INTRODUCTION

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Background

Myocardial infarction (MI) is the irreversible necrosis of heart muscle secondary to prolonged ischemia. This usually results from an imbalance of oxygen supply and demand. The appearance of cardiac enzymes in the circulation generally indicates myocardial necrosis. MI is considered, more appropriately, part of a spectrum referred to as acute coronary syndromes (ACSs), which also includes unstable angina and non–ST-elevation MI (NSTEMI). Patients with ischemic discomfort may or may not have ST-segment elevation. Most of those with ST-segment elevation will develop Q waves. Those without ST elevations will ultimately be diagnosed with unstable angina or NSTEMI based on the presence of cardiac enzymes.

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

Pathophysiology

Atherosclerosis is the disease primarily responsible for most ACS cases. Approximately 90% of MIs result from an acute thrombus that obstructs an atherosclerotic coronary artery. Plaque rupture is considered to be the major trigger of coronary thrombosis. Following plaque rupture, platelet activation and aggregation, coagulation pathway activation, and endothelial vasoconstriction occur and lead to coronary thrombosis and occlusion.

Consider nonatherosclerotic causes of acute MIs in younger patients or if no evidence of atherosclerosis is noted. Such causes include coronary emboli from sources such as an infected cardiac valve through a patent foramen ovale (PFO), coronary occlusion secondary to vasculitis, primary coronary vasospasm (variant angina), cocaine use, or other factors leading to mismatch of oxygen supply and demand, as may occur with a significant GI bleed.

Frequency

United States

Approximately 1.5 million cases of MI occur each year.

International

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 developed countries and are one of the main causes of death in many developing countries; they are the major cause of death in adults everywhere.

Mortality/Morbidity

• 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.
• Ischemic heart disease is the leading cause of death worldwide.
• Approximately 6.3 million deaths due to heart disease occurred in 1990 worldwide, which represents 29% of all deaths. The prevalence of coronary artery disease (CAD) is increasing rapidly in nonindustrialized countries.

Race

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

Sex

• A male predominance in incidence 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

• Incidence increases with age.
• Most patients who develop an acute MI are older than 60 years. Elderly people also tend to have higher rates of morbidity and mortality from their infarcts.

CLINICAL

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History

Symptoms of myocardial infarction include the following:

• Chest pain
• • This is usually described as a substernal pressure sensation that also may be described as squeezing, aching, burning, or even sharp pain.
  • Prolonged chest discomfort lasting longer than 30 minutes is most compatible with infarction.
  • Radiation to the left arm or neck is common.
  • The sensation is precipitated by exertion and relieved by rest and nitroglycerin.
  • Chest pain may be associated with nausea, vomiting, diaphoresis, dyspnea, fatigue, or palpitations.
  • Atypical chest pain is common, especially in patients with diabetes and in elderly patients. However, any patient may present with atypical symptoms. These symptoms are considered the anginal equivalent for that patient.
• Shortness of breath
• • Shortness of breath may be the patient's anginal equivalent or a symptom of heart failure. See Medscape's Heart Failure Resource Center.
  • It is due to elevated end-diastolic pressures secondary to ischemia, which may then lead to elevated pulmonary pressures.
• Atypical presentations
• • 20% of patients are asymptomatic or have atypical symptoms.
  • Atypical presentations are common and frequently lead to misdiagnoses.
  • A patient may, for example, present with abdominal discomfort or jaw pain as his or her anginal equivalent.
  • An elderly patient may present with altered mental status.
  • Low threshold should be maintained when evaluating high- and moderate-risk patients, as their anginal equivalents may mimic other presentations.
  • Women tend to present more commonly with atypical symptoms such as sharp pain, fatigue, weakness, and other nonspecific complaints.

Physical

Physical examination findings for myocardial infarction can vary; one patient may be comfortable in bed, with normal examination results, while another may be in severe pain with significant respiratory distress requiring ventilatory support.

