Cardiovascular risk-factor reduction in elderly patients with cardiac disease.

[Williams MA. Cardiovascular risk-factor reduction in elderly patients with cardiac disease. Phys Ther. 1996;76:469-480. Key words: Cardiac, general; Cardiovascular system; Coronary disease, Geriatrics; Risk factors.

Elderly persons (65 years of age and older) are the fastest growing age group in the United States. Individuals join the ranks of the elderly population at the rate of approximately 1,000 per day, and that number is likely to increase because the average life expectancy for persons reaching age 65 years is now an additional 15 years.[1-3] In 1991, there were 30 million persons aged 65 years or greater in the United States, and this figure is expected to increase to almost 50 million by the year 2020 (20% of the population).[4,5]

Currently, the 12% of the population considered elderly use 30% of all health care resources and a much larger proportion of resources related to cardiovascular disease.[6] The majority of patients with coronary heart disease (CHD), which is the manifestation of coronary artery disease (CAD), are older than 65 years, and nearly one half of persons aged 65 years or older have cardiovascular disease.[7] Coronary artery disease is the most common cause of death in the elderly population. The prevalence of CAD is greatest and similar in women and men by age 70 years.[6-8] The mean age of patients in coronary care programs following a myocardial infarction (MI) is now greater than 65 years.[5] One third of cardiac operations on adults are performed on patients aged 65 years or greater.[9] Additionally, cardiac disease is rarely isolated. Disability associated with cardiovascular disease is pervasive and often linked with other structural and functional changes associated with aging, with concomitant diseases such as pulmonary disease or arthritis, and with inactivity. In the United States, use of coronary artery bypass grafting (CABG) and angioplasty is on the rise in elderly patients, but there appears to be some reluctance to manage risk factors in this group.

Four major modifiable risk factors for the development and progression of CAD have been identified: hypertension, hypercholesterolemia, habitual smoking, and physical inactivity.[10] The effectiveness of risk-factor modification for the secondary prevention of events of cardiac morbidity and mortality has been described for younger persons; however, less is known for elderly persons.[11,12] The purpose of this review is to focus on these four major risk factors in elderly patients with cardiac disease by describing the effectiveness of modification of these factors, methodologies for doing so, and considerations for the future of such interventions.

Distribution of Cardiovascular Risk Factors in the Elderly Population

The distribution of hypertension, hypercholesterolemia, habitual smoking, and physical inactivity in the elderly population and subsets of this group are reviewed in Table 1. Data are from three separate databases--Omaha,[3] Framingham,[13] and New York City[14]--and describe the extent of risk factors in elderly persons. The Framingham (Mass) data represent individuals from a community setting of a cross-sectional age range among the elderly population, whereas data from New York City were obtained from a long-term health care center with generally older patients (mean age=82 years). Omaha (Neb) data were obtained from elderly patients (mean age=71 years) who were referred for participation in a standard early outpatient cardiac rehabilitation program. Both Framingham and New York City cohorts included individuals with and without diagnosed cardiovascular disease. All patients in the Omaha database had a diagnosis of CHD. Demographic differences between the study populations exist, but their frequencies of the various risk factors are similar.

[TABULAR DATA 1 OMITTED]

Comparisons of elderly patients with cardiac disease (mean age [[+ or -]SD]=71.0[+ or -]3.1 years) and younger patients with cardiac disease (mean age=54.5[+ or -]6.3 years), with both groups participating in the same cardiac rehabilitation program, suggest different frequencies of hypertension, habitual smoking, and reduced exercise capacity (Tab. 2). Data suggest that elderly patients have statistically significant increases in frequency of hypertension and physical inactivity but a decreased frequency of habitual smoking. Both groups appear to have similar frequencies of hypercholesterolemia.

Table 2.
Risk-factor Frequency Data for Elderly Versus Younger Patient Groups
at Phase II [Entry.sup.3](a)
                                      Elderly Group   Younger Group
Variable                                 (N= 191         (N=414)
Hypertension (%)                           41               21
Hypercholesterolemia                       18               23
  (% > 240 mg/dL)
Habitual smoking                           17(*)            50
Physical inactivity                        41(*)            32
  (% [less than or equal to]4 METs)

(*) One metabolic equivalent (MET) is defined as the oxygen uptake
while sitting quietly. Peak exercise is defined in terms of
multiples of resting MET level. (Asterisk (*) indicates
significantly different from younger group
(P <.05) Subjects in the elderly were 65 years of age or older;
subjects in the younger group were less than 65 years of age.

Hypertension

The mechanisms of hypertension in elderly persons are similar to those in younger individuals.[15] Increased peripheral vascular resistance (PVR) plays a major role, and both mean arterial pressure and PVR increase with advancing age. The reduced production of the protein elastin, atherosclerosis, and calcific changes in the aorta and other large arteries reduce distensibility and elasticity, decrease compliance, increase PVR, and contribute to hypertension in this age group.[16]

Framingham data suggest that systolic hypertension [greater than or equal to] 160 mm Hg) is a statistically significant risk factor for CHD in elderly men and women, whereas diastolic hypertension )[greater than or equal to] 95 mm Hg) is a statistically significant risk factor only in elderly women.[13] In contrast, Aronow et al[14] have suggested that hypertension is significantly correlated with CAD in elderly women but not in elderly men. These authors also demonstrated that hypertension in elderly subjects with previously documented CAD correlated with new coronary events.[17] In people aged 65 to 85 years, the frequency of hypertension is 20% to 46% in men and 37% to 65% in women.[3,13,14]

