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Management of the Elderly Person After Myocardial Infarction

Divisions of Cardiology and Geriatrics, Department of Medicine, New York Medical College, Valhalla.

Address correspondence to Wilbert S. Aronow, MD, Cardiology Division, New York Medical College, Macy Pavilion, Rm. 138, Valhalla, NY 10595. E-mail: wsaronow{at}aol.com

	Abstract

Top Abstract Management of Coronary Risk... Aspirin Anticoagulants Beta Blockers Nitrates Angiotensin-Converting Enzyme... Calcium Channel Blockers Antiarrhythmic Therapy Hormone Replacement Therapy Revascularization References

 
Elderly persons after myocardial infarction should have their modifiable coronary artery risk factors intensively treated. Hypertension should be treated with beta blockers and angiotensin-converting enzyme inhibitors. The blood pressure should be reduced to <140/85 mmHg and to 130/80 mmHg in persons with diabetes or renal insufficiency. The serum low-density lipoprotein cholesterol should be reduced to <100 mg/dl with statins if necessary. Aspirin or clopidogrel, beta blockers, and angiotensin-converting enzyme inhibitors should be given indefinitely unless contraindications exist to the use of these drugs. Long-acting nitrates are effective antianginal and antiischemic drugs. There are no Class I indications for the use of calcium channel blockers after myocardial infarction. Postinfarction patients should not receive Class I antiarrhythmic drugs, sotalol, or amiodarone. An automatic implantable cardioverter-defibrillator should be implanted in postinfarction patients at very high risk for sudden cardiac death. Hormonal therapy should not be used in postmenopausal women after myocardial infarction. The two indications for coronary revascularization are prolongation of life and relief of unacceptable symptoms despite optimal medical management.

	MANAGEMENT OF CORONARY RISK FACTORS

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Cigarette Smoking
The Chicago Stroke Study showed that current cigarette smokers aged 65–74 years had a 52% higher mortality from CAD than nonsmokers, ex-smokers, and pipe and cigar smokers (5). Ex-smokers who had stopped smoking for 1 to 5 years had a similar mortality from CAD as did nonsmokers (5). The Systolic Hypertension in the Elderly Program pilot project demonstrated that smoking was a predictor of first cardiovascular event and MI/sudden death (6). At 30-year follow-up of persons 65 years of age and older in the Framingham Study, cigarette smoking was not associated with the incidence of CAD in older men and women but was associated with mortality from CAD in older men and women (7).

At 12-year follow-up of men aged 65–74 years in the Honolulu Heart Program, cigarette smoking was an independent risk factor for nonfatal MI and fatal CAD (8). The absolute excess risk associated with cigarette smoking was 1.9 times higher in older men than in middle-aged men. At 5-year follow-up of 7178 persons aged 65 years or older in three communities, current cigarette smokers had a higher incidence of cardiovascular mortality than nonsmokers (relative risk = 2.0 for men and 1.6 for women) (9). The incidence of cardiovascular death in former smokers was similar to those who had never smoked (9). At 6-year follow-up of older men and women in the Coronary Artery Surgery Study registry, the relative risk of MI or death was 1.5 for persons aged 65–69 years and 2.9 for persons 70 years of age or older who continued smoking compared with quitters during the year before study enrollment (10).

At 40-month follow-up of 664 elderly men, mean age 80 years, and at 48-month follow-up of 1488 elderly women, mean age 82 years, current cigarette smoking increased the relative risk of new coronary events (nonfatal or fatal MI or sudden cardiac death) 2.2 times in older men and 2.0 times in older women (Table 1) (11). We have also observed that cigarette smoking aggravates angina pectoris and precipitates silent myocardial ischemia in elderly persons with CAD.

Hypertension
Systolic hypertension in older persons is diagnosed if the systolic blood pressure is 140 mmHg or higher on three occasions (12). Diastolic hypertension in older persons is diagnosed if the diastolic blood pressure is 90 mmHg or higher on three occasions (12). Isolated systolic hypertension in older persons is diagnosed if the systolic blood pressure is 140 mmHg or higher on three occasions, and the diastolic blood pressure is normal (12). Isolated systolic hypertension occurred in 65% of 1051 older persons with hypertension (13).

Isolated systolic hypertension and diastolic hypertension are both associated with increased cardiovascular morbidity and mortality in elderly persons (14). Increased systolic blood pressure is a greater risk factor for cardiovascular morbidity and mortality than is increased diastolic blood pressure (14). The higher the systolic or diastolic blood pressure, the greater the morbidity and mortality from CAD in elderly men and women.

