medical Center, Phoenix, Arizona

Disclosure: Nothing to disclose.

Claudia Dima, MD  Fellow in Interventional Cardiology, Department of Cardiology, Banner Good Samaritan Medical Center

Disclosure: Nothing to disclose.

Samer Garas, MD, FACC  Chief of Cardiology, Department of Interventional Cardiology, St Vincent's Hospital

Samer Garas, MD, FACC is a member of the following medical societies: Alpha Omega Alpha, American College of Cardiology, and American Medical Association

Disclosure: Nothing to disclose.

Pawan Hari, MD, MPH  Resident Physician, Department of Internal Medicine, Wayne State University School of Medicine

Disclosure: Nothing to disclose.

Ahmad M Jeroudi, MD  Fellow in Cardiovascular Disease, Emory University School of Medicine

Disclosure: Nothing to disclose.

Ashok K Kondur, MD  Clinical Assistant Professor, Department of Internal Medicine, Detroit Medical Center, Wayne State University

Ashok K Kondur, MD is a member of the following medical societies: American College of Physicians and Michigan State Medical Society

Disclosure: Nothing to disclose.

David S Levey, MD, PhD  Orthopedic/Neurospinal MRI TeleRadiologist, Poolside MRI, San Antonio, TX

David S Levey, MD, PhD is a member of the following medical societies: American Roentgen Ray Society, Radiological Society of North America, and Texas Medical Association

Disclosure: Nothing to disclose.

Suzanne M Miller, MD  Clinical Instructor, Emergency Medicine, George Washington University School of Medicine and Health Sciences; Attending Physician, Department of Emergency Medicine, INOVA Fairfax Hospital; Chief Executive Officer, MDadmit

Suzanne M Miller, MD is a member of the following medical societies: American Academy of Emergency Medicine and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Brian Olshansky, MD  Professor of Medicine, Department of Internal Medicine, University of Iowa College of Medicine

Brian Olshansky, MD is a member of the following medical societies: American Autonomic Society, American College of Cardiology, American College of Chest Physicians, American College of Physicians, American College of Sports Medicine, American Federation for Clinical Research, American Heart Association, Cardiac Electrophysiology Society, Heart Rhythm Society, and New York Academy of Sciences

Disclosure: Guidant/Boston Scientific Honoraria Speaking and teaching; Medtronic Honoraria Speaking and teaching; Guidant/Boston Scientific Consulting fee Consulting; Novartis Honoraria Speaking and teaching; Novartis Consulting fee Consulting

Justin D Pearlman, MD, ME, PhD, FACC, MA  Chief, Division of Cardiology, Director of Cardiology Consultative Service, Director of Cardiology Clinic Service, Director of Cardiology Non-Invasive Laboratory, Director of Cardiology Quality Program KMC, Dartmouth-Hitchcock Medical Center, Dartmouth Medical School

Justin D Pearlman, MD, ME, PhD, FACC, MA is a member of the following medical societies: American College of Cardiology, American College of Physicians, American Federation for Medical Research, International Society for Magnetic Resonance in Medicine, and Radiological Society of North America

Disclosure: Nothing to disclose.

Ashish Pershad, MD  Consulting Staff, Heart and Vascular Center of Arizona

Ashish Pershad, MD is a member of the following medical societies: American College of Cardiology

Disclosure: Nothing to disclose.

Donald Schreiber, MD, CM  Associate Professor of Surgery (Emergency Medicine), Stanford University School of Medicine

Donald Schreiber, MD, CM is a member of the following medical societies: American College of Emergency Physicians

Disclosure: Abbott Point of Care Inc Research Grant and Speakers Bureau Speaking and teaching; Nanosphere Inc Grant/research funds Research; Singulex Inc Grant/research funds Research; Abbott Diagnostics Inc Grant/research funds None

Gary Setnik, MD  Chair, Department of Emergency Medicine, Mount Auburn Hospital; Assistant Professor, Division of Emergency Medicine, Harvard Medical School