Treatment

A number of randomized clinical trials performed over the last two decades with older patients have demonstrated reductions in cardiovascular morbidity and mortality associated with treatment of both systolic and diastolic hypertension, although no investigation has focused on elderly patients with cardiac disease.[18] In the Hypertension Detection and Follow-up Program, patients experienced a 45% decrease in the incidence of fatal and nonfatal strokes after receiving antihypertensive therapy for diastolic blood pressures (DBPs) greater than 90 mm Hg.[19] In the National Heart Foundation of Australia study of mild hypertension, treatment for DBPs ranging from 95 to 109 mm Hg resulted in a 39% reduction in fatal and nonfatal sequela, including stroke, MI, and cardiac death, in the treatment group versus the standard care group.[20] The European Working Party on High Blood Pressure in the Elderly focused on patients with DBPs of 90 to 109 mm Hg or systolic blood pressures (SBPs) of 160 to 239 mm Hg. A statistically significant 38% reduction in total cardiovascular mortality in actively treated patients, including a 60% reduction in fatal MI, was observed.[21] The Systolic Hypertension in the Elderly Program (SHEP) studied patients with SBPs ranging from 160 to 219 mm Hg and DBPs of less than 90 mm Hg.[22] A 36% reduction in fatal and nonfatal stroke rate was observed in treated patients. Reductions in CAD incidence and deaths, left ventricular failure, and total mortality also were observed. Similar to the findings of each of these studies, the Swedish Trial in Old Patients With Hypertension (STOP-Hypertension) demonstrated the effects of antihypertensive treatment in patients with SBPs of 180 to 230 mm Hg and DBPs of at least 90 mm Hg and in patients with DBPs of 105 to 120 mm Hg who were 70 to 84 years of age.[23] Statistically significant reductions in stroke morbidity and mortality (38%) and total mortality (43%), including deaths resulting from MI and other cardiovascular conditions, were noted. Finally, the multicenter Medical Research Council Working Party study conducted in the United Kingdom, although limited by several design flaws, demonstrated statistically significant reductions in stroke and all other cardiovascular events.[24]

Although none of the reports regarding cardiovascular morbidity and mortality associated with treatment of hypertension are specific to elderly patients with cardiac disease, treatment recommendations for such patients are based on these data. Cheting and Weber[18] recommend treatment for elderly patients when the DBP is greater than 90 mm Hg or the SBP is greater than 160 mm Hg. These authors also suggest that therapy should be considered for patients with borderline systolic hypertension (SBP=140-159 mm Hg) who also exhibit multiple risk factors. The goal of treatment should be to reduce the DBP to below 90 mm Hg or by at least 10 mm Hg or to reduce the SBP to below 160 mm Hg while maintaining a DBP of 70 mm Hg or above.[25] Reducing SBP to less than 140 mm Hg may result in additional benefit without excess risk but should not be attempted at the expense of adverse effects or unnecessary complexity of treatment.[26] In addition, because sluggish baroreceptor and sympathetic nervous system responsiveness as well as impaired cerebral autoregulation may be present in these patients, Langer et al[27] recommend that blood pressure goals be achieved over periods of months rather than days or weeks.

According to Cheung and Weber,[18] nonpharmacological therapy should be the initial approach to therapy in elderly patients with mild to moderate hypertension and certainly a feature of any treatment regimen that also requires pharmacologic intervention. Recommendations should include weight reduction, sodium restriction, decreased alcohol intake, and regular aerobic exercise.[28,29] Because elderly patients may already have borderline appropriate dietary intake, it is important to ensure the adequacy of any prescribed caloric-restricted diet. As suggested previously, it is usually appropriate to continue nonpharmacological measures in conjunction with drug therapy because of the beneficial effects on cardiovascular risk and the potential reduction of the amount of medication required to achieve blood pressure control.

Pharmacologic therapy of all types is more difficult in elderly patients than in younger patients because the aging process is associated with altered pharmacokinetics and drug responses.[18] Both hepatic and renal function are often reduced, which may result in decreased clearance of pharmacological agents. Low blood volume, potentially leading to higher initial plasma drug concentration, and reduced baroreflex sensitivity, which may lead to less responsiveness to volume-pressure changes, also are frequently present and may increase responsiveness to these medications in these patients.[30] As a result, a comparatively high incidence of symptomatic side effects, including hypotension, dizziness, and fatigue, can be anticipated.[31-33] Most often, however, adverse effects of drug therapy in elderly persons are not unique but are simply exaggerated responses to problems that also are observed in younger patients.[18] Reduced dosages and careful titrations may minimize undesired side effects.

The association of antihypertensive therapy with undesirable changes in blood lipids has been suggested.[18] Results from both the European Working Party in High Blood Pressure in the Elderly study and the SHEP study, however, suggested only transient adverse effects in this age group.[34,35] Although a lipid-related increase in cardiovascular risk theoretically may offset the benefits of antihypertensive therapy, the clinical significance of this effect is unclear. Certainly, lipid profiles should be monitored during therapy. Conversely, selection of antihypertensive agents not associated with adverse effects on lipids, including calcium channel blockers, angiotensin-converting enzyme (ACE) inhibitors, and centrally and peripherally acting antiadrenergic agents may be necessary.

Diuretics have provided the basis for treatment in all major trials of antihypertensive therapy in the elderly population.[18] In view of the cardiovascular benefits demonstrated in these studies, initial therapy with diuretics appears to be appropriate in this patient group.[36] Unless the patient has renal insufficiency or diabetes mellitus, thiazide diuretics are preferred to loop diuretics because they are at least as effective and need to be given only once daily.[37] More frequent monitoring to detect the hypokalemia and hypomagnesemia may be required.[37,38] Because hypokalemia has been linked to the development of potentially hazardous cardiac dysrhythmias, such monitoring may be particularly important in elderly patients with CAD who have a propensity for arrhythmias.[18]

The value of beta-blockers in treating elderly patients with hypertension who require therapy in addition to or in place of diuretic agents is not clear.[18] Beta-blockers reduce cardiac output and heart rate and produce the short-term effect of increased PVR, the latter effect being of particular concern in elderly patients. Although many clinicians have found these agents to work satisfactorily in elderly patients, it has been reported that they are less effective in older patients than in young patients.[24,39] The success of the SHEP trial, however, suggests that beta-blockers can have a role in the treatment of elderly patients.[35] When beta-blockers are used for treating hypertension in elderly patients, plasma concentrations of the drug may be higher as a consequence of the slower metabolism of these patients compared with that of younger patients. Unless smaller dosages are used initially, the incidence of adverse effects during treatment may be relatively high in older patients with hypertension. Fatigue and exercise intolerance sometimes associated with these agents may be more frequent and may further limit the patient with poor functional capacity.

