Principles of Ambulatory Medicine, 7th Edition

Chapter 63

Postmyocardial Infarction Care and Cardiac Rehabilitation

Kerry J. Stewart

Roy C. Ziegelstein

Epidemiology of Myocardial Infarction

Overview

Cardiovascular diseases are the major cause of mortality in the United States, accounting for more than one million deaths annually. These conditions are responsible for approximately 40% of all deaths in this country (1). Approximately 35% of these deaths are caused by myocardial infarction (MI). Approximately 25% of men and 38% of women will die within 1 year after having an MI (1). Although the overall death rate after MI has decreased, the rate of hospitalizations for MI has been relatively stable. The greater number of patients surviving an MI has increased the number of individuals with chronic heart failure (see Chapter 66) and the number of individuals who should be considered for cardiac rehabilitation and secondary prevention (2). In both older and younger patients, mortality after MI could be reduced still further with more consistent use of interventions known to benefit patients after MI, which is the focus of this chapter (3).

Patients who survive an acute MI are far more likely to suffer recurring illness or death from coronary artery disease (CAD). Approximately 7.1 million people alive today in the United States have a history of heart attack (1). Two of every three survivors of MIs do not make a complete recovery but still have a good long-term prognosis. The longitudinal care of the patient who has survived an MI usually is the responsibility of the patient's primary care provider.

Demographic Subgroups

The average age of a person having a first heart attack is 65.8 years for men and 70.4 years for women (1). Aging of the population undoubtedly will result in greater numbers of individuals with chronic diseases, including CAD, congestive heart failure (CHF), and stroke (4).

Death rates from CAD are highest among African American men and women. Whereas the mortality from cardiovascular disease has declined for men over the last two decades, it has increased for women during this period (1). For patients hospitalized with an acute MI, women, particularly African-American women, have higher case mortality than men both during hospitalization and in the 48 months after discharge (5). The higher mortality in women admitted for acute MI has been found in all age groups irrespective of type of treatment (6).

Prognosis of Patients Discharged From Coronary Care Units

Survivors of Myocardial Infarction

Mortality

Over the last several decades, the in-hospital mortality rate for patients with acute MI has decreased to approximately 10% (1,7). Although the in-hospital mortality rate is higher for patients with Q-wave MI, there is a higher

P.972


long-term mortality for those with non–Q-wave MI. The overall first-year mortality for hospital survivors of an MI is approximately 10% to 15% (7,8). Most of the deaths in the first year occur during the 3 months after discharge, and they occur chiefly in patients with one or more of the high-risk characteristics listed in Table 63.1.

TABLE 63.1 Characteristics Associated with Increased Mortality after Discharge of Patients Who Have Had an MI

Admission characteristics
History of a previous MI
CHF (chest x-ray or Killip classification)
History of hypertension
Extent of LV ischemia (radionuclide scintigraphy, cardiac enzymes)
Characteristics at discharge
Early (within 10 days) post-MI angina, with transient ST–T changesa
LV ejection fraction ≤40% (echocardiography, radionuclide ventriculography, arteriography)
Complex ventricular arrhythmiab (Holter monitor)
Left main, proximal left anterior descending, or three-vessel CAD (arteriography)
Positive limited early post-MI ECG stress test (within 2–3 weeks after MI)
Ventricular aneurysm developing in acute stage of MI
Characteristics after discharge
ECG abnormalities, especially ischemic ST-segment depression, 1 month after MI
Decreased heart rate variability
Cigarette smoking
Depression

aMortality risk highest when ECG shows ischemia at a distance (i.e., transient ischemic ST changes in myocardial location that is different from the location of the patient's MI).
bMultifocal premature ventricular contractions (PVCs), runs of two or more sequential ectopic ventricular beats, or PVCs with R-on-T pattern. CAD, coronary artery disease; CHF, congestive heart failure; ECG, electrocardiogram; LV, left ventricular; MI, myocardial infarction.

The classification of acute MI developed by Killip according to the presence and severity of CHF on admission to the hospital is one of the most useful prognostic indices. Class I patients have no evidence of CHF on admission, class II patients have mild CHF, class III patients present with pulmonary edema, and class IV patients have cardiogenic shock. Figure 63.1 shows the strikingly different survival rates among patients in these four classes (9). Improvement in survival rates in each of the Killip classes has been observed, but the classification remains a valid index of morbidity and mortality after MI (10,11).

Table 63.1 lists the clinical factors predictive of an increased mortality after hospital discharge. Patients with the greatest risk of mortality during the first year after an MI have one or more of the following factors: previous MI; development of early (within 10 days) post-MI angina accompanied by transient ST-segment or T-wave changes; ejection fraction ≤40%; late hospital phase (predischarge) complex ventricular arrhythmia; left main, proximal left anterior, left anterior descending, or three-vessel CAD; positive stress test at low workload within a few weeks after MI; presence of ischemic ST changes on resting electrocardiogram (ECG) taken ≥1 month after MI; and low heart rate variability (amount of heart rate fluctuation around the mean heart rate) (12). The Gruppo Italiano per lo Studio della Sopravvivenza nell’Infarto Miocardico (GISSI)-2 study also clearly showed that the significantly increased risk of in-hospital mortality with older age persists after discharge (13). Left ventricular (LV) aneurysm developing within 2 days of acute MI also brings a high risk of death during the first year, independent of LV function (14). In addition to these cardiac complications, post-MI depression is strongly associated with post-MI mortality, even after controlling for other known predictors of survival (15).

FIGURE 63.1. Survival after acute myocardial infarction based on Killip classification (810 patients admitted to the Duke Medical Center Coronary Care Unit from 1967 to 1978). (From

Rosati RA, Harris PJ. Acute myocardial infarction. In: Fries J, Ehrlich GE, eds. Prognosis: contemporary outcomes of disease. Bowie, MD: Charles Press, 1981:275

, with permission.)

In patients who are clinically stable 1 to 6 months after hospitalization for an acute MI or unstable angina, the presence of ischemic ST-segment depression on the resting ECG is the strongest predictor of morbidity and mortality over the ensuing 3 years. Posthospitalization stress testing is predictive of future coronary events in stable patients only when ischemia (≥1 mm ST-segment depression on exercise ECG) or a reversible perfusion defect (on thallium exercise test) is present at a low workload (5 metabolic equivalents [METs] or less) or when there is evidence of exercise-induced LV dysfunction (LV cavity dilation and/or increased thallium uptake by the lung during exercise) (16). Each of these high-risk subsets has made up <3% of study populations.

Morbidity

Postinfarction angina occurs during the year after an MI in many patients, and cardiac stress testing can help

P.973


anticipate who will develop this symptom. Stress testing, during the hospitalization, after discharge, or both, is recommended for many patients who have sustained an MI (17,18). The American College of Cardiology (ACC)/American Heart Association (AHA) guidelines list three class I recommendations for stress testing after MI (19): (a) before discharge for prognostic assessment, activity prescription, and evaluation of medical therapy; (b) early after discharge for prognostic assessment, activity prescription, evaluation of medical therapy, and cardiac rehabilitation if the predischarge exercise test was not done; and (c) late after discharge for prognostic assessment, activity prescription, evaluation of medical therapy, and cardiac rehabilitation if the early exercise test was submaximal. Despite these recommendations, only one of every 10 patients hospitalized in this country undergoes a stress test before hospital discharge (20). The limited utilization of stress testing as part of the care of patients with acute MI may relate to the perception that the test is not as useful in patients who have received reperfusion therapy (i.e., percutaneous coronary intervention or thrombolytic therapy) as it was in patients in the pre-reperfusion era. However, exercise testing after contemporary reperfusion therapies for MI still confers important prognostic information (21).

Patients who can exercise to 5 to 6 METs or to 70% to 80% of their age-predicted maximal heart rate without an abnormal ECG or blood pressure response have a low 1-year mortality (22). Patients with a post-MI symptom-limited stress test that shows early ischemic ST-segment changes (≥1 mm exercise-induced ST-segment depression) or limited work capacity (≤5 METs) have two or more times the risk of recurrent MI and of death over the ensuing year (23).

Postinfarction medical complications other than angina include CHF, life-threatening arrhythmias and sudden death, intracavity thrombi with stroke and systemic emboli, and post-MI syndrome (Dressler syndrome).

The psychologic and social sequelae during the year after an MI depend on both the severity of the patient's MI and the patient's premorbid psychosocial situation (see later in this chapter for a more detailed discussion of this topic).

Patients with Unstable Angina

Unstable angina is defined as pain caused by cardiac ischemia that is occurring more frequently, is being provoked by less effort, is occurring at rest, or is being relieved less readily by nitroglycerin. Chapter 62 describes other characteristics.

Patients discharged from the cardiac care unit with the diagnosis of unstable angina have 1-year morbidity and mortality rates similar to the rates of patients discharged with the diagnosis of a completed MI (24). Studies show that the resting ECG and the response to exercise stress testing are especially helpful in predicting future events in patients who are clinically stable after admission for unstable angina (16). The lack of ischemic ST-segment changes during exercise testing helps to identify patients at lower risk.

In an individual patient with unstable angina, a more precise prognosis often can be given by defining the coronary anatomy by cardiac catheterization and coronary angiography. In studies of patients with unstable angina, coronary angiography has shown CAD in the left main artery is more common in patients discharged with the diagnosis of unstable angina than in patients discharged with the diagnosis of a completed MI (15% vs. 5%, respectively). Another 10% have diffuse CAD, 10% have normal coronary arteries and are presumed to have coronary artery spasm or small-vessel disease as the cause of their chest pain, and the remaining 65% are equally divided among single-vessel, double-vessel, and triple-vessel CAD (25). This information is clinically important because of the demonstrated superiority of surgical over medical treatment of CAD in the left main artery. Chapter 62 describes the prognoses associated with each of the patterns and the management of unstable angina.

Survivors of Cardiac Arrest Who Have Not Had a Myocardial Infarction

The first-year mortality rate of survivors of out-of-hospital cardiac arrest who have not had an MI is approximately three times the mortality rate of survivors of out-of-hospital cardiac arrest who subsequently are shown to have completed an MI. In a study of >200 survivors of out-of-hospital cardiac arrest followed for >4 years, the rate of recurrence of ventricular fibrillation or sudden death in patients without an acute MI was 31%, compared with 5% for out-of-hospital survivors of cardiac arrest who subsequently evolved ECG changes of acute MI. The median time to recurrent circulatory arrest was 20 weeks. More than 70% of the episodes of ventricular fibrillation were unexpected or occurred during sleep or during the usual activities of daily living (26).

Because the survivors of ventricular fibrillation not associated with an MI have a high risk of sudden death, they require aggressive and highly individualized treatment. Advances in electrophysiology, antiarrhythmics, automatic implantable defibrillators, and the many innovative surgical approaches to ventricular dysrhythmias dictate prompt referral of such high-risk patients to a consulting cardiologist. Survivors of ventricular fibrillation not associated with an MI often receive an implantable cardioverter-defibrillator (ICD). The widespread use of ICDs is likely to produce issues for primary care providers who care for patients with these devices. Increased levels of anxiety and depression have been described in patients after ICD placement (27, 28, 29). The experience of a shock may

P.974


contribute to psychological distress and diminished quality of life (30,31). Chapter 64 discusses this topic in detail.