• Low-grade fever may be present.
• Hypotension or hypertension can be observed depending on the extent of the MI.
• Fourth heart sound (S4) may be heard in patients with ischemia. With ischemia, diastolic dysfunction is the first physiologically measurable effect and this can then cause a stiff ventricle and an audible S4.
• Dyskinetic cardiac bulge (in anterior wall MI) can occasionally be palpated.
• Systolic murmur can be heard if mitral regurgitation (MR) or ventricular septal defect (VSD) develops.
• Other findings include cool, clammy skin and diaphoresis.
• Signs of congestive heart failure (CHF) may be found, including the following:
• • Third heart sound (S3) gallop
  • Pulmonary rales
  • Lower extremity edema
  • Elevated jugular venous pressure

Causes

• Atherosclerosis with occlusive or partially occlusive thrombus formation
• Nonmodifiable risk factors for atherosclerosis
• • Age
  • Sex
  • Family history of premature coronary heart disease
• Modifiable risk factors for atherosclerosis
• • Smoking or other tobacco use
  • Diabetes mellitus
  • Hypertension (See Medscape's Hypertension Resource Center.)
  • Dyslipidemia
  • Obesity (See Medscape's Obesity Resource Center.)
• New and other risk factors for atherosclerosis
• • Elevated homocysteine levels
  • Male pattern baldness
  • Sedentary lifestyle and/or lack of exercise
  • Psychosocial stress
  • Presence of peripheral vascular disease
  • Poor oral hygiene
• Nonatherosclerotic causes
• • Vasculitis
  • Coronary emboli
  • Congenital coronary anomalies
  • Coronary trauma
  • Coronary spasm
  • Drug use (cocaine)
  • Factors that increase oxygen requirement, such as heavy exertion, fever, or hyperthyroidism
  • Factors that decrease oxygen delivery, such as hypoxemia of severe anemia

DIFFERENTIALS

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Other Problems to be Considered

Pneumonia
Pancreatitis

WORKUP

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Lab Studies

Lab studies for patients with myocardial infarction include the following:

• Cardiac enzymes: In patients with suspected MI, obtain cardiac enzymes at regular intervals, starting upon admission and serially for as long as 24 hours.
• Troponin levels
• • Troponin levels are now considered the criterion standard in defining and diagnosing MI, according to the American College of Cardiology (ACC)/American Heart Association (AHA) consensus statement on MI.^{1, 2}
  • Cardiac troponin levels (troponin-T and troponin-I) have a greater sensitivity and specificity than CK-MB levels in detecting MI. They have important diagnostic and prognostic roles. Positive troponin levels are considered virtually diagnostic of MI in the most recent ACC/AHA revisions, as they are without equal in combined specificity and sensitivity in this diagnosis.
  • Serum levels increase within 3-12 hours from the onset of chest pain, peak at 24-48 hours, and return to baseline over 5-14 days.
• Creatine kinase level
• • Creatine kinase comprises 3 isoenzymes, including creatine kinase with muscle subunits (CK-MM), which is found mainly in skeletal muscle; creatine kinase with brain subunits (CK-BB), predominantly found in the brain; and myocardial muscle creatine kinase (CK-MB), which is found mainly in the heart.
  • Serial measurements of CK-MB isoenzyme levels were previously the standard criterion for diagnosis of MI. CK-MB levels increase within 3-12 hours of onset of chest pain, reach peak values within 24 hours, and return to baseline after 48-72 hours. Levels peak earlier (wash out) if reperfusion occurs. Sensitivity is approximately 95%, with high specificity. However, sensitivity and specificity are not as high as for troponin levels, and the trend has favored using troponins for the diagnosis of MI.
• Myoglobin levels
• • Urine myoglobin levels rise within 1-4 hours from the onset of chest pain.
  • Myoglobin levels are highly sensitive but not specific, and they may be useful within the context of other studies and in early detection of MI in the ED.
• Complete blood cell count
• • Obtain a CBC count if MI is suspected to rule out anemia as a cause of decreased oxygen supply and prior to giving thrombolytics.
  • Leukocytosis is also common, but not universal, in the setting of acute MI.
  • A platelet count is necessary if a IIb/IIIa agent is considered; furthermore, the patient's WBC count may be elevated modestly in the setting of MI, signifying an acute inflammatory state.
• Chemistry profile
• • In the setting of MI, closely monitor potassium and magnesium levels.
  • Creatinine level is also needed prior to initiating treatment with an angiotensin-converting enzyme (ACE) inhibitor.
• Lipid level profile: This may be helpful if obtained upon presentation because levels can change after 12-24 hours of an acute illness.
• C-reactive protein (CRP) levels: Consider measuring CRP levels and other markers of inflammation upon presentation if an ACS is suspected.

