Clinical and physiologic benefits

Numerous small studies have demonstrated that a supervised exercise program for patients with a variety of cardiac diagnoses improves quality of life, decreases the rate of reinfarction, reduces rehospitalization, and prevents ischemia. In 1989 a meta-analysis of several randomized studies also showed a significant decrease in mortality of myocardial infarction survivors who participated in a comprehensive cardiac rehabilitation program compared with controls. The odds ratios for 1-, 2-, and 3-year survival were 0.77, 0.74, and 0.80, respectively. Although this landmark study was done before the advent of current medical and invasive therapies now used to treat myocardial infarctions, a more recent study also found that cardiac rehabilitation had a similar effect on mortality in heart attack survivors. In fact, the degree of benefit continued to increase in recent years, as those patients who participated in cardiac rehabilitation in 1998 fared better than controls compared with those who participated in 1982. The most recent meta-analysis, consisting of 7683 patients, showed a 31% relative risk reduction in mortality for those who participated in an exercise-only form of cardiac rehabilitation. Based on this analysis, 72 patients would have to participate in an exercise training program to save one life over 2.5 years.

Exercise training improves outcomes and mortality in cardiac patients through a host of mechanisms. By directly measuring coronary atherosclerosis, Kramsch and colleagues showed that exercise causes a regression in plaque burden. This effect is likely achieved by improving several atherogenic clinical parameters, such as by correcting dyslipidemia, reducing blood pressure, increasing insulin sensitivity, reducing adiposity, decreasing vascular inflammation, and augmenting endothelial function.

Exercise improves lipid profiles by causing a modest increase in high-density lipoprotein (HDL) and a decrease in low-density lipoprotein (LDL). HDL, the so-called good cholesterol, is an LDL scavenger and high levels are important to decrease atherogenesis. Although diet alone has little effect on HDL, a low-fat diet in combination with moderate exercise increases HDL levels by up to 5% to 13%. LDL is the bad cholesterol. It is directly atherosclerotic and a major component in vessel injury. A 10% reduction in LDL levels is seen with an exercise and diet combination. Less is known about the effects of exercise on triglycerides. Most studies show little effect in those patients with baseline normal triglyceride levels. Among those with diabetes or high triglyceride levels, however, exercise does improve hypertriglyceremia.

By increasing muscle mass and efficient glucose utilization, exercise training specifically lowers insulin resistance. In fact, low basal levels of insulin are seen in well-trained nondiabetic subjects, despite a high carbohydrate and caloric diet. Exercise begins to lower insulin resistance after only one exercise session, although its effect wanes after as few as 3 days of inactivity. Chronic conditioning leads to chronically low insulin levels, signifying high insulin sensitivity. This effect is independent of body weight, percentage of body fat, and caloric intake. In diabetics especially, decreasing insulin resistance has important clinical consequences. For example, 22 weeks of aerobic exercise training in type 2 diabetics reduces hemoglobin A1c values by 0.51%. A further decrease of hemoglobin A1c by 0.46% is seen if aerobic exercise is combined with resistance training. The effect is greater for those with a baseline A1c greater than 7.5%. In this group, an average decrease of more than 1% was demonstrated without changing diet or medications.

In hypertensive patients, exercise has an acute effect on blood pressure. Mean blood pressure is reduced an average of 7 mm Hg on days when patients participate in 30 minutes of moderate exercise. Long-term exercise training has a sustained effect on blood pressure. After 32 weeks of supervised training in severely hypertensive patients, mean blood pressure was reduced by 5 mm Hg and allowed for a reduction in blood pressure medications. These patients also demonstrated beneficial cardiac reverse remodeling on echo, showing a reduction in left ventricular hypertrophy and left ventricular mass.

Improvements in atherogenic indices such as dyslipidemia, insulin resistance, and hypertension are seen despite only a small change in body mass index. In studies of weight loss during supervised exercise programs, the results are mixed. Although there is likely a small decrease in weight (around 2 kg) with exercise alone, obese patients must combine intensive diet with a moderate exercise program to achieve a more reasonable 8.5 kg weight loss or a 1.3 kg/m ² drop in body mass index.