Calcium channel blockers are clearly effective in elderly patients.[40-42] These agents are at least as efficacious as diuretics and perhaps are better tolerated.[43] Postural hypotension, sedation, depression, and biochemical abnormalities generally are not associated with these agents. In addition, Buhler[44] has suggested that a greater percentage of older patients with hypertension respond to calcium channel blockers than to beta-adrenergic blockers. Hypotension, dizzyness, light-headedness, and ankle edema, however, may be associated with these medications, as well as a potential increase in risk of MI and stroke (see article by Ciccone in this issue). Angiotensin-converting enzyme inhibitors also appear to be effective in this age group even though low serum renin values are characteristic of elderly individuals with hypertension and thus suggest that these agents might be expected to be less effective in this Angiotensin-converting enzyme inhibitors reduce total PVR without reflex stimulation of heart rate and cardiac output. The appear to be particularly effective in elderly patients when combined with diuretic therapy, with a potential added advantage of a tendency to raise serum potassium levels.[46] Because of the possibility of hyperkalemia, ACE inhibitors should be used carefully in patients with renal impairment and in patients who are taking potassium-retaining diuretics, potassium salts, or nonsteroidal anti-inflammatory drugs. Furthermore, ACE inhibitors may be useful in managing coexisting congestive heart failure, and, like beta-blockers and calcium channel blockers, they appear to be beneficial in the treatment of patients post-MI.[47,48]

If these pharmacological agents have not been effective or well tolerated, the use of alternative or additional drugs may be indicated. [18] The [alpha.sub.1]-blockers and anti-adrenergic agents produce antihypertensive effects in elderly individuals.[49] Concerns that treatment with these drugs may be associated with detrimental effects on quality of life and reports of postural hypotension, however, have been cited as reasons for avoiding the use of these medications in elderly patients.[50] Hypotension during therapy may be more frequent in the presence of volume depletion or concomitant use of other antihypertensive medications. Starting dose or increases in dosage initiated at bedtime while the patient is positioned supine appear to reduce hypotensive episodes associated with this therapy. Use of the [alpha1] blocker doxazosin or terazosin appears to decrease the incidence of first-dose syncope because of delayed onset of effects.[51.52] In summary, hypertension should be treated in elderly patients post-MI. With this recommendation, however, is the caution to avoid excessively low blood pressure because of the increased potential for a poor outcome.[53] Analysis of patients with preexisting hypertension or those developing hypertension post-MI indicates a greater risk of mortality, recurrent MI, and stroke compared with those without hypertension.[54] Treatment clearly reduces this risk.

Hypercholesterolemia

Hypercholesterolemia appears to be an important risk factor in the elderly population, although findings from two recent studies suggest that this remains controversial.[14,17,55-63] From guidelines developed for younger individuals, it is clear that lipid abnormalities are common even in elderly individuals.[64] Elevated serum total cholesterol (T-CHOL), has been shown to be a statistically significant risk factor for mortality from CHD in elderly persons and predictive of new coronary events in elderly men and women with CAD.[13,17,57] Additionally, a recent analysis revealed that among patients with prior MI, elevated T-CHOL was most strongly related to death from coronary disease and to all-cause mortality (ie, death from all causes) in persons 65 years of age or older.61 Criteria for abnormal lipid levels in elderly patients with cardiac disease are yet to be established, although values greater than 250 mg/dL appear to warrant attention in this age group. Findings suggest that as many as 9% to 23% of elderly men and 18% to 40% of elderly women have T-CHOL levels in excess of 250 mg/dL.[3,13,14]

Whether preventive measures such as dietary modification or use of drugs that decrease T-CHOL while increasing or maintaining high-density lipoprotein cholesterol (HDL-C) levels have an important impact on CHD in the elderly population remains to be demonstrated. Results from a few studies[65-67] are favorable. The Stockholm Ischemic Heart Disease Secondary Prevention Study showed a 28% decrease in both ischemic heart disease and total mortality in a small number of patients greater than 60 years of age when treated with a combination of clofibrate and niacin.[65] The pilot study for the Cholesterol Reduction in Seniors Program indicated safe and effective lowering of T-CHOL, but the definitive study to document the benefits in patients over 65 years of age has not been initiated.[68] Gordon and Rifkind[69] have calculated the theoretical benefit of T-CHOL lowering in older individuals on morbidity and mortality. Their projections suggest that cholesterol lowering should be beneficial in older patients, although documentation of these benefits is still needed. It does appear, however, that if a patient has CHD or other cardiovascular disease, treatment should be initiated irrespective of current age.[70] Again, treatment should be administered only if there are no severe functional limitations, quality-of-life restrictions, or concomitant diseases that would severely limit life expectancy.

Treatment

According to Morley et al,[71] the initial consideration for the treatment of hypercholesterolemia should always be dietary and lifestyle modification. There is marked variation, however, in the ability of older patients to make such modifications. Elderly patients who are physically and mentally alert, living with a spouse, and sharing meals and who have diverse culinary interests can be treated in a manner similar to that for younger patients. In others, however, inadequate dietary intakes or poor socioeconomic conditions will be incompatible with risk reduction.72 Negative factors such as depression, isolation, or concomitant diseases also affect the patients' ability to institute such changes. Additionally, some' individuals who have had a lifetime of certain dietary habits are unlikely to accept dietary changes and new foods.

The current dietary recommendations of National Cholesterol Education Program are the Step 1 (less than 10% of calories from saturated fat, 30% or less of total calories from fat, and less than 300 mg of cholesterol per day) and Step 2 (less than 7% of calories from saturated fat and less than 200 mg of cholesterol per day) diets of the American Heart Association,[70] although others[73,74] have suggested more stringent dietary restriction of fat, particularly as it relates to the potential for disease reversibility. In many older patients, the Step 1 diet is not only adequate but all that is realistic. For those willing and able to pursue a more aggressive path, this should be done under the supervision of a dietitian. Costs related to this tv e of supervision and to the purchase and preparation of the food itself may be higher, but it is essential that nutritional adequacy be maintained. A gradual change from high-fat to lower-fat foods is recommended. Because they are an important source of calcium, the elimination or substantial reduction of dairy products in the diet should only be recommended in the most carefully considered cases, especially in older women who are at increased risk of osteoporosis.

Unfortunately, there is limited evidence of the benefit of T-CHOL-lowering diets in older patients.[70] In one encouraging investigation, Dayton et al[66] studied the effect of a high polyunsaturated fat-low saturated fat diet in 846 men ranging in age from 50 to 89 years. The results suggested a reduction in mortality from CHD and cerebral infarction over an 8-year period of follow-up in treated patients with T-CHOL levels above 223 mg/dL at the study outset. The beneficial effects appeared to be equal for both the younger and older age groups. According to Hunninghake,[70] drug therapy should be considered for patients who can reasonably expect some long-term benefit because conclusive evidence of a reduction in risk for CHD has not been shown in this age group. This decision should be based on clinical expectation. The decision to initiate drug therapy should be made jointly by the patient and the physician. The patient should understand that evidence of benefit from therapy in the elderly population has not been clearly established and that the costs and side effects of drug therapy are serious considerations. Older patients may be more susceptible to the side effects of drugs because of decreased hepatic metabolism or renal excretion or presence of concomitant diseases. The following is a summary of the effectiveness and limitations of specific pharmacologic agents.

