Structural bases of myocardial hypertrophy.

Hypertrophy is undoubtedly the most important problem in the structural adaptation of heart muscle. It stands at the centre of medical discussion because it is just the hypertrophic heart muscle that, after performing efficiently for a long time, finally fails. For this reason structural researches into hypertrophy include those of myocardial failure (Buchner, I950, I96I). According to the macroscopical findings we speak of left-sided hypertrophy if mainly the left ventricle and the septum belonging to it increase in size, or of right-sided hypertrophy if the burden falls almost exclusively on the right ventricle. There are also forms, however, in which the hypertrophy involves the whole myocardium for example, in cases of macrosplanchnia in acromegaly or in idiopathic cardiomegaly. From the macroscopical findings we can distinguish concentric hypertrophy with normal or even reduced lumen of the chamber. Concentric hypertrophy is especially found in hypertrophy due to raised pressure for example, as a consequence of aortic stenosis, hypertension, etc. Eccentric hypertrophy, on the other hand, is found in the cardiac hypertrophy of athletes and in volume hypertrophy for example, as a result of a shunt or a chronic lack of oxygen. In concentric hypertrophy with good cardiac efficiency the sarcomeres of the heart muscle contract extremely in systole, starting from a mean intensity in diastole; in eccentric hypertrophy, on the other hand, the diastolic active dilatation is greatest and the contraction only average in systole (Fig. i). Even if the heart volume is not increased, heart failure may be present in concentric hypertrophy and may be absent in spite of large heart volumes in eccentric volume hypertrophy (Reindell, Keul, and Doll, I968). Teare (I968) divides idiopathic hypertrophic subaortic stenosis into an asymmetrical form, which chiefly involves the region of the ventricular septum and anterior wall of the left ventricle, and a diffuse form. From our investigations (Meessen and Poche, I967) with the electron microscope, however, even inparts oftheasymmetrically formed heart which to the naked eye are not hypertrophied, growth process can be seen. We may therefore assume that both Teare's forms are only the expression of an often focal accentuated growth. A limit of the extent of hypertrophy is reached when the whole heart weighs often 500 g., and sometimes iooo g. or more, instead of the normal 300 g. In the extreme weights, however, not only the muscle mass but also the connective tissue is considerably increased. In I0 cases of cardiac hypertrophy with AV block and a mean heart weight of 6oo g. the proportion of connective tissue amounted to 22 per cent (Knieriem and Effert, I966). Linzbach (1950, I960) set the 'critical weight of the heart' for the isolated left chamber at 200 to 250 g. and for the whole heart at 500 g., while Schoenmackers (I963) thought the upper limit of weight for the heart muscle to be 550 g.