In addition to contributing to a direct decrease in atherogenesis, exercise training may also have antithrombotic effects. There are increased serum levels of fibrinogen, a coagulant, after a myocardial infarction. Among survivors of a heart attack, this increased fibrinogen level is associated with additional events. Fibrinolysis is mediated by tissue-type plasminogen activator (t-PA) and inhibited by plasminogen activator inhibitor type 1 (PAI-1). The activity of t-PA is increased in older men after a 6-week program of moderate exercise. This result is accompanied by a decrease in t-PA antibodies, PAI-1, and fibrinogen. In contrast, platelet activation may actually increase temporarily in sedentary individuals who undergo strenuous exercise acutely, increasing their short-term risk of an event. Long-term conditioning, however, mitigates the risk and leads to a chronic decrease in platelet activity and clot formation.

Conditioning also has important anti-inflammatory effects. Markers of inflammation are higher in patients with coronary artery disease. Abnormal levels of highly sensitive C-reactive protein (hsCRP), tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6) have all correlated with an increased risk of future events. In several studies, exercise training has been shown to decrease the levels of all these markers of vascular inflammation independent of weight loss, lipid management, or blood pressure. In one study, patients with obstructive coronary artery disease were randomized to 2 years of exercise training without invasive intervention or percutaneous revascularization. Those in the exercise group decreased their hsCRP and IL-6 levels by 41% and 18%, respectively compared with no improvement in the stented group. Furthermore, the exercise group had fewer cardiovascular events and showed a greater improvement in exercise tolerance and ischemic threshold compared with the angioplasty group.

A decrease in vascular inflammation, blood pressure, and LDL may contribute to better endothelial function, but there is also evidence that exercise training independently improves vascular function by promoting vasodilatation. Arterial dilatation is mediated by endothelial release of nitric oxide which is impaired in atherosclerotic vessels, leading to a decrease in arterial area and blood flow. Exercise training attenuates this effect. Indeed, a 4-week exercise program has shown to reduce the abnormal acetylcholine-induced vasoconstriction in diseased coronary arteries. Compared with the control group, the trained group also had an increase in coronary blood flow reserve by demonstrating a more vigorous response to vasodilators. Other evidence has shown that exercise training in diabetics improves vascular function better than pharmacologic therapy. In patients with coronary artery disease, exercise has a direct positive effect on brachial artery reactivity and nitric oxide levels.

In part through its effects on endothelial function, exercise training reduces ischemia and increases the ischemic threshold in patients with obstructive coronary artery disease. The combination of increased blood flow with more efficient cardiac metabolic capacity can decrease ischemic episodes despite an increase in workload. Patients with chronic angina and documented ST depressions who participated in regular moderate exercise for 6 months were able to exercise longer and at higher workloads at the end of the training period. They were able also to generate a higher heart rate, blood pressure, and myocardial oxygen demand before the onset of chest pain or electrocardiographic signs of ischemia. More intense exercise training, with sessions that actually induce ischemia, is safe and leads to increase coronary blood flow by promoting collateral formation.

Physical conditioning also has a distinct antiarrhythmic effect, reducing the risk of sudden death. This effect is particularly important in patients with coronary artery disease or cardiomyopathies who have up to a 10% chance of developing fatal ventricular tachycardias or fibrillation within 1 year. In animals susceptible to sudden death, exercise training significantly reduces the risk of developing a ventricular arrhythmia during electrophysiology testing. This reduction in arrhythmic potential is in part mediated by altering the automatic nervous system. Patients with heart disease who have a high sympathetic tone are at increased risk of sudden death, and exercise helps mitigate this risk by lowering sympathetic activity while increasing parasympathetic activity. Exercise training has been shown to lower resting heart rates, increase heart rate variability, and increase serum acetylcholine levels, all of which are associated with enhanced vagal tone and lower risk of sudden death. There is also evidence that physical training has a direct effect on cardiac myocytes. Similar to β-blocker therapy, exercise reduces the abnormally high level of β2-adrenoceptor responsiveness seen in cardiac tissue after a myocardial infarct. Exercise has also been shown to lengthen the refractory period of ventricular tissue, increasing electrical stability. Thus, some investigators advocate that the decrease in mortality seen with cardiac rehabilitation may be entirely due to a reduction in arrhythmias leading to sudden death.