FIGURE 63.2. Flow diagram of risk stratification after myocardial infarction. CCU, coronary care unit; CHF, congestive heart failure; LBBB, left bundle branch block; MI, myocardial infarction; PTCA, percutaneous transluminal coronary angioplasty; ST, ST segment. (From

Clinical Guidelines Parts I and II. Guidelines for risk stratification after myocardial infarction [American College of Physicians]. Ann Intern Med 1997;126:561

, with permission.)

Risk Stratification Before Hospital Discharge

The American College of Physicians has published recommendations for in-hospital risk stratification of MI patients, and the recommendations are summarized in Figs. 63.2 and 63.3 (see American College of Physicians,http://www.hopkinsbayview.org/PAMreferences). This three-phase scheme delineates decision-making that is supported by outcome data from clinical trials. It was published to guide the care of MI patients before they are discharged from the hospital. It draws on a mix ofbaseline characteristics and findings from continuous reevaluation of the patient. Depending on clinical findings, a patient may have undergone thrombolysis, revascularization, or neither in the acute and nonacute phases of risk stratification. In the predischarge evaluation, patients at intermediate or low risk (60%–70% of MI patients) should undergo assessment of LV function and noninvasive stress testing. Often, those patients can be discharged after stays as short as 4 to 5 days. The postdischarge prognosis of MI patients and their appropriate management depend on the predischarge evaluation, postdischarge reevaluations, and the rehabilitation and medical approaches described in this chapter.

Rehabilitation and Management After Myocardial Infarction

Most patients discharged after MI can expect to return to most of their usual activities within a few weeks to months. For a smaller number of patients, complications of their MI make this outcome impossible. In either situation, an organized plan for care should be followed (Table 63.2). This plan should include the education of the

P.975


patient and the patient's family. Because of shorter hospital stays, much of the patient education previously included in inpatient cardiac rehabilitation now is conducted in outpatient programs.

FIGURE 63.3. Flow diagram for predischarge risk stratification after myocardial infarction. LVEF, left ventricular ejection fraction. (From

Clinical Guidelines Parts I and II. Guidelines for risk stratification after myocardial infarction [American College of Physicians]. Ann Intern Med 1997;126:561

, with permission.)

Patient Education

Many hospitals initiate education about MI when the patient is clinically stable. The educational program often is the responsibility of a cardiac rehabilitation professional. Patient education should cover the nature of coronary heart disease, cardiac symptoms, cardiac drugs, modification of major risk factors (smoking, hypertension, hyperlipidemia, obesity, and inactivity), and guidelines for resumption of physical activities (including sexual activity) and return to work. It should be emphasized that MI is a manifestation of a disease process that has been ongoing for many years. Many patients attribute their MI to what they were doing at the moment it actually occurred. Patients must understand that the MI very likely would have occurred regardless of what they were doing that particular day and that the likelihood of a recurrence may best be diminished by following prescribed medical therapy and making lifestyle changes.

Individualized information should be provided in a predischarge conference at which the patient and the patient's family members are encouraged to ask questions. The conference should include review of any adverse prognostic features identified before discharge (Table 63.1); the medications prescribed at discharge; discussion of specific plans for cardiac rehabilitation, diet, and smoking modification; a chance for ventilation about emotional stress-laden issues; and realistic appraisal of expectations of return to work or usual levels of physical activity. Because of the possibility of postinfarction angina, it is important to describe this symptom to patients who have never experienced it and to point out to all patients that postinfarction angina may occur with the increased activity recommended for the coming weeks. Every patient should be given sublingual nitroglycerin, and the correct use of this drug should be reviewed.

TABLE 63.2 Plan of Care for MI Survivors after Hospital Discharge

Patient education (objectives for all patients)a
Understands disease process (damage to the heart that heals in a few months, leaves a scar)
Understands likely prognosis
Understands and follows progressive activity scheduleb
Understands approximate timetable for return to workb
Understands importance of controlling major risk factors (smoking, hypercholesterolemia, hypertension) and takes action to control them
Knows how to recognize key cardiac symptoms (angina, tachycardia, heart failure, hypotension) and understands how to use sublingual nitroglycerin
Participates in group classes after dischargec
Gets answers to questions specific to his or her lifestyle
Medical management
Review in-hospital course for prognosis characteristics (see Table 63.1) and for medications prescribed at discharge
Assess and reinforce above patient education
Check periodically for complications of infarction (see Table 63.5)
Check for behavioral/psychiatric complications
Check ECG 2–3 months after discharge
Consider β-blocker, ACE inhibitor, statin, and aspirin treatmentd
Referral for cardiac rehabilitationd

aEssential to include the patient's partner in all aspects of education.
bSerial exercise stress tests can be used to plan progressive activity (see text).
cIf programs are available in the community.
dSee text for details.
ACE, angiotensin-converting enzyme; ECG, electrocardiogram; MI, myocardial infarction.

It is important to provide written information and to assess and reinforce patient understanding of the information after discharge. This has perhaps become even more important as length of stay for MI has decreased, resulting in fewer in-hospital opportunities for education and for providing postdischarge recommendations. The patient education booklet After a Heart Attack (single copies

P.976


available without charge from local chapters of the AHA) gives a useful general account of the disease process, prognosis, coronary risk factors, and rehabilitation process.

Many hospitals have developed group classes for MI survivors and their families. Typically, they are invited to participate in a number of weekly meetings during the first or second month after discharge. Sessions usually are led by a cardiac rehabilitation professional such as a nurse, social worker, clinical exercise physiologist, or cardiologist, with the objective of having participants raise questions about the recovery period to provide mutual support by sharing experiences with each other. Additional resources available in many communities are patient-run heart clubs and supervised physical conditioning programs (see Physical Conditioning After Myocardial Infarction). The American Association of Cardiovascular and Pulmonary Rehabilitation (401 North Michigan Avenue, Chicago, IL 60611-4267; 312-321-5146;http://www.aacvpr.org) publishes a national directory of cardiac rehabilitation programs and is an excellent source of patient materials and professional publications, such as Guidelines for Cardiac Rehabilitation and Secondary Prevention Programs (see American Association of Cardiovascular and Pulmonary Rehabilitation, http://www.hopkinsbayview.org/PAMreferences). In addition, several resources for patients are available on the Internet, including the sites of the Johns Hopkins Bayview Medical Center and Johns Hopkins Greenspring Station (http://www.hopkinsbayview.org/cardiology) and of the AHA (http://www.americanheart.org). Patients also can be directed to support groups such as The Mended Hearts (http://www.mendedhearts.org/). Many of these sites provide links to other sources of patient information, support, and online newsletters.

Postdischarge Appointments

In general, each patient who has had an MI should be encouraged to contact his or her primary care provider or cardiologist at least once during the first week at home to discuss any questions that arise. An office visit should be scheduled within 2 to 3 weeks. Before this visit, it is important to review the patient's hospital summary to determine whether adverse prognostic features were present (Table 63.1) and to identify the medications prescribed at discharge. The visit should be divided between an assessment of the patient's progress in rehabilitation (physical activity level, diet and smoking modifications, emotional status, understanding of the overall plan of care, expectation about return to work) and an assessment of the patient's medical status (manifestations of ischemia and heart failure, blood pressure status, and review of current medications). Two or more additional office visits, similar to the first visit, should be scheduled during the 3 months after an MI, and the patient should be encouraged to telephone at any time about new symptoms or questions.

Risk Stratification at 3 to 6 Weeks

Approximately 3 to 6 weeks after MI, a maximal exercise stress test should be considered, because this test can provide helpful therapeutic and prognostic information regarding the patient's disease (see discussion of stress testing after MI earlier in this chapter). Table 63.3summarizes the criteria and recommendations of the American College of Physicians, based on stratification into low-risk and moderate-risk findings in this stress test. The stress test is also used to assess functional capacity, to guide the return to work, and to provide goals (e.g., target heart rate, MET level) for an exercise prescription. Approximately 3 months after hospital discharge, an ECG should be obtained and used as the patient's new baseline tracing.

Activity Schedule

Table 63.4 provides a practical summary of symptom recognition for use by the patient and a schedule of progressive physical activities for the first 2 months after MI.

P.977

P.978


In Chapter 16, Table 16.1 lists a broad array of activities corresponding to the recommended energy levels during and after the recuperation period. Resumption of activities with increasing energy requirements should be gradual; in particular, the duration of new activities should be brief at first, with gradual increase, according to how the patient feels. The schedule given in Table 63.4 can be given to most patients. A more aggressive plan can be tailored for the patient if an early physical conditioning program, guided by early stress testing, is available. Similarly, stress test-guided conditioning also can be planned for patients after the first 1 to 2 weeks of convalescence from an MI. Supervised programs that enroll patients soon after MI are widely available. In addition to the American Association of Cardiovascular and Pulmonary Rehabilitation, affiliates of the AHA commonly maintain lists of local exercise programs. A comprehensive discussion of exercise conditioning is found below (see Physical Conditioning After Myocardial Infarction).

TABLE 63.3 Recommendations According to Stress Test Risk Stratification 3 to 6 Weeks After MI

Low-risk patients
These patients have a peak workload ≥5 METsa in the absence of exercise-induced angina pectoris or ST-segment depression.
Recommendations: Further diagnostic testing is unlikely to identify patients at an even lower risk and therefore is not indicated. The effect, if any, of medical or surgical therapy on the prognosis of these patients is difficult to demonstrate because of their very low risk. Treatment should emphasize the reduction of risk factors, especially control of hypertension, smoking cessation, diet modification, and exercise training.
Moderate-risk patients
These patients have a peak workload <5 METs, peak systolic pressure <110 mm Hg, or severe myocardial ischemia, defined as angina or ischemic ST-segment depression ≥2 mm appearing at a heart rate ≤130–140 bpm.
Indication for coronary arteriography: In patients at moderate risk, coronary arteriography is indicated.

aMET (metabolic equivalent) is the energy requirement for a certain level of activity. One MET is the energy requirement at rest. METs for common activities are given in Table 16.1.
MI, myocardial infarction.
Data from American College of Physicians. Evaluation of patients after recent acute myocardial infarction (position paper). Ann Intern Med 1989;110:485.

