Myocardial Infarction

Ischemic myocardial necrosis usually resulting from abrupt reduction in coronary blood flow to a segment of myocardium.

Clinically recognized or unrecognized MI occurs in 35% of elderly persons; 60% of hospitalizations due to acute MI occur in persons >= 65.

Symptoms and Signs

Of elderly patients with documented acute MI, 19 to 66% present with chest pain, 20 to 59% with dyspnea, 15 to 33% with neurologic symptoms, and 0 to 19% with gastrointestinal symptoms (eg, epigastric distress, vomiting, nausea, heartburn, indigestion). Other symptoms and signs include peripheral gangrene, increased claudication, palpitations, renal failure, weakness, pulmonary embolism, restlessness, sweating, and sudden cardiac death. Elderly patients with acute MI tend to delay longer than younger patients in seeking medical assistance after the onset of chest pain or other presenting symptoms of MI.

Elderly patients with acute MI are more likely than younger ones to die of MI and to have pulmonary edema, heart failure, left ventricular dysfunction, cardiogenic shock, conduction disturbances requiring insertion of a pacemaker, and atrial fibrillation or atrial flutter. In such patients, rupture of the left ventricular free wall, of a papillary muscle (which results in severe mitral regurgitation), or of the interventricular septum is also more likely. These ruptures are more common among women and among patients with persistent peri-infarctional hypertension. The rupture usually occurs without warning, most commonly 1 to 4 days after MI.

Diagnosis

Non-Q-wave MI, which is more common among elderly patients with acute MI than among younger ones, may be diagnosed in a symptomatic elderly patient when the plasma level of the MB-isoenzyme of creatine kinase is increased >= 5% or when serial ECGs show

• a new ST-segment elevation of >= 0.1 millivolt (measured 0.02 second after the J point),
• a new ST-segment depression of >= 0.1 millivolt (measured 0.08 second after the J point), or
• a new T-wave inversion of at least 0.1 millivolt in leads II, III, and aVF, in at least two precordial leads, or in leads I and aVL plus an increase of >= 5% in the plasma level of the MB-isoenzyme of creatine kinase

The total creatine kinase level is not necessarily increased after MI.

Q-wave MI may be diagnosed in a symptomatic elderly patient when serial ECGs show pathologic Q waves with a depth of >= 0.2 millivolt and a duration of >= 0.04 seconds. If pathologic Q waves occur on a resting ECG in a patient with no history of MI, the diagnosis is unrecognized Q-wave MI, which is common among elderly patients with documented MI (prevalence, 31 to 68%; incidence, 21 to 43%). The incidence of new coronary events among elderly patients with Q-wave MI is similar whether the MI is clinically recognized or unrecognized and whether the patients are men or women.

Treatment

Unless contraindicated, aspirin (or if contraindicated, ticlopidine or clopidogrel) should be given. The role of glycoprotein IIb/IIIa inhibitors (eg, tirofiban, abciximab) in the treatment of elderly patients with acute MI is under study.

For chest pain associated with acute MI, morphine sulfate 2 to 4 mg IV is the drug of choice, but nitrates and -blockers may also be used. Oxygen may be given but is unlikely to help if the oxygen saturation exceeds 94%. For heart failure, oxygen therapy, furosemide 20 to 80 mg IV, and nitrates may be used. For hypotension, IV fluids or dobutamine may be needed.

Subcutaneous heparin 7500 U q 12 h should be given to reduce the incidence of venous thromboembolism after treatment of acute MI.

The role of IV heparin in treatment of these patients is controversial, and that of low-molecular-weight heparin is under study.

Unless contraindicated, a -blocker should be given to patients at admission. It is given IV initially, then orally. Such therapy can reduce the mortality rate by 23% in elderly patients who have had an MI (but it has not been shown to significantly reduce the mortality rate in younger patients). Risk of recurrent MI is also reduced. Early IV -blocker therapy may be given with or without thrombolytic therapy.

Nitrates probably do not reduce mortality in patients with acute MI but may be used for treatment of chest pain and heart failure.

Early and continued use of an angiotensin-converting enzyme (ACE) inhibitor is recommended for patients with acute MI who are hemodynamically stable (systolic blood pressure >= 100 mm Hg) and who have heart failure, a large anterior MI, or a left ventricular ejection fraction of <= 40%. Such therapy can reduce the risk of death, severe heart failure, and severe left ventricular systolic dysfunction. The reduction in risk of death and severe heart failure is greater among elderly than among younger patients. When ACE inhibitor therapy is initiated during acute MI, the patient's blood pressure, renal function, and serum potassium should be closely monitored.

Use of calcium channel blockers during acute MI is not recommended, because these drugs do not benefit and may harm patients with acute MI. Switching elderly patients who have been taking calcium channel blockers to -blockers may be advisable.