Through a variety of mechanisms, the exercise-training portion of cardiac rehabilitation has many clinical and physiologic benefits that directly prolong life in cardiac patients. Some benefits, such as a reduction in LDL levels, hemoglobin A1c, blood pressure, and body mass index, can be easily measured and have a direct effect on reducing coronary atheromas. Other physiologic benefits, such as a reduction in thrombosis, inflammation, poor endothelial function, ischemia, and arrhythmias, may be harder to quantify but also play a role in improving health and survival.

Indications, contraindications, and safety

Exercise training is safe and effective for a variety of patient populations. Traditional indications for cardiac rehabilitation include patients recovering from a myocardial infarction or coronary artery bypass surgery; however, in 1995 a guideline statement jointly issued by the Agency for Health Care Policy and Research and the National Institutes of Health broadened the indications to include patients with stable angina and congestive heart failure. In March of 2006, the Centers of Medicare and Medicaid issued a memorandum expanding coverage to patients who have had valve surgery or cardiac transplant. Table 1 lists the indications reimbursed by Medicare and the research studies cited to include each group. Despite clear evidence supporting exercise training in patients with nonischemic congestive heart failure, the committee did not expand coverage for a diagnosis of heart failure alone. As the Centers for Medicare and Medicaid usually sets the standards of coverage for the health insurance industry as a whole, most people outside the groups listed in Table 1 are not covered. Some insurers, however, have recognized the clinical benefits and cost-effectiveness of cardiac rehabilitation and have agreed to cover other patient populations, including those with heart failure, peripheral artery disease, congenital heart disease, left ventricular assist devices, valvular disease, pacemakers, pulmonary hypertension, and cardiac arrhythmias.

To determine an individual’s risk of starting an exercise program, a 4-category risk assessment has been proposed:

• 
  

  Class A: Men younger than 45 years of age or women younger than 55 years with no known cardiac problems and no cardiovascular symptoms, or older individuals with no known symptoms and normal exercise tolerance demonstrated by stress testing

  
  
• 
  

  Class B: Those with known coronary artery disease, valve disease, congenital heart disease, or heart failure with stable New York Heart Association Class 1 or 2 symptoms

  
  
• 
  

  Class C: Patients with known coronary artery disease, valve disease, congenital heart disease, or heart failure with stable New York Heart Association Class 3 or 4 symptoms, evidence of ischemia at a low workload (less than 6 metabolic equivalents [METs]), a drop in blood pressure, or nonsustained ventricular tachycardia with exercise

  
  
• 
  

  Class D: Patients with known cardiovascular disease with unstable symptoms or angina, severe and symptomatic valvular disease, uncontrolled arrhythmias, or those with congenital heart disease for which there is a contraindication for exercise (like hypertrophic cardiomyopathy).

Supervised exercise training is designed for patients in classes B and C. Initially electrocardiography (EKG) and blood pressure monitoring should be performed during exercise sessions for those in class C. Individuals in class A can likely start an exercise program without supervision. Those in class D should not exercise until further medical care can stabilize their symptoms and lower their risk.

Using this classification, supervised exercise training is very safe even in those with significant cardiovascular disease. The likelihood of a major event such as a cardiac arrest or myocardial infarction is less than 1 per 67,126 patient-hours of exercise. Less severe complications (the development of chest pain, shortness of breath, or non–life-threatening arrhythmias which cause termination of the exercise session) occur at a rate of 1 per 320 hours. The rate of death is about 1 per 783,972 patient-hours. This mortality risk compares favorably to the rate of death in a control population of healthy joggers (1 per 396,000 hours). Indeed, at 1 mortal event per approximately 80 exercise years, dying during a supervised exercise session may even be attributed to chance alone. The small rate of major complications has led some investigators to advocate that the current risk classification system is too strict. Perhaps more patients should be allowed to exercise without monitoring, thus allowing for the establishment of more off-site, low-cost, and convenient exercise facilities.

