eMedicine Specialties > Cardiology > Coronary Artery Disease

Myocardial Infarction: Follow-up

Author: Samer Garas, MD, FACC, Chief of Cardiology, Department of Interventional Cardiology, St Vincent's Hospital
Coauthor(s): A Maziar Zafari, MD, PhD, FACC, Associate Professor, Department of Medicine, Emory University School of Medicine; Chief, Section of Cardiology, Atlanta Veterans Affairs Medical Center
Contributor Information and Disclosures

Updated: Oct 5, 2009

Follow-up

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 myocardial infarction. 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.
  • To stratify mortality risk after PCI for acute myocardial infarction, Negassa et al have developed a prognostic classification model. Patients can be readily stratified into risk categories using this tree-structured model.10

Further Outpatient Care

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

Inpatient & Outpatient Medications

  • The long-term use of aspirin in patients who have had an myocardial infarction results in significant reduction in subsequent mortality rate.
  • Beta-blocker therapy has confirmed therapeutic benefit in survivors of acute myocardial infarction. This therapy is most beneficial in patients with the highest risk.
  • ACE inhibitor use in patients with known coronary artery disease 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 coronary artery disease. The National Cholesterol Education Panel has set guidelines for target cholesterol levels. In general, patients who have experienced myocardial infarction 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 acute coronary syndrome, 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, myocardial infarction, or worsening unstable angina requiring hospitalization.11
  • 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 coronary artery disease. 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 myocardial infarction.
    • 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–myocardial infarction 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.
  • Low-dose aspirin has shown substantial benefit for primary prevention of myocardial infarction and stroke, but its use must be weighed against the risk for hemorrhagic stroke and gastrointestinal bleeding. The Antithrombotic Trialists’ (ATT) Collaboration conducted meta-analyses of serious vascular events, including myocardial infarction, stroke, and vascular death, and major bleeds in 6 primary prevention trials and in 16 secondary prevention trials that compared long-term aspirin versus control. The primary prevention trials included 95,000 individuals at low average risk, and the secondary prevention trials included 17,000 individuals at high average risk.

    Aspirin was associated with significant reduction (12% proportional reduction) for serious vascular events (0.51% aspirin vs 0.57% control annually, p = 0.0001), but the net effect on stroke was not significant. This reduction was largely due to a 20% reduction in nonfatal myocardial infarction (0.18% vs 0.23% annually, p <0.0001). Aspirin increased risk for major gastrointestinal and extracranial bleeding. The use of aspirin for primary prevention must be advised in context with the patient’s personal risks and history.12
  • Do not start post–myocardial infarction patients on postmenopausal hormone therapy (HT). Patients already taking HT for more than 1 year may be continued on this therapy without increased risk.

Complications

  • A number of arrhythmias occur after myocardial infarction, ranging from benign to fatal. Arrhythmias are common in the setting of myocardial infarction 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–myocardial infarction 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 myocardial infarction 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.
  • Congestive heart failure can be due to systolic dysfunction or diastolic dysfunction in the setting of myocardial infarction. 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 congestive heart failure 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 mitral regurgitation is most common in the setting of an inferoposterior myocardial infarction. 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 mitral regurgitation with congestive heart failure. 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 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 an myocardial infarction 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

Miscellaneous

Medicolegal Pitfalls

  • Failure to diagnosis a myocardial infarction is the leading cause of litigation against emergency department 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 myocardial infarction 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 V 3 R or V 4 R 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 S 3 , 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 myocardial infarction 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.
 


More on Myocardial Infarction

Overview: Myocardial Infarction
Differential Diagnoses & Workup: Myocardial Infarction
Treatment & Medication: Myocardial Infarction
Follow-up: Myocardial Infarction
Multimedia: Myocardial Infarction
References

References

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Further Reading

Keywords

myocardial infarction, heart attack, acute coronary syndromes, ACS, MIunstable angina, non–ST-elevation MI, NSTEMI, coronary artery disease, CAD, ischemic heart disease, chest pain, impaired systolic function, impaired diastolic function, myocardial necrosis, atherosclerosis, coronary thrombus, plaque rupture, coronary emboli, infected cardiac valve, coronary occlusion secondary to vasculitis, primary coronary vasospasm, variant angina

cardiovascular disease, congestive heart failure, CHF, coronary heart disease, smoking, diabetes mellitus, hypertension, dyslipidemia, obesity, elevated homocysteine levels, male pattern baldness, sedentary lifestyle, psychosocial stress, peripheral vascular disease, poor oral hygiene

vasculitis, congenital coronary anomalies, coronary trauma, coronary spasm, necrosis of heart muscle, coronary thrombosis, pulmonary rales, lower extremity edema, elevated jugularvenous pressure, cocaine use, heavy exertion, hyperthyroidism, severe anemia

Contributor Information and Disclosures

Author

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.

Coauthor(s)

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

Medical Editor

Eric Vanderbush, MD, FACC, MD, Chief, Department of Internal Medicine, Division of Cardiology, Clinical Assistant Professor, Harlem Hospital Center and Columbia University
Eric Vanderbush, MD, FACC, MD is a member of the following medical societies: American College of Cardiology and American Heart Association
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Marschall S Runge, MD, PhD, Charles and Anne Sanders Distinguished Professor of Medicine, Chairman, Department of Medicine, Vice Dean for Clinical Affairs, University of North Carolina at Chapel Hill School of Medicine
Marschall S Runge, MD, PhD is a member of the following medical societies: American Association for the Advancement of Science, American College of Cardiology, American College of Physicians-American Society of Internal Medicine, American Federation for Clinical Research, American Federation for Medical Research, American Heart Association, American Physiological Society, American Society for Clinical Investigation, American Society for Investigative Pathology, Association of American Physicians, Association of Professors of Cardiology, Association of Professors of Medicine, Southern Society for Clinical Investigation, and Texas Medical Association
Disclosure: Pfizer Honoraria Speaking and teaching; Merck Honoraria Speaking and teaching; Orthoclinica Diagnostica Consulting fee Consulting

CME Editor

Eleftherios Mylonakis, MD, Clinical and Research Fellow, Department of Internal Medicine, Division of Infectious Diseases, Massachusetts General Hospital
Eleftherios Mylonakis, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Physicians, American Society for Microbiology, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.

Chief Editor

Eric H Yang, MD, Assistant Professor of Medicine, Director of Coronary Care Unit, University of North Carolina at Chapel Hill School of Medicine
Eric H Yang, MD is a member of the following medical societies: Alpha Omega Alpha
Disclosure: Up to Date Royalty Review panel membership

 
 
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