TABLE 63.4 Activity Schedule and Symptom Recognition for Patients Convalescing from MIa

General points
All activities, including sitting and lying down, require energy. The amount of energy required to perform a specific activity is expressed as METs. One MET is your resting energy requirement. As activities become more strenuous, the amount of energy required (METs) also increases, as does the workload imposed on your heart.
The schedule recommended in this program is based on the number of METs needed for various activities. Some specific recommendations are given for each of the first 3 months after your return to home. Table 16.1 gives the energy requirements for a wide variety of additional activities. If the table omits your favorite activities, ask your doctor about them.
Warnings: Generally the following activities impose an added strain on your heart and should be avoided, especially during the first 3 months after a heart attack:
Taking very hot or cold showers or baths
Extended breath-holding while exercising, lifting, or straining
Working in a bent or stooped position or with arms held above your head
Doing work that requires continuous tensing of your muscles
Working or exercising during very hot, cold, humid, or windy weather (in bad weather, plan your regular exercise at a nearby shopping mall)
Working or exercising during the first hour after a meal or after consuming alcohol
Consuming excessive amounts of alcohol (e.g., >1–2 oz of whiskey, 2–3 beers, 1–2 glasses of wine per day)
Walking or exercising on a hill or an inclined surface
Engaging in any activity that creates emotional stress or worry for you
Recommended activity scheduleb
First month (1–3 METs)
From discharge to 1 week
Regular exercise: Walk 5 min at a leisurely pace once per day on a level surface.
Some specific advice: This week, primarily get used to being at home. Occupy yourself with sit-down activities, such as watching television, playing cards, sewing, painting, or sketching. Avoid lifting objects heavier than 5 lb or doing activities that require reaching above your head. You may go up and down the stairs. However, take your time and limit the number of times you need to climb them. Do all of the things you were doing in the hospital. Get up and get dressed each day. You may be surprised at how tired and weak you feel. This is natural. Be sure to take rest periods when you need them, particularly after meals and before you exercise or climb the stairs.
Week 2
Regular exercise: Walk 10 min at a leisurely pace twice per day.
Some specific advice: Continue all of your previous activities and add others, such as taking rides in the car (however, no driving yet), cooking a meal, washing clothes in a machine (have someone else remove them), making your bed, attending a relaxing movie, going out to dinner, going shopping with your family (let others lift things from the shelves to the basket and carry the groceries), shooting pool, playing shuffleboard, throwing a softball underhand, and playing a piano or organ.
Weeks 3 and 4
Regular exercise: Advance gradually to walking 15 min at a leisurely pace twice per day.
Some specific advice: Continue your previous activities and others, such as going to religious services, sweeping floors, polishing furniture, and driving the car (beginning with short drives, avoiding heavy traffic).
Second month (3–5 METs)
Regular physical exercise: Progressively increase leisurely walking from 20 min once per day at a slightly faster pace to 30 min once or twice per day.
Some specific advice: Table 16.1 lists the approximate energy requirements of each activity. You may gradually increase your activities by adding other activities and spending more time at them; seeTable 16.1 for activities requiring ≤5 METs or ≥5 METs.
Recognizing heart symptoms
Your heart will give you warning signs if it is not ready for increased activity. Here are some guidelines to use:
Pulse: Locate your pulse and count the number of times it beats for 15 s and multiply that number by 4. This is your heart rate for 1 min. Take your pulse before you begin your walk or any new activity and at the end of the activity. Contact your health care provider before resuming exercise if:
There is an increase ≥20 bpm in pulse after exercise compared with before exercise pulse
Your heart rate exceeds 120/minc
You detect abnormal heart action: pulse becomes irregular, fluttering or jumping in chest or throat, very slow pulse rate, sudden burst of rapid heartbeats
Chest pain: Contact your health care provider before resuming exercise if you experience pain or pressure in the chest, arm, or throat precipitated by exercise or following exercise. Remember to take your nitroglycerin and rest if you do experience pain.
Dizziness: Contact your health care provider before resuming exercise if you become dizzy, light-headed, or faint during exercise.
Breathing difficulty: Contact your health care provider before resuming exercise if you become short of breath during or after a new exercise, or if you awaken from sleep short of breath.

aInformation in Chapter 16, Table 16.1 should be given to patients who receive the instructions in this table.
bPace of these activities may be scaled up or down by results of early post-MI stress test when available.
cThese figures may be markedly modified by results of early stress test or medication.
MI, myocardial infarction.

Return to Work

Because many patients will have their first MI during their active working years, they are commonly concerned about returning to work. After an MI, 10% to 20% of patients are unable to return to their former occupational and recreational activities. Fortunately, the remaining 80% to 90% of patients are able to do so within 2 to 6 months. In fact, 88% of those younger than 65 years are able to return to their usual work after an MI (1). Patients who do not return to work within 6 months of MI are unlikely ever to return to work (32), and this often is caused by psychological rather than physical factors (see Psychological Problems). Psychological distress is common even in individuals who are able to return to work after an MI (33).

Many factors determine whether an individual returns to work after an MI. Health care providers should be aware that only some of these factors are related to the patient's cardiac or medical condition. An individual's employment history and societal factors are important determinants of the likelihood of returning to work. Local unemployment rates, working conditions, employer attitudes about adjusting workloads, employer return-to-work policies, and medical care benefits are all important determinants (34). Obviously, the type of work is also an essential consideration. Patients whose occupations involve mental stress and hectic schedules should be advised to return to work on a part-time basis at first, leaving plenty of time for rest and relaxation. For patients whose work involves significant physical exertion, the timing of return to work can be based on the information given in Tables 16.1 and 63.4 and guided by the results of exercise stress testing and monitored responses during a supervised rehabilitation program. It is evident from Table 16.1 that most occupations require an energy level of ≤6 METs. Occupational activities classified as heavy work require energy expenditure of ≤7 METs. Certain activities may produce an increased workload on the heart because of psychological stress (e.g., driving a vehicle in heavy traffic) or because they entail significant resistive exercise (e.g., carpentry, plumbing, shoveling, operating pneumatic tools, or carrying objects heavier than 30 lb).

Patients with MIs complicated by poorly controlled angina, CHF, or arrhythmias should be evaluated in conjunction with a consulting cardiologist (see Medical Complications) before a plan for returning to work and other activities is formulated. Some of these patients may qualify for permanent medical disability (see Chapter 9) or for job retraining through vocational rehabilitation. The fundamental difference between impairment and disability caused by CAD was underscored in the report of the 1989 Bethesda Conference on Insurability and Employability of the Patient with Ischemic Heart Disease (35). Impairment is a medically defined disorder and is a key component of disability, but it is just one of several factors that determine the overall ability of a person to perform meaningful work. Additional factors that affect disability include other medical disorders, age, sex, education, training, and psychosocial support. The main points in the report state that most MI patients can return to work; prognosis can be estimated by clinical examination and noninvasive studies that evaluate LV function (echocardiogram), myocardial jeopardy (thallium stress test), and electrical instability (Holter monitor); cardiac catheterization is not routinely required; special assessment may be needed for jobs requiring sudden or sustained high effort or heat exposure (e.g., firefighters) or for those in whom sudden disability may endanger others (e.g., airline pilots); a trial period of progressively increasing part-time work may be necessary for smooth transition from total disability to full-time work; and maximal functional capacity should be evaluated as soon as the clinical status is stable, usually 3 to 5 weeks after uncomplicated MI, 7 weeks after coronary bypass surgery, and 1 week after coronary angioplasty in patients who have not had an MI.

Although cardiac rehabilitation, including education, counseling, and behavioral intervention, has many benefits, it has not been shown to alter the rates of return to work. This was the conclusion of the 1995 Cardiac Rehabilitation Clinical Guideline No. 17 of the Agency for Health Care Policy and Research (see Wenger et al., http://www.hopkinsbayview.org/PAMreferences). The expert panel reported that although education and counseling may improve a patient's potential for return to work, many other factors play a role in return to work, including willingness of the employer to rehire the patient, the patient's level of job satisfaction, economic incentives, and perceived stress of the job.

P.979

Sexual Activity

It is safe for patients who are symptom-free during usual activities of daily living to resume sexual intercourse within 4 to 6 weeks of MI. Available data suggest that the energy requirement approximates 3 METs during foreplay and afterplay and 5 METs at climax (36). These are equivalent to the oxygen demands of a brisk walk around the block or climbing one flight of stairs.

The Myocardial Infarction Onset Study provides information about the risk of sexual activity in patients with cardiac disease and is of particular benefit to those counseling individuals about sexual activity after an MI (37). Although this study confirmed that sexual activity can trigger MI, the risk appears to be small and transient. Notably, the relative risk of triggering an MI in individuals with a history of angina or previous MI is not greater than the relative risk in individuals without prior cardiac disease.

The same study indicated that regular exercise appears to reduce, and possibly to eliminate, the small increased risk of MI associated with sexual activity. Thus, health care providers who counsel patients after an MI can reassure them that the risk of triggering an MI during sexual activity is particularly low for those who exercise regularly. When counseling patients about resumption of sexual activity, the health cared provider should give specific advice and encourage questions. The pamphlet Sex and Heart Disease, available from the AHA (http://www.americanheart.org), is a helpful adjunct to counseling. Frequency of sexual intercourse can be similar to the frequency before the patient's MI. Sexual foreplay without completion of intercourse can be recommended to patients who wish to resume sex cautiously. In general, sexual activity can be resumed in the position that was most gratifying before the MI; however, patients should avoid positions in which they support their weight on their arms because this requires sustained static type of work (see Physical Conditioning After Myocardial Infarction) and may put extra stress on the heart by increasing the blood pressure. Sexual activity should be engaged in when both partners are relaxed. It is best to abstain from intercourse for 2 or 3 hours after eating a large meal because eating increases the work of the heart.

Inability to return to a previous pattern of sexual activity may be caused by angina (precipitated by intercourse), new medications, or psychological stress associated with the recent MI. If an otherwise stable patient develops angina during intercourse, sublingual nitroglycerin can be taken just before sexual activity.

Erectile dysfunction may be particularly common in men with CAD because the two conditions share common risk factors. For this reason, patients recovering from an MI may ask their practitioner about the use of medications to treat erectile dysfunction. Three drugs approved for erectile dysfunction are sildenafil (Viagra), tadalafil (Cialis), and vardenafil (Levitra). These drugs work by inhibiting the action of cyclic guanosine monophosphate (cGMP)-specific phosphodiesterase type 5, thereby blocking the breakdown of cGMP and allowing it to accumulate in the corpus cavernosum of the penis. A study in men with severe coronary stenosis showed that oral sildenafil did not produce any adverse cardiovascular effects, even in coronary flow (38). When patients with CAD were given sildenafil, vardenafil, or tadalafil before exercise stress testing to a level of cardiac work at least as great as that experienced during sexual intercourse, no significant cardiovascular problems were encountered (39, 40, 41, 42). Although caution should be used when prescribing sildenafil, tadalafil, and vardenafil to patients with CAD, particularly if the individual is not physically active on a regular basis, these drugs appear safe in the absence of low blood pressure or aortic stenosis. It must be emphasized, however, that these drugs should be used cautiously by men who are taking medicines that contain organic nitrates of any kind, including nitroglycerin. Because nitrates increase cGMP, the concomitant use of an organic nitrate and sildenafil, tadalafil, or vardenafil may result in dramatic, and potentially dangerous, reductions in arterial blood pressure. Chapter 6 discusses the evaluation and management of drug-induced and psychological sexual dysfunction, both of which may occur after MI.

Psychological Problems

It is normal for patients to experience symptoms of anxiety and depression during the first few weeks after discharge from the hospital. Some of these symptoms are caused by misconceptions about the nature and prognosis of MI and may respond to simple reassurance and clarification. Most patients do well when they are encouraged to express their concerns and are reassured that their response is normal. A small supply of a minor tranquilizer (see Chapter 22) or a short-acting hypnotic (see Chapter 7) can be prescribed if needed. Participation in group classes and group exercise programs can help patients adjust to changes in their lives after MI (see Patient Education).

