Preventing Reinfarction: Basic Elements of an Effective Cardiac Rehabilitation Program

About 38% of persons who experience a myocardial infarction (MI) in a given year will die as a result.¹ Among persons who survive, cardiovascular mortality in those who do not receive treatment after hospital discharge is almost 10% in the first year after the MI and increases about 5% per year thereafter.² The rate of sudden death in patients who have had an MI is 4 to 6 times the rate in the general population.¹ Thus, immediate implementation of risk factor modification is of urgent importance in patients who have sustained an MI.

Here we outline the basic elements of an effective cardiac rehabilitation program and highlight the role of the primary care physician in such programs. We also summarize the latest recommendations for cardioprotective drug therapy and offer tips on how to help patients quit smoking.

In a second article, on page 569, we describe a heart-healthy diet and effective exercise programs, and we discuss ways to motivate patients to make necessary lifestyle changes.

CARDIAC REHABILITATION: SCOPE AND RATIONALE

Cardiac rehabilitation encompasses a broad spectrum of protective and preventive interventions that address the underlying causes of cardiac disease. The objectives of rehabilitation are to:

• Increase functional capacity.
• Decrease symptoms.
• Stop cigarette smoking.
• Modify the lipid profile.
• Reduce body weight and fat stores.
• Lower blood pressure.
• Promote psychosocial well-being.

Interventions that aim for aggressive risk-factor reductions are individually associated with reductions in mortality of 18% to 45% in patients with known heart disease (Table).^3-5 A recent meta-analysis of 48 randomized, controlled trials encompassing nearly 9000 patients examined whether current thrombolytic and revascularization procedures, which markedly reduce postinfarction mortality, together with better pharmacological therapies, diminish the impact of adjunctive cardiac rehabilitation programs on survival.⁶ The authors reported that:

• Compared with usual care, cardiac rehabilitation reduced cardiac mortality by 26% and all-cause mortality by 20%.

Cardiac rehabilitation was associated with substantial reductions in total cholesterol levels, triglyceride levels, systolic blood pressure, and self- reported cigarette smoking, compared with usual care.

This systematic review confirmed the findings of previous meta-analyses^7-9 that exercise-based cardiac rehabilitation reduces both cardiac and total mortality, and that the benefits persist in the current era of advanced acute care, independent of the specific type of heart disease diagnosed, type of cardiac rehabilitation, amount of exercise involved, length of follow-up, trial quality, and trial publication date.

ROLE OF THE PRIMARY CARE PHYSICIAN

Despite the strong evidence of benefit, cardiac rehabilitation programs in the United States remain vastly underutilized.¹⁰ Characteristics of patients who are less likely to participate in cardiac rehabilitation include:

• Female sex.
• Age 62 years or older.
• Single marital status.
• Low personal income.
• Blue-collar work history.
• Presence of comorbid disease.
• History of depression.
• Denial of disease severity.
• Lack of access.
• Poor motivation.^11-15

Of note, the fervor of the primary care physician's recommendation appears to be the single most powerful predictor of participation in cardiac rehabilitation.⁶ For patients who decline or are unable to participate in a formal program, home-based exercise rehabilitation is an acceptable alternative because of its lower cost, greater practicability, convenience, and potential for promoting independence and self-responsibility.¹⁰

PHARMACOTHERAPY

Aggressive lipid lowering; control of hypertension and diabetes; and prophylactic use of antiplatelet agents, ß-blockers, and angiotensin-converting enzyme (ACE) inhibitors all have a demonstrated benefit in patients who have had an MI. In addition, a combination of evidence-based therapies (eg, aspirin, a ß-blocker, lipid-lowering medications, and an ACE inhibitor together) is independently and strongly associated with lower 6-month mortality in patients with acute coronary syndromes.¹⁷

Many evidence-based guidelines exist for drug therapy for secondary prevention, but these regimens have to be tailored to the needs of each patient. If possible, make sure drug therapy is started before hospital discharge; this has been shown to enhance adherence.¹⁸

Keep in mind that medications are an adjunct-not an alternative-to lifestyle changes; the effects of drug therapy and lifestyle changes on cardiovascular risk reduction are independent and additive.¹⁹

Cardioprotective drugs and devices. Have all patients who have sustained an MI-and in whom the therapy is not contraindicated- continue to take aspirin indefinitely. Clopidogrel can be substituted in patients who are allergic to or intolerant of aspirin.

