Am Fam Physician. 1998;57(8):1901-1904
The morbidity, mortality and health care costs associated with congestive heart failure make prevention a more attractive public health strategy than treatment. Aggressive management of etiologic factors, including hypertension, coronary artery disease, valvular disease and excessive alcohol intake, can prevent the left ventricular remodeling and dysfunction that lead to heart failure. Early intervention with angiotensin converting enzyme inhibitors in patients with chronic left ventricular dysfunction can prevent, as well as treat, the syndrome. Several intervention strategies in patients with acute myocardial infarction can slow or prevent the left ventricular remodeling process that antedates congestive heart failure. The primary care physician must be alert to the need for aggressive intervention to reduce the burden of heart failure syndrome on the patient and on society.
Congestive heart failure is a complex clinical syndrome characterized by exertional dyspnea, fatigue and, often, peripheral edema resulting from left ventricular dysfunction. Although the extent of the abnormal function of the left ventricle can be quantitated, it is more difficult to measure the severity of symptoms; furthermore, the specific mechanism underlying the symptoms remains poorly understood. Since neurohormonal systems are often stimulated in the heart failure syndrome, activation of the sympathetic nervous system and the renin angiotensin system is often implicated in sodium retention, edema formation and some other symptoms of heart failure.
Etiology
Congestive heart failure always occurs within the setting of cardiac disease. Dysfunction of the left ventricle usually precedes the development of noticeable symptoms. Thus, efforts to prevent left ventricular dysfunction by treating etiologic factors may be very rewarding. The following etiologic factors should be considered when devising a strategy for the prevention of congestive heart failure (Table 1).
| Predisposing factor | Intervention |
|---|---|
| Hypertension | Blood pressure control |
| Coronary artery disease | Smoking cessation, weight reduction, exercise, lipid lowering, blood pressure control, aspirin prophylaxis |
| Valvular disease | Surgery |
| Cardiomyopathy | Alcohol abstention |
| Left ventricular hypertrophy | Blood pressure control, ACE inhibitor therapy |
| Myocardial infarction (especially patients with dilated left ventricles and/or evidence of ventricular dysfunction) | ACE inhibitor therapy, nitrates (?), beta blockers (?) |
Hypertension
Left ventricular hypertrophy as a complication of longstanding hypertension is a common factor in heart failure, even though the patient's blood pressure may be normal at the time congestive heart failure is diagnosed. In the absence of coronary artery disease and myocardial infarction, the left ventricular dysfunction in patients with hypertension often is predominantly a diastolic dysfunction with well-preserved chamber size and a normal ejection fraction. Good control of blood pressure can slow or prevent the development of left ventricular hypertrophy and can bring about regression of established hypertrophy. Such therapy can effectively prevent the development of heart failure.1
Coronary Artery Disease
Coronary artery disease is the most common etiology for left ventricular systolic dysfunction. Preventing plaque from developing in the coronary arteries could have a profound effect on the incidence of heart failure. Lipid reduction, as well as blood pressure control, smoking cessation, weight reduction and exercise, may be effective in preventing or slowing the development of coronary atherosclerosis in high-risk patients and thus may prevent congestive heart failure.2 Aspirin therapy can prevent myocardial infarction in patients with atherosclerosis, and it is also an important consideration in the prevention of congestive heart failure.3
Valvular Disease
Stenotic and regurgitant valvular deformities have been well documented as contributing factors in ventricular dysfunction. Identification of the lesions and surgical correction before the development of irreversible ventricular dysfunction should be effective in preventing the onset of heart failure.
Cardiomyopathy
Many diseases and toxins directly affect the myocardium, causing ventricular dysfunction. Excessive consumption of alcohol, diabetes mellitus and viral infections are associated with some causes of cardiomyopathy, whereas other cases may be genetic or idiopathic in nature. The effectiveness of abstention from alcohol has been established, but specific interventions for the prevention of heart failure in patients with other cardiomyopathies have not been established.4
Even in the absence of a specific etiologic approach, the progression of ventricular dysfunction and the symptoms of congestive heart failure can be delayed with proper therapy. The Studies of Left Ventricular Dysfunction (SOLVD) Prevention Trial5 recently demonstrated that therapy initiated during the asymptomatic phase of left ventricular dysfunction can significantly delay the development of overt symptoms. The study evaluated the efficacy of enalapril (Vasotec), an angiotensin converting enzyme (ACE) inhibitor, 10 mg twice daily, for the prevention of congestive heart failure symptoms. Patients receiving enalapril had a striking reduction in the risk of developing new-onset heart failure. Results from this study demonstrated for the first time that heart failure could be prevented if pharmacologic therapy is introduced after the ventricle is already dysfunctional.