Bile acid sequestrants appear to be effective in elderly persons. The reductions in low-density lipoprotein cholesterol (LDL-C) levels are dose dependent, as are the side effects.[70] The side effects are primarily gastrointestinal (both upper and lower tracts) in nature. Constipation is frequent and is one of the major reasons for poor acceptance in older patients.[75]

Nicotinic acid, although seemingly effective, is associated with multiple side effects, including upper gastrointestinal effects such as nausea and heartburn.[70] Other major forms of toxicity include hypcrglycemia, hyperuricemia, and hepatotoxicity. Hepatotoxicity is of particular concern for sustained release form of this agent.[76] The risk of these complications increases with increasing dosage and is generally believed to be significantly elevated if the total daily dosage is 3 g or more. Older patients appear to be especially vulnerable to these effects. They tend to have much more hyperglycemia, and any decreased renal function predisposes them to the development of hyperuricemia and possibly gout, especially in men. Flushing is more prominent with alcohol intake and may be improved with prophylactic use of aspirin.[77]

In general, hepatic hydroxymethyl glutaryl coenzyme A-reductase inhibitors are effective for lowering LDL-C levels and are well tolerated by older patients. These drugs also produce modest increases in HDL-C.[70] Older patients, especially women, tend to have slightly greater decreases in LDL-C than do younger patients. The risk of side effects appears to be increased in patients with multiple disease states and is probably increased in any condition that tends to decrease excretion of the drug. Because older patients more frequently exhibit multiple disease states, these patients may be at greater risk for developing liver toxicity, myopathy, and optic nerve degeneration. In addition, the added cost of patient monitoring for potential side effects and increased medication costs are of particular concern in this age group.

Smoking

The prevalence of cigarette smoking appears to decrease with advancing age. This decrease can be attributed not only to higher mortality rates in smokers but also to discontinuation of smoking because of health problems or concerns in older persons. Statistically significant associations, however, are apparent between cigarette smoking and death due to CHD.[59] Thirty-year follow-up data from the Framingham Heart Study in persons who reached age 65 years or greater demonstrated that smoking was not associated with total CAD incidence but was a statistically significant factor for cardiac death.[13] Smoking has been significantly correlated with new coronary events in elderly persons who have CAD.[17] The prevalence of smokers in the elderly population ranges from 9% to 22% for men and 3% to 23% for women, although there are few data for elderly women.[3,13,14]

Smoking cessation lowers the risk of death or MI similarly in young and elderly patients with CAD.[78,79] In patients aged 65 years or greater with documented CAD, 6-year follow-up data showed that continuation of a smoking habit was associated with an 18% increase in death or MI compared with those patients who had quit smoking.[78] Considerable inferential data also suggest a beneficial effect of smoking cessation for elderly patients with cardiac disease. Although these data are not specific to elderly persons, the mean population age at follow-up was greater than 60 years in most studies.[80-82] In the Coronary Drug Project, patients who continued smoking after MI had a 29% higher mortality rate at 5 years than did those who quit smoking.[80] The Framingham data demonstrated fewer recurrent MIs and reduced mortality in those who stopped smoking.[81] Other work[82] has resulted in similar findings.

Treatment

Little information is available for programs of smoking cessation, specifically for the elderly population.[83] Standard programs of counseling intervention appear to be as effective with elderly persons as with younger participants. Nicotine replacement therapy is probably effective, although theoretically, elderly individuals may have an increased side-effect profile, including increased drug sensitivity and increased skin sensitivity to patches. Patients with CHD at any age do not appear to be at increased risk for associated symptoms or events related to this therapy.[84]

Physical Inactivity

Although adults, including those with heart disease, have been encouraged to become physically active, the Centers for Disease Control and Prevention and the American College of Sports Medicine have suggested that 24% of elderly persons are completely sedentary and another 54% are inadequately active.[85-89] Data from the Omaha cohort suggest that 41% of elderly patients with cardiac disease have less than a 4-MET (metabolic equivalent) exercise capacity at entrance into exercise rehabilitation.[3] These data indicate the extensive level of physical inactivity present in this population.

Studies of the effects of short-term exercise training (3 months) in elderly patients with cardiac disease have demonstrated a variety of training benefits.[90-4] Data have demonstrated statistically significant increases in maximal exercise tolerance, decreases in submaximal exercise myocardial work as estimated by the rate-pressure product, and decreases in ratings of perceived exertion at standardized work intensities. Increased maximal rate-pressure product after training also was observed, suggesting that trained elderly patients with cardiac disease are able to perform at higher levels of myocardial oxygen demand.[90] These results appear achievable regardless of whether elderly patients are taking beta-blocker medications or are post-MI or post-CABG. Elderly patients with cardiac disease appear to make modest but statistically significant improvements in weight, percentage of body fat, forced expiratory ventilation in 1 second, resting heart rate, and resting rate-pressure product.[90] Resting SBP and DBP have not been reported to exhibit a training effect. Findings suggest that both elderly male and female patients with cardiac disease improve similarly even though the female patients studied were generally less fit, having nearly a 20% lower maximal oxygen uptake.[93,95,96]

Despite these findings, subjective and objective observations have suggested that "older" elderly patients with cardiac disease, those patients 75 years of age or greater, may not improve as much as "younger" elderly patients with cardiac disease following exercise training. Only limited improvements in submaximal and maximal responses to exercise were exhibited in patients with cardiac disease aged 75 years or greater, with even lesser change in patients aged 80 years or greater.[97] More recent work has suggested that there is a subgroup of this latter patient population that is capable of training benefits similar to those observed in younger elderly patients.[98] This subgroup of older elderly patients was characterized as capable of completing an extended period of exercise training and increasing exercise training intensity throughout the entire period of early and extended exercise training.

In many instances, the response to long-term exercise training ([greater than or equal to]6 months) is maintenance of previously made gains., Nevertheless, additional modest improvements have been reported in weight, resting heart rate, resting SBP, and maximal exercise capacity.[99] Furthermore, statistically significant decreases in resting DBP also have been observed, a finding not previously noted with short-term exercise training.[99] Improved physiological and perceptual responses to standardized submaximal effort have been reported and suggest that continued reduction in submaximal myocardial oxygen demand at standardized work loads is possible.[99] Improvements derived from both short- and long-term exercise rehabilitation will allow elderly patients to function at higher work levels during daily activities and may result in fewer cardiac symptoms and improved quality of life.