Another common psychological complication of MI is an inappropriate fear of physical activity of any kind (i.e., the so-called cardiac crippleor ergophobic). Early participation in supervised physical activity, including the exercise stress test, and exercise conditioning have been shown to enhance the patient's self-confidence and ability to perform physical tasks (43). Having the partner or family member observe an exercise test may help to establish confidence that the patient is not a cardiac cripple. In some medical centers, partners or family members are offered an opportunity to walk on the treadmill. This serves to establish a reference point for estimating ability to engage in activity. Engaging in a wide range of

P.980


activities in the months after an MI is important because self-confidence is task specific (43,44). Most cardiac exercise programs (see below) initially emphasize activities using the legs, such as walking and jogging. Although these activities increase self-confidence in tasks requiring leg work, they do little for arm self-confidence. To increase arm self-confidence, patients must practice separate arm exercises (44,45). This is especially important for patients who plan to return to work that may require upper-body and arm efforts. The use of resistance training in cardiac rehabilitation now is routinely recommended for physiologic benefits and may help to increase self-confidence (46,47).

Another common problem is denial of illness persisting beyond the first few days in the hospital. The behavior associated with persistent denial may create substantial risks. This is especially true of patients who are extremely competitive and are used to controlling most of the circumstances of their lives (48). Typically they are determined to return to work as soon as possible and will refuse cardiac rehabilitation on the basis that they can do it better on their own. This behavior arouses anxiety, fear, and concern in the family and may lead to significant interpersonal conflict. An open discussion with patient and partner, with each acknowledging the other's concerns, often can lead to resolution of these conflicts and more appropriate behavior from each of them.

At times it is useful to teach patients to use various forms of feedback to guide their activities. Specifically, patients are taught to use a target heart rate based on an exercise stress test; to observe themselves and how they feel, with the basic instruction to rest if fatigue or any cardiac symptoms occur during exercise; to call their primary care provider or cardiologist if symptoms persist after using nitroglycerin; and to view family members as a source of feedback. In most cases, family members’ observation on how the patient looks is remarkably accurate. If a partner says his or her partner looks tired or does not look right, he or she probably is correct (and vice versa). By having the patient agree to consider these comments as well-meaning, the patient usually will comply with the partner's advice. Thereafter, the number of reminding behaviors is reduced progressively, and the rehabilitation process can proceed with greater enthusiasm from both partners. With more difficult patients or with partners having pre-existing interpersonal strife, the consultation of a psychiatrist or psychologist may be helpful in managing adjustment problems.

Some patients have severe psychological and behavioral problems after MI that may interfere with their rehabilitation. The most common problem is persistent depression, which may have characteristics of a major or minor depressive illness or may present as an adjustment disorder characterized by anxiety, depression, somatization, or a mixture of these responses (49). Chapters 21, 22, and 24 discuss the diagnosis and management of these problems.

Approximately 40% of patients have either minor or major depression soon after an MI (49). Major depression occurs in 15% to 20% of patients and is associated with a threefold to fourfold increased cardiovascular mortality at 6 months (13). Individuals with major depression soon after an MI are likely to remain depressed for at least several months and possibly longer (49). Thus, the practitioner who views depression as an expected reaction that is likely to improve and not likely to influence recovery may be missing an opportunity to improve the patient's quality of life and health. Because major depression typically does not resolve spontaneously, the patient who leaves the hospital depressed may continue to experience mood disturbance at the very time when participation in risk-reducing behaviors is critical. It is important for health care providers to recognize that patients with depression after an MI are less likely to adhere to recommended behavior and lifestyle changes intended to reduce the risk of subsequent cardiac events (50).

These findings highlight the importance of recognizing symptoms of depression and offering patients appropriate treatment, which should include a program of cardiac rehabilitation. A study in which depressive symptoms were present in 20% of patients after a major coronary event showed that symptoms resolved in two thirds of these patients after a program of cardiac rehabilitation (51). Unfortunately, patients with depression are more difficult to recruit and retain in these programs than are individuals without depression (52,53). When depression is identified in a patient recovering from an MI, the practitioner should encourage the individual to socialize and to increase interactions with friends and family. Depression resolves more rapidly after an MI when patients have good social support (54). Social support may even buffer the adverse effects of depression on prognosis. The 1-year cardiac mortality of depressed patients with the lowest levels of perceived social support has been observed to be more than five times that of depressed patients with the highest levels of perceived social support (54).

The selective serotonin reuptake inhibitors (SSRIs) can be used safely by patients with ischemic heart disease (55, 56, 57, 58). In light of these studies and the general absence of significant cardiovascular side effects of the SSRIs, antidepressants in this class are preferable to tricyclic antidepressants (TCAs) in patients with depression after an MI who require antidepressant therapy. TCAs may increase resting heart rate, produce orthostatic hypotension, and adversely affect intracardiac conduction and, possibly, the susceptibility to ventricular arrhythmias (59). In a study that compared the effects of the SSRI paroxetine to the effects of the TCA nortriptyline in patients with ischemic heart disease and major depression, patients treated with the TCA experienced significantly more adverse cardiac events than

P.981


patients treated with paroxetine (56). Although concerns about the safety of SSRIs in patients with ischemic heart disease have been allayed, no trial to date has shown that treatment of depression with either an SSRI (58) or with cognitive behavior therapy (60) improves survival. Chapter 24 discusses in detail the treatment of depression.

Medical Therapy

Overview

There is evidence that β-blockers and aspirin reduce the risk of morbidity and mortality after MI. For certain subgroups of patients, long-term treatment with angiotensin-converting enzyme (ACE) inhibitors also improves prognosis. Despite the widespread use of calcium channel blockers after MI, there is no evidence that this class of drug improves prognosis. The evidence for current recommendations regarding each of these classes of drugs is thoroughly reviewed by Hennekens et al. (see http://www.hopkinsbayview.org/PAMreferences).

β-Adrenoreceptor Blockers

β-Blocker therapy is recommended for all patients who have had an MI. Treatment should begin during the initial hospitalization and should be continued indefinitely. Although the benefits of β-blocker therapy are modest in low-risk patients (i.e., younger patients without a prior MI, those who have not had an anterior MI, or those who do not now have complex ventricular ectopy or significant LV dysfunction) (61), it is generally recommended that unless a clear contraindication exists, even low-risk patients should receive β-blockers indefinitely. When initiated early in the course of an infarction (within 6 hours), β-blockers may limit or reduce infarct size. Later in the postinfarct time period, the mechanism for reduction in mortality is prevention of reinfarction and the antiarrhythmic property of β-blockers. The overall magnitude of benefit from the use of β-blockers seems to be an approximately one-third reduction in first-year mortality and about the same magnitude of reduction in reinfarction during the first post-MI year. These benefits may extend beyond 1 year in some subgroups.Contraindications or relative contraindications to the use of β-blockers include asthma, bradycardia, and insulin-treated diabetes mellitus. The recommended dosage of a β-blocker is the amount required to produce attenuation of heart rate and blood pressure response to exercise without producing side effects. Chapter 67 summarizes the characteristics of the available β-blocking drugs.

Antiplatelet Therapy

Daily aspirin (75–325 mg) is recommended for all patients who have had an MI. Although the efficacy of other types of antiplatelet therapy is less well established, clopidogrel (75 mg/day) may be substituted for aspirin if the patient has an aspirin allergy or aspirin intolerance. Clopidogrel often is recommended in addition to aspirin for patients who have had an MI, particularly if they have been treated with percutaneous coronary intervention (PCI). Clopidogrel is usually given for at least one month, although the optimal duration of clopidogrel therapy is debated. Because many patients have drug-eluting stents placed during PCI, which often require prolonged use of clopidogrel and aspirin, the decision about how long to continue this drug should be made in conjunction with the consulting cardiologist. If the risk is acceptable, warfarin anticoagulation is a reasonable alternative for secondary prevention of MI in patients unable to take aspirin or for those with atrial fibrillation, LV thrombus, or extensive wall-motion abnormality. Multiple randomized trials of antiplatelet therapy for secondary prevention of vascular disease show that prolonged treatment with aspirin has no effect on nonvascular mortality but reduces vascularmortality by approximately 15% and nonfatal vascular events (stroke or MI) by approximately 30% in patients with pre-existing cardiac or cerebral vascular diseases (62). Post-MI benefits are similar to the benefits in patients after stroke and transient ischemic attack. In absolute terms, the benefits of antiplatelet therapy accrued to approximately 40 per 1,000 treated patients during the first month of treatment after an acute MI and to approximately 40 per 1,000 patients with a history of MI who were treated for 3 years. There is no difference in the degree of protection afforded by aspirin alone at a dosage of 325 mg/day and that afforded by higher aspirin dosages or other antiplatelet agents. Aspirin 100 mg/day has been shown to improve coronary artery bypass graft patency at 4 months (90% of grafts patent vs. 68% in the placebo group) (63) and to decrease significantly the frequency of restenosis after percutaneous transluminal coronary angioplasty (64) and thrombolysis (65). Chapter 57 provides additional details on antiplatelet agents.

Angiotensin-Converting Enzyme Inhibitors

All patients who have had an MI and whose LV ejection fraction is <40% should receive an ACE inhibitor in the absence of specific contraindications (see Hennekens, et al., MI management guidelines, http://www.hopkinsbayview.org/PAMreferences). Although the benefit of ACE inhibitors may be less in those with normal or mildly reduced LV function, even these patients should be considered for treatment with ACE inhibitors, in addition to aspirin and beta blockers. The purpose of using these agents after an MI is to prevent adverse LV remodeling and recurrent ischemic events.

Long-term use of ACE inhibitors by patients with chronic ischemic congestive cardiomyopathy is associated with significant improvement in morbidity and mortality

P.982


irrespective of severity and symptoms of failure. A large placebo-controlled study showed that patients with recent MI and LV dysfunction (ejection fraction ≤40% by radionuclide ventriculography) who were randomized to captopril experienced a modest reduction in cardiovascular and overall mortality, progression to severe heart failure, and recurrent MI during 3 years of treatment (66). Another large study showed that asymptomatic patients with LV ejection fraction ≤35% who were randomized to enalapril also experienced a reduction in mortality or progression to heart failure during 3 years of treatment (67). The benefits accrued chiefly to patients with the lowest ejection fractions. In asymptomatic patients with reduced ejection fractions, ACE inhibitors should be started at low dosages (e.g., enalapril 2.5 mg/day; captopril 6.25 mg three times daily) with gradual increases (e.g., enalapril up to 10 mg/day; captopril up to 25 or 50 mg three times daily) guided by blood pressure response and renal function. An angiotensin II receptor blocker (ARB) is an acceptable alternative for patients who have sustained an MI or who have CHF and who are intolerant of ACE inhibitors. Chapter 67 summarizes the characteristics of ACE inhibitors.

Calcium Channel Blockers

Calcium channel blockers are not recommended for secondary prevention after an MI. Because calcium channel blockers have not been demonstrated to significantly reduce mortality in MI survivors, they should be used only in patients with symptomatic ischemia or hypertension that is not controlled despite treatment with β-blockers and ACE inhibitors or ARBs. Calcium channel blockers may be appropriate for patients with good LV function who have specific contraindications to beta blockers or who tolerate them poorly.

Smoking, Hyperlipidemia, Hypertension, and Exercise

Smoking

All patients who smoke after an MI should be counseled to stop. Post-MI morbidity and mortality are significantly reduced in patients who discontinue smoking. Smokers who have survived an MI usually are motivated to stop. Chapter 27 describes practical ways to assist patients who desire to stop smoking, including the prescription of nicotine substitution products.

