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Exercise Rehabilitation for Cardiac Patients

A Beneficial but Underused Therapy

Paul D. Thompson, MD
Exercise and Sports Cardiology Series Editor

THE PHYSICIAN AND SPORTSMEDICINE - VOL 29 - NO. 1 - JANUARY 2021


In Brief: Exercise-based cardiac rehabilitation is currently underused, even though exercise is one of the few nonsurgical interventions that can make heart disease patients feel better physically and mentally. Benefits include increased muscle strength, lowered heart rate, increased stroke volume, and increased submaximal and maximal working capacity. Patients in cardiac rehabilitation programs, however, often do not exercise enough to obtain maximal benefit. Programs should ideally be initiated under supervision to provide the correct regimen and requisite vigorous activity. Subsequent moderate exercise regimens can be done at home. All patients should engage in lifelong maintenance programs.

The benefit of exercise for heart disease patients continues to be rediscovered, and its utility has extended to sicker patients, such as those with congestive heart failure. Despite its documented benefits, exercise remains underused in patients who have coronary artery disease (CAD). Only approximately 15% of the eligible CAD patients are referred to exercise-based cardiac rehabilitation programs (1), and the standard exercise program rarely exceeds 3 months.

Although exercise training for CAD patients is called cardiac rehabilitation, exercise is only one component of postdischarge intensive cardiac care. Currently, many hospitalizations for CAD acute myocardial infarction (MI) last only several days because of newer therapies and cost containment. Shortened hospitalizations for MI and other cardiac problems have shifted the intensive care for these patients from the hospital to the outpatient setting.

Heart Disease and Exercise

Goals. Any postdischarge intensive cardiac care program has three main goals: (1) maintain or improve the patient's functional capacity, (2) improve the patient's quality of life, and (3) prevent recurrent cardiac events. In addition to exercise, critical elements of rehabilitation include aggressive dietary and pharmacologic treatment of serum lipids, smoking cessation, routine use of antiplatelets agents such as aspirin, selective use of other anticoagulants such as warfarin, the routine use of beta-blockers, and the use of angiotensin-converting enzyme (ACE) inhibitors in patients with reduced left ventricular ejection fraction (2). Most programs now also include counseling and education. Some physicians now recommend the routine use of ACE inhibitors post-MI because of the HOPE Trial results. Several problems limit this trial's application to maximally managed CAD patients, including the fact that less than 50% of the patients had CAD, only 40% were treated with beta-blockers, only 75% were receiving aspirin, and only 29% were on lipid-lowering therapy.

Cardiac oxygen demand. The myocardium's oxygen extraction without physical activity is high and is 70% to 80% of the available arterial oxygen "at rest" (3). Thus, oxygen needs of physical exercise must be met primarily by augmented coronary blood flow.

Maximal oxygen uptake or VO2max is an excellent measure of exercise capacity (4), but VO2 can underestimate an individual's ability for sustained submaximal exercise. Measuring only VO2max when assessing a patient's effort tolerance represents a critical shortcoming because few tasks are performed at maximum exercise capacity. However, in sedentary individuals, maximal capacity generally correlates with submaximal endurance capacity.

Exercise in Patients With CAD

Although inactivity (5) and low exercise capacity (6) are important CAD risk factors, patients who have CAD without coronary heart disease (CHD) often have exercise capacities that are within the average range for their age and sex. (See "CAD vs CHD Nomenclature," page 72.) Patients with CHD, however, usually demonstrate reduced maximal exercise capacities, with the reductions dependant on the severity of the myocardial damage and the degree that damage reduces the ability to increase cardiac output. Similarly, patients with asymptomatic myocardial ischemia are often limited by exercise dyspnea.

Patients with classic angina pectoris experience exercise-induced chest discomfort at a highly reproducible rate pressure product (RPP) that occurs when myocardial oxygen demand exceeds the ability of narrowed coronary arteries to supply adequate coronary flow. Many patients do not experience classic angina, however, and have considerable variation in the RPP at the onset of symptoms. Coronary artery vasomotion probably accounts for much of this variation since the coronary arteries alter their internal diameter in response to various stimuli. Exercise induces arterial dilation in normal coronary arteries but vasoconstriction in atherosclerotic coronary segments (7). Other factors include the time of day exercise occurs since the coronary arteries are more constricted in the morning (8), and ventricular volume, which is larger during supine exercise, for example (9).

How CAD Patients Adapt to Exercise

Exercise effects. Exercise training increases VO2max (4), but the magnitude of the change varies among subjects. Increases in VO2max are greater with increased duration and intensity of exercise but are smaller in more fit and older individuals. Healthy subjects who engage in exercise for 3 to 12 months have about a 20% increase in VO2max (10). Thus, the same external workload or exercise task after training represents less of a workload relative to that person's now higher VO2 and consequently, less physical stress for the individual.