At 30-year follow-up of persons aged 65 years and older in the Framingham Study, systolic hypertension correlated with the incidence of CAD in older men and women (7). Diastolic hypertension correlated with CAD in older men but not in older women (7). At 40-month follow-up of elderly men and 48-month follow-up of elderly women, systolic or diastolic hypertension increased the relative risk of new coronary events 2.0 times in men and 1.6 times in women (Table 1) (11).

Elderly persons with hypertension should be treated initially with salt restriction, weight reduction if necessary, cessation of drugs that increase blood pressure, avoidance of alcohol and tobacco, increase in physical activity, decrease of dietary saturated fat and cholesterol, and maintenance of adequate dietary potassium, calcium, and magnesium intake.

Antihypertensive drugs have been documented to reduce new coronary events in older men and women with hypertension (Table 2) (15–19). Persons with prior MI should be treated with beta blockers and angiotensin-converting enzyme (ACE) inhibitors and not treated with calcium channel blockers or alpha blockers (20–31). In an observational prospective study of 1212 elderly men and women, mean age 80 years, with prior MI and hypertension treated with beta blockers, ACE inhibitors, diuretics, calcium channel blockers, or alpha blockers, at 40-month follow-up, the incidence of new coronary events in persons treated with one antihypertensive drug was lowest in persons treated with beta blockers or ACE inhibitors (29). In elderly persons treated with two antihypertensive drugs, the incidence of new coronary events was lowest in persons treated with beta blockers plus ACE inhibitors (29).

In addition to beta blockers, elderly persons with hypertension and CHF should be treated with diuretics and ACE inhibitors (41,42). ACE inhibitors should also be administered to persons with diabetes or renal insufficiency (20). The blood pressure should be lowered to <140/85 mmHg in persons after MI and to 130/80 mmHg or lower in persons with diabetes or renal insufficiency (20).

Dyslipidemia
Serum total cholesterol.-- In the Framingham Study, serum total cholesterol was an independent risk factor for CAD in older men and women (43). Among persons aged 65 years or older with prior MI in the Framingham Study, serum total cholesterol was most strongly related to death from CAD and to all-cause mortality (44). Many other studies have demonstrated that a high serum total cholesterol is a risk factor for new coronary events in elderly men and women (6,11,45–47).

During 9-year follow-up of 350 men and women, mean age 79 years, in the Bronx Aging Study, a consistently increased serum low-density lipoprotein (LDL) cholesterol was associated with the development of MI in elderly women (48). In the Established Populations for Epidemiologic Studies of the Elderly study, serum total cholesterol was a risk factor for mortality from CAD in elderly women but not in elderly men (49). At 40-month follow-up of elderly men and 48-month follow-up of elderly women, an increase of 10 mg/dl of serum total cholesterol increased the relative risk of new coronary events 1.12 times in men and 1.12 times in women (Table 1) (11).

Serum high-density lipoprotein cholesterol.-- A low serum high-density lipoprotein (HDL) cholesterol is a risk factor for new coronary events in elderly men and women (6,11,43,48–51). In the Framingham Study (43), in the Established Populations for Epidemiologic Studies of the Elderly Study (49), and in our study (11), a low serum HDL cholesterol was a more powerful predictor of new coronary events than was serum total cholesterol.

During 9-year follow-up of 350 men and women in the Bronx Aging Study, a consistently low serum HDL cholesterol level was independently associated with the development of MI, cardiovascular disease, or death in men (48). At 40-month follow-up of 664 elderly men and 48-month follow-up of 1488 elderly women, multivariate analysis showed that there was a 1.70 times higher probability of developing new coronary events in men and a 1.95 times higher probability of developing new coronary events in women for a decrease of 10 mg/dl of serum HDL cholesterol (Table 1) (11).

Serum triglycerides.-- Hypertriglyceridemia has been reported to be a risk factor for new coronary events in elderly women but not in elderly men (11,43). At 40-month follow-up of elderly men and at 48-month follow-up of elderly women, multivariate analysis demonstrated that serum triglycerides was not a risk factor for new coronary events in elderly men and was a very weak risk factor for new coronary events in elderly women (Table 1) (11).

Drug Therapy of Hypercholesterolemia
At 5.4-year median follow-up of 4444 men and women (1021 aged 65–70 years) with CAD and hypercholesterolemia in the Scandinavian Simvastatin Survival Study, compared with placebo, simvastatin 20–40 mg daily significantly reduced in patients aged 65–70 years total mortality by 34%, CAD mortality by 43%, major coronary events by 34%, nonfatal MI by 33%, any acute CAD-related endpoint by 33%, any atherosclerosis-related endpoint by 34%, and coronary revascularization by 41% (Table 3) (52). The absolute risk reduction for both all-cause mortality and CAD mortality was approximately twice as great in persons 65–70 years of age at study entry as in those younger than 65 years (52).

