Myocardial Infarction

Practice Essentials

Myocardial infarction (MI; ie, heart attack) is the irreversible necrosis of heart muscle secondary to prolonged ischemia. Approximately 1.5 million cases of MI occur annually in the United States.

Essential update: Aldosterone antagonists underutilized after MI

Although current guidelines strongly recommend the use of aldosterone antagonists after MI for patients with left ventricular systolic dysfunction concomitant with either clinical heart failure or diabetes mellitus, an analysis of data on 202,213 US patients discharged following an acute MIs found that only 14.5% of eligible patients received aldosterone antagonists at the time of discharge. Among eligible patients who were discharged on otherwise optimal medical therapy (68.9%), 16.1% were prescribed aldosterone antagonists.[1]

Signs and symptoms

Patients with typical myocardial infarction may have the following prodromal symptoms in the days preceding the event (although typical STEMI may occur suddenly, without warning):

FatigueChest discomfortMalaise

Typical chest pain in acute myocardial infarction has the following characteristics:

Intense and unremitting for 30-60 minutesRetrosternal and often radiates up to the neck, shoulder, and jaw and down to the ulnar aspect of the left armUsually described as a substernal pressure sensation that also may be characterized as squeezing, aching, burning, or even sharp In some patients, the symptom is epigastric, with a feeling of indigestion or of fullness and gas

The patient’s vital signs may demonstrate the following in myocardial infarction:

The patient’s heart rate is often increased secondary to sympathoadrenal dischargeThe pulse may be irregular because of ventricular ectopy, an accelerated idioventricular rhythm, ventricular tachycardia, atrial fibrillation or flutter, or other supraventricular arrhythmias; bradyarrhythmias may be present In general, the patient's blood pressure is initially elevated because of peripheral arterial vasoconstriction resulting from an adrenergic response to pain and ventricular dysfunction However, with right ventricular myocardial infarction or severe left ventricular dysfunction, hypotension is seenThe respiratory rate may be increased in response to pulmonary congestion or anxietyCoughing, wheezing, and the production of frothy sputum may occurFever is usually present within 24-48 hours, with the temperature curve generally parallel to the time course of elevations of creatine kinase (CK) levels in the blood. Body temperature may occasionally exceed 102°F

See Clinical Presentation for more detail.

Diagnosis

Laboratory studies

Laboratory tests used in the diagnosis of myocardial infarction include the following:

Cardiac biomarkers/enzymes: The American College of Cardiology/American Heart Association (ACC/AHA) guidelines on unstable angina/NSTEMI (non–ST-segment elevation myocardial infarction) recommend that in patients with suspected myocardial infarction, cardiac biomarkers should be measured at presentation Troponin levels: Troponin is a contractile protein that normally is not found in serum; it is released only when myocardial necrosis occurs Creatine kinase (CK) levels: CK-MB levels increase within 3-12 hours of the onset of chest pain, reach peak values within 24 hours, and return to baseline after 48-72 hours Myoglobin levels: Myoglobin is released more rapidly from infarcted myocardium than is troponin; urine myoglobin levels rise within 1-4 hours from the onset of chest pain Complete blood countChemistry profileLipid profileC-reactive protein and other inflammation markers

Electrocardiography

The ECG is the most important tool in the initial evaluation and triage of patients in whom an acute coronary syndrome (ACS), such as myocardial infarction, is suspected. It is confirmatory of the diagnosis in approximately 80% of cases.

Cardiac imaging

For individuals with highly probable or confirmed ACS, a coronary angiogram can be used to definitively diagnose or rule out coronary artery disease.

See Workup for more detail.

Management

Prehospital care

For patients with chest pain, prehospital care includes the following:

Intravenous access, supplemental oxygen, pulse oximetryImmediate administration of aspirin en routeNitroglycerin for active chest pain, given sublingually or by sprayTelemetry and prehospital ECG, if available

Emergency department and inpatient care

Initial stabilization of patients with suspected myocardial infarction and ongoing acute chest pain should include administration of sublingual nitroglycerin if patients have no contraindications to it.

The American Heart Association (AHA) recommends the initiation of beta blockers to all patients with STEMI (unless beta blockers are contraindicated).

If STEMI is present, the decision must be made quickly as to whether the patient should be treated with thrombolysis or with primary percutaneous coronary intervention (PCI).[2, 3]

Although patients presenting with no ST-segment elevation are not candidates for immediate thrombolytics, they should receive anti-ischemic therapy and may be candidates for PCI urgently or during admission.

