Cardiac muscle cell hypertrophy, hyperplasia of connective tissue, abnormal peripheral circulation and metabolic changes in the cardiac fibre and in the smooth muscle cell as a consequence of mechanic overload are described in variable proportions in heart failure. These changes in turn are essential factors for progression of the disease. Results of early drug intervention in patients with few or no symptoms suggest that decrease of mechanic overload by vasodilator therapy slows down the progression of the disease. In late stages, treatment with diuretics and vasodilators improves the symptoms and the outcome of heart failure. Diuretics alone and inotropic positive substances bring about some improvement of symptoms and maximal oxygen consumption, but they have no favourable effect on the outcome. Positive inotropic substances remain restricted to late forms of heart failure, in which they seem to ameliorate symptoms but have a rather unfavourable effect on the outcome. The role of diuretics, ACE inhibitors and digoxin is well defined. This is not the case for newer calcium-channel blockers from the dihydropyridine group, of beta blockers, of phosphodiesterase inhibitors and of substances with partial beta agonist and partial beta blocking activity. These drugs must still be classified as experimental agents for the treatment of heart failure.