Start an ACE inhibitor soon after patients become stable; in those who have either clinical or radiological signs of heart failure or a left ventricular ejection fraction of less than 0.40, continue this therapy indefinitely. Prescribe angiotensin receptor blockers for patients who cannot tolerate ACE inhibitors.¹⁸

Long-term aldosterone blockade is recommended for patients who have sustained an ST-segment-elevation MI and who meet the following criteria:

• Are receiving therapeutic doses of an ACE inhibitor or have a left ventricular ejection fraction of 0.40 or less.
• Have either symptomatic heart failure or diabetes.
• Do not have significant renal dysfunction (creatinine level no higher than 2.5 mg/dL in men or 2.0 mg/dL in women).
• Do not have hyperkalemia (potassium level no higher than 5.0 mEq/L).¹⁸

Prescribe a ß-blocker for all patients who have had an MI unless there is an absolute contraindication. The benefits of ß-blockers (reducing mortality and lowering rates of reinfarction) outweigh the risks. Although more intense monitoring is required, consider use of these agents even in patients with the following conditions:

• Mild asthma that is not currently active.
• Insulin-dependent diabetes.
• Chronic obstructive pulmonary disease.
• Severe peripheral vascular disease.
• PR interval greater than 0.24 seconds.
• Moderate left ventricular failure.¹⁸

Assess left ventricular function in all patients who have sustained an MI to determine whether an implantable cardioverter-defibrillator is warranted. In patients whose ejection fraction shortly after their MI was 0.40 or lower, consider reevaluation of ventricular function for a return in viability (use echocardiography or another test).¹⁸

Modification of lipids. Because patients who have had an MI are at very high risk for cardiovascular events, a low-density lipoprotein cholesterol (LDL-C) level of less than 70 mg/dL is the preferred goal.²⁰ The results of a recent cholesterol panel determine the choice of drug and dosage. The largest reductions in LDL-C seen with statins occur at the starting dosage; with each successive doubling of the dosage, the LDL-C falls by about another 6%.²¹

In patients whose LDL-C level is initially greater than 100 mg/dL, the standard starting dosage of a statin is rarely sufficient to lower the level to less than 70 mg/dL. Achieving the target level may require a higher dosage of the statin; a standard dosage together with ezetimibe, a bile acid sequestrant, or nicotinic acid; or both a higher dosage and a second agent.²⁰ In patients with elevated triglyceride levels or low high-density lipoprotein cholesterol levels, consider adding a fibrate or niacin.²¹

SMOKING CESSATION

For smokers with a history of MI, quitting is the single most important change they can make to reduce future risk.^22-24 The risk of coronary artery disease (CAD) and sudden death after an infarction is 2 to 4 times greater in cigarette smokers than it is in nonsmokers.²⁵

An increasing number of behavioral and pharmacological options are available to help smokers achieve and maintain smoking cessation. Bupropion and nicotine replacement products (ie, the transdermal patch) are appropriate for first-line treatment in smokers who have had an MI. In 2006, varenicline became the first prescription medication for smoking cessation to be approved by the FDA in 10 years.²⁶ Two randomized, double-blind, placebo-controlled studies of about 2000 smokers showed that after 3 months of treatment, about 44% of those receiving varenicline had quit smoking, compared with 30% of those receiving bupropion and 17.7% of those receiving placebo.²⁶ Several drugs now in development (eg, rimonabant) have also shown promise as smoking cessation aids.²⁷

Nondrug approaches can also help. As little as 3 minutes or less of physician counseling increases cessation rates by as much as 30% in some patients.^28,29 Informing smokers who have had an MI that their risk of another MI will be reduced to that of nonsmokers 3 years after they quit can provide additional motivation.³⁰

Keep in mind that most patients must make several attempts before they succeed in quitting permanently. After a relapse, remind the patient that it is possible to quit smoking, and that the majority of successful quitters report going through multiple relapses before they are able to quit for good.

Advising patients to avoid second-hand smoke is as important as encouraging them to stop smoking. It may also be as difficult as quitting; patients may need to avoid poorly ventilated places, such as bowling allies and bars, or their spouse may need to be treated for tobacco dependence.³¹

References:

REFERENCES:

1.

Law MR, Watt HC, Wald NJ. The underlying risk of death after myocardial infarction in the absence of treatment. 2002;162:2405-2410.

2.

Heart Disease and Stroke Statistics--2007 Update. A Report from the American Heart Association Statistics Committee and Stroke Statistics Subcommittee.

Circulation.

2007;115:69-171. Available at:

http://circ.ahajournals.org/cgi/content/full/115/ 5/e69

. Accessed March 26, 2007.

3.

Iestra JA, Kromhout D, van der Schouw YT, et al. Effect size estimates of lifestyle and dietary changes on all-cause mortality in coronary artery disease patients: a systematic review.

Circulation.

2005;112: 924-934.

4.

Franklin BA, Gordon NF.

Contemporary Diagnosis and Management in Cardiovascular Exercise.

Newton, Pa: Handbooks in Health Care Co; 2005.

5.

Myers J, Kaykha A, George S, et al. Fitness ver-sus physical activity patterns in predicting mortality in men.

Am J Med.

2004;117:912-918.

6.

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: 682-692.

7.

Oldridge NB, Guyatt GH, Fischer ME, et al. Cardiac rehabilitation after myocardial infarction.