Imaging Studies

• Chest radiography
• • Upon presentation, obtain a chest radiograph to assess the patient's heart size and the presence or absence of decompensated CHF with or without pulmonary edema.
  • A chest radiograph may also assist in diagnosing concomitant disease, such as pneumonia in an elderly patient, as a precipitating cause for MI.
  • A chest radiograph may be helpful in evaluation for aortic dissection.
• Echocardiography
• • An echocardiogram may play an important role in the setting of MI.
  • Regional wall motion abnormalities can be identified, which are especially helpful if the diagnosis is questionable.
  • An echocardiogram can also define the extent of the infarction and assess overall left ventricle (LV) and right ventricle (RV) function. In addition, an echocardiogram can identify complications, such as acute MR, LV rupture, or pericardial effusion.
• Myocardial perfusion imaging
• • Prior to discharge, obtain myocardial perfusion imaging to assess the extent of residual ischemia if the patient has not undergone cardiac catheterization. The extent of ischemia can guide further therapy as to whether to proceed with catheterization or to continue conservative therapy.
  • Myocardial perfusion has been shown to be a valuable method for triage of patients with chest pain in the ED. Significant variability exists among centers, and the results of the trials can be applied only to those centers with proven reliability and experience.
• Cardiac angiography
• • Cardiac catheterization defines the patient's coronary anatomy and the extent of the disease. Most investigators recommend that all patients with MI should undergo cardiac catheterization, if it is available.
  • Patients with cardiogenic shock, intractable angina despite medications, or severe pulmonary congestion should undergo cardiac catheterization immediately.

Other Tests

• The electrocardiogram (ECG) is the most important tool in the initial evaluation and triage of patients in whom an ACS is suspected (see Media files 1-3). It is confirmatory of the diagnosis in approximately 80% of cases.
• • Obtain an ECG immediately if MI is considered or suspected.
  • In patients with inferior MI, record a right-sided ECG to rule out RV infarct.
  • Qualified personnel should review the ECG as soon as possible.
  • Perform ECGs serially upon presentation to evaluate progression and assess changes with and without pain.
  • Obtain daily serial ECGs for the first 2-3 days and additionally as needed.
  • Convex ST-segment elevation with upright or inverted T waves is generally indicative of MI in the appropriate clinical setting.
  • ST depression and T-wave changes may also indicate evolution of NSTEMI.

TREATMENT

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Medical Care

Initial therapy for acute myocardial infarction is directed toward restoration of perfusion as soon as possible to salvage as much of the jeopardized myocardium as possible. This may be accomplished through medical or mechanical means, such as percutaneous coronary intervention or coronary artery bypass grafting.

Further treatment is based on (1) restoration of the balance between the oxygen supply and demand to prevent further ischemia, (2) pain relief, and (3) prevention and treatment of any complications that may arise.

