Cardiac hypertrophy in heart disease is associated with a deterioration of the patient's prognosis. From experimental work it is known that hypertrophy can recede, sometimes it is, however, associated with an undesirable increase of fibrous tissue in the heart muscle. In clinical practice we can reduce cardiac hypertrophy (assessed mainly by echocardiography), at least in some patients, by reducing or eliminating the evoking cause (e.g. in sportsmen terminate training, in aortic valve disease by replacement of the valve, in hypertonic patients we reduce the pressure by drugs). After regression of hypertrophy later also the amount of fibrous tissue recedes and as a rule the function does not deteriorate. Lately we are trying to influence factors which directly participate in the hypertrophy of the myocytes, in particular in hypertonic subjects by preferential action on the adrenergic system and the renin angiotensin system.