by Tak W. Kwan, MD FACC, FACP

Congestive Heart Failure (CHF) is a common disorder in the U.S. It affects more than 4 million people and over 400,000 new cases are diagnosed each year. It has a major effect on the quality of life and productivity. Any disorder that im-pairs blood ejection can cause CHF. In the past, hypertension and valvular heart disease were the most likely causes of heart failure. However, nowadays with the widespread use of coronary angiography, coronary heart disease is the most common etiology; and accounts for about 60-70% cases of CHF. From all previous multicenter studies, CHF has a wide spectrum of morbidity and mortality. Every NYHA class has a different mortality curve. In NYHA IV patients, the mortality is as high as 60% in 12 months. But in asymptomatic or NYHA I patients, the 12 months mortality is less than 10%.

CHF is a progressive disease. It is due to a change in the geometry of the left ventricle. After acute infarction or any damage to the heart muscle, there is an initial structural change of the ventricular contour, for infarct expansion. The distorted ventricle will undergo further remodel-ing as a consequence of elevated neurohormone factors and cytokines. As a result, wall stress on the remaining viable myocardium is increased. This can lead to further cavity enlargement and shape distortion. This process is called cardiac remodeling. It is associated with a greater likelihood of cardiac morbi-dity and mortality in patients with CHF.

When we plan for therapy in patients with CHF, we have to treat symptoms of heart failure, to improve quality of life, to reduce hospitalization and most importantly, to reduce mor-tality. Several drugs can achieve these goals. Digitalis is an important drug to treat heart failure. PROVED and RADIANCE trials showed that digoxin can improve exercise capacity. DIG study did not show mortality reduction when compared to placebo. Based on the evidence, digoxin can alleviate symptom, improve clinical status, and thereby decrease the risk of hospitalization for heart failure. Digoxin appears to have little or no effect on survival.

Diuretic is the only drug that can adequately control the fluid retention of heart failure. The most common diuretics is loop diuretics. It can provide a massive natriuresis in a short period of time. Another important diuretic is aldosterone receptor anta-gonist which can exert favorable effects on sodium and potassium balance and may decrease the risk of the progression of heart failure. RALES study showed that Altactone can cause a 27% reduction in mortality and 36% reduction in hospitalization for heart failure. A postulate mechanism is that Aldactone can inhibit fibrosis of the surrounding myocytes.

Angiotension converting enzyme inhibitor is the most important therapy in the history of CHF. The mechanism is inhibition of the formation of angio-tension II and aldosterone synthesis. Another mechanism is to inhibit local hypertrophy and infarct expansion. As expected, cardiac remodeling will be inhibited. Most of the ACE studies demonstrated that ACE inhibitor benefits patients in NYHA IV heart failure (CONSENUS), NYHA II/III (SOLVD), NYHA I or asymptomatic patient (SOLVD-prevention), acute MI (SAVE, AIRE). Except in SOLVD-prevention trial, which showed delayed development of heart failure, all other studies demonstrated mortality benefit. The dosage for ACE inhibitor should be maximized as showed in ALTAS study. In this study, high dose patients produced greater hemodynamic, neurohormonal, symptomatic and prognostic benefits than patients with low doses of ACE inhibitors.

Angiotension receptor blocker is a new class of drug. ELITE I study showed a 46% reduction in mortality with Losartan when compared to Captopril. However, this is not a mortality study. ELITE II is a better design trial in terms of mortality. The result should be presented in the American Heart Association Meeting in November this year.

Beta-blocker was thought to be contraindicated in patients with CHF because of its acute effect in reducing ventricular function. Nowadays, Beta-blocker is a main stay of therapy in CHF because of the following mechanisms: 1) Reduction in norepinephine release. 2) Reduction in peripheral vascular resistance. 3) Inhibition of renin. 4) Attenuation of arrhythmias. 5) Reduction of wall stress. 6) Amelioration of ischemia. The largest Beta-blocker trial in CHF is MERIT-HF study. It showed 34% reduction in all causes of mortality, 38% reduction in cardiovascular mortality, 49% reduction in heart failure, and 41% reduction in sudden death. The benefit of metoprolol was apparent in all patients regardless of NYHA class, left ventricular ejection fraction, gender, or presence of ischemic heart disease. It is appropriate to use beta-blocker in all patients with CHF. One important thing to remember is to start beta-blocker in the lowest possible dose and to titrate upward slowly.

Revascularization is a very important therapy in patients with CHF. Patients with coronary artery disease and CHF have a very high mortality. After revascularization, angina and heart failure are usually improved. After reviewing all data in medical and surgical therapy in coronary artery disease, the greatest mortality benefit is amongst patients with severely reduced ventricular function. In the absence of fatal non-cardiac disease, any patients with coronary artery disease and CHF should be considered for revascularization. ðP