• Thrombolytic therapy has been shown to improve survival rates in patients with acute MI if administered in a timely fashion in the appropriate group of patients. If percutaneous coronary intervention (PCI) capability is not available or will cause a delay greater than 90 minutes, then the optimal approach is to administer thrombolytics within 12 hours of onset of symptoms in patients with ST-segment elevation greater than 0.1 mV in 2 or more contiguous ECG leads, new left bundle-branch block (LBBB), or anterior ST depression consistent with posterior infarction. Tissue plasminogen activator (t-PA) is superior to streptokinase in achieving a higher rate of coronary artery patency; however, the key to efficacy lies in the speed of the delivery of therapy.
• Aspirin and/or antiplatelet therapy
• • Aspirin has been shown to decrease mortality and re-infarction rates after MI. Administer aspirin immediately, which the patient should chew if possible upon presentation. Continue aspirin indefinitely unless an obvious contraindication, such as a bleeding tendency or an allergy, is present. Clopidogrel may be used as an alternative in cases of a resistance or allergy to aspirin. Recent data from the CLARITY trial (CLopidogrel as Adjunctive ReperfusIon Therapy Thrombolysis in Myocardial Infarction [TIMI] 28) suggest that adding clopidogrel to this regimen is safe and effective.³ The clopidogrel dose used was 300 mg. Further studies suggest that a higher dose of clopidogrel may have added benefit.⁴
  • Administer a platelet glycoprotein (GP) IIb/IIIa-receptor antagonist, in addition to acetylsalicylic acid and unfractionated heparin (UFH), to patients with continuing ischemia or with other high-risk features and to patients in whom a percutaneous coronary intervention (PCI) is planned. Eptifibatide and tirofiban are approved for this use. Abciximab also can be used for 12-24 hours in patients with unstable angina or NSTEMI in whom a PCI is planned within the next 24 hours.
• Heparin (and other anticoagulant agents) has an established role as an adjunctive agent in patients receiving t-PA, but not in patients receiving streptokinase. Heparin is also indicated in patients undergoing primary angioplasty. Few data exist with regard to efficacy in patients not receiving thrombolytic therapy in the setting of acute MI. Low molecular-weight heparins (LMWHs) have been shown to be superior to UFHs in patients with unstable angina or NSTEMI. Bivalirudin (a direct thrombin inhibitor) has shown some promise in the setting of STEMI if combined with high-dose clopidogrel load and may be an appropriate alternative strategy.
• Nitrates have no apparent impact on mortality rate in patients with ischemic syndromes. Their utility is in symptomatic relief and preload reduction. Administer to all patients with acute MI within the first 48 hours of presentation, unless contraindicated (ie, in RV infarction).
• ACE inhibitors reduce mortality rates after MI. Administer ACE inhibitors as soon as possible as long as the patient has no contraindications and remains in stable condition. ACE inhibitors have the greatest benefit in patients with ventricular dysfunction. Continue ACE inhibitors indefinitely after MI. Angiotensin-receptor blockers may be used as an alternative in patients who develop adverse effects, such as a persistent cough, although initial trials need to be confirmed.
• Beta-blockers may reduce the rates of reinfarction and recurrent ischemia. Administer to patients with MI unless a contraindication is present. However, a large chinese trial showed no benefit to beta-blockade. This has created some doubt as to the benefit and may lead to a change in the guidelines.⁵

Surgical Care

• Percutaneous coronary intervention
• • PCI is the treatment of choice in most patients with STEMI, assuming a door to balloon time of less than 90 minutes in at least 75% of the patients presenting with STEMI. PCI provides greater coronary patency (>96% thrombolysis in myocardial infarction [TIMI] 3 flow), lower risk of bleeding, and instant knowledge about the extent of the underlying disease. Studies have shown that primary PCI has a mortality benefit over thrombolytic therapy. Door to balloon times correlate closely with mortality rates, making this the key measurement for any successful interventional program.
  • The choice of primary PCI should be individualized to each institution and to the patient's presentation and timing. PCI in patients with occluded arteries for more than 24 hours appears to offer no added benefit over medical treatment.
  • The widespread use of stenting and adjunctive IIb/IIIa therapy are improving the results of primary PCI. One trial showed that, in patients with acute MI, coronary stenting and abciximab lead to a greater degree of myocardial salvage and a better clinical outcome than fibrinolysis with thrombolytic therapy.^{6, 7} Improvement of long- and short-term outcomes, however, depends highly on the speed with which reperfusion is achieved.
  • Primary PCI is also the treatment of choice in patients with cardiogenic shock, patients in whom thrombolysis failed, and those with high risk of bleeding or contraindications to thrombolytic therapy.
  • Only an experienced operator should perform primary PTCA, and PTCA should be performed only where the appropriate facilities are available. Operators should have at least 75 cases per year, while the center should perform at least 200 cases per year as per the recommendations of the ACC.
• Emergent or urgent coronary artery graft bypass surgery is indicated in patients in whom angioplasty fails and in patients who develop mechanical complications such as a VSD, LV, or papillary muscle rupture.