Indications, contraindications, and safety

Exercise training is safe and effective for a variety of patient populations. Traditional indications for cardiac rehabilitation include patients recovering from a myocardial infarction or coronary artery bypass surgery; however, in 1995 a guideline statement jointly issued by the Agency for Health Care Policy and Research and the National Institutes of Health broadened the indications to include patients with stable angina and congestive heart failure. In March of 2006, the Centers of Medicare and Medicaid issued a memorandum expanding coverage to patients who have had valve surgery or cardiac transplant. Table 1 lists the indications reimbursed by Medicare and the research studies cited to include each group. Despite clear evidence supporting exercise training in patients with nonischemic congestive heart failure, the committee did not expand coverage for a diagnosis of heart failure alone. As the Centers for Medicare and Medicaid usually sets the standards of coverage for the health insurance industry as a whole, most people outside the groups listed in Table 1 are not covered. Some insurers, however, have recognized the clinical benefits and cost-effectiveness of cardiac rehabilitation and have agreed to cover other patient populations, including those with heart failure, peripheral artery disease, congenital heart disease, left ventricular assist devices, valvular disease, pacemakers, pulmonary hypertension, and cardiac arrhythmias.

To determine an individual’s risk of starting an exercise program, a 4-category risk assessment has been proposed:

• 
  

  Class A: Men younger than 45 years of age or women younger than 55 years with no known cardiac problems and no cardiovascular symptoms, or older individuals with no known symptoms and normal exercise tolerance demonstrated by stress testing

  
  
• 
  

  Class B: Those with known coronary artery disease, valve disease, congenital heart disease, or heart failure with stable New York Heart Association Class 1 or 2 symptoms

  
  
• 
  

  Class C: Patients with known coronary artery disease, valve disease, congenital heart disease, or heart failure with stable New York Heart Association Class 3 or 4 symptoms, evidence of ischemia at a low workload (less than 6 metabolic equivalents [METs]), a drop in blood pressure, or nonsustained ventricular tachycardia with exercise

  
  
• 
  

  Class D: Patients with known cardiovascular disease with unstable symptoms or angina, severe and symptomatic valvular disease, uncontrolled arrhythmias, or those with congenital heart disease for which there is a contraindication for exercise (like hypertrophic cardiomyopathy).

Supervised exercise training is designed for patients in classes B and C. Initially electrocardiography (EKG) and blood pressure monitoring should be performed during exercise sessions for those in class C. Individuals in class A can likely start an exercise program without supervision. Those in class D should not exercise until further medical care can stabilize their symptoms and lower their risk.

Using this classification, supervised exercise training is very safe even in those with significant cardiovascular disease. The likelihood of a major event such as a cardiac arrest or myocardial infarction is less than 1 per 67,126 patient-hours of exercise. Less severe complications (the development of chest pain, shortness of breath, or non–life-threatening arrhythmias which cause termination of the exercise session) occur at a rate of 1 per 320 hours. The rate of death is about 1 per 783,972 patient-hours. This mortality risk compares favorably to the rate of death in a control population of healthy joggers (1 per 396,000 hours). Indeed, at 1 mortal event per approximately 80 exercise years, dying during a supervised exercise session may even be attributed to chance alone. The small rate of major complications has led some investigators to advocate that the current risk classification system is too strict. Perhaps more patients should be allowed to exercise without monitoring, thus allowing for the establishment of more off-site, low-cost, and convenient exercise facilities.

Exercise protocols

There are 3 sequential phases of cardiac rehabilitation. Phase 1 focuses on the inpatient setting, and includes early mobilization and walking with nursing or physical therapy support 24 to 48 hours after an acute event. Phase 2 is a supervised exercise and counseling program that usually starts 2 to 6 weeks after discharge from the hospital. Phase 3 focuses on maintaining fitness at home or in a private gym after completion of a cardiac rehabilitation program.

On referral to cardiac rehabilitation (phase 2), an exercise prescription should be individualized for each patient based on his or her medical diagnoses and baseline stamina. An initial history and physical should define medical conditions and identify those with unstable symptoms. It should also pinpoint each patient’s modifiable risk factors, such as ongoing smoking or obesity, to customize the education programs. A baseline symptom-limited exercise stress test is also recommended. This test determines the patient’s maximum exercise tolerance and heart rate in order to tailor future workouts. If ischemia (>1 mm of horizontal ST depression on EKG monitoring) or arrhythmias develop during exercise testing, this level of exercise and heart rate should be recorded. These patients warrant EKG and blood pressure monitoring during exercise. Future sessions should target a heart rate 10 to 15 beats below the ischemic threshold. Patients with internal cardiac defibrillators should also have close monitoring of their heart rate during exercise testing and rehabilitation sessions. The heart rate should be kept below the set threshold that would trigger device therapy or shocks.