Adaptations. Similar adaptations to exercise training occur in patients with CAD and CHD. The average increase in VO2max ranges from 11% to 56% (3). CHD severity and length of training influence exercise effects. Patients with severely impaired cardiac function may only be able to achieve an attenuated increase in maximal exercise capacity.

Patients with angina provide the clearest example of the physiologic adaptations to exercise training in patients with CAD. Exercise-induced increases in stroke volume mean that the same absolute external workload, which determines cardiac output, can occur at a lower heart rate. The lower rate requires less oxygen and coronary blood flow (figure 1). The net effect is that after exercise training, the same task can be done with a lower heart rate and delayed onset of angina.

Most studies (11,12) of exercise training in angina patients show that angina occurs at the same RPP after training, though exercise capacity at onset of angina is higher. Other studies (13,14), however, clearly demonstrate increases in the RPP at angina onset. Improved myocardial oxygen supply after short-term exercise is likely related to changes in vasomotor tone rather than to reductions in the coronary artery lesion or to collateral artery development.

Sim and Neill (14) speculated that training improved vasomotor tone when they noted exercise training increases the RPP at angina during exercise but not during cardiac pacing. More recently, studies of exercise's effect on ST-segment depression (15) and on myocardial perfusion images (16) have also suggested improvements in myocardial oxygen supply. Studies in animals (17,18) and humans (19) have documented this vasodilatory effect. These effects make exercise an effective adjunctive therapy for angina patients who are not candidates for revascularization. Among 17 CAD patients whose exercise was limited by angina, participation in a 12-week exercise program reduced the number who had angina by 11 (61%) (20). Others have reported similar but less dramatic results (15).

Physiologic measures. Few real-life tasks require maximal effort, so assessing only maximal effort capacity can underestimate many of the benefits of exercise. Exercise can have dramatic effects on submaximal working capacity in CAD and CHD patients, though this parameter has rarely been examined. Ades et al (21) found that 33 of 45 patients were able to complete a 45-minute exercise session after 3 months of training, whereas only 10 had been able to do so before training (10 of 45). Although the average time to exhaustion increased 37%, VO2max increased only 16%.

Predicting which CAD patients are most likely to have improved effort tolerance is controversial (22). Fioretti et al (23) found no significant relationship between baseline exercise capacity and the change in exercise tolerance in post-MI patients after 3 months of training. Another study (20) noted less improvement with the same period of exercise in patients who had exercise-induced ischemia, even though both patients and controls had similar baseline exercise performance. Some have suggested that the greatest improvement in patients with exercise-induced angina is among those whose angina occurred at a pretraining RPP of greater than 20,000 (12). Others (15) suggest that to improve exercise tolerance in CAD patients, leisure-time physical energy expenditure must exceed 1,400 kcal/day.

Muscle changes. Many exercise adaptations are related to skeletal muscle changes and include increased capillary density, increased mitochondrial size and function, and increased muscle strength. Exercise training effects have been separated into central (cardiac) adaptations and peripheral (muscle) changes, though the division is somewhat arbitrary. Muscle-specific and generalized exercise training effects may be better terms to use (24) because many of the physiologic (11,12), neurologic (25), and vascular changes (18,26,27) reflect both cardiac and skeletal muscle changes.

Coronary artery flow, collaterals, and stenosis. Although increasingly strong evidence indicates that exercise training can reduce the coronary artery vasoconstrictor response to exercise and thereby increase coronary artery flow, no conclusive evidence shows that exercise training can either increase coronary collateral flow in CAD patients or reduce the severity of stenotic lesions.

Exercise and Survival

There is persuasive evidence suggesting that exercise training can reduce repeat cardiac events in CAD patients, but no single study has had sufficient power to test this hypothesis. This contrasts to several large studies of pharmacologic interventions in CAD patients. Unfortunately, no group has sufficient financial incentive to test directly the exercise training hypothesis in CAD patients.

Decreased mortality. Meta-analysis can address some of the drawbacks of small trials. O'Connor et al (28) used meta-analysis to demonstrate that cardiac rehabilitation significantly decreased total mortality at 2- and 3-year follow-up. Sudden death in the first year after randomization was 37% lower, but total 1-year mortality was not significantly reduced.

This meta-analysis has multiple limitations. Only post-MI patients were examined, so results may not be applicable to other CAD and CHD patients. Subjects were primarily middle-aged men, so the benefit for women and older patients cannot be assessed. Component studies were conducted between 1960 and 120214 and may not be reproducible in the current medical climate. Fewer post-MI patients in the present era incur myocardial damage because of reperfusion therapies or have residual ischemia because they undergo aggressive bypass surgery and angioplasty. In addition, some physiologic effects of exercise training can be mimicked with drugs such as beta-blockers and vasodilatory agents.