Consultations

• ED personnel should initiate evaluation and treatment, including administering a thrombolytic agent.
• Obtain cardiology consultation immediately if primary PCI is considered. Otherwise, cardiology consultation may be obtained as needed and upon admission. Consultation may be obtained sooner if the patient presents with significant heart failure, mechanical complications, arrhythmias, or other complicating factors.

Diet

• Initially, keep the patient on nothing by mouth (NPO) until his or her condition has been stabilized and treated. Following initial therapy and admission, a dietitian should instruct the patient regarding appropriate diet, as recommended by the AHA.
• A low-salt, low-fat, and low-cholesterol diet is generally recommended.

Activity

• Confine patients to bed rest to minimize oxygen consumption until reperfusion and initial therapy are complete. This usually lasts about 24-48 hours; after that, the patient's activity may be accelerated slowly as tolerated and as the clinical situation allows.
• Initiate cardiac rehabilitation prior to discharge.

MEDICATION

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The goals of pharmacotherapy for myocardial infarction are to reduce morbidity and to prevent complications.

Drug Category: Salicylates

The antiplatelet effects of these agents may improve mortality rate.

Drug Category: Antiplatelet agent

Strong mortality benefit. Increased risk of bleeding in case of emergent CABG.

Drug Category: Anticoagulants

Unfractionated intravenous heparin and fractionated low molecular weight subcutaneous heparins are the two choices for initial anticoagulation therapy.

Drug Category: Platelet aggregation inhibitors

These agents prevent acute cardiac ischemic complications in unstable angina unresponsive to conventional therapy.

Drug Category: Vasodilators

These agents relieve chest discomfort by improving myocardial oxygen supply, which in turn dilates epicardial and collateral vessels, improving blood supply to the ischemic myocardium.

Drug Category: Beta-adrenergic blockers

This category of drugs has the potential to suppress ventricular ectopy due to ischemia or excess catecholamines. In the setting of myocardial ischemia, beta-blockers have antiarrhythmic properties and reduce myocardial oxygen demand secondary to elevations in heart rate and inotropy.

See related Medscape CME Activity New Statement on Cocaine-Associated MI Urges Caution With Beta Blockers, Emphasizes Kicking the Habit.

Drug Category: Angiotensin-converting enzyme (ACE) inhibitors

These agents may prevent conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in lower aldosterone secretion.

Drug Category: Thrombolytics

The main objective is to restore circulation through a previously occluded vessel by the rapid and complete removal of a pathologic intraluminal thrombus or embolus that has not been dissolved by the endogenous fibrinolytic system.

Drug Category: Analgesics

Pain control is essential to quality patient care. Analgesics ensure patient comfort, promote pulmonary toilet, and have sedating properties, which are beneficial for patients who experience pain.

FOLLOW-UP

Section 8 of 11  

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Further Inpatient Care

• Admit patients with myocardial infarction to a coronary care unit. Monitor patients carefully for arrhythmia, recurrent ischemia, and other possible complications. The patient may be transferred to a telemetry unit 24-48 hours after admission if no complications occur. Hospitalize the patient for approximately 4-5 days after MI. Patients who undergo primary PCI or have an immediate cardiac catheterization may be discharged sooner if their hospital course is without incident.
• Perform a coronary angiography on high-risk patients prior to discharge to evaluate their need for revascularization.
• In the case of patients who have not had a cardiac catheterization and have no complications, perform a submaximal stress test prior to discharge to assess their subsequent risk.

Further Outpatient Care

• Arrange for follow-up within 2 weeks of discharge.
• Arrange for cardiac rehabilitation.