Gary Setnik, MD is a member of the following medical societies: American College of Emergency Physicians, National Association of EMS Physicians, and Society for Academic Emergency Medicine

Disclosure: SironaHealth Salary Management position; South Middlesex EMS Consortium Salary Management position; ProceduresConsult.com Royalty Other

George A Stouffer III, MD  Henry A Foscue Distinguished Professor of Medicine and Cardiology, Director of Interventional Cardiology, Cardiac Catheterization Laboratory, Chief of Clinical Cardiology, Division of Cardiology, University of North Carolina Medical Center

George A Stouffer III, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Cardiology, American College of Physicians, American Heart Association, Phi Beta Kappa, and Society for Cardiac Angiography and Interventions

Disclosure: Nothing to disclose.

Specialty Editor Board

Eric Vanderbush, MD, FACC  Chief, Department of Internal Medicine, Division of Cardiology, Harlem Hospital Center; Clinical Assistant Professor of Cardiology, Columbia University College of Physicians and Surgeons

Eric Vanderbush, MD, FACC is a member of the following medical societies: American College of Cardiology and American Heart Association

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

David FM Brown, MD  Associate Professor, Division of Emergency Medicine, Harvard Medical School; Vice Chair, Department of Emergency Medicine, Massachusetts General Hospital

David FM Brown, MD is a member of the following medical societies: American College of Emergency Physicians and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Eugene C Lin, MD  Attending Radiologist, Teaching Coordinator for Cardiac Imaging, Radiology Residency Program, Virginia Mason Medical Center; Clinical Assistant Professor of Radiology, University of Washington School of Medicine

Eugene C Lin, MD is a member of the following medical societies: American College of Nuclear Medicine, American College of Radiology, Radiological Society of North America, and Society of Nuclear Medicine

Disclosure: Nothing to disclose.

Chief Editor

Eric H Yang, MD  Associate Professor of Medicine, Director of Interventional Cardiology Fellowship Program, Henry Ford Hospital

Eric H Yang, MD is a member of the following medical societies: Alpha Omega Alpha

Disclosure: Nothing to disclose.

Additional Contributors

The authors and editors of eMedicine gratefully acknowledge the contributions of previous authors Sumanth R Daram, MD, Rex C Liu, MD, Sridevi R Pitta, MD, and Vibhuti N Singh, MD, MPH, FACC, FSCAI, to the development and writing of the source articles.

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Acute anterior myocardial infarction.
Acute inferior myocardial infarction.
Posterolateral myocardial infarction.
A 53-year-old patient who had experienced 3 hours of chest pain had a 12-lead electrocardiogram performed, and the results are as shown. He was given sublingual nitroglycerin and developed severe symptomatic hypotension. His blood pressure normalized with volume resuscitation.
The right-sided leads indicate ST-segment elevations in RV4 and RV5, which are consistent with a right ventricular infarct.
The electrocardiogram shows lateral ST-segment elevation that is consistent with a lateral wall acute myocardial infarction.
This patient has a symptom duration of fewer than 12 hours. In the setting of active chest pain and electrocardiographic changes showing acute myocardial infarction, he would still benefit from thrombolysis. His history of surgery is not a contraindication and his blood pressure can be controlled with nitrates and beta-blockers.
This patient has an inferior wall myocardial infarction indicated on the ECG. Approximately 20% of inferior myocardial infarctions are right ventricular. Nitroglycerin will drop the preload; right ventricular (RV) output is very preload-dependent. Right-sided chest leads would be useful in demonstrating ST-segment elevations in RV4 and RV5.
Acute inferior myocardial infarction on an electrocardiogram.
After thrombolytic therapy, reperfusion arrhythmias, such as an accelerated idioventricular rhythm, may occur.
Hypokinesis of the anteroseptal wall observed during echocardiography in a patient presenting with an acute anteroseptal myocardial infarction.
Apical left ventricular dyskinesis (ventricular aneurysm) after an anterior myocardial infarction.
Image shows a scar in the anterior wall.
Graph
 
 
 
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