The 37% reduction of sudden cardiac death at 1 year in this meta-analysis has several possible explanations. Exercise training reduces the incidence of ventricular fibrillation during ischemia (29), and this correlates with increases in parasympathetic tone (30). Alternatively, the availability of defibrillators and trained personnel to resuscitate stricken exercisers may have been responsible. If so, the purported benefits may not be valid for CAD patients in unsupervised or home programs.

Ischemic conditioning. Reduction in fatal infarctions without a reduction in recurrent nonfatal events also suggests that exercise training may represent ischemic preconditioning, the observation that brief periods of ischemia before coronary occlusion can reduce subsequent infarct size (31). Ischemic preconditioning is of growing importance in cardiology since it is second only to early reperfusion as a mechanism to protect the myocardium from ischemic injury.

Exercise may represent ischemic preconditioning that helps lessen subsequent ischemic effects (32). Interestingly, doses of endogenous or exogenous norepinephrine or other catecholamines produce changes that mimic this phenomenon (33). Three implications arise from the postulated ischemic preconditioning benefits of exercise in CAD patients: (1) Exercise must be frequent and sustained because the effect is transient; (2) benefits may be valid only for patients with exercise-induced ischemia since only these patients experience the phenomenon and resultant adaptations; and (3) when no ischemia is present, exercise must be sufficiently intense to increase circulating catecholamine levels to elicit the effect.

Cost-Effectiveness of Rehabilitation

Cost-benefit analyses. Ades et al (34) showed that post-MI or bypass surgery patients who participated in a cardiac exercise program had fewer hospital admissions and shorter stays, resulting in a $739 savings per patient per year. Ades et al (35) also estimated a value for cardiac rehabilitation of $4,950 per year of life saved based on 1995 dollars. These benefits compare favorably with interventions such as thrombolytic therapy, coronary bypass surgery, and lipid-lowering medications.

Staff interaction. Much of the cardiac rehabilitation cost savings may be related to frequent contact with the rehabilitation staff. Patients are repeatedly admonished to monitor themselves for chest discomfort and to report persistent symptoms. Patients in supervised programs can relay symptoms to staff for evaluation. The exercise session itself can be used as a modified stress test for evaluating symptoms and for appropriately triaging patients. Prompted more by concern than discomfort, unsupervised patients often seek emergency or other care, and are often admitted. Bondestam et al (36) showed that rehabilitation patients had a lower incidence of emergency department visits and rehospitalizations than unsupervised patients. Emergency department visits were generally justified among the rehabilitation participants, but visits of unsupervised patient were often prompted by vague symptoms.

Exercise Risks for CAD Patients

Infarction and death. The primary risks of exercise training are cardiac arrest, MI, and death, but these are rare (37). In supervised programs, approximately 85% of patients who have a cardiac arrest are successfully resuscitated (37), but the risks of exercise during vigorous cardiac rehabilitation should not be ignored. Sudden deaths have occurred in studies involving vigorous rehabilitation (15,38).

Although exercise has therapeutic benefits and low risks, physicians must be cautious about permitting CAD patients to compete in vigorous athletics. Such exercise clearly increases the risk of cardiac arrest and MI (39,40). We encourage cardiac patients to participate in rehabilitation programs and engage in moderate exercise in unsupervised settings, but discourage them from competing in athletics in which their ability to restrict their competitive instincts might be compromised. Examples of such sports include basketball, racquetball, and competitive singles tennis. For many competitive patients, curtailed participation diminishes self-esteem.

Left ventricular function. There has been a question as to which vigorous exercise is beneficial or deleterious to ventricular performance in patients with anterior wall MI and reduced left ventricular function (LVF). Jugdutt et al (41) examined the effect of 12 weeks of exercise on left ventricular size and function in patients after Q-wave anterior wall MI and in nonrandomized, matched controls. After the exercise program, the training group and controls were subdivided into two additional groups depending on whether or not their functional status had remained constant or had deteriorated. Among the exercisers, the group whose functional status decreased had greater pretraining left ventricular asynergy that increased with training, and they also experienced decreased left ventricular ejection fractions. This suggests that exercise training worsened LVF and that this effect results from incomplete infarct healing.

Although this report (41) initiated concern in the cardiac rehabilitation community, subsequent studies have not confirmed the finding. Giannuzzi et al (42) showed that left ventricular volumes expanded only in controls, perhaps to compensate for reduced LVF. Exercisers exhibited increased ejection fractions rather than left ventricular dilatation, suggesting that vigorous exercise training increased left ventricular contractibility and prevented LVF deterioration. Most patients took beta-blockers and ACE inhibitors; thus, exercise contributed to improved LVF despite maximal medical therapy. This finding may indicate that prolonged exercise enhances the effects of ACE inhibition, perhaps by a vasodilatory effect.

