[The natural history of dilated cardiomyopathy and pathophysiology of congestive heart failure].

To clarify the natural history and mechanisms of compensation and decompensation in dilated cardiomyopathy (DCM), the hemodynamic and follow-up data of 52 patients who underwent cardiac catheterization between April 1976 and July 1984 were evaluated. The symptoms of the majority of 42 patients who were in severe congestive heart failure (CHF) (New York Heart Association Functional Class IV) on admission were improved. Two were in Class I, 22 in Class I, 22 in Class III, only six remaining in Class IV at the times of their catheterizations one to two months post admission. The patients were categorized as compensated (Class I and II) and decompensated (Class III and IV), and their data were compared with those of 30 normal subjects. Cardiac status was evaluated at the end of August 1984, and the mean follow-up period was 44 months. The hemodynamic and angiographic characteristics of DCM consisted of an enlarged and poorly contracting left ventricle, with an increased left ventricular (LV) muscle mass, low LV systolic pressure, reduced cardiac output, and elevated systemic vascular resistance. LV volume was larger, and the ejection fraction (EF) was more reduced in the decompensated group in association with elevated preload and afterload. Preload and afterload were within the normal range in the compensated group. LV wall thickness tended to decrease in the decompensated group, and the LV muscle masses did not differ between these two groups. There was a significant inverse correlation between afterload and EF (r = -0.57, p less than 0.01) in DCM. There were five sudden deaths and five CHF deaths, and cardiac symptoms improved in the majority of the survivors. One, two and five year survival rates were 91.2%, 79.8%, and 72.5%, respectively. No hemodynamic variables could be available to predict the prognosis except for the LV end-diastolic pressure and stress. It is concluded that the absence of adequate compensatory hypertrophy and the inappropriate elevation of afterload, or so-called "afterload mismatch" plays an important role in the development of CHF, in addition to depressed contractility in DCM. Persistent elevation of preload despite vigorous medical treatment indicates a poor prognosis. No other hemodynamic variables were good indicators of prognosis.