At 6.1-year mean follow-up of 9014 men and women (3514 of whom were aged 65–75 years) with MI (64%) or unstable angina pectoris (36%) and serum total cholesterol levels of 155–271 mg/dl in the Long-Term Intervention With Pravastatin in Ischaemic Disease Study, compared with placebo, pravastatin 40 mg daily significantly decreased all-cause mortality by 22%, death from CAD by 24%, fatal and nonfatal MI by 29%, death from cardiovascular disease by 25%, need for coronary artery bypass surgery by 22%, need for coronary angioplasty by 19%, hospitalization for unstable angina pectoris by 12%, and stroke by 19% (Table 3) (54). The absolute benefits of treatment with pravastatin were greater in groups of persons at higher absolute risk for a major coronary event such as elderly persons, those with a higher serum LDL cholesterol level, those with a lower serum HDL cholesterol level, and those with a history of diabetes mellitus or smoking (54).

At 5-year follow-up of 20,536 British men and women (10,697 of whom were aged 65–80 years) with either CAD, occlusive arterial disease of noncoronary arteries, diabetes mellitus, or treated hypertension and no serum lipid requirement in the Heart Protection Study, compared with placebo, simvastatin 40 mg daily significantly decreased all-cause mortality by 13%, any vascular mortality by 17%, major coronary events by 27%, any stroke by 25%, any revascularization by 24%, and any major vascular event by 24% (Table 3) (55). In the 1263 persons aged 75–80 years at study entry and 80–85 years at follow-up, any major vascular event was significantly decreased 28% by simvastatin. Lowering serum LDL cholesterol from <116 mg/dl to <77 mg/dl by simvastatin caused a 25% significant decrease in vascular events (55).

At 3.2-year follow-up of 5804 men and women aged 70–82 years with a history of or risk factors for vascular disease and a serum total cholesterol 155 mg/dl, compared with placebo, pravastatin significantly reduced coronary death, nonfatal MI, and fatal or nonfatal stroke by 15% (Table 3) (56).

In an observational prospective study of 1410 elderly persons, mean age 81 years, with prior MI and a serum LDL cholesterol of 125 mg/dl, 48% of persons were treated with a statin and 52% with no lipid-lowering drugs. At 36-month follow-up, persons treated with statins had a significant independent reduction in new coronary events of 50% (57), a significant independent reduction in new stroke of 60% (58), and a significant independent reduction in new CHF of 48% (59). In 529 elderly diabetics, mean age 79 years, with prior MI and a serum LDL cholesterol of 125 mg/dl, 53% of persons were treated with statins and 47% with no lipid-lowering drugs (60). At 29-month follow-up, statins caused a 37% significant independent reduction in the incidence of new coronary events and a 47% significant independent reduction in the incidence of new stroke (60).

On the basis of the available data, the serum LDL cholesterol should be reduced to <100 mg/dl in persons with CAD (21,61–63). However, data from the Heart Protection Study favor treating all postinfarction patients with statins, regardless of the initial serum lipid values (55). An educational program on dyslipidemia treatment needs to be administered to physicians to improve the use of lipid-lowering drugs in elderly persons after MI (64–66).

Diabetes Mellitus
Diabetes mellitus is a risk factor for new coronary events in elderly men and in elderly women (11,67,68). At 40-month follow-up of elderly men and 48-month follow-up of elderly women, diabetes mellitus was found by multivariate analysis to increase the relative risk of new coronary events 1.9 times in men and 1.8 times in women (Table 1) (11).

Diabetics are more often obese and have higher serum LDL cholesterol and triglycerides levels and lower serum HDL cholesterol levels than do nondiabetics. Diabetics also have a higher prevalence of hypertension and left ventricular hypertrophy than do nondiabetics. These risk factors contribute to the higher incidence of new coronary events in diabetics than in nondiabetics.

Elderly persons after MI who have diabetes should be treated with dietary therapy, weight reduction if necessary, and appropriate drugs if needed to control hyperglycemia. Other coronary risk factors such as smoking, hypertension, dyslipidemia, obesity, and physical inactivity should be controlled. The blood pressure should be lowered to 130/80 mmHg or lower by an ACE inhibitor (20) or by an angiotensin II receptor blocker (69) if the ACE inhibitor cannot be tolerated. The serum LDL cholesterol level should be reduced to <100 mg/dl (61). Because there are data showing an increased incidence of coronary events and of mortality in diabetics with CAD treated with sulfonylureas (70–72), these drugs should be avoided if possible in postinfarction diabetics.