Comparisons of the exercise training benefits between young and elderly patients with cardiac disease have demonstrated that magnitudes of changes and exercise training responses are similar.[90] One observation has suggested that elderly patients with cardiac disease might make greater relative improvement in submaximal response to exertion than their younger counterparts.[92] A possible explanation for this finding is that regular physical activity has not been a part of many elderly patients' lives for many years; hence, improvements may represent a larger percentage of change when compared with baseline measurements. Additionally, as suggested by Hakki and coworkers,[100] status of left ventricular function may be more important than age in determining exercise capacity in patients with CAD.

Treatment

More than for other age groups, activity programs for elderly patients with cardiac disease must be tailored to the individual's age, fitness level, and health status, and these variables vary widely among elderly individuals.[4] The most critical factor in an elderly patient's ability to function independently in society is the ability to be mobile without assistance.[101] Thus, the overall focus for exercise training should be to enhance health-related fitness components, including cardiorespiratory and muscular endurance, flexibility, strength, and body composition. The cardiorespiratory system of the older patient with cardiac disease is capable of exercise training, and valuable improvement of functional capacity is achievable. Regular exercise also can lead to increased strength and muscle mass, a loss of fat, and maintenance of an acceptable level of body composition in this population. Limiting the deterioration of functional capacity is a prerequisite to enabling preservation of an independent, active, and energetic lifestyle. Attaining this objective is a goal of the physical activity program for elderly patients.

Table 3 presents guidelines for prescribing exercise for elderly patients with cardiac disease. The recommendations are not substantially different from those for younger patients. Some specific cautions and modifications to these general guidelines, however, should be noted. Of particular importance is the caution to start and progress slowly to prevent injury and allow for steady progression. Having patients exercise at the lower end of the intensity range while making increases in duration of the exercise session over time appears to be the most beneficial course. When exercise training has not been performed prior to training, which may be the case for as many as 50% of elderly patients, alternative methods can be used to prescribe exercise.[3] These methods include the use of reduced exercise work loads and ratings of perceived exertion early in the program. These alternative methods allow the patient to continue to exercise in a supervised setting while the exercise prescription is modified based on the results from several sessions. Evaluation should begin at very low work loads (2-3 METs) to ensure safety until appropriate safe levels are identified. Patients should be encouraged to increase caloric expenditure to 1,000 kcal/wk (4,200 kJ/wk) and beyond and to accomplish this through increased frequency and duration of exercise of mild-to-moderate intensity rather than increasing to high-intensity effort as a mechanism to achieve health benefits.[85]

Table 3
General Recommendations for Initiating an Exercise Training Program
for Elderly Patients With Cardiac Disease[3,103]

Warm-up-5-10 min of stretching and light activity involving the
large muscle groups prior to each exercise session

Intensity--50%-80% of the peak oxygen uptake attained at the
most recent exercise test corresponding to 60%-85% of the
peak heart rate at same test

Frequency--Participation 3-5 d/wk

Duration--20-40 min of aerobic exercise, broken up into shorter
periods allowing for 1- to 2-min rest intervals when appropriate

Mode--Upper- and lower-extremity exercise using treadmill
walking, leg ergometry, and arm ergometry

Cool-down--5-10 min of activity similar to warm-up activities

Flexibility--10-15 min of static stretching "of the muscles of each
major body section," including head and neck, shoulders,
chest, trunk, hips, legs, knees, and ankles

Resistive training--12-15 repetitions of a modest work load (25%.
of body weight for larger muscle groups, such as the
quadriceps femoris muscles, and 10% of body weight for
smaller muscle groups, such as the triceps muscles), 4-8
stations, 2-3 sessions per week; always performed after the
regular exercise session to provide for adequate warming of
various muscle groups and to reduce the likelihood of injury

Although cardiac rehabilitation programs may be best begun in a supervised setting, these types of programs are not always available and some patients must exercise without direct supervision. In these instances, exercise programs for elderly patient with cardiac disease must be developed under specific advise from the patients' primary care physician.[102] The exercise prescription can closely follow the recommendations shown in Table 3.[3,103] Health care professionals, however, should advise elderly patients with cardiac disease to adhere to a more cautious exercise prescription because of the unsupervised nature of the exercise program. These patients need to become comfortable with monitoring their own exercise response and potential cardiac symptoms and should contact their physician or other appropriately designated health care professional with any change in response or at the occurrence of symptoms. Written materials should be provided to assist these patients in understanding these recommendations. Exercise logbooks for recording type of exercise, exercise response, and any symptoms are helpful and can be reviewed through the mail or at the patients' next visit.

Summary

Recent advances in the care of elderly patients with cardiac disease will probably extend longevity an additional 10 to 20 years following the initial diagnosis of CHD. Thus, cardiac rehabilitation professionals will be challenged to increase the quantity and quality of programs dealing with risk-factor management for these patients. The impact of an aging society, the evolving economic climate, and the cost-benefit ratios of health care spanning into the next century will directly affect the provision of such programs for these patients. The cost-effectiveness of such programs must be related to quality-of-life outcomes in this patient population. Although little attention has been paid to these issues in this group, it is probable that, as with younger patients, education and physical activity will be a part of any quality-of-life outcome measures. It is also likely that elderly persons may not be able to afford such inventions at the current levels of cost and copayments. The health care community must develop creative methods to allow these individuals to participate in both lifestyle and exercise programs and at the same time reduce costs for both patients and programs.

Quality of life is an important aspect of program outcomes. This fact is especially important for elderly patients with cardiac disease. Whereas exercise and health-related education programs for younger patients have resulted in decreased mortality levels, a reduction in mortality levels may be less demonstrable for elderly patients; thus, more basic issues regarding desired levels of health, independence, and productivity become major factors in maintaining effective and individualized patient care.[11,12] Determining desired patient outcomes is the first step in designing risk-factor intervention programs. Evaluating the quality of life can be highly subjective because the values and expectations of the participants will affect program outcomes and thus must be defined at the program's outset. The patient's sense of well-being, life satisfaction, and ability to participate in valued activities in the home, workplace, or community must be given paramount importance.

Finally, the health care community is challenged not only to provide such care but to stringently evaluate methodologies and outcomes and to document the effectiveness of such programming. We are only now beginning to see some of the results of such scientifically based investigations of this patient population, and we should look forward to learning more and sharing our experiences in this growing arena of patient care.

Acknowledgements

I thank Daniel Hilleman, PharmD, for his assistance in reviewing the manuscript and Stephanie Rockwell for manuscript preparation.