Critical care units have reduced early mortality rates from acute myocardial infarction by approximately 50% by providing immediate defibrillation and by facilitating the implementation of beneficial interventions. These interventions include the administration of IV medications and therapy designed to do the following:

Limit the extent of myocardial infarctionSalvage jeopardized ischemic myocardiumRecanalize infarct-related arteries

See Treatment and Medication for more detail.

Image libraryApical left ventricular dyskinesis (ventricular aneurysm) after an anterior myocardial infarction. NextBackground

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. (See Etiology.) The electrocardiographic result of an acute myocardial infarction is seen below.

The 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 ofcardiac enzymes. Both these conditions mayormaynothavechangesonthesurfaceECG,includingST-segmentdepressionorT-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.[4, 5, 6, 7, 8]

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

The American College of Cardiology (ACC)/American Heart Association (AHA)/European Society of Cardiology/World Heart Federation released the Observations From the TRITON-TIMI 38 Trial (Trial to Assess Improvement in Therapeutic Outcomes by Optimizing Platelet Inhibition With Prasugrel–Thrombolysis in Myocardial Infarction 38), which better outlines a universal definition of myocardial infarction, along with a classification system and risk factors for cardiovascular death.[9]

PreviousNextAnatomy

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.)

PreviousNextPathophysiology

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 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.

PreviousNextEtiology

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.[10] Evidence indicates that in numerous cases, culprit lesions are stenoses of less than 70% and are located proximally within the coronary tree.[11, 12] Coronary atherosclerosis is especially prominent near branching points of vessels.[13] 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:

AgeSexFamily history of premature coronary heart diseaseMale-pattern baldness

Modifiable risk factors for atherosclerosis include the following:

Smoking or other tobacco useDiabetes mellitusHypertensionHypercholesterolemia and hypertriglyceridemia, including inherited lipoprotein disordersDyslipidemiaObesitySedentary lifestyle and/or lack of exercisePsychosocial stressPoor oral hygieneType 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 vasculitisVentricular hypertrophy (eg, left ventricular hypertrophy, idiopathic hypertrophic subaortic stenosis [IHSS], underlying valve disease) Coronary artery emboli, secondary to cholesterol, air, or the products of sepsisCongenital coronary anomaliesCoronary traumaPrimary coronary vasospasm (variant angina)Drug use (eg, cocaine, amphetamines, ephedrine)ArteritisCoronary anomalies, including aneurysms of coronary arteriesFactors that increase oxygen requirement, such as heavy exertion, fever, or hyperthyroidismFactors that decrease oxygen delivery, such as hypoxemia of severe anemiaAortic dissection, with retrograde involvement of the coronary arteriesInfected 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.[14]

PreviousNextEpidemiologyUnited 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.[15] A continued focus on improving outcomes for these high-risk patients is needed.

PreviousNextPrognosis

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."[16] 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 functionShort-term and long-term treatment with beta-blockers, aspirin, and ACE inhibitors

Poorer prognosis is associated with the following factors:

Increasing ageDiabetesPrevious 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)[17] Delayed or unsuccessful reperfusionPoorly preserved left ventricular function (the strongest predictor of outcome)Evidence of congestive heart failure (Killip classification ≥II)[18] or frank pulmonary edema (Killip classification ≥III)[19] Elevated B-type natriuretic peptide (BNP) levels[20, 21, 22] Elevated high sensitive C-reactive protein (hs-CRP), a nonspecific inflammatory marker[23] Secretory-associated phospholipase A2 activity is related to atherosclerosis and predicts all-cause mortality in elderly patients; it also predicts mortality or MI in post-MI patients.[24]

A study by Alherbish et al found that in patients with STEMI, the presence of ST deviation in ECG lead aVR indicates an increased mortality risk. Data from the APEX-AMI (Pexelizumab in Conjunction With Angioplasty in Acute Myocardial Infarction) trial were examined to determine the incidence and prognostic value of aVR ST deviation in STEMI patients undergoing primary percutaneous coronary intervention within 6 hours of symptom onset; the investigators determined that aVR ST deviation was associated with a 50% relative increase in the risk of death within 90 days in patients with noninferior MI, while aVR ST elevation in patients with inferior MI was associated with a nearly 6-fold increase in such risk.[25, 26]

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.[27]

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. PreviousNextPatient 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.[28]

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.[29]

A Norwegian randomized trial found that aerobic interval training (treadmill) increased peak oxygen uptake more than the usual care rehabilitation (aerobic exercise training) after myocardial infarction.[30]

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 eMedicineHealth's Cholesterol Center. Also, see eMedicineHealth'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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