In/Out Patient Meds

• The long-term use of aspirin in patients who have had an MI results in significant reduction in subsequent mortality rate.
• Beta-blocker therapy has confirmed therapeutic benefit in survivors of acute MI. This therapy is most beneficial in patients with the highest risk.
• ACE inhibitor use in patients with known CAD has been shown to reduce mortality rate.
• Many trials have shown a clear benefit of lipid-lowering therapy in the secondary and primary prevention of CAD. The National Cholesterol Education Panel has set guidelines for target cholesterol levels. In general, patients who have experienced MI should achieve low-density lipoprotein (LDL) level less than 100 mg/dL, high-density lipoprotein (HDL) level greater than 40 mg/dL, and triglyceride level less than 200 mg/dL. High-risk patients should be treated to a target LDL level of less than 70 mg/dL.
• Schwartz et al recently showed in the MIRACL trial that initiating atorvastatin during hospitalization for an ACS, irrespective of lipid levels, reduces the frequency of recurrent ischemic events. This treatment significantly reduced the frequency of the combined end point of death, recurrent death, MI, or worsening unstable angina requiring hospitalization.⁸
• Clopidogrel should be prescribed for a year following discharge if the patient has no contraindications and cost is not prohibitive. To reduce the risk of bleeding, the aspirin dose can be reduced to 81 mg.

Transfer

A patient in whom thrombolytic therapy fails should be transferred to a facility where cardiac catheterization and angioplasty facilities are available.

Deterrence/Prevention

• Smoking cessation
• • Cigarette smoking is a major risk factor for CAD. Risk of recurrent coronary events decreases 50% at 1 year after smoking cessation.
  • Provide all patients who smoke with guidance, education, and the support needed to avoid smoking.
  • Bupropion has been shown to increase the chances of patients' success in achieving smoking cessation.
• Alcohol consumption
• • Mild alcohol consumption has been associated with a decreased risk of stroke and MI.
  • Cautiously consider recommending and discussing alcohol use on a case-by-case basis.
• Antioxidant therapy, including vitamin E, has not shown clear benefit in the prevention of coronary events.
• Do not use long-term anticoagulant (ie, warfarin) therapy routinely in post-MI patients but as an alternative in patients who cannot take antiplatelet agents. Patients with known LV thrombus, atrial fibrillation, or severe wall motion abnormalities have shown benefit from long-term anticoagulation, maintaining the international normalized ratio (INR) between 2 and 3.
• Do not start post-MI patients on postmenopausal hormone therapy (HRT). Patients already taking HRT for more than 1 year may be continued on this therapy without increased risk.

Complications

• A number of arrhythmias occur after MI, ranging from benign to fatal. Arrhythmias are common in the setting of MI and are a major cause of morbidity and mortality. Close monitoring and immediate treatment of arrhythmias may be the most important part of the treatment of a post-MI patient within the first 48 hours. Pay close attention to exacerbating factors, such as electrolyte disturbances (especially potassium and magnesium), hypoxemia, drugs, or acidosis, and correct them accordingly.
• Ventricular fibrillation and/or ventricular tachycardia occurring within the first 48 hours may be due to ischemia; however, if ventricular arrhythmias occur later, then further workup is indicated. Immediate cardioversion is the treatment of choice. Accelerated idioventricular arrhythmia is a ventricular arrhythmia that may occur in response to reperfusion. This rhythm has a benign prognosis and usually does not require therapy.
• Supraventricular arrhythmias are also common. Sinus bradycardia may be due to drugs, ischemia, or a vagal response. Sinus tachycardia may be due to pain, anxiety, drugs, or other causes. Atrial fibrillation and other atrial tachycardias may also occur. Treat any tachycardia by correcting the cause first or by pharmacotherapy, because persistent tachycardias may lead to further ischemia.
• Conduction abnormalities may result from ischemia, necrosis, or chronotropic drugs, or as a vagal response. Recognition and treatment of these abnormalities are important in short- and long-term outcomes. Possible therapies include medications, such as atropine, or even placement of a transvenous pacemaker if indicated. Conduction disturbances are seen more commonly in the setting of inferior MI but are more ominous when seen with an anterior infarct.
• Recurrent ischemia may be due to incomplete reperfusion. Postinfarct angina occurs in 20-30% of patients. This is an indication to proceed to cardiac catheterization followed by mechanical revascularization as needed.
• CHF can be due to systolic dysfunction or diastolic dysfunction in the setting of MI. The severity of the heart failure and systolic dysfunction depends on the extent of the infarct and the presence of any other complications, such as acute mitral regurgitation. Aggressive treatment is indicated to avoid worsening of the situation. Treatment may include any or all of the following: nitrates, morphine, diuretics, ACE inhibitors, and other vasodilators if needed. Digoxin has no role in the setting of acute CHF due to ischemia.
• Cardiogenic shock is defined as a systolic BP less than 90 mm Hg in the presence of organ hypoperfusion. The mortality rate due to cardiogenic shock is as high as 70% in some series. Patients usually require inotropic agents, such as dopamine or dobutamine, and occasionally an intraaortic balloon pump is required. Patients presenting with cardiogenic shock should proceed directly to the catheterization lab, if available, for mechanical revascularization.
• Acute MR is most common in the setting of an inferoposterior MI. This is secondary to ischemia, necrosis, or rupture of the LV papillary muscle (especially the posteromedial papillary muscle). This can lead to mild-to-severe MR with CHF. Diagnosis can be made on physical examination, but an echocardiogram is necessary to confirm the diagnosis and assess the severity, which helps in the choice of therapy. Treatment consists of aggressive afterload reduction, intraaortic balloon pump insertion, and immediate surgical repair.
• Ventricular rupture occurs in the interventricular septum or the LV free wall. Both are catastrophic events with mortality rates greater than 90%. Prompt recognition, stabilization, and surgical repair are crucial to any hope of survival. Ventricular rupture is more common in women, patients with hypertension, and those receiving NSAIDs or steroids. An echocardiogram can usually define the abnormality, and a right heart catheterization can show an oxygen saturation step-up in the case of a septal rupture.
• Other complications include pericarditis, ventricular aneurysms, mural thrombi, and hypertension. Recognition and treatment can be life saving.