References

[1] Council on Scientific Affairs, American Heart Association. Exercise programs for the elderly. JAMA. 1984;252:544-546. [2] Jamy PP. Prescribing for the Elderly. Littleton, Mass: PSG Publishing Co Inc; 1980. [3] Williams MA. Exercise Testing and Training in the Elderly Cardiac Patient. Champaign, Ill: Human Kinetics Inc; 1994:1-2. [4] Elia EA. Exercise and the elderly. Clin Sports Med. 1991;10:141-155. [5] National Center for Health Statistics. 1986 Summary: National Hospital Discharge Survey--Advance Data From Vital and Health Services Statistics. Hyattsville, Md: US Public Health Service, Dept of Health and Human Services publication no. 145. 1987;6:87-1250. [6] Wenger NK. Introductory remarks, Ill: 18th Bethesda Conference report-cardiovascular disease in the elderly. J Am Call Cardiol 1987; 10:8A-9A. [7] Balady GJ, Weiner DA. Exercise testing in healthy elderly subjects and elderly patients with cardiac disease. Journal of Cardiopulmonary Rehabilitation. 1989;9:35-39. [8] O'Rourke RA, Chatterjee K, Wei JY. Coronary heart disease: 18th Bethesda Conference report-cardiovascular disease in the elderly. Am Coll Cardiol 1987;10:52A-56A. [9] Satler LF, Green CE, Wallace RB, Rackley CE. Coronary artery disease in the elderly. Am J Cardiol. 1989;63:245-248. [10] Fletcher GF, Blair SN, Blumenthal J, et al. Statement on exercise: benefits and recommendations for physical activity programs for all Americans--a statement for health professionals by the Committee on Exercise and Cardiac Rehabilitation of the Council on Clinical Cardiology, American Heart Association. Circulation. 1992;86:340-344. [11] Oldridge NB, Guyatt GH, Fischer MS, Rimm AA. Cardiac rehabilitation after myocardial infarction: combined experience of randomized clinical trials, JAMA. 1988,260:945-950. [12] O'Connor GT, Buring JE, Yusuf S, et al. An overview of randomized trials of rehabilitation with exercise after myocardial infarction. Circulation. 1989;80:234-244. [13] Kannel WB, Vokonas PS. Primary risk factors for coronary heart disease in the elderly: The Framingham Study. In: Wenger NK, Furberg CD, Pitt E, eds. Coronary Heart Disease in the Elderly. New York, NY: Elsevier Science Inc; 1986:60-92. [14] Aronow WS, Starling L, Etienne F, et al. Risk factors for coronary artery disease in persons older than 62 years in a long-term health care facility. Am J Cardiol. 1986;57:518-520. [15] Lund-Johansen P. Age, hemodynamics, and exercise in essential hypertension: difference between beta-blockers and dihydropyridine calcium antagonists. J Cardiovasc Pharmacol. 1989;14(suppl 10):S7-S13. [16] Pearson AC, Gudipati C, Nagelhout D, et al. Echocardiographic evaluation of cardiac structure and function in elderly subjects with isolated systolic hypertension. Jam Coll Cardiol 1991;17:422-430. [17] Aronow WS, Herzig AH, Etienne F, et al. 41-Month follow-up of risk factors-correlated with new coronary events in 708 elderly patients. J Am Genatr Soc. 1989;37:501-506. [18] Cheung DG, Weber MA. Hypertension in the elderly. In: Tresch DD, Aranow WS, eds. Cardiovascular Disease in the Elderly Patient. New York, NY: Marcel Dekker Inc; 1994:149-181. [19] Hypertension Detection and Follow-up Program Cooperative Group: Five-year findings of the Hypertension Detection and Follow-up Program, II: mortality by race, sex, and age. JAMA. 1979; 242:2572-2577. [20] National Heart Foundation of Australia. Treatment of mild hypertension in the elderly: report by the management committee. Med J Aust. 1981;2:398-402. [21] Amery A, Birkenhager W, Brixko P, et al. Mortality and morbidity results from the European Working Party on High Blood Pressure in the Elderly Trial. Lancet. 1985;1:1349-1354. [22] SHEP Research Cooperative Group. Final results of the Systolic Hypertension in the Elderly Program (SHEP): prevention of stroke by antihypertensive drug treatment in older persons with isolated systolic hypertension. JAMa. 1991;265:3255-3264. [23] Dahlof B, Lindhom LH, Hansson L, et al. Morbidity and mortality in the Swedish Trial in Old Patients With Hypertension (STOP-Hypertension). Lancet. 1991;338:1281-1285. [24] Medical Research Council Working Party. Medical Research Council trial of treatment of hypertension in older adults: principle results. BMJ. 1992;304:405-412. [25] Working Group on Hypertension in the Elderly. Statement on hypertension in the elderly. JAMA. 1986;256:70-74. [26] Fletcher AE, Bulpitt CJ. How far should blood pressure be lowered? N Engl J Med. 1992;326:251-254. [27] Langer RD, Criqui MH, Barrett-Connor EL, et al. Blood pressure change and survival after age 75. Hypertension. 1993;22:551-559. [28] Kaplan NM. Non-drug treatment of hypertension. Ann Intern Med. 1985;102:359-373. [29] Subcommittee on Nonpharmacological Therapy of the 1984 joint National Committee on Detection, Evaluation, and Treatment of High Blood Pressure. Nonpharmacological approaches to the control of high blood pressure: final report. Hypertension. 1986;8:444-467. [30] Lipsitz LA, Nyquist Rp Jr, Wei JY, Rowe JW. Postpravdial reduction in blood pressure in the elderly. N Engl J Med. 1983;309:8.1-83. [31] Hurwitz N. Predisposing factors in adverse reactions to drugs. BMJ. 1969;1:536-539. [32] Jackson G, Pierscianowski TA, Mahon W. Inappropriate antihypertensive therapy in the elderly. Lancet. 1976;2:1317-1318. [33] Montamat SC, Cusack BJ, Vestal RE. Management of drug therapy in the elderly. N Engl J Med. 1989;321:303-308. [34] Hulley SB, Furberg CD, Gurland B, et al. Systolic Hypertension in the Elderly Program: antihypertensive efficacy of chlorthalidone. Am J Cardiol 1985;56:913-920. [35] Amery A, Birkenhager W, Bulpitt C, et al. Influence of antihypertensive therapy on serum cholesterol in elderly hypertensive patients. Acta Cardiol 1982;37:235-244. [36] Joint National Committee on Detection, Evaluation, and Treatment of High Blood Pressure. The 1988 Report of the Joint National Committee on Detection, Evaluation, and Treatment of High Blood Pressure. Arch Intern Med. 1988;148:1023-1038. [37] Sowers JR. Managing geriatric hypertension: a brief overview. Geriatrics. 