JAMA.

1988;260:945-950.

8.

O'Connor GT, Buring JE, Yusuf S, et al. An overview of randomized trials of rehabilitation with exercise after myocardial infarction.

Circulation.

1989;80: 234-244.

9.

Lau J, Antman EM, Jimenez-Silva J, et al. Cumulative meta-analysis of therapeutic trials for myocardial infarction.

N Engl J Med.

1992;327:248-254.

10.

Franklin BA, Hall L, Timmis GC. Contemporary cardiac rehabilitation services.

Am J Cardiol.

1997;79:1075-1077.

11.

Grace SL, Evindar A, Abramson B, et al. Physician management preferences for cardiac patients: factors affecting referral to cardiac rehabilitation.

Can J Cardiol.

2004;20:1101-1107.

12.

Ades PA, Waldmann ML, Polk DM, et al. Referral patterns and exercise response in the rehabilitation of female coronary patients aged 62 years. Am J Cardiol. 1992;69:1422-1425.

13.

Cannistra LB, Balady GJ, O'Malley CJ, et al. Comparison of the clinical profile and outcome of women and men in cardiac rehabilitation.

Am J Cardiol.

1992;69:1274-1279.

14.

Doolan-Noble F, Broad J, Riddell T, North D. Cardiac rehabilitation services in New Zealand: access and utilisation.

N Z Med J.

2004;117:U955.

15.

Higgins JC, Ades PA. Cardiac rehabilitation: clinical benefits and referral patterns.

Intern Med.

1993;14:10-16.

16.

Ades PA, Waldmann ML, McCann WJ, et al. Predictors of cardiac rehabilitation participation in older coronary patients.

Arch Intern Med.

1992;152: 1033-1035.

17.

Mukherjee D, Fang J, Chetcuti S, et al. Impact of combination evidence-based medical therapy on mortality in patients with acute coronary syndromes.

Circulation.

2004;109:745-749.

18.

Antman EM, Anbe DT, Armstrong PW, et al. ACC/AHA guidelines for the management of patients with ST-elevation myocardial infarction: a report of the American College of Cardiology/ American Heart Association Task Force on Practice Guidelines (Committee to Revise the 1999 Guidelines for the Management of Patients With Acute Myocardial Infarction). 2004.

19.

Franklin BA, Kahn JK, Gordon NF, Bonow RO. A cardioprotective "polypill"? Independent and additive benefits of lifestyle modification.

Am J Cardiol.

2004;94:162-166.

20.

Grundy SM, Cleeman JI, Merz NB, et al; for the Coordinating Committee of the National Cholesterol Education Program. Implications of Recent Clinical Trials for the National Cholesterol Education Program Adult Treatment Panel III Guidelines.

Circulation.

2004;100:227-239.

21.

Executive Summary of 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).

JAMA.

2001:285;2486-2496.

22.

Willhelmsson C, Vedin JA, Elmfeldt D, et al. Smoking and myocardial infarction.

Lancet.

1975; 1:415-420.

23.

Sparrow D, Dawber TR, Colton T. The influence of cigarette smoking on prognosis after a first myocardial infarction.

J Chronic Dis.

1978;31: 425-432.

24.

Grines CL, Topol EJ, O'Neill WW, et al. Effect of cigarette smoking on outcome after thrombolytic therapy for myocardial infarction.

Circulation.

1995;91:298-303.

25.

Sherman CB. Health effects of cigarette smoking.

Clin Chest Med.

1991;12:643-658.A clinical practice guideline for treating tobacco use and dependence: a US Public Health Service Report. The Tobacco Use and Dependence Clinical Practice Guideline Panel, Staff, and Consortium Representatives.

JAMA.

2000;283:3244-3254.

26.

Kuehn BM. FDA speeds smoking cessation drug review.

JAMA.

2006;295:614.

27.

Henningfield JE, Fant RV, Buchhalter AR, Stitzer ML. Pharmacotherapy for nicotine dependence.

CA Cancer J Clin.

2005;55:281-299.

28.

The Tobacco Use and Dependence Clinical Practice Guideline Panel, Staff, and Consortium Representatives. A clinical practice guideline for treating tobacco use and dependence: a US Public Health Service Report.

JAMA.

2000;283:3244-3254.

29.

Fiore MC. Treating tobacco use and dependence: an introduction to the US Public Health Service Clinical Practice Guideline.

Respir Care.

2000;45: 1196-1199.

30.

Rea TD, Heckbert SR, Kaplan RC, et al. Smoking status and risk for recurrent coronary events after myocardial infarction.

Ann Intern Med.

2002; 137:494-500.

31.

He J, Vupputuri S, Allen K, et al. Passive smoking and the risk of coronary heart disease: a meta-analysis of epidemiologic studies.

N Engl J Med.

1999;340:920-926.