The use of IV magnesium during acute MI is controversial. Magnesium should not be routinely used in the treatment of elderly patients with acute MI.

The prophylactic use of antiarrhythmic drugs other than -blockers does not improve the clinical outcome in patients with acute MI. In a meta-analysis, prophylactic lidocaine, once commonly used, did not improve survival and was associated with an increased incidence of asystolic cardiac arrest. Also, the elderly are at increased risk of lidocaine toxicity. Therefore, the use of lidocaine during acute MI should be limited to treatment of patients with life-threatening ventricular arrhythmias. Patients with supraventricular tachyarrhythmias may be treated with -blockers or direct-current cardioversion.

The need for a pacemaker may be temporary (during acute MI by transvenous pacing) or permanent (after acute MI).

Reperfusion therapy (thrombolytics or PTCA) during acute MI can reduce the absolute and percent mortality rate more among elderly patients than among younger patients. In patients > 80 who had had an MI, the mortality rate was 41% lower for patients given streptokinase than for those given placebo, and 14.1 lives per 100 treated patients were saved. Medical therapy alone is preferred for most elderly patients who have had an MI, but if revascularization is indicated, PTCA is generally preferred to CABG.

Unless contraindicated, reperfusion therapy should be considered for elderly patients who have ischemic symptoms that last >= 30 minutes and that occur within 6 to 12 hours of clinical presentation and who have an ST-segment elevation of at least 1 to 2 mm in >= 2 ECG leads or who have left bundle branch block. Elderly patients with persistent myocardial ischemia, hypotension, or cardiogenic shock occurring > 12 hours after the onset of symptoms may still benefit from PTCA. Intracoronary stent placement decreases the risk of restenosis after PTCA. The potential benefit of reperfusion therapy is higher for elderly patients with a large anterior acute MI.

Streptokinase (1.5 million U IV over 1 hour) may be preferable to recombinant human tissue plasminogen activator (rt-PA) for the elderly because it causes fewer episodes of stroke and cerebral hemorrhage; it is also less expensive. However, the choice of thrombolytic drug is controversial. Minimization of delays in treatment is more important than drug choice.

Long-term management (see Table 88-1): Modifiable risk factors should be controlled. Long-term drug therapy may include antiplatelet drugs, anticoagulants, -blockers, nitrates, and ACE inhibitors. Calcium channel blockers are generally avoided; use of a calcium channel blocker instead of a -blocker after MI doubled the risk of mortality in one study. Automatic implantable cardioverter-defibrillators and surgical treatment (revascularization with PTCA or CABG) are appropriate for some patients.

Long-term use of the -blockers propranolol, timolol, and metoprolol reduces rates of recurrent MI and sudden cardiac death more in elderly patients than in younger ones, regardless of whether the initial MI was non-Q-wave or Q-wave.

Class I antiarrhythmic drugs and d-sotalol (not clinically available) increase mortality rates after MI and should not be used in elderly patients after MI. Amiodarone and d,l-sotalol (which is available) do not significantly affect mortality rates after MI. -Blockers are the only antiarrhythmic drugs that reduce mortality rates in elderly patients with nonsustained ventricular tachycardia or complex ventricular arrhythmias after MI; unless specifically contraindicated, -blockers should be used to treat these patients after MI.

Because estrogen replacement therapy does not appear to improve outcome after MI and may increase the incidence of venous thromboembolic events and of gallbladder disease, it is not recommended for postmenopausal women who have had an MI.

Complications: When the left ventricular free wall, papillary muscle, or interventricular septum ruptures after acute MI, mortality risk is very high unless surgical repair is promptly performed.

When the left ventricular free wall ruptures suddenly, emergency surgery is not feasible. If the rupture is subacute, emergency cardiac surgery, perhaps after rapid stabilization with pericardiocentesis, volume expansion, intra-aortic balloon pump placement, and other medical therapy, offers hope of survival.

For patients with rupture of the papillary muscle, an overall operative mortality rate of 27% has been reported. The short-term and long-term mortality rates were slightly higher for those with ejection fractions < 45%; age did not predict survival. Patients with papillary muscle rupture and severe mitral regurgitation require prompt surgery because they may deteriorate rapidly, and surgery generally has good results. Age should not be a major consideration in the decision to perform surgery.

The results of surgery for rupture of the interventricular septum are somewhat less encouraging. Among one group of patients with cardiogenic shock, the only survivors were those who underwent prompt surgical repair, with a mortality rate of 62%. Age appears to be an independent predictor of survival. Operative mortality rates of 27 to 47% for early repair of septal rupture have been reported. Patients who survive the operation seem to have a favorable prognosis. Prompt surgery is therefore advised for most patients with postinfarction rupture of the interventricular septum.