Unfortunately, many patients at risk for the development of heart failure (patients with hypertension) were excluded in the SOLVD trial. Although the Framingham study6 identified hypertension as the most prevalent risk factor for heart failure, patients with hypertension have been systematically omitted from most trials because of their need for vasodilator antihypertensive therapy, which excludes them from many protocols. Also, the type of heart failure found in patients with hypertension is often a complication of diastolic dysfunction with a normal ejection fraction. This is an exclusion criterion in many trials.7 Moreover, aggressive control of blood pressure has already been shown to be very effective in preventing overt heart failure.8
Mechanism of ACE Inhibitor Effect
A number of potential mechanisms have been suggested to explain the efficacy of ACE inhibitors in preventing congestive heart failure. The simplest explanation is that ACE inhibitors reduce vascular tone and, by lowering impedance, improve emptying of the left ventricle.9 Improved left ventricular systolic performance may reduce the risk of symptomatic heart failure.
Another suggested mechanism is more attractive. Progressive structural changes occur in the left ventricular myocardium in patients who develop overt heart failure. This myocardial remodeling process is characterized by an enlargement of the chamber and an increase in muscle mass.10 The chamber dilation is associated with a progressive reduction in wall motion, eventually resulting in a globally hypokinetic ventricle. ACE inhibitors have been demonstrated to inhibit the remodeling process associated with the progressive decline of ejection fraction and overt symptoms of heart failure in both animal and human studies.11,12
Thus, the first line of defense in the prevention of overt heart failure is to identify patients who have already developed a remodeled left ventricle or who are likely to develop a remodeled left ventricle and to institute preventive therapy with an ACE inhibitor.
Early Intervention in Patients at Risk for Coronary Heart Failure
The patient with a dilated left ventricle already has a reduced life expectancy that can only modestly be prolonged with ACE inhibitor therapy.13 Identification of high-risk patients and early intervention before ventricular dysfunction has developed is an attractive public health strategy. This strategy has already been demonstrated to be effective in patients with acute myocardial infarction. Some patients, especially those who develop infarcts of the anterior wall, develop late ventricular dilation, which significantly increases morbidity and reduces survival rate. Early intervention with ACE inhibitors has been demonstrated to slow the progression of left ventricular enlargement and reduce morbidity and mortality.14,15
A number of large-scale clinical trials have been completed that document the efficacy of such intervention. What remains unresolved is whether intervention with ACE inhibitor therapy should be applied to all patients who sustain an acute myocardial infarction, to only those with an infarction of the anterior wall, or to only a subgroup of that population, based on their likelihood of developing a remodeling process and impaired global ventricular function.16 The greatest efficacy has been demonstrated in patients who have presented with either overt heart failure at the time of infarction or with early evidence of ventricular dysfunction that is likely to progress. In studies of these patients, intervention within the first week after infarction has been associated with a striking reduction in morbidity and mortality. Earlier intervention, even before documentation of the severity of the infarction or the consequent ventricular dysfunction, has demonstrated benefit in all but one large trial.17 Clear evidence for incremental benefit from earlier intervention needs to be established before routine administration of ACE inhibitors within the first 24 hours of a myocardial infarction can be recommended. It is, however, clear that intervention within 72 hours in a high-risk population has a long-term salutary effect.
Other interventions, including the early administration of nitroglycerin and the early administration of beta blockers, have also been tested in patients with acute myocardial infarction with varying results. Some studies have shown early administration of nitrates to be beneficial18 and others have not.19 It is likely that selective administration of these drugs would be effective in responsive patient populations, but the criteria for identifying these populations are not yet available.
Final Comment
Heart failure is a progressive and lethal disease if left untreated. Even with existing therapy, the mortality rate remains high, and the quality of life and morbidity are significantly impaired. The management of advanced heart failure requires pharmacologic and mechanistic insight. Prevention of heart failure is an important agenda for the family physician. Our growing understanding of the natural history of left ventricular dysfunction provides the opportunity to intervene effectively and prolong the productive lives of patients.