It will be found that this new-formation of muscular tissue is in nearly all cases Compensatory, that is, intended to make up for some defect in the heart itself or in the circulation. The needs of the organism assert themselves by the nervous connections of the body on the cardiac ganglia, and the contractions become more forcible. Within the limits of health, and without any increase of the volume of the cardiac muscles, there are great variations possible in the force of the cardiac contractions. But where the heart is for a long period impelled to unusually violent exertion, it becomes hypertrophied.
In many of these conditions there is a mechanical interference with the flow of the blood either in the heart itself or in the arteries, and as a consequence the heart is overloaded with blood, but in some the mechanical cause is not very obvious. As a general rule the cavities are dilated, -and the dilatation may indeed be the primary condition, the hypertrophy occurring as a secondary consequence. It is usual, therefore, to consider dilatation and hypertrophy together, there being commonly some dilatation along with the hypertrophy.
Pathologists have frequently observed that hypertrophy of the heart has existed without any mechanical hindrance in the circulation being-discoverable. Some of these cases have been traced to functional disorders of the heart, the organ contracting more frequently and violently than it should. But some cases are really due to frequent and violent exercise, which has been so prolonged as to have taxed the contractile power of the heart beyond its normal ability. An acute overstrain may be produced by prolonged muscular exertion, such as in hill-climbing (Allbutt), athletic exercises, etc. It has been induced experimentally by Roy and Adami, by narrowing the aorta. In that case dilatation of the heart, followed by incompetence of the auriculo-ventricular valve, was the result.
When frequently repeated, such overstrain will lead to hypertrophy, which may only partly compensate, and there may be a permanent over-dilatation with incompetence of the valves.
This has been observed under a variety of circumstances. It has been described as occurring amongst the Cornish miners, who after their work was over had to reach the surface of the earth by climbing ladders for an hour (Peacock), or in the case of people in hilly countries who are in the habit of carrying loads uphill (Miinzinger). It has been observed also in young soldiers, who, as a result of severe drill, have frequently attacks of palpitation. The ability of the heart varies greatly in different individuals; in some the strain of drill reveals a weakness which has come to be recognized in the army as "irritable heart" (Da Costa, Maclean and Myers). During campaigns, also, long marches may so overstrain the heart as to lead to dilatation and hypertrophy (Friintzel).
Adhesion of the pericardium and Valvular disease are further causes of hypertrophy. In both of them interference with the circulation exists, as will be seen further on.
Obstruction of the coronary arteries, leading to permanent loss of a portion of the muscular wall, will cause hypertrophy, both on account of the loss of tissue and of the derangement of the muscular apparatus of the wall.
Hypertrophy is a frequent result of Obstruction to the circulation in the lungs. In emphysema, for instance, there is great obliteration of the pulmonary vessels, and the right ventricle contracts more vigorously to compensate. A similar result may follow other chronic diseases of the lung, and even extensive pleural adhesions.
Interferences with the systemic circulation, especially Aneurysms and Rigidity of the arteries, are frequent causes of hypertrophy of the left ventricle.
From what has gone before, it will be apparent that hypertrophies of the heart vary greatly in amount and in the distribution of the enlargement. The term General hypertrophy is used to express an enlargement of the heart in all its parts, while Partial hypertrophy expresses an enlargement limited to a part of the organ. As it is the ventricles which are specially exposed to the causes of hypertrophy, the partial forms are divisible into two, namely, hypertrophy of the right and left ventricles respectively.
In General hypertrophy the general shape of the heart is not much altered. The heart is enlarged in all its parts, the ventricles and auricles are increased in capacity, and their walls thickened. The heart is like that of a bullock in size, so that the name cm bovis is often applied to it.
When the right ventricle is mainly affected, the heart assumes a somewhat quadrilateral form (see Fig. 215). On examining the normal heart as it lies on its posterior surface, after removal from the body, the right ventricle is seen to occupy the greater part of the anterior aspect. The normal position of the septum, as shown in the accompanying figure, is slightly to the right of the left border, and it reaches the apex region slightly to the right of the true apex. In the heart the position of the septum is always indicated on the surface by a coronary artery, which, with its padding of fat, occupies a groove corresponding with the anterior border of the septum. In hypertrophy of the right ventricle, as shown by the dotted line in the figure, the apex is unduly obtuse, and it is often difficult to determine what is its exact seat. The septum is nearer the left border than usual, and it reaches the apex region rather to the left than the right of the most projecting point. The right ventricle also monopolizes the anterior aspect of the heart still more than in the normal condition. When the heart is laid open, the undue thickness of the right ventricle, as well as the enlargement of its cavity, become apparent.
Fig. 215. - Hypertrophy of right ventricle. The alteration in shape is indicated by the dotted line: «, superior vena cava; b, aorta; c, conus arteriosus; d, right auricle; e, left auricle; f, left ventricle.
Fig. 216. - Hypertrophy of left ventricle. The alteration in shape indicated by dotted lines; g, the hypertrophied ventricle. (BlWDFLEISCH).
In Hypertrophy of the left ventricle the relations are very different, as shown in Fig. 216. The heart as a whole is more elongated and pointed than normal, and this is often very striking. The apex part especially appears greatly prolonged. When the heart is viewed on its anterior aspect the septum is seen to lie more to the right than is normal, and the true apex is much further to the left of the point at which the septum reaches the apex region. On laying open the heart, the thickening of the wall of the left ventricle is very obvious, and the septum is often greatly thickened. The septum belongs partly to the left and partly to the right ventricle, but as the left ventricle is much thicker than the right, the septum belongs more to the left. It will partake in the hypertrophy of either ventricle, and, in the case we are considering the thickening is often very striking. The thickened septum frequently bulges into the right ventricle, sometimes diminishing its capacity greatly, and even producing actual obstruction of the conus arteriosus. In transverse section the hypertrophy of the left ventricle is sometimes very manifest, the right forming merely a crescentic appendage (see Fig. 217).
Fig. 217. - Transverse section of ventricles of heart showing hypertrophy of the left, from a case of chronic Bright's disease.
Hypertrophy and dilatation of the auricles is less common, but may be very marked. The right auricle is specially liable to dilatation, in consequence of mitral or tricuspid stenosis (see Fig. 218), or obstruction to the pulmonary circulation. This dilatation may reach an extraordinary amount, as in Fig. 218, and in a case recorded by Middleton. Dilatation of the left auricle is less frequent. It occurs by no means regularly as a result of mitral stenosis, but occasionally does so.
Fig. 21S. - Great dilatation of