Lipid-Lowering Diet and Drugs

A diet low in saturated fat and cholesterol (the AHA Step II diet) should be recommended to all patients after an MI. As noted in the Third Report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III) (see Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults, http://www.hopkinsbayview.org/PAMreferences), most patients with CAD require drug therapy to reduce low-density-lipoprotein (LDL) cholesterol. Lipid-lowering therapy should be recommended to reduce LDL cholesterol to <100 mg/dL. In general, treatment should begin with a statin, although whether reducing LDL cholesterol to <100 mg/dL by other means, including the use of other lipid-lowering drugs, produces similar reductions in coronary events in patients who have sustained an MI is not clear. Whereas a target LDL cholesterol of <100 mg/dL has been established by the expert panel, later data suggest that the optimal LDL level may be even lower, perhaps in the 75 to 80 mg/dL range (68). For patients who have normal total and LDL cholesterol levels but whose high-density lipoprotein (HDL) cholesterol is <35 mg/dL, an exercise program should be recommended in an attempt to raise HDL cholesterol. Drug therapy (e.g., with niacin or a fibrate) also may be considered for this purpose.

As pointed out in the American College of Physicians’ risk stratification report (see American College of Physicians,http://www.hopkinsbayview.org/PAMreferences), lipid levels measured within 24 to 48 hours of an MI are accurate and can guide post-MI secondary prevention decisions. Chapter 82 provides detailed information on cholesterol and atherosclerotic disease.

Exercise

The role of formal exercise programs in rehabilitation after MI is described in detail in Physical Conditioning after Myocardial Infarction.

Medical Complications

Table 63.5 lists the principal medical complications of MI, the procedures that may be useful in diagnosing or evaluating them, and potential therapies. As noted earlier (see Risk Stratification Before Hospital Discharge), complications identified early are addressed very aggressively before or shortly after discharge. In general, use of advanced and costly procedures to evaluate the complications listed in Table 63.5should be coordinated with a consulting cardiologist.

Postinfarction Angina

As discussed in the prognosis, angina is common in survivors of MI. Chapter 62 describes in detail the evaluation and medical management of angina. Because protection of the heart from transient ischemia may be especially important during recovery from an MI, it is advisable to

P.983


prescribe β-blockers in most patients (see above) and to undertake aggressive evaluation and management of patients who develop angina within the first 3 months after MI. Because of the poor prognosis associated with angina that occurs very early after an MI, patients with this problem after hospital discharge should be referred to a cardiologist for consideration of coronary catheterization and possible coronary revascularization.

TABLE 63.5 Medical Complications of MI

Complications

Diagnostic Procedures for Selected Patientsa

Management Approaches

Angina or other evidence of reversible ischemia

ECG stress testing, echocardiographic or radionuclide stress testing, Holter monitor for silent ischemia, coronary arteriography

Standard antianginal therapy (see Chapter 62), coronary artery bypass or PTCA for selected patients, physical conditioning

CHF

Radionuclide ventriculography or echocardiography (reduced ejection fraction, segmental dysfunction, rupture, ventricular aneurysm)

Afterload reduction, diuretics, ?β-blockers, ?anticoagulants (see Chapter 66 for treatment of heart failure), surgery in a few selected patients

Arrhythmias

Holter monitor, ECG stress testing, electrophysiologic study in selected patients

β-Blockers, other antiarrhythmics (seeChapter 64), surgery or implantable defibrillator in selected patients

Post-MI syndrome (Dressler syndrome)

Echocardiography (pericardial effusion)

Aspirin or other anti-inflammatory agents (see text)

Systemic emboli

Echocardiography (intracardiac thrombus)

Anticoagulant therapy (see Chapter 57), surgery in selected patients

aShould be coordinated with and interpreted by consulting cardiologist.
CHF, congestive heart failure; ECG, electrocardiogram; MI, myocardial infarction; PTCA, percutaneous transluminal coronary angioplasty.

Postinfarction Symptomatic Congestive Heart Failure

Postinfarction symptomatic CHF usually develops before hospital discharge. Currently, most patients undergo measurement of LV ejection fraction as part of their evaluation before discharge so that those at increased risk for developing symptomatic CHF after discharge are known. As noted above, ACE inhibitors delay deterioration in functional capacity and improve survival in patients with CHF after MI (66).Chapter 66 describes in detail the use of ACE inhibitors and other agents for CHF. Selected patients with persistent CHF may have segmental or global LV dysfunction or mitral regurgitation that may improve after cardiac surgery and may benefit from referral to a cardiologist.

Postinfarction Arrhythmias

A substantial proportion of MI survivors have complex ventricular arrhythmias (see criteria in Table 63.1) on 24-hour ambulatory ECG monitoring after the first week of hospitalization. Controlled trials do not show that suppression of ventricular ectopy with drug therapy improves mortality. Therefore, routine testing to determine whether ventricular arrhythmia is present after an MI is not recommended. Studies evaluating the benefits of implantable defibrillators in specific high-risk populations have shown that defibrillators prolong life compared with use of antiarrhythmic drugs (69,70). Chapter 64 provides a comprehensive discussion of the management of symptomatic arrhythmias.

Postmyocardial Infarction (Dressler) Syndrome

An estimated 3% to 4% of patients develop this complication, usually within 1 to 8 weeks after an MI. The syndrome is characterized by the pain of pericarditis (substernal pain relieved by leaning forward and increased with inspiration), presence of a friction rub, pericardial effusion (which can best be demonstrated by echocardiography), malaise, fever, leukocytosis, and often unilateral or bilateral pleural effusion. The principal considerations in the differential diagnosis are pulmonary embolism and recurrence or extension of the recent MI.

A patient with suspected Dressler syndrome should be considered for hospitalization. A possible recurrent MI should be addressed by monitoring, serial ECGs, and measurement of cardiac enzymes. Evaluation for pulmonary embolization requires ventilation–perfusion lung scanning or spiral computed tomography. If these tests do not explain the patient's symptoms, the clinical diagnosis of Dressler syndrome can be made with reasonable assurance. Echocardiographic evidence of a pericardial effusion and an elevated erythrocyte sedimentation rate may be present.

P.984

Dressler syndrome usually responds to salicylates or indomethacin. In patients who do not respond to these drugs, prednisone provides prompt relief of symptoms. However, use of steroids within 4 weeks of an MI may interfere with postinfarction healing and may increase the risk of myocardial rupture; therefore, use of steroids should be limited to patients who are >4 weeks postinfarction. Once the diagnosis is secure and symptoms are controlled, the patient can be discharged. The anti-inflammatory drug chosen in the hospital should be administered for a few weeks after discharge. Patients who have recurrent symptoms when anti-inflammatory treatment is discontinued should resume treatment for another month or longer.

Arterial Embolization

Arterial embolization occurs after hospitalization in 5% to 10% of MI survivors. The emboli seem to originate from mural thrombi that typically are seen in the LV apex adjacent to akinetic or dyskinetic wall segments. Approximately 30% to 40% of hearts with akinetic or dyskinetic LV apices show mural thrombi on the echocardiogram. Thus, anticoagulation (see Chapter 57) in patients with mural thrombi is generally recommended, although the impact and appropriate duration of anticoagulation have not been assessed in a prospective trial. However, most cardiologists recommend anticoagulation therapy for 3 to 6 months for MI survivors who have mural thrombi. In patients with LV systolic dysfunction, warfarin use is associated with improved survival and reduced morbidity (71). Patients with atrial fibrillation or a history of embolic events also should be considered for systemic anticoagulation with warfarin.

Referral for Cardiology Consultation

Selected MI survivors may benefit from coronary angioplasty or cardiac surgery by symptom reduction or improved prognosis. Patients in the following groups should be referred promptly to a cardiologist to ensure optimal medical therapy and to obtain an opinion about the advisability and the timing of invasive procedures:

  • Patients with uncontrolled anginarefractory to medical therapy, with a markedly positive exercise stress test at low workload or with evidence of LV dysfunction during exercise (e.g., increased lung uptake of thallium during exercise)
  • Patients with a ventricular aneurysm
  • Patients with CHF refractory to medical therapy (ACE inhibitors, digitalis, and diuretics)
  • Patients with structural complications, such as ventricular septal defect (suggested by holosystolic murmur and thrill at the left sternal border), papillary muscle rupture (suggested by refractory CHF and holosystolic apical murmur), segmental akinesis, or ventricular aneurysm
  • Patients with electrical instability(e.g., symptomatic bradycardia, high-grade atrioventricular blocks, ventricular tachycardia, or other arrhythmias)

Home Care for Acute Myocardial Infarction

Although not generally advisable, management at home may be appropriate for an occasional patient who has a stable acute MI and objects to hospitalization, a patient who is predicted to have a high likelihood of becoming very disoriented and agitated in a cardiac care unit, or a patient who consults a health care provider several days after the onset of symptoms of infarction. The scheme for rehabilitation after MI described in this chapter can be adapted to these situations.

Management of Unstable Angina After Discharge From Hospital

Of patients admitted to a hospital with unstable angina but without MI, 15% to 30% continue to have pain despite vigorous medical management. Patients in this group have an estimated 1-year mortality rate of 25%. Therefore, most are evaluated and referred for coronary angioplasty or coronary artery bypass surgery. These interventions relieve or eliminate symptoms in most cases and improve survival for those with left main CAD, three-vessel disease, and two-vessel disease with LV dysfunction.

To date, the rehabilitation of the medically managed patient with unstable angina has not been studied as systematically as the rehabilitation of the patient after MI. These patients should receive education similar to that recommended for patients after MI regarding the nature of CAD, the recognition of symptoms, and the control of risk factors (see above). Because these patients have not sustained an ischemic injury that typically would require ≥2 months to heal, they often return to their usual activities more rapidly than patients who have had an MI. This is true particularly if the angina is well controlled and a stress test shows good effort tolerance (≥9 METs) and minimal or no changes caused by ischemia or LV dysfunction. Chapter 62 provides additional information regarding the management of unstable angina.

Physical Conditioning After Myocardial Infarction

Regular exercise, with the goal of attaining the physiologic adaptation known as the conditioning effect, is safe and

P.985


beneficial for almost all patients after MI (46), just as it is for healthy people and patients with most chronic diseases. The basic principles of exercise training are applicable to people with and without heart disease. Low-intensity exercise that does not produce a conditioning effect may be associated with health benefits (see Chapter 16). Cardiac rehabilitation programs are excellent resources to which patients can be referred for a supervised exercise program. Contemporary programs also are experienced in addressing the individualized exercise and learning needs of each patient in the rehabilitation setting.

Chapter 16 describes in considerable details the cardiovascular principles related to exercise; Chapter 68 describes important principles regarding the musculoskeletal system. A brief summary of these principles is provided here.

The body adapts to the kind and amount of physical demands placed on it. The response is specific, with the greatest changes observed only in those parts of the body on which demands are placed. For exercise to improve fitness, it must overload the muscles or organ system involved in the exercise. To overload is to exercise at a greater intensity than the intensity to which a person is accustomed. Threshold of training is the amount of exercise that must be done to produce fitness improvements. Because the effects of exercise are specific to the type of activity engaged, an optimal exercise program should include a variety of activities designed to improve each of the major components of fitness: cardiovascular endurance, muscle strength, muscle endurance, and flexibility.

