In embryonic life, and for a time after birth, the heart grows by increase in size and by division of the muscle-cells. Later, the growth of the heart depends essentially upon the enlargement of the muscle-cells alone. In hypertrophy of the heart, produced by artificial lesions of the valves, true dilatation of the left ventricle always precedes the hypertrophy. Hypertrophy may develop even when the general nutrition of the body is very unfavorable, and in hyper trophy the increase of the weight of the heart and of the transverse diameter of the muscle-cells is proportional. Tangl (Virchow's Archly, June, '89).
Heart-hypertrophy follows any condi tion or set of conditions increasing the amount of work done by the heart. The causes of heart-hypertrophy may be di vided into two broad classes: (1) causes lying in lesions of the heart itself, inter fering with proper function; (2) causes outside the heart.
The first class is subdivided into (a) lesions of the valves, and (b) lesions of the heart-wall. Of 105 cases of heart hypertrophy valvular lesions were pres ent in 13. Of lesions affecting the heart wall there were found myocarditis, tuberculosis, am' aneurism. In some cases of localized myocarditis there is a compensatory nypertrophy of other por tions of the same wall. An aneurism of the heart-wall may throw out of function so large an area of muscle that the re mainder must hypertrophy to make up for the portion lost. Again, an aneurism may be so situated in the heart-wall that the function of one or more of the valves may be interfered with.
The second class of causes of heart hypertrophy may be subdivided into (a) causes acting directly and interfering mechanically with the contraction of the heart, and (b) causes acting by increas ing the general arterial blood-pressure.
Cases of the first class resolve themselves into pericardial adhesions. There were S examples of this lesion, and of these 4 were tuberculous.
In 7 out of S cases there were hyper trophy and dilatation of the right ven tricle,—in most cases extreme,—and in 5 cases uniform dilatation of the whole heart.
Of the causes acting by increasing the general arterial blood-pressure, some offer mechanical obstruction to the blood flow in territorial areas, others to the blood-flow in the whole general arterial system. To the former class belong (a) nephritis, and (b) pressure of tumors and the like upon vascular trunks.
There were 14 cases of left-ventricle hypertrophy associated with nephritis without arteriosclerosis. This number included only 1 case of acute nephritis.
Causes producing mechanical obstruc tion to the blood-flow in the whole ar terial system include (a) the action of drugs and poisons (as alcohol, digitalis, and tobacco) ; (b) excessive work; (c) hydrannic plethora (including general arterial hypoplasia) ; (4) cardio-nervous influences; (e) arteriosclerosis.
Arteriosclerosis was found to be by far the most common cause of left-ventricle hypertrophy-. It is the most frequent of all causes of heart-hypertrophy due to conditions lying outside the heart, oc curring in subjects over thirty years of age. Of the 105 cases of heart-hyper trophy from all causes, there are 62 cases dependent upon arteriosclerosis. Of these 62 eases, 3S had well-marked chronic diffuse nephritis, 17 slight chronic diffuse nephritis, 3 subacute nephritis, 1 acute glomerulonephritis, and 3 normal kidneys. Aneurism of the aorta occurred in 4 cases. In 20 cases there were valvular lesions. In most of these hearts the coronary arteries were dilated, thickened, and tortuous, and the seat of recent or chronic endarteritis. W. T. Howard (Johns Hopkins Hosp. Reports. vol. iii, Nos. 4, 5, 6, '93).
Hypertrophy is never primary, and dilatation always precedes hypertrophy in a hard-working heart, whether the in creased labor be due to resistance from within or from without or to nervous stimulation and augmented action. J. G. Adami (Montreal Med. Jour., May, '95).
Statistics showing the proportion in which the various causes manifested themselves in 360 cases. Cardiac hyper trophy, due to some cause or other, was found to exist in no less than 10.5 cases. Of these arterial sclerosis was found to be the cause in 59 per cent.; chronic nephri tis in 13.4 per cent.; valvular lesions in 12.4 per cent.; adhesions of the peri cardium in 7.6 per cent.; excessive mus cular work in 3.S per cent.: tumors in 1.9 per cent.; aneurisms in 0.95 per cent.; hremic plethora in 0.9.3 per cent. More than 50 per cent. of the cases of cardiac hypertrophy iu general hospital work were due to arterial disease. La flenr (Montreal Med. Jour., May, '95).