1985;40:63-66. [38] Drayer JI, Weber MA, DeYoung JL, Wyle FA. Circadian blood pressure patterns in ambulatory hypertensive patients. Am J Med. 1982;73:493-499. [39] Buhler FR, Burkhart F, Lutold BE, Kung M. Antihypertensive beta-blocking action as related to renin and age: a pharmacologic tool to identify mechanisms in essential hypertension. Am J Cardiol. 1975; 36:653-669. [40] Fritschka E, Distler A, Gotzen R, et al. Crossover comparison of nitrendipine with propranolol in patients with essential hypertension. J Cardiovasc Pharmacol. 1984;6(suppl 7):S1100-S1104. [41] Kiowski W, Buhler FR, Fadayomi MO. Age, race, blood pressure, and renin: predictors for antihypertensive treatment with calcium antagonists. Am J Cardiol 1985;56:81H-85H. [42] Materson BJ, Reda DJ, Cushman WC, etal. Single-drug therapy hypertension in men: a comparison of six antihypertensive agents with placebo. N Engl J Med. 1993;328:914-921. [43] Ryyny RL, Loverde M, Mitchell W. Treatment of hypertension in the elderly with a new calcium channel blocking drug, nitrendipine. Am J Med. 1989;86:49-55. [44] Buhler FR. Age and cardiovascular response adaptation: determinants of an antihypertensive concept primarily based on beta-blockers and calcium entry blockers. Hypertension. 1983;5(suppl 3):III94-III100. [45] Veterans Administration Cooperative Study Group on Antihypertensive Agents: low-dose captopril for the treatment of mild to moderate hypertension. Hypertension. 1983;5(suppl):III36-III144. [46] Cheung DG, Gasster JL, Weber MA. Assessing duration of antihypertensive effects with whole-day blood pressure monitoring. Arch Intern Med. 1989;149:2021-2025. [47] Schulman SP, Weiss JL, Becker LC, et al. The effects of antihypertensive therapy on left ventricular mass in elderly patients. N Engl J Med. 1990;322:1350-1356. [48] Ventura HO, Frohlich ED, Mersserli FH, etal. Cardiovascular effects and regional blood flow distribution associated with angiotensin-converting enzyme inhibition (captopril) in essential hypertension. Am J Cardiol. 1985;55:1023-1026. [49] Cheung DG, Hoffman CA, Ricci ST, Weber MA. Mild hypertension in the elderly: a comparison of prazosin and enalapril. Am J Med. 1989;86(suppl IB):87-90. [50] Croog SH, Levine S, Testa MA, et al. The effects of antihypertensive therapy on the quality of life. N Engij Med. 1986;314:1657-1664. [51] Studer JA, Piepho RW. Antihypertensive therapy in the geriatric patient, 11: a review of the [alpha.sub.1]-adrenergic blocking agents. J Clin Pharmacol 1993;33:2-13. [52] Khoury AF, Kaplan NM. [alpha]-blocker therapy of hypertension: an unfulfilled promise. JAMA. 1991;266:394-398. [53] The Coronary Drug Project Research Group. Blood pressure in survivors of myocardial infarction. J Am Coll Cardiol 1984;4:1135-1147. [54] Connolly DC, Elveback LR, Oxman HA. Coronary heart disease in residents of Rochester, Minnesota, 1950-1975, III: effect of hypertension and its treatment on survival of patients with coronary artery disease. Mayo Clin Proc. 1983;58:249-254. [55] Aronow WS, Ahn C, Kronzon I, Koenigsberg M. Congestive heart failure, coronary, events, and atherothrombotic brain infarction in elderly blacks and whites with systemic hypertension and with and without echocardiographic and electrocardiographic evidence of left ventricular hypertrophy. Am J Cardiol 1991;67:295-299. [56] Aronow WS, Sales FF, Etienne F, Lee NH. Prevalence of peripheral arterial disease and its correlation with risk factors for peripheral arterial disease in elderly patients in a long-term health care facility. Am J Cardiol. 1988;62:644-646. [57] Barrett-Connor E, Suarez L, Khaw KT, et al. Ischemic heart disease risk factors after age 50. J Chronic Dis. 1984;37:903-908. [58] Castelli WP, Wilson PWF, Levy D, Anderson & Cardiovascular risk factors in the elderly. Am J Cardiol. 1989;63:12H-19H. [59] Rubin SM, Sidney S, Black DM, et al. High cholesterol in elderly men and the excess risk for coronary heart disease. Ann Intern Med. 1990;113:916-920. [60] Siegel D, Kuller L, Lazarus NB, et al. Predictors of cardiovascular events and mortality in the Systolic Hypertension in the Elderly Program Pilot Project. Am J Epidemiol 1987;126:385-399. [61] Wong ND, Wilson PW, Kannel WB. Serum cholesterol as a prognostic factor after myocardial infarction: The Framingham Study. Ann Intern Med. 1991;115:687-693. [62] Krumholz HM, Seeman TE, Merrill SS, et al. Lack of association between cholesterol and coronary heart disease mortality and morbidity and all-cause mortality in persons older than 70 years. JAMA. 1994;272:1335-1340. [63] Corti MC, Guralnik JM, Salive ME, et al. HDL cholesterol predicts coronary heart disease mortality in older persons. JAMA. 1995;274: 539-544. [64] Aronow WS, Kronzon I. Prevalence of coronary risk factors in elderly blacks and whites. J Am Geriatr Soc. 1991;39:567-570. [65] Carlson LA, Rosenhamer G. Reduction in mortality in the Stockholm Ischemic Heart Disease Secondary Prevention Study by combined treatment with clofibrate and nicotinic acid. Acta Med Scand. 1988;223:405-418. [66] Dayton S, Pearce ML, Hoshimoto S, et al. A controlled trial of a diet high in unsaturated fat in preventing complications of atherosclerosis. Circulation. 1969;60(suppl 2):I-63. [67] Snowdon DA, Phillips RL, Fraser GE. Meat consumption and fatal ischemic heart disease. Prev Med. 1984;13:490-500. [68] LaRosa JC, Applegate W, Crouse JR III, et al. Cholesterol lowering in the elderly: results of the Cholesterol Reduction in Seniors Program (CRISP) pilot study. Arch Intern Med. 1994;154:529-539. [69] Gordon DJ, Rifkind BM. Treating high blood cholesterol in the older patient. Am J Cardiol. 