The principal hemodynamic adaptation to cardiovascular or aerobic exercise in patients with heart disease takes place in the peripheral vascular and muscular systems. Trained muscles can extract more oxygen from a given blood flow, and there is a better distribution of the cardiac output. Heart rate and blood pressure are lower at rest and at a given submaximal workload. As a result, the patient can do more work with less cardiac effort (i.e., less myocardial oxygen demand). This is extremely beneficial to cardiac patients who have limited coronary artery blood supply or poor LV function. Angina may occur at the same threshold, that is, the same double product (heart rate × systolic blood pressure), but this threshold is reached at a higher level of body work or MET level. METs are used to rate the energy requirement of different physical activities, as indicated by the amount of oxygen extracted during those activities. One MET is 3.5 mL O2/kg body weight per minute and is equivalent to oxygen requirement at rest, 2 METs are twice the resting requirements, and so on (METs required for a broad range of activities are given in Table 16.1). In patients with CAD, the increase in angina-free exercise capacity with regular exercise is achieved through some of the same mechanisms by which β-blockers and nitrates increase work capacity. Similar to the effect of these drugs, the effect of exercise training is to reduce heart rate and blood pressure at rest and during work. In healthy people who perform aerobic exercise, changes occur in the heart itself, including increased diastolic volume, increased ejection fraction at rest and to a greater extent during exercise, and enhanced contractility. Few studies show any of this central effect in cardiac patients. However, there is evidence that cardiac patients may achieve central changes if they train hard and long enough (72). Improvement in coronary collateral circulation or myocardial perfusion has been shown in patients who participate in regular physical exercise and adhere to a low-fat diet (73). However, the independent effect of exercise on CAD progression is not yet known.

In recent years, there is increased recognition of the importance of resistive training for individuals with and without cardiovascular disease. The AHA issued a Scientific Advisory on “Resistance Exercise in Individuals With and Without Cardiovascular Disease” (seehttp://www.hopkinsbayview.org/PAMreferences). This advisory, which has been endorsed by the American College of Sports Medicine, notes that after careful screening and risk stratification, and when appropriately prescribed, resistance training is an effective method for improving muscular strength and endurance, preventing and managing a variety of chronic medical conditions, modifying cardiac risk factors, and enhancing psychosocial well-being. Examples of resistance training are weight lifting, pushups, situps, isometrics, and use of elastic stretch bands. Most activities requiring lifting and straining, such as weight training, have a large static component. In such activities there is increased peripheral vascular resistance, with subsequent increase in blood pressure but little increase in heart rate or cardiac output. Such exercises do not bring about enhancement in oxygen extraction, so they are generally not aerobic. Brief periods of moderate resistive exercise appear safe. In fact, studies show that cardiac patients who were required to carry or lift weights or to perform isometric exercise after MI had fewer ischemic electrocardiographic changes and arrhythmias during resistive exercise than during aerobic exercises (74). Therefore, gradual involvement in resistive training may be beneficial and desirable, especially for patients whose jobs or recreational activities require static efforts.

Cardiac Rehabilitation

Participation in a formal cardiac rehabilitation program should be recommended to all patients after an MI (46). These programs reduce cardiovascular mortality and the risk of subsequent cardiac events, improve symptoms and exercise tolerance, improve blood lipids, increase the likelihood of smoking cessation, improve quality of

P.986


life and psychosocial outcomes, and promote compliance. Cardiac Rehabilitation Clinical Guideline No. 17 (see Wenger et al.,http://www.hopkinsbayview.org/PAMreferences) from the Agency for Health Care Policy and Research defined the scientific basis for recommendations for multifactorial cardiac rehabilitation services that include medical evaluation, prescribed exercise, cardiac risk factor modification, and education, counseling, and behavioral interventions. Provision of these services is physician directed and typically is implemented by a team of health care professionals that may include nurses, clinical exercise physiologists, and physical therapists. Unfortunately, despite the scientific evidence demonstrating the benefits of cardiac rehabilitation, the report points out that only 11% to 20% of the several millions of patients with coronary heart disease participate in cardiac rehabilitation programs.

Benefits of Conditioning

Cardiac patients who exercise regularly and have become conditioned show better control of angina and enhancement of physical working capacity. Because of the peripheral cardiovascular adaptations described earlier, angina pectoris occurs at higher exercise levels. This increased anginal threshold allows the patient to do more work, and at any given level of work the patient feels more comfortable because the work represents a lower percentage of a now higher maximal capacity. Similar benefits for patients with LV dysfunction and chronic heart failure also have been demonstrated (75,76). Rating of perceived exertion (RPE) is a scale that measures how hard any given level of work feels (Table 63.6). The RPE is administered during exercise testing. The patient is asked to rate the work at each stage of the test. After conditioning, the RPE is lower at any given stage and is associated with a lower heart rate and blood pressure (77). RPE is also a useful way to prescribe exercise. This approach focuses on how the patient actually feels and correlates closely with the target heart rate and desired MET level. For most cardiac patients, a prescription at 13 to 14 (“somewhat hard” to “hard”) on the RPE scale is both safe and effective for cardiovascular conditioning.

TABLE 63.6 Rate of Perceived Exertion (RPE) Scale

6
7 Very, very light
8
9 Very light
10
11 Fairly light
12
13 Somewhat hard
14
15 Hard
16
17 Very hard
18
19 Very, very hard
20

From Borg G. Subjective effort in relation to physical performance and working capacity. In: Pick HL, ed. Psychology: from research to practice. New York: Plenum, 1978:333, with permission.

The effect of exercise training on longevity in patients after MI has been established. Meta-analysis of the combined results of 10 randomized clinical trials demonstrates a 25% reduction in cardiovascular mortality, although not in nonfatal reinfarction, for patients in rehabilitation programs (78). Benefits of exercise conditioning on the psychometric profile are not firmly established (78).

Risks of Conditioning

With proper selection, supervision, monitoring, and precautions, physical conditioning for cardiac patients is remarkably safe. Cumulative data from >1.5 million person-hours of exercise, done predominantly 3 months after MI, show that the risks of ventricular fibrillation, acute MI, and death are one in 10,000 to one in 32,000, one in 253,000, and one in 100,000 to one in 212,000 person-hours of exercise, respectively (79). There is no comparable large series on exercise conditioning earlier than 3 months after MI. In the authors’ experience with exercise programs beginning an average of 7 to 10 days after hospital discharge, there have been few serious complications during exercise over a 30-year period. These patients exercise under supervision three times per week, for up to 12 weeks, at a conditioning heart rate of approximately 80% of what they safely achieved on a post-MI stress test, performed before starting the exercise program.

Cardiovascular Medications and Conditioning

Many patients who enroll in exercise programs are taking multiple medications. Many of these medications alter the cardiovascular response to exercise. Patients enrolled in a conditioning program should ideally undergo stress testing (see below) while taking their regular medications, and the effects of their drugs should be considered in interpreting test results. For example, β-blockers attenuate the heart rate response to exercise. Thus, heart rate is not useful as an end point for stress testing or as a parameter for the patient to monitor during exercise conditioning. In a patient taking a β-blocker, symptoms, ECG changes, fatigue, and RPE (Table 63.6) are used as end points during

P.987


stress testing. These parameters also are useful for establishing the exercise prescription in patients on certain medications. Table 63.7summarizes the effects of a number of commonly prescribed cardiac drugs on the hemodynamic response to exercise.

TABLE 63.7 Effect of Various Classes of Medications on Hemodynamic Status during Exercise

Drug

Peak Heart Rate

Peak Systolic
Blood Pressure

Antihypertensive

ACE inhibitor, ARB

=

Hydralazine

Minoxidil

Clonidine

Methyldopa

Prazosin

Nitrate

β-Blocker

Digitalisa

=

Calcium channel blocker

Nifedipine

Diltiazem

=

Verapamil

aPatients with congestive heart failure.
↓, decreased;↑, increased; =, no discernible effect; ACE, angiotensin-converting enzyme; ARB, angiotensin II receptor blocker.
Modified from Powles ACP. The effect of drugs on the cardiovascular response to exercise. Med Sci Sports Exerc 1981;13:252, with permission.

Patients taking a variety of drugs have been evaluated and have participated safely in physical conditioning programs. Some controversy exists regarding the effect of β-blockers on the response to training. It has been suggested that β-blockers attenuate the beneficial effects of training. A clinical trial to establish whether a β-blocker or calcium channel blocker limits exercise capacity and training effect showed that neither drug interfered with muscle strength (80). After starting the β-blocker, maximal aerobic capacity was reduced by 20%, whereas a 20% increase in aerobic capacity from this reduced level occurred with training while subjects continued to use the drug. Thus, although a training effect can be achieved while a patient is taking a β-blocker, its use may limit the full benefit of exercise training as measured by maximal aerobic capacity. On the other hand, for patients who are limited by ischemia, use of a β-blocker typically allows the patient to achieve workloads that may not otherwise be attained without anti-ischemic medication.

Referral for Conditioning

The decision to refer a patient for physical conditioning after MI depends on the patient's clinical status and motivation and the availability of well-supervised and staffed programs designed for such patients. Whereas patient participation often is limited by third-party insurance reimbursement, a key factor in increasing compliance to cardiac rehabilitation is a specific instruction from the health care provider to the patient to participate in such a program. No data support the efficacy of the informal “get more exercise” advice that often is the exercise prescription received by patients with CAD. Medically supervised programs that offer ECG monitoring and the immediate availability of emergency care often accept patients within 1 to 2 weeks of hospital discharge. If such a program is not available, cautious guidelines such as those shown in Table 63.4 are appropriate. After 2 months, if no supervised program is available, patients with uncomplicated MI can be advised to increase their exercise levels gradually, using the results of a stress test to establish target heart rates or RPE.

Before beginning a conditioning program, the patient should undergo an ECG stress test (see Chapter 62 for a description of the patient's experience), the results of which are used in planning the exercise program. In general, the conditioning target heart rate is 70% to 85% of the maximal heart rate safely achieved on the stress test.

Contraindications

A patient should not be enrolled in or should discontinue a conditioning program if the following problems are present: poorly controlled angina, severe dyspnea at low workloads, moderate to severe uncontrolled hypertension at rest (systolic >160 mm Hg or diastolic >110 mm Hg), complex arrhythmias (Table 63.1), atrial fibrillation with a rapid ventricular response, second- or third-degree heart block, significant valvular or congenital heart disease, significant orthopedic or pulmonary limitations, chronic alcoholism, or recent acute physical or mental illness.

Exercise Programs

Exercise sessions should be supervised by personnel trained in clinical exercise physiology and cardiopulmonary resuscitation, with immediate availability of monitoring and resuscitative equipment. Programs for patients soon after MI should have equipment for continuous ECG monitoring. Sessions usually are held three times per week, typically on nonconsecutive days. The total duration of an average session is approximately 45 to 60 minutes. The pattern for an aerobic workout is illustrated in Figure 63.4. During the stimulus phase, the patient exercises at an intensity that elicits a heart rate or RPE (see above) that falls within the prescribed target zone. Figure 63.5 shows recommendations for exercise intensity based on heart rate response during an exercise stress test. Exercising near the 70% level, for 20 to 30 minutes, promotes fitness, and

P.988


beginners should be instructed to maintain intensity near this level. Experienced exercisers can advance to the 85% level if a more intense workout is desired. The stimulus, or period at the target heart rate, is preceded by 5 to 10 minutes of warmup and is followed by 5 to 10 minutes of cooldown (Fig. 63.4). Warmup and cooldown should include stretching and range-of-motion calisthenic exercises (see Chapter 68). Warmup provides for gradual acceleration of the heart and circulation; it is beneficial to joints and muscles and helps prevent musculoskeletal injuries.