Prognosis

• Acute MI 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 MI.
• Approximately half of all patients with an MI are rehospitalized within 1 year of their index event.
• Overall, prognosis is highly variable and depends largely on the extent of the infarct, the residual LV function, and whether the patient underwent revascularization.

Patient Education

• Diet
• • Diet plays an important role in the development of CAD. Educate post-MI patients about the role of a low-cholesterol and low-salt diet.
  • Educate patients about the AHA dietary guidelines regarding a low-fat, low-cholesterol diet.
  • A dietitian should see and evaluate all post-MI patients prior to their discharge.
• Smoking cessation
• • Educate all post-MI patients regarding the critical role of smoking in the development of CAD.
  • Smoking cessation classes should be offered to help patients avoid smoking after their MI.
• 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.

MISCELLANEOUS

Section 9 of 11  

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• Miscellaneous
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Medical/Legal Pitfalls

• Failure to diagnosis a myocardial infarction is the leading cause of litigation against ED clinicians and cardiologists.
• Consider atypical presentations in elderly patients, patients with diabetes, and women. Assess all patients carefully, especially if they have significant cardiac risk factors.
• Review all ECGs that are obtained in a prompt fashion because time is crucial.
• Obtain cardiology consultation whenever the diagnosis is questionable.
• Consider an echocardiogram to assess wall motion abnormalities in difficult cases with nondiagnostic ECGs, such as with an LBBB.

Special Concerns

• Right ventricular infarction
• • Approximately one third of patients with inferior MI develop RV infarction. RV infarction presents a special challenge because the adjunctive therapy, other than reperfusion, is somewhat different.
  • A right-sided ECG with greater than 1 mm ST elevation in V3R or V4R leads describes an RV infarct. An echocardiogram may be helpful in confirming the diagnosis. On physical examination, signs of right heart failure, such as elevated jugular venous pulsation, right-sided S3, Kussmaul sign, or hypotension, may be present, and the patient may have clear lung fields.
  • The patient becomes volume dependent to maintain adequate LV and RV filling. Occasionally, dobutamine may be needed, or even an intraaortic balloon pump for hemodynamic support.
  • Avoid nitrates or any medications that lower preload in this setting. A pulmonary artery catheter can be helpful in guiding therapy.
• Elderly patients
• • Elderly patients with acute MI are at increased risk of developing complications. Treat these patients aggressively.
  • Elderly patients have an increased risk of bleeding with thrombolytic therapy, but they also have the most to gain from this therapy.
  • Very elderly patients should undergo primary angioplasty if available, but they should receive thrombolytics if excessive delay is anticipated before angioplasty can be performed.

MULTIMEDIA

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Media file 1:  Acute anterior myocardial infarction.
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