Exercise intensity can be determined in an individual by measuring the maximum oxygen uptake (V o _2max ). V o _2max is defined as the maximum oxygen uptake that can be achieved in an individual with progressive exercise. This value can be quantified using gas analyzers that measure the breath-by-breath concentration of oxygen and carbon dioxide. During standard exercise testing and cardiac rehabilitation, however, these sophisticated tests are not usually needed. Instead, exercise intensity is more often expressed in METs, which is defined as the uptake of oxygen for the average individual for a given activity. One MET is equal to a V o ₂ of 3.5 mL O ₂ /kg/min and is the amount of oxygen uptake for the average person at rest. Table 2 lists the average maximum exercise intensity by age and compares it with standard activities and METs. An average sedentary man can achieve a maximum of 10 METs, whereas many well-trained distance runners can reach up to 24 METs. The failure to achieve at least 6 METs in patients less than 80 years of age is a marker of severe deconditioning or disease and carries a poor prognosis.

Exercise intensity can also be measured by the rating of perceived exertion. On this Borg Scale, a patient rates his or her level of perceived work from 6 to 20. A level of 12 to 13 is rated “somewhat hard” and generally corresponds to 60% of V o _2max . A rating of 18, “very hard,” corresponds to 85% of V o _2max . This method of determining exercise intensity is particularly helpful in patients who are on high-dose b-blockers or in heart transplant patients, in whom the heart rate is a less reliable indicator of exertion level. Otherwise, the rating of perceived exertion, V o _2max , maximum achieved METs, and maximum heart rate are closely correlated in most groups of cardiac patients.

During a supervised exercise program, patients typically meet for an exercise session 3 to 5 times a week. Each exercise session should begin with a 5- to 10-minute warm-up period during which they participate in light stretches. Sessions should then include 20 to 60 minutes of endurance aerobic activity. Another 5 to 10 minutes of cool-down with walking and stretching are important to prevent dizziness associated with the sudden cessation of moderate exercise. Most sessions (2–3 times a week) should also include resistance training with specific exercises to strengthen each muscle group.

The endurance portion of the session usually progresses in stages. The first 4 to 6 weeks are focused on exercises with a light intensity level. Light intensity is defined as 20% to 40% of the maximum METs, a perceived exertion score of 10 to 11, or 35% to 55% of the maximum heart rate. During this time the participant may have limited endurance (20 minutes or less). Over the next 4 to 6 months the exercise sessions should progress to a moderate intensity level (40% to 60% of maximum METs, a perceived exertion score of 12 to 13, or 55% to 70% of maximum heart rate). During this time, the participant should also focus on endurance, gradually increasing the aerobic workout to 40 to 60 minutes. After 6 to 12 months, the goal is to maintain the achieved fitness level by continuing the program at home or in a private gym. Although a treadmill has been the traditional mode for endurance exercise testing and training in the United States, patients may prefer other modes of aerobic exercise such as elliptical machines, stair climbers, bicycling, or even swimming. During a cardiac rehabilitation session they may often switch between several of these modalities. Indeed, several 10-minute sessions are as beneficial as one longer session.

Resistance and strength training are an important part of a cardiac rehabilitation program. Although it has little effect on V o _2max , resistance training helps increase strength, basal metabolic rate, endurance time, and functional capacity, while reducing injuries. It is especially important in the frail and elderly. Recommended exercises include the chest press, shoulder press, triceps extension, biceps curl, arm pull-down (for the upper back), low back extension, abdominal curl, quadriceps extension, hamstring curl, and calf raise. A prescription of one set of 10 to 15 repetitions with light weight (for a goal perceived exertion score of 10–11) for 8 of these exercises per session is recommended for patients with cardiac disease. Patients who have had a sternotomy should avoid weight training with the upper extremities for 3 months after the operation, and stability of the sternum should be examined before starting upper-body weight lifting. Table 3 gives a sample workout schedule for a training session.

Table 3

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