FIGURE 63.4. Exercise training program.

Cooldown provides for gradual deceleration of the cardiovascular system and prevents pooling of blood in the muscles when exercise stops abruptly. Pooling can lead to a precipitous drop in venous return and, consequently, postexercise hypotension.

As discussed earlier, training is specific to the muscles used in a particular exercise. Therefore, a training session should consist of a variety of activities designed to provide a well-rounded workout. Exercises for both the legs and the arms can be incorporated into the session. Aerobic training of the legs can be achieved through bicycling, walking, jogging, and stair stepping. The arms can be trained with shoulder wheels, rowing machines, and arm ergometers. Swimming, cross-country ski machines, and combination arm–leg cycles are excellent for exercising both lower and upper extremities at the same time.

For most cardiac patients, combined resistance and aerobic training can be used to improve aerobic capacity and upper-body and lower-body strength (46,47,81). Three-year experience with combined training indicates increased muscle strength and self-efficacy, enhanced compliance with the exercise program, and no cardiac or orthopedic complications (82). In combined training (also known as circuit weight training), the patient uses machines, each of which stresses a different muscle group, and moves from weight machine to weight machine, performing for 30 seconds at 40% of maximal capacity, with 30 seconds of rest between each exercise, for a total of 20 minutes. This type of exercise combines elements of dynamic and static forms of exercise. Published exercise guidelines recommend that patients selected for this type of exercise should be preconditioned in a traditional program of walking and jogging for at least 3 months and achieve at least 6 METs during exercise without symptoms or ischemic ECG changes. However, our research has demonstrated the safety and efficacy of combined training incorporated into cardiac rehabilitation as soon as 4 weeks after acute MI in selected patients (83). Reviews on the use of weight training in CAD and hypertension can be found elsewhere (see ref. 47, Stewart et al.,http://www.hopkinsbayview.org/PAMreferences). Alternatives to weight machines, particularly for patients at high risk or for those who are markedly deconditioned or who are participating very soon after MI, are rubber-band devices, pulley weights, wrist weights, and light dumbbells.

FIGURE 63.5. Target pulse rates for 10-second counts that should be measured the first 10 seconds after exercise (to convert the count to beats per minute, multiply by 6). To determine a patient's target pulse rate range, identify the highest rate safely achieved during the most recent exercise test on the top line (maximum pulse line) and then locate the corresponding 10-second counts on the 85% and 70% lines directly below. These two values represent the limits of target rate range for exercise conditioning. (From

Haskell WL. Design and implementation of cardiac conditioning programs. In: Wenger NK, Hellerstein HK, eds. Rehabilitation of the coronary patient. New York: Wiley, 1978:209, with permission

.)

P.989

Termination of Supervised Training

Criteria for terminating supervised exercise training and transfer to nonsupervised maintenance programs are not clearly established. ECG monitoring in cardiac rehabilitation programs for up to 12 weeks has been approved by Medicare, and patients often begin programs without continuous monitoring after this period. Clinical stability and functional capacity above 7 to 8 METs (Chapter 16, Table 16.1) are generally accepted exit criteria.

After a few months of supervised exercise, repeated stress testing is useful for measuring the change in physical working capacity and for adjusting more accurately the optimal exercise training intensity.

Long-Term Maintenance of Physical Conditioning

Long-term compliance with formal exercise programs often is poor. Regular exercise at the proper intensity, frequency, and duration is necessary for maintenance of physical fitness. Measurable deterioration in the conditioning effect occurs after missing exercise for only a few weeks. The time required to retrieve lost benefits seems to be directly related to the length of time without exercise and the degree of physical fitness achieved before cessation of exercise. Exercise must become a part of a person's weekly routine, not something that is done only sporadically or only during the recovery from MI.

Specific References*

For annotated General References and resources related to this chapter, visit http://www.hopkinsbayview.org/PAMreferences.

  1. American Heart Association. 2005 Heart and stroke statistical update. Dallas, TX: American Heart Association, 2005.
  2. Rosamond WD, Chambless LE, Folsom AR, et al. Trends in the incidence of myocardial infarction and in mortality due to coronary heart disease, 1987 to 1994. N Engl J Med 1998;339:861.
  3. Ellerbeck EF, Jencks SF, Radford MJ, et al. Quality of care for Medicare patients with acute myocardial infarction: a four-state pilot study from the cooperative cardiovascular project. JAMA 1995;273:1509.
  4. Bonow RO, Smaha LA, Smith SC Jr, et al. World Heart Day 2002: The international burden of cardiovascular disease: responding to the emerging global epidemic. Circulation 2002;106:1602.

P.990

  1. Tofler GH, Stone PH, Muller JE, et al. Effects of gender and race on prognosis after myocardial infarction: adverse prognosis for women, particularly black women. J Am Coll Cardiol 1987;9:473.
  2. Chandra NC, Ziegelstein RC, Rogers WJ, et al. Observations of the treatment of women in the United States with myocardial infarction: a report from the National Registry of Myocardial Infarction. I. Arch Intern Med 1998;158:981.
  3. Furman MI, Dauerman HL, Goldberg RJ, et al. Twenty-two year (1975 to 1997) trends in the incidence, in-hospital and long-term case fatality rates from initial Q-wave and non-Q-wave myocardial infarction: a multi-hospital, community-wide perspective. J Am Coll Cardiol 2001;37:1571.
  4. McGovern PG, Pankow JS, Shahar E, et al. Recent trends in acute coronary heart disease—mortality, morbidity, medical care, and risk factors. The Minnesota Heart Survey Investigators. N Engl J Med 1996;334:884.
  5. Rosati RA, Harris PJ. Acute myocardial infarction. In: Fries JF, Ehrlich GE, eds. Prognosis: contemporary outcomes of disease. Bowie, MD: Charles Press, 1981.
  6. Steg PG, Dabbous OH, Feldman LJ, et al. Determinants and prognostic impact of heart failure complicating acute coronary syndromes: observations from the Global Registry of Acute Coronary Events (GRACE). Circulation 2004;109:494.
  7. Werns SW, Bates ER. The enduring value of Killip classification. Am Heart J 1999;137: 213.
  8. van Ravenswaaij CMA, Kollee LAA, Hopman JCW, et al. Heart rate variability. Ann Intern Med 1993;118:436.
  9. Maggioni AP, Maseri A, Fresco C, et al. Age-related increase in mortality among patients with first myocardial infarctions treated with thrombolysis. The Investigators of the Gruppo Italiano per lo Studio della Sopravvivenza nell’Infarto Miocardico (GISSI-2). N Engl J Med 1993;329:1442.
  10. Meizlish JL, Berger HJ, Plankey M, et al. Functional left ventricular aneurysm after acute myocardial infarction. N Engl J Med 1984;16:1001.
  11. Frasure-Smith N, Lesperance F, Talajic M. Depression following myocardial infarction. Impact on 6-month survival. JAMA 1993;270:1819.
  12. Moss AJ, Goldstein RE, Hall J, et al. Detection and significance of myocardial ischemia in stable patients after recovery from acute event. JAMA 1993;269:2379.
  13. Antman EM, Anbe DT, Armstrong PW, et al. American College of Cardiology; American Heart Association Task Force on Practice Guidelines. ACC/AHA guidelines for the management of patients with ST-elevation myocardial infarction—executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 1999 Guidelines for the Management of Patients With Acute Myocardial Infarction). Circulation 2004;110:588.
  14. Braunwald E, Antman EM, Beasley JW, et al. American College of Cardiology; American Heart Association. Committee on the Management of Patients With Unstable Angina. ACC/AHA 2002 guideline update for the management of patients with unstable angina and non-ST-segment elevation myocardial infarction—summary article: a report of the American College of Cardiology/American Heart Association task force on practice guidelines (Committee on the Management of Patients With Unstable Angina). J Am Coll Cardiol 2002;40:1366.
  15. Gibbons RJ, Balady GJ, Bricker JT, et al. American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee to Update the 1997 Exercise Testing Guidelines). ACC/AHA 2002 guideline update for exercise testing: summary article: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee to Update the 1997 Exercise Testing Guidelines). Circulation 2002;106:1883.
  16. Blomkalns AL, Chen AY, Hochman JS, et al.; CRUSADE Investigators. Gender disparities in the diagnosis and treatment of non-ST-segment elevation acute coronary syndromes: large-scale observations from the CRUSADE (Can Rapid Risk Stratification of Unstable Angina Patients Suppress Adverse Outcomes With Early Implementation of the American College of Cardiology/American Heart Association Guidelines) National Quality Improvement Initiative. J Am Coll Cardiol 2005;45:832.
  17. Valeur N, Clemmensen P, Saunamäki K, Grande P; DANAMI-2 Investigators. The prognostic value of pre-discharge exercise testing after myocardial infarction treated with either primary PCI or fibrinolysis: a DANAMI-2 sub-study. Eur Heart J 2005;26:119.
  18. Mark D, Froelicher V. Exercise treadmill testing and ambulatory monitoring.In:Califf R, Mark D, Wagner G, eds. Acute coronary care. St. Louis: CV Mosby, 1995:767.
  19. Theroux P, Marpole DGF, Bourassa MG. Exercise stress testing in the postmyocardial infarction patient. Am J Cardiol 1983;52:664.
  20. Anderson HV, Cannon CP, Stone PH, et al. One-year results of the Thrombolysis in Myocardial Infarction (TIMI) IIIB clinical trial. A randomized comparison of tissue-type plasminogen activator versus placebo and early invasive versus early conservative strategies in unstable angina and non-Q wave myocardial infarction. J Am Coll Cardiol 1995;26:1643.
  21. Plotnick GD. Approach to the management of unstable angina. Am Heart J 1979;98:243.
  22. Schaffer WA, Cobb LA. Recurrent ventricular fibrillation and modes of death in survivors of out-of-hospital ventricular fibrillation. N Engl J Med 1975;293:259.
  23. Hegel MT, Griegel LE, Black C, et al. Anxiety and depression in patients receiving implanted cardioverter-defibrillators: a longitudinal investigation. Int J Psychiatry Med 1997;27:57.
  24. Heller SS, Ormont AM, Lidagoster L, et al. Psychosocial outcome after ICD implantation: a current perspective. Pacing Clin Electrophysiol 1998;21:1207.
  25. Schuster PH, Phillips S, Dillon DL, et al. The psychosocial and physiological experiences of patients with an implantable cardioverter defibrillator. Rehabil Nurs 1998;23:30.
  26. Kamphuis HC, de Leeuw JR, Derksen R, et al. Implantable cardioverter defibrillator recipients: quality of life in recipients with and without ICD shock delivery: a prospective study. Europace 2003;5:381.
  27. Namerow PB, Firth BR, Heywood GM, et al. Quality-of-life six months after CABG surgery in patients randomized to ICD versus no ICD therapy: findings from the CABG Patch Trial. Pacing Clin Electrophysiol 1999;22:1305.
  28. Russell RO Jr, Abi-Mansour P, Wenger NK, et al. Return to work after coronary artery bypass surgery and percutaneous transluminal angioplasty: issues and potential solutions. Cardiology 1986;73:306.
  29. Brisson C, Leblanc R, Bourbonnais R, et al. Psychologic distress in postmyocardial infarction patients who have returned to work. Psychosom Med 2005;67:59.
  30. Mital A, Desai A, Mital A. Return to work after a coronary event. J Cardiopulm Rehabil 2004;24:365.
  31. DeBusk RF. Report of the twentieth Bethesda Conference. Insurability and employability of the patient with ischemic heart disease. 38th Annual Scientific Session. Anaheim, CA: American College of Cardiology, March 1989.
  32. Hellerstein HK, Friedman EH. Sexual activity in the post-coronary patient. Arch Intern Med 1970;125:987.
  33. Muller JE, Mittleman A, Maclure M, et al. Triggering myocardial infarction by sexual activity. Low absolute risk and prevention by regular physical exertion. Determinants of Myocardial Infarction Onset Study Investigators. JAMA 1996;275:1405.
  34. Herrmann HC, Chang G, Klugherz BD, et al. Hemodynamic effects of sildenafil in men with severe coronary artery disease. N Engl J Med 2000;342:1622.
  35. Fox KM, Thadani U, Ma PT, et al., on behalf of the CAESAR 1 (Clinical American and European Studies of Angina And Revascularization) Investigators. Sildenafil citrate does not reduce exercise tolerance in men with erectile dysfunction and chronic stable angina. Eur Heart J 2003;24:2206.
  36. Arruda-Olson AM, Mahoney DW, Nehra A, et al. Cardiovascular effects of sildenafil during exercise in men with known or probable coronary artery disease: a randomized crossover trial. JAMA 2002;287:719.
  37. Thadani U, Smith W, Nash S, et al. The effect of vardenafil, a potent and highly selective phosphodiesterase-5 inhibitor for the treatment of erectile dysfunction, on the cardiovascular response to exercise in patients with coronary artery disease. J Am Coll Cardiol 2002;40:2006.
  38. Patterson D, MacDonald TM, Effron MB, et al. Tadalafil does not affect time to ischemia during exercise stress testing in patients with coronary artery disease. Circulation 2002;106[Suppl II]:II–330.
  39. Ewart CK, Taylor CB, Reese LB, et al. Effects of early postmyocardial infarction exercise testing on self-perception and subsequent physical activity. Am J Cardiol 1983;51:1076.
  40. Ewart CK, Stewart KJ, Kelemen MH, et al. Self-efficacy mediates strength gains during circuit weight training in men with coronary artery disease. Med Sci Sports Exerc 1986;18:531.
  41. Gillilan RE, Chopra AK, Kelemen MH, et al. Prediction of compliance to target heart rate during walk-job exercise in cardiac patients by a self-efficacy scale. Med Sci Sports Exerc 1984;16:115.
  42. Leon AS, Franklin BA, Costa F et al. Cardiac rehabilitation and secondary prevention of coronary heart disease: an American Heart Association scientific statement from the Council on Clinical Cardiology (Subcommittee on Exercise, Cardiac Rehabilitation, and Prevention) and the Council on Nutrition, Physical Activity, and Metabolism (Subcommittee on Physical Activity), in collaboration with the American Association of Cardiovascular and Pulmonary Rehabilitation. Circulation 2005;111:369.
  43. Pollock ML, Franklin BA, Balady GJ, et al. AHA Science Advisory. Resistance exercise in individuals with and without cardiovascular disease: benefits, rationale, safety, and prescription: an advisory from the Committee on Exercise, Rehabilitation, and Prevention, Council on Clinical Cardiology, American Heart Association; Position paper endorsed by the American College of Sports Medicine. Circulation 2000;101:828.
  44. Baile WF, Engel BT. A behavioral strategy for promoting treatment compliance following myocardial infarction. Psychosom Med 1978;40:412.
  45. Schleifer SJ, Macari-Hinson MM, Coyle DA, et al. The nature and course of depression following myocardial infarction. Arch Intern Med 1989;149:1785.