1989;63:48H-52H. [70] Hunninghake DB. Hyperlipidemia in the elderly. In: Tresch DD, Aronow WS, eds. Cardiovascular Disease in the Elderly. New York, NY: Marcel Dekker Inc; 1994:183-211. [71] Morley JE, Mooradian AD, Silver AJ, et al. Nutrition the elderly. Ann Intern Med. 1988;109:890-904. [72] Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults: Report of the National Cholesterol Education Program Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults. JAMA. 1993;269:3015-3023. [73] Ornish D, Brown SE, Scherwitz LW, et al. Can lifestyle changes reverse coronary heart disease? Lancet. 1990;2:129-133. [74] Schuler G, Hambrecht R, Schlierf G, et al. Regular physical exercise and low-fat diet: effects on progression of coronary artery disease. Circulation. 1992;86:1-11. [75] Tikkanen MJ. Hypercholesterolemia in the elderly: Is drug treatment justified? Eur Heart J 1988;9:79-82. [76] McKenney JM, Proctor JD, Harris S, Chinchili VM. A comparison of the efficacy and toxic effects of sustained- vs immediate-release niacin in hypercholesterolemic patients. JAMA. 1994;271:672-677. [77] Jay RH, Dickson AC, Betteridge DJ. Effects of aspirin upon the flushing reaction induced by niceritrol. Br J Clin Pharmacol. 1990;29: 120-122. [78] Hermanson B, Omenn GS, Kronmal RA, Gersh BJ. Beneficial six-year outcome of smoking cessation in older men and women with coronary artery disease: results from the CASS Registr. N Engl J Med. 1988;319:1365-1369. [79] Jajich CL, Ostfeld AM, Freeman DH Jr. Smoking and coronary heart disease mortality in the elderly. JAMA. 1984;252:2831-2834. [80] The Coronary Drug Project Research Group: cigarette smoking as a risk factor in men with a prior history of myocardial infarction. J Chronic Dis. 1979;32:415-425. [81] Sparrow D, Dawber TR, Colton T. The influence of cigarette smoking on prognosis after a first myocardial infarction. J Chronic Dis. 1978;31:425-432. [82] Wilhelmsson L, Elmfeldt D, Vedin JA, et al. Smoking and myocardial infarction. Lancet. 1975;1:415-420. [83] Orleans CT, Resch N, Noll E, et al. Use of transdermal nicotine in a state-level prescription plan for the elderly: a first look at "real-world" patch users. JAMA. 1994;271:601-607. [84] Working Group for the Study of Transdermal Nicotine in Patients With Coronary Artery Disease. Nicotine replacement therapy for patients with coronary artery disease. Arch Intern Med. 1994;154:989-995. [85] Fletcher GF, Balady G, Froelicher VF, et al. Exercise standards: a statement for health care professionals from the American Heart Association. Circulation. 1995;91:580-615. [86] Balady GJ, Fletcher BJ, Froelicher ES, et al. Cardiac rehabilitation programs: a statement for health care professionals from the American Heart Association. Circulation. 1994;90:1602-1610. [87] American Association of Cardiovascular and Pulmonary Rehabilitation. Guidelines for Cardiac Rehabilitation Programs. Champaign, Ill: Human Kinetics Inc; 1995:27-56. [88] US Centers for Disease Control and Prevention, American College of Sports Medicine. Physical activity and public health. Sports Medicine Bulletin. 1993;28:7. [89] American College of Sports Medicine. ACSM's Guidelines for Exercise Testing and Prescription. Baltimore, Md: Williams & Wilkins; 1995:3-6. [90] Williams MA, Maresh CM, Esterbrooks DJ, et al. Early exercise training in patients older than age 65 years compared with that in younger patients after acute myocardial infarction or coronary artery bypass grafting. Am J Cardiol. 1985;55:263-266. [91] Ades PA, Hanson JS, Gunther PGS, Tonino RP. Exercise conditioning in the elderly coronary patient. J Am Geriatr Soc. 1987;35:121-124. [92] Ades PA, Grunvald MH. Cardiopulmonary exercise testing before and after conditioning in older coronary patients. Am Heart J 1990; 120:585-589. [93] Ades PA, Waldman ML, Polk DA, Coflesky JT. Referral patterns and exercise response in the rehabilitation of female coronary patients aged -62 years. Am J Cardiol. 1992;69:1422-1425. [94] Lavie CJ, Milani RV, Littman AB. Benefits of cardiac rehabilitation and exercise training in secondary coronary prevention in the elderly. J Am Coll Cardiol. 1993;22:678-683. [95] Oldridge NB, Lasalle D, Jones NL. Exercise rehabilitation of female patients with coronary artery disease. Am Heart 1980;100:755-757. [96] Petratis MM, Williams MA, Fogland TL, Esterbrooks DJ. The benefits of early exercise training in female cardiac patients. Journal of Cardiac Rehabilitation. 1987;7:503. Abstract. [97] Williams MA, Esterbrooks LJ, Sketch MH. Limitations of phase 11 exercise training in the "older" elderly cardiac patient. Circulation. 1990;82:111-576. Abstract. [98] Williams MA, Thalken LJ, Esterbrooks DJ, Sketch MH. Effects of short-term and long-term exercise training in older elderly cardiac patients. Circulation. 1992;86:1-670. Abstract. [99] Williams MA, Maresh CM, Esterbrooks DJ, Sketch MH. Characteristics of exercise responses following short- and long-term aerobic training in elderly cardiac patients. J Am Getiatr Soc. 1987;35:904. Abstract. [100] Hakki AH, Depace NL, Iskandrian AS. Effect of age on left ventricular function during exercise in patients with coronary artery disease. J Am Coll Cardiol. 1983;2:645- 651. [101] Abrams WB. Cardiovascular drugs in the elderly. Chest. 1990;98: 980-986. [102] Williams MA, Sketch MH. After a heart attack: prescribing exercise to speed recovery. Senior Patient. 1990;2:16-20. [103] Williams MA, Esterbrooks DJ, Aronow WS, Sketch MH. Guidelines to exercise therapy of the elderly after myocardial infarction. Eur Heart J. 1984;5(suppl E):121-123.

MA Williams PhD, is Professor of Medicine and Director, Cardiovascular Disease Prevention and Rehabilitation Program, Division of Cardiology, Creighton University School of Medicine, Omaha NE 68131. Address all correspondence to Dr Williams at Cardiac Center of Creighton University, 3006 Webster St, Omaha, NE 68131 (USA).