Obesity
In the Framingham Study, obesity was an independent risk factor for new coronary events in older men and in older women (67). Disproportionate distribution of fat to the abdomen assessed by the waist-to-hip circumference ratio has also found to be a risk factor for cardiovascular disease, mortality from CAD, and total mortality in elderly men and women (73,74).

Obese persons who have had an MI must undergo weight reduction. Weight reduction is also a first approach to controlling hyperglycemia, mild hypertension, and dyslipidemia before placing persons on long-term drug therapy. Regular aerobic exercise should be added to diet in treating obesity.

Physical Inactivity
Physical inactivity is associated with obesity, dyslipidemia, hyperglycemia, and hypertension. At 12-year follow-up in the Honolulu Heart Program, physically active men aged 65 years or older had a relative risk of 0.43 for CAD compared with inactive men (75). Exercise training programs are not only beneficial in preventing CAD (76) but also have been shown to improve endurance and functional capacity in elderly persons after MI (77,78). Moderate exercise programs suitable for elderly persons after MI include walking, climbing stairs, bicycling, or swimming.

	ASPIRIN

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Aspirin reduces the aggregation of platelets exposed to thrombogenic stimuli by inhibiting the cyclooxygenase enzyme reaction within the platelet and thereby blocking synthesis of thromboxane A₂, a powerful stimulus to platelet aggregation and vasoconstriction (79).

Randomized trials involving 20,006 patients showed that aspirin and other antiplatelet drugs administered to patients after MI decreased the incidence of recurrent MI, stroke, or vascular death by 36 events per 1000 patients treated for 2 years (80). The benefit of aspirin in reducing MI, stroke, or vascular death in patients after MI was irrespective of age, sex, blood pressure, and diabetes (80).

Data from the Multicenter Study of Myocardial Ischemia in 936 patients enrolled 1 to 6 months after an acute MI (70% of patients) or unstable angina pectoris (30% of patients) showed at 23-month follow-up that the cardiac mortality rate was 1.6% for aspirin users and 5.4% for nonusers of aspirin (81). Cardiac mortality was decreased 90% in aspirin users who underwent thrombolytic therapy compared with nonusers of aspirin who underwent thrombolytic therapy (81).

The Coumadin Aspirin Reinfarction Study (CARS) randomized 8803 low-risk patients after MI to aspirin 160 mg daily, aspirin 80 mg plus warfarin 1 mg daily, or to aspirin 80 mg plus warfarin 3 mg daily (82). At follow-up, the combined incidence of cardiovascular death, recurrent MI, and stroke was similar in the three treatment groups (82). The incidence of mortality was similar in the three treatment groups. However, the incidence of nonfatal stroke was decreased by aspirin 160 mg daily (82). Data from the Combination Hemotherapy and Mortality and Prevention Study showed in 5059 postinfarction patients that warfarin administered in a dose to achieve an international normalized ration (INR) of 1.8 combined with low-dose aspirin did not provide a clinical benefit beyond that achieved with aspirin alone (83).

Of 5490 survivors of acute MI aged 65 years with no contraindications to aspirin, 4149 patients (76%) received aspirin at the time of hospital discharge (84). At 6-month follow-up, aspirin users had a significant 23% decrease in mortality (84).

In an observational prospective study of 1410 patients, mean age 81 years, with prior MI and a serum LDL cholesterol of 125 mg/dL or higher, 832 patients (59%) were treated with aspirin (85). At 3-year follow-up, use of aspirin caused a 52% significant independent reduction in new coronary events (85). Use of statins caused a 54% significant independent reduction in the incidence of new coronary events (85).

On the basis of the available data, all patients should receive aspirin in a dose of 160 mg to 325 mg daily on day 1 of an acute MI and continue this dose of aspirin for an indefinite period unless there is a specific contraindication to its use (86).

Clopidogrel is also an excellent antiplatelet drug that is effective in reducing MI, ischemic stroke, and vascular death in postinfarction patients (87). The American College of Cardiology (ACC)/American Heart Association (AHA) guidelines recommend the use of clopidogrel for an indefinite period in postinfarction patients unless there is a specific contraindication to its use (86).

	ANTICOAGULANTS

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The routine use of warfarin after MI is controversial (88). However, three well-controlled studies have shown a decrease in mortality and/or morbidity in patients receiving long-term oral anticoagulation therapy after MI (89–91). The Sixty Plus Reinfarction Study Group reported at 2-year follow-up after MI of persons, mean age 68 years, that compared with placebo, acenocoumarin, or phenprocoumon caused a 26% nonsignificant decrease in mortality, a 55% significant decrease in recurrent MI, and a 40% nonsignificant decrease in stroke (89). The Warfarin Reinfarction Study Group showed at 37-month follow-up after MI of persons 75 years of age or younger that compared with placebo, warfarin caused significant decreases in mortality (24%), recurrent MI (34%), and stroke (55%) (90). The Anticoagulation in the Secondary Prevention of Events in Coronary Thrombosis Research Group reported at 37-month follow-up after MI of persons, mean age 61 years, that compared with placebo, nicoumalone, or phenprocoumon caused a 10% nonsignificant decrease in mortality, a 53% significant decrease in recurrent MI, and a 42% significant decrease in stroke (91).

The ACC/AHA guidelines recommend as Class I indications for long-term oral anticoagulant therapy after MI: 1) secondary prevention of MI in post-MI patients unable to tolerate daily aspirin or clopidogrel, 2) post-MI patients with persistent atrial fibrillation, and 3) post-MI patients with left ventricular thrombus (70). Long-term warfarin should be given in a dose to achieve an INR between 2.0 and 3.0 (86).

	BETA BLOCKERS

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Beta blockers are very effective antianginal and antiischemic agents and should be given to all patients with angina pectoris or silent myocardial ischemia due to CAD unless there are specific contraindications to their use. Teo and colleagues (92) analyzed 55 randomized controlled trials, which included 53,268 patients, that investigated the use of beta blockers after MI. Beta blockers significantly reduced mortality by 19% in these studies (92). A randomized, double-blind, placebo-controlled study of propranolol in high-risk survivors of acute MI at 12 Norwegian hospitals showed a 52% decrease in sudden cardiac death in persons treated with propranolol for 1 year (93).

Table 4 shows that metoprolol, timolol, propranolol, and carvedilol caused a greater decrease in mortality after MI in older persons than in younger persons (94–98). The decrease in mortality after MI in patients treated with beta blockers was due both to a reduction in sudden cardiac death and recurrent MI (95–98). A retrospective cohort study also showed that MI patients aged 60 to 89 years treated with metoprolol had an age-adjusted mortality reduction of 76% (99).

In the Beta-Blocker Pooling Project, results from 9 studies involving 3519 patients with CHF at the time of acute MI showed that beta blockers caused a 25% decrease in mortality (101). In the Multicenter Diltiazem Post-Infarction Trial, the 2.5-year risk of total mortality in patients with an LVEF <30% was 24% for patients receiving beta blockers (relative risk = 0.53) versus 45% for patients not receiving beta blockers (102). Beta blockers have also been shown to reduce mortality in patients with CAD and CHF associated with an LVEF 35% (103) or 40% (36).

An observational prospective study was performed in 477 persons, mean age 79 years, with prior MI and an LVEF <40% (mean LVEF 31%) (24). At 34-month follow-up, persons treated with beta blockers without ACE inhibitors had a 25% significant decrease in new coronary events and a 41% significant decrease in CHF (24). At 41-month follow-up, persons treated with both beta blockers and ACE inhibitors had a significant 37% reduction in new coronary events and a significant 60% reduction in CHF (24).

A retrospective analysis of the use of beta blockers after MI in a New Jersey Medicare population from 1987 to 1992 showed that only 21% of elderly persons after MI without contraindications to beta blockers were treated with beta blockers (104). Elderly persons who were treated with beta blockers after MI had a 43% decrease in 2-year mortality and a 22% decrease in 2-year cardiac hospital readmissions than elderly persons who were not treated with beta blockers (104). Use of a calcium channel blocker instead of a beta blocker after MI doubled the risk of mortality (104).

Beta blockers have also been demonstrated to decrease mortality in elderly persons with complex ventricular arrhythmias after MI and an LVEF 40% (34) or 40% (33). The decrease in mortality in elderly persons with heart disease and complex ventricular arrhythmias caused by propranolol is due more to an antiischemic effect than to an antiarrhythmic effect (38). In these persons, propranolol also markedly decreased the circadian variation of ventricular arrhythmias (105), abolished the circadian variation of myocardial ischemia (106), and abolished the circadian variation of sudden cardiac death or fatal MI (107).

A meta-analysis of trials also showed that the use of beta blockers after non-Q-wave MI is likely to decrease mortality and recurrent MI by 25% (108). Therefore, elderly persons with Q-wave MI or non-Q-wave MI without contraindications to beta blockers should be treated with beta blockers indefinitely after MI. Beta blockers with intrinsic sympathomimetic activity should not be used. Propranol, timolol, metoprolol, or carvedilol should be used to treat post-MI persons (109). The ACC/AHA guidelines recommend that patients without a clear contraindication to beta blocker therapy should receive beta blockers within a few days of MI (if not initiated acutely) and continue them indefinitely (86).

	NITRATES

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Long-acting nitrates are effective antianginal and antiischemic drugs (110). These drugs should be administered along with beta blockers to persons after MI who have angina. The dose of oral isosorbide dinitrate prescribed should be gradually increased to a dose of 30–40 mg given three times daily if tolerated. Isosorbide-5-mononitrate in a dose of 60 mg may also be given once daily. To avoid nitrate tolerance, there should be a nitrate-free interval of 12 hours each day (111). Beta blockers should be used to prevent angina pectoris and rebound myocardial ischemia during the nitrate-free interval.

	ANGIOTENSIN-CONVERTING ENZYME INHIBITORS

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ACE inhibitors improve symptoms, quality of life, and exercise tolerance in patients with CHF and an abnormal LVEF (112) or a normal LVEF (113). An overview of 32 randomized trials that included 7105 patients with CHF showed that ACE inhibitors significantly reduced mortality by 23% and mortality or hospitalization for CHF by 35% (114). Persons who develop CHF after MI should be treated with ACE inhibitors unless there are specific contraindications to their use.

Table 5 shows that ACE inhibitors decrease mortality in persons after MI (22,23,115–118). In the Survival and Ventricular Enlargement Trial, asymptomatic patients with an LVEF 40% treated with captopril 3 to 16 days after MI had at 42-month follow-up compared with placebo, a 19% decrease in mortality, a 21% decrease in death from cardiovascular causes, a 37% decrease in development of severe CHF, a 22% decrease in development of CHF requiring hospitalization, and a 25% decrease in recurrent MI (115). Captopril reduced mortality independent of age, sex, blood pressure, LVEF, and use of thrombolytic therapy, aspirin, or beta blockers (115). In the Heart Outcomes Prevention Evaluation Study, 9217 persons aged 55 years (55% aged 65 years) with MI (53%), cardiovascular disease (88%), or diabetes mellitus (38%) but no CHF or abnormal LVEF were randomized to ramipril 10 mg daily or placebo (22). At 4.5-year follow-up, compared with placebo, ramipril significantly decreased the incidence of MI, stroke, and cardiovascular death by 22% (22).

	CALCIUM CHANNEL BLOCKERS

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Teo and colleagues (92) analyzed randomized controlled trials, which including 20,342 persons, that investigated the use of calcium channel blockers after MI. Mortality was insignificantly higher (relative risk = 1.04) in persons treated with calcium channel blockers (92). A meta-analysis of randomized clinical trials of the use of calcium channel blockers in persons with MI, unstable angina pectoris, and stable angina pectoris showed that the relative risk for mortality in the trials using dihydropyridines such as nifedipine, which increase heart rate, was 1.16 (119). The calcium channel blockers diltiazem and verapamil, which decrease heart rate, had no effect on survival (119).

Furberg and colleagues (120) performed a meta-analysis of the effect of nifedipine on mortality in 16 randomized secondary prevention clinical trials in persons with CAD. In this study, the relative risk for mortality was 1.06 for persons treated with nifedipine 30 mg to 50 mg daily, 1.18 for persons treated with nifedipine 60 mg daily, and 2.83 for persons treated with nifedipine 80 mg daily (120).

The Multicenter Diltiazem Postinfarction Trial demonstrated at 25-month follow-up in persons after MI that, compared with placebo, diltiazem caused no significant effect on mortality or recurrent MI (121). However, in persons with pulmonary congestion at baseline or an LVEF <40%, diltiazem caused a significant increase in new cardiac events (hazard ratios = 1.41 and 1.31, respectively) (121). In this study, diltiazem also increased the incidence of late-onset CHF in persons with an LVEF <40% (122). Use of a calcium channel blocker instead of a beta blocker after MI in a New Jersey Medicare population also doubled the risk of mortality (104).

Since no calcium channel blocker has been demonstrated to improve survival after MI, except for the subgroup of patients with a normal LVEF treated with verapamil in the Danish Verapamil Infarction Trial II (123), calcium channel blockers should not be used in the treatment of patients after MI. However, if patients after MI have persistent angina despite treatment with beta blockers and nitrates, a nondihydropyridine calcium channel blocker such as verapamil or diltiazem should be added to the therapeutic regimen if the LVEF is normal. If the LVEF is abnormal, amlodipine or felodipine should be added to the therapeutic regimen. The ACC/AHA guidelines state that there are no Class I indications for the use of calcium channel blockers after MI (21).

	ANTIARRHYTHMIC THERAPY

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Class I Drugs
A meta-analysis of 59 randomized controlled trials composed of 23,229 persons, which investigated the use of quinidine, procainamide, disopyramide, imipramine, moricizine, lidocaine, tocainide, phenytoin, mexiletine, aprindine, encainide, and flecainide after MI, showed that mortality was significantly higher in persons receiving class I antiarrhythmic drugs than in persons receiving no antiarrhythmic drugs (odds ratio = 1.14) (92). None of the 59 studies showed a reduction in mortality by class I antiarrhythmic drugs (92).

In the Cardiac Arrhythmia Suppression Trials I and II, older age also increased the likelihood of adverse effects including death in persons after MI receiving encainide, flecainide, or moricizine (124). Compared with no antiarrhythmic drug, quinidine or procainamide did not reduce mortality in elderly persons with CAD, a normal or abnormal LVEF, and presence versus absence of ventricular tachycardia (125). On the basis of the available data, persons after MI should not receive class I antiarrhythmic drugs.

D, L-Sotalol, and D-Sotalol
Studies comparing the effect of d, l-sotalol with placebo on mortality in persons with complex ventricular arrhythmias have not been performed. Compared with placebo, d, l-sotalol did not reduce mortality in post-MI persons followed for 1 year (126). In the Survival with Oral d-Sotalol (SWORD) trial, 3121 survivors of MI with an LVEF 40% were randomized to d-sotalol or placebo (127). Mortality was significantly higher at 148-day follow-up in persons treated with d-sotalol (5.0%) than in persons treated with placebo (3.1%) (127). On the basis of the available data, d, l-sotalol and d-sotalol should not be used to treat persons after MI.

Amiodarone
In the European Myocardial Infarction Amiodarone Trial, 1486 survivors of MI with an LVEF 40% were randomized to amiodarone (743 patients) or to placebo (743 patients) (128). At 2-year follow-up, 103 patients treated with amiodarone and 102 patients treated with placebo had died (128). In the Canadian Amiodarone Myocardial Infarction Arrhythmia Trial, 1202 survivors of MI with nonsustained ventricular tachycardia or complex ventricular arrhythmias were randomized to amiodarone or to placebo (129). Amiodarone was very effective in suppressing ventricular tachycardia and complex ventricular arrhythmias. However, the mortality rate at 1.8-year follow-up was not significantly different in the persons treated with amiodarone or placebo (129). In addition, early permanent discontinuation of drug for reasons other than outcome events occurred in 36% of persons taking amiodarone (129).

In the Cardiac Arrest in Seattle: Conventional Versus Amiodarone Drug Evaluation Study, the incidence of pulmonary toxicity was 10% at 2 years in persons receiving amiodarone in a mean dose of 158 mg daily (130). The incidence of adverse effects for amiodarone also approaches 90% after 5 years of treatment (131). On the basis of the available data, amiodarone should not be used in the treatment of persons after MI.

Beta Blockers
However, beta blockers have been demonstrated to reduce mortality in persons with nonsustained ventricular tachycardia or complex ventricular arrhythmias after MI in patients with a normal or abnormal LVEF (33,34,132,133). On the basis of the available data, beta blockers should be used in the therapy of elderly persons after MI, especially if nonsustained ventricular tachycardia or complex ventricular arrhythmias are present, unless there are specific contraindications to their use.

Automatic Implantable Cardioverter-Defibrillator
In the Antiarrhythmics Versus Implantable Defibrillators (AVID) trial, 1016 persons, mean age 65 years, with a history of ventricular fibrillation or serious sustained ventricular tachycardia were randomized to an automatic implantable cardioverter defibrillator (AICD) or to drug therapy with amiodarone or d, l-sotalol (134). Persons treated with an AICD had a 39% decrease in mortality at 1 year, a 27% decrease in mortality at 2 years, and a 31% decrease in mortality at 3 years (134). If persons after MI have life-threatening ventricular tachycardia or ventricular fibrillation, an AICD should be inserted. The efficacy of the AICD implanted for ventricular fibrillation or recurrent sustained ventricular tachycardia on survival is similar in older and younger persons (135).

The Multicenter Automatic Defibrillator Implantation Trial (MADIT) randomized 196 persons with prior MI, an LVEF 35%, a documented episode of asymptomatic nonsustained ventricular tachycardia, and inducible ventricular tachycardia or ventricular fibrillation not suppressed by intravenous procainamide or an equivalent drug at electrophysiologic study to conventional medical therapy or implantation of an AICD (136). At 27-month follow-up, persons treated with an AICD had a 54% reduction in mortality (136). These data favor the prophylactic implantation of an AICD in post-MI persons at very high risk for sudden cardiac death.

MADIT II randomized 1,232 persons, mean age 64 years, with a prior MI and an LVEF of 30% to an AICD or to conventional medical therapy (137). At 20-month follow-up, compared with conventional medical therapy, the AICD significantly decreased all-cause mortality 31% from 19.8% to 14.2% (137). The effect of AICD therapy in improving survival was similar in persons stratified according to age, sex, LVEF, New York Heart Association class, and QRS interval (137). These data favor considering the prophylactic implantation of an AICD in post-MI persons with an LVEF of 30%.

	HORMONE REPLACEMENT THERAPY

Top Abstract Management of Coronary Risk... Aspirin Anticoagulants Beta Blockers Nitrates Angiotensin-Converting Enzyme... Calcium Channel Blockers Antiarrhythmic Therapy Hormone Replacement Therapy Revascularization References

 
The Heart Estrogen/Progestin Replacement Study (HERS) investigated, in 2763 women with documented CAD, the effect of hormonal therapy versus double-blind placebo on coronary events (138). At 4.1-year follow-up, there were no significant differences between hormonal therapy and placebo in the primary outcome (nonfatal MI or CAD death) or in any of the secondary cardiovascular outcomes. However, there was a 52% significantly higher incidence of nonfatal MI or death from CAD in the first year in persons treated with hormonal therapy than in persons treated with placebo (138). Women on hormonal therapy had a 289% significantly higher incidence of venous thromboembolic events and a 38% significantly higher incidence of gallbladder disease requiring surgery than women on placebo.

The Estrogen Replacement and Atherosclerosis trial randomized 309 postmenopausal women, mean age 66 years, with coronary angiographic evidence of significant CAD to estrogen plus progestin, estrogen alone, or double-blind placebo (139). At 3.2-year follow-up, quantitative coronary angiography showed no between-group differences in progression of coronary atherosclerosis (139).

At 6.8-year follow-up in the HERS trial, hormonal therapy did not decrease the risk of cardiovascular events in women with CAD (140). The investigators concluded that hormonal therapy should not be used to decrease the risk of coronary events in women with CAD (140). At 6.8-year follow-up in the HERS trial, all-cause mortality was insignificantly increased 10% by hormonal therapy (141). The overall incidence of venous thromboembolism at 6.8-year follow-up was significantly increased 208% by hormonal therapy (141). At 6.8-year follow-up, the overall incidence of biliary tract surgery was significantly increased 48%, the overall incidence for any cancer was insignificantly increased 19%, and the overall incidence for any fracture was insignificantly increased 4% (141).

The estrogen plus progestin component of the Women's Health Initiative (WHI) study included 16,608 healthy postmenopausal women aged 50–79 years with an intact uterus who were randomized to estrogen plus progestin or to placebo (142). At 5.2-year follow-up, this component of the WHI study was prematurely discontinued because the excess risk of events included in the global index was 19 per 10,000 person-years (142). Absolute excess risks per 10.000 person-years included 7 more coronary events, 8 more strokes, 8 more episodes of pulmonary embolism, and 8 more invasive breast cancers, while absolute risk reductions per 10,000 person-years were 6 fewer colorectal cancers and 5 fewer hip fractures (142).

On the basis of the available data, hormonal therapy should not be used in postmenopausal women with CAD (21,142,143).

	REVASCULARIZATION

Top Abstract Management of Coronary Risk... Aspirin Anticoagulants Beta Blockers Nitrates Angiotensin-Converting Enzyme... Calcium Channel Blockers Antiarrhythmic Therapy Hormone Replacement Therapy Revascularization References

 
Medical therapy alone is the preferred treatment in elderly persons after MI. The two indications for revascularization in elderly persons after MI are prolongation of life and relief of unacceptable symptoms despite optimal medical management. In a prospective study of 305 patients aged 75 years with chest pain refractory to at least two antianginal drugs, 150 patients were randomized to optimal medical therapy and 155 patients to invasive therapy (144,145). In the invasive group, 74% had coronary revascularization (54% coronary angioplasty and 20% coronary artery bypass graft surgery). During the 6-month follow-up, one third of the medically treated group needed coronary revascularization for uncontrollable symptoms. At 6-month follow-up, death, nonfatal MI, or hospital admission for an acute coronary syndrome was significantly higher in the medically treated group (49%) than in the invasive group (19%) (144,145). Revascularization by percutaneous transluminal coronary angioplasty (145) or by coronary artery bypass graft surgery (146) in elderly persons is extensively discussed elsewhere. If coronary revascularization is performed, aggressive medical therapy must be continued.

Summary
Table 6 summarizes the overall management approach to elderly persons after MI.

Received December 24, 2003

Accepted March 2, 2004

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Top Abstract Management of Coronary Risk... Aspirin Anticoagulants Beta Blockers Nitrates Angiotensin-Converting Enzyme... Calcium Channel Blockers Antiarrhythmic Therapy Hormone Replacement Therapy Revascularization References

 

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