P.991

  1. Ziegelstein RC, Fauerbach JA, Stevens SS, et al. Patients with depression are less likely to follow recommendations to reduce cardiac risk during recovery from a myocardial infarction. Arch Intern Med 2000;160:1818.
  2. Milani RV, Lavie CJ, Cassidy MM. Effects of cardiac rehabilitation and exercise training programs on depression in patients after major coronary events. Am Heart J 1996;132:726.
  3. Guiry E, Conroy RM, Hickey N, et al. Psychological response to an acute coronary event and its effect on subsequent rehabilitation and lifestyle change. Clin Cardiol 1987;10:256.
  4. Blumenthal JA, Williams RS, Wallace AG, et al. Physiological and psychological variables predict compliance to prescribed exercise therapy in patients recovering from myocardial infarction. Psychosomatic Med 1982;44:519.
  5. Frasure-Smith N, Lespèrance F, Gravel G, et al. Social support, depression, and mortality during the first year after myocardial infarction. Circulation 2000;101:1919.
  6. Shapiro PA, Lesperance F, Frasure-Smith N, et al. An open-label preliminary trial of sertraline for treatment of major depression after acute myocardial infarction (the SADHAT Trial). Sertraline Anti-Depressant Heart Attack Trial. Am Heart J 1999;137:1100.
  7. Roose SP, Laghrissi-Thode F, Kennedy JS, et al. Comparison of paroxetine and nortriptyline in depressed patients with ischemic heart disease. JAMA 1998;279:287.
  8. Strik JJ, Honig A, Lousberg R, et al. Efficacy and safety of fluoxetine in the treatment of patients with major depression after first myocardial infarction: findings from a double-blind, placebo-controlled trial. Psychosom Med 2000;62:783.
  9. Glassman AH, O’Connor CM, Califf RM, et al. Sertraline antidepressant heart attack randomized trial (SADHEART) group. Sertraline treatment of major depression in patients with acute MI or unstable angina. JAMA 2002;288:701.
  10. Roose SP, Glassman AH. Cardiovascular effects of tricyclic antidepressants in depressed patients with and without heart disease. J Clin Psychiatry 1989;50[Suppl]:1.
  11. Berkman LF, Blumenthal J, Burg M, et al. Enhancing Recovery in Coronary Heart Disease Patients Investigators (ENRICHD). Effects of treating depression and low perceived social support on clinical events after myocardial infarction: the Enhancing Recovery in Coronary Heart Disease Patients (ENRICHD) Randomized Trial. JAMA 2003;289:3106.
  12. Furberg CD, Friedwald WT, Eberlein KA. Proceedings of the workshop on the implications of recent beta-blocker trials for postmyocardial infarction patients. Circulation 1983;67:1.
  13. Antiplatelet Trialists’ Collaboration. Collaborative overview of randomized trials of antiplatelet therapy. I. Prevention of death, myocardial infarction, and stroke by prolonged antiplatelet therapy in various categories of patients. BMJ 1994;308:81.
  14. Lorenz RL, Schacky CV, Weber M, et al. Improved aortocoronary bypass patency by low-dose aspirin (100 mg daily): effects on platelet aggregation and thromboxane formation. Lancet 1984;1:1261.
  15. Thornton MA, Greventzig AR, Hollman J, et al. Coumadin and aspirin in prevention of recurrence after transluminal coronary angioplasty: a randomized study. Circulation 1984;69:72.
  16. ISIS-2. Randomised trial of intravenous streptokinase, oral aspirin, both or neither among 17,187 cases of suspected acute myocardial infarction. Lancet 1988;2:349.
  17. Pfeffer M, Braunwald E, Moye L, et al. Effect of captopril on mortality and morbidity in patients with left ventricular dysfunction after myocardial infarction. N Engl J Med 1992;327:669.
  18. SOLVD Investigators. Effects of enalapril on mortality and development of heart failure in asymptomatic patients with reduced left ventricular ejection fractions. N Engl J Med 1992;32:685.
  19. LaRosa JC, Grundy SM, Waters DD, et al. Intensive lipid lowering with atorvastatin in patients with stable coronary disease. N Engl J Med 2005;352:1425.
  20. Moss AJ, Hall WJ, Cannom DS, et al. Improved survival with an implanted defibrillator in patients with coronary disease at high risk for ventricular arrhythmias. N Engl J Med 1996; 335:1933.
  21. The Antiarrhythmic versus Implantable Defibrillator (AVID) Investigators. A comparison of antiarrhythmic-drug therapy with implantable defibrillator in patients resuscitated form near-fatal ventricular arrhythmias. N Engl J Med 1997;337:1576.
  22. Al-Khadra AS, Salem DN, Rand WM, et al. Warfarin anticoagulation and survival: a cohort analysis from the Studies of Left Ventricular Dysfunction. J Am Coll Cardiol 1998;31:749.
  23. Ehsani AA, Heath GH, Hagberg JM, et al. Effects of 12 months of intense exercise training on ischemic ST-depression in patients with coronary artery disease. Circulation 1981;64: 1116.
  24. Schuler G, Hambrecht R, Schlierf G, et al. Regular exercise and low fat diet: effects on progression of coronary artery disease. Circulation 1992;86:1.
  25. Taylor JL, Copeland RB, Cousin AL, et al. The effect of isometric exercise on the graded exercise test in patients with stable angina. J Cardiopulm Rehab 1981;1:450.
  26. Coats AJS, Adampoulos S, Meyer TC, et al. Effects of physical training in chronic heart failure. Lancet 1990;335:63.
  27. Sullivan MJ, Higgambotham MB, Cobb FR. Exercise training in patients with severe left ventricular dysfunction: hemodynamics and metabolic effects. Circulation 1988;78:506.
  28. Gutmann MC, Squires RW, Pollack ML, et al. Perceived exertion–heart rate relationship during exercise testing and training in cardiac patients. J Cardiovasc Rehab 1981;1:52.
  29. Taylor RS, Brown A, Ebrahim S, et al. Exercise-based rehabilitation for patients with coronary heart disease: systematic review and meta-analysis of randomized controlled trials. Am J Med 2004;116:682.
  30. Council on Scientific Affairs, American Medical Association. Physician-supervised exercise programs in rehabilitation of patients with coronary heart disease. JAMA 1981;245:1463.
  31. Stewart KJ, Effron MB, Vaeni SA, et al. Effects of diltiazem or propranolol during exercise training of hypertensive men. Med Sci Sports Exerc 1990;22:171.
  32. Kelemen MH, Stewart KJ, Gillilan RE, et al. Circuit weight training in cardiac patients. J Am Coll Cardiol 1986;7:38.
  33. Stewart KJ, Mason M, Kelemen MH. Three year participation in circuit weight training improves muscular strength and self-efficacy in cardiac patients. J Cardiopulm Rehab 1988;8:292.
  34. Stewart KJ, McFarland LD, Weinhofer JJ, et al. Safety and efficacy of weight training soon after acute myocardial Infarction. J Cardiopulm Rehabil 1998;18:37.


If you find an error or have any questions, please email us at admin@doctorlib.org. Thank you!