Practical Aspects of Exercise Programs

Program structure. Most exercise-based cardiac rehabilitation programs have a similar structure and exercise training schedule. Most require a baseline exercise stress test to determine maximal exercise heart rate, document baseline exercise performance, and exclude significant cardiac ischemia. Testing may be waived if patients have recently undergone revascularization, and symptoms and rating of perceived exertion can be used to guide training intensity.

Exercise starts as soon as possible after MI or intervention. Post-MI and angioplasty patients whose conditions are uncomplicated can begin moderate exertion within a week of discharge, and post-bypass-graft patients within 3 weeks of discharge. Usually, patients exercise three times a week in 20- to 40-minute sessions at 70% to 85% of their baseline maximal heart rate. The program lasts for 12 or more weeks, and patients are usually monitored with electrocardiography during exercise.

Patients with exercise-induced ischemia or angina exercising on their own should exercise below their ischemic threshold. In a supervised program, patients can exercise to angina onset or to the predetermined ischemic RPP. Sublingual or spray nitroglycerin can be used liberally to increase the tolerated exercise intensity; however, this approach is not recommended routinely for home-based exercise. Some patients with stable angina can exercise to the onset of pain during unsupervised sessions, but patients with silent exercise-induced ischemia should restrict activity to intensity less than their ischemic RPP. Most programs also include education and counseling sessions.

Resistance exercise. Rehabilitation programs previously prohibited resistance exercise because of misguided concerns about increased systolic blood pressure (43). Now, almost all programs include some strength training to help patients more adequately meet the demands of daily household tasks. Exercises include modified push-ups, biceps curls, military presses, bench presses, quadriceps extensions, hamstring curls, and bent-knee sit-ups.

The Rehabilitation Viewpoint

Few patients are referred to exercise-based cardiac rehabilitation programs (1), probably because many physicians are uncomfortable with exercise and are not familiar with its benefits. Many patients who have stable angina occurring at a high RPP and who have only one- or two-vessel disease can be treated as well with exercise therapy as with prompt angioplasty. If exercise treatment fails, patients can seek interventional therapy. My views are summarized in table 1.


TABLE 1. Characteristics and Evidence for Prescribing Exercise-Based CAD Rehabilitation

Characteristic Evidence Author's Observations

Exercise usage Only 15% of eligible patients are referred Physicians often unfamiliar with exercise and its benefits
Exercise intensity Moderate rather than vigorous exercise has been emphasized Emphasis on public health rather than CAD patient; benefits may be greatest with vigorous activity
Cost reductions Home-based training and heart rhythm telephone monitoring often used rather than supervised program Cost savings may be due to supervision and staff interaction
Flexible programs Every patient is different Patients can be better served with individualized programs
Economics vs clinical care principles ECG monitoring is used in training; usual length is 12 weeks Monitoring and length are determined by insurers' reimbursement policies and not medical need
Long-term maintenance needed for patient benefit Exercise benefits do not persist if patient becomes inactive Short programs are good for getting patient started; benefits are probably lifelong programs

CAD = coronary artery disease; ECG = electrocardiographic


What Remains to Be Done

Exercise-based cardiac rehabilitation should be critically reevaluated in a randomized, controlled clinical trial modeled after that of O'Connor et al (28). The reduction in mortality with cardiac rehabilitation compares favorably with that observed with other interventions (eg, simvastatin (44) or pravastatin sodium (45)) and is especially impressive given the short exercise intervention, limited follow-up, and the fact that patients often exercised on their own. Cardiac rehabilitation may prove even more successful with contemporary medical care if the exercise intervention is lifelong.

References

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CAD vs CHD Nomenclature

Coronary artery disease (CAD) refers to any abnormality of the coronary arteries. The predominant cause of CAD is atherosclerosis, but other conditions such as vasculitis, anomalous coronary artery origin or course, and coronary artery aneurysms from prior vasculitis can also cause CAD. Coronary heart disease (CHD) is often used interchangeably with CAD, but CHD more correctly refers to myocardial dysfunction produced by CAD from myocardial infarction or chronic ischemia. Not all patients with CAD have CHD, but all CHD patients have CAD as the proximate cause of myocardial dysfunction.


Dr Thompson is the director of preventive cardiology in the Division of Cardiology at the Hartford Hospital in Hartford, Connecticut. Address correspondence to Paul D. Thompson, MD, 80 Seymour St, Hartford, CT 06102; e-mail to [email protected].

This article was adapted from the recently published book: Thompson PD (ed): Exercise and Sports Cardiology. New York City, McGraw-Hill Medical Publishing, 2021 (to order: 1-800-262-4729 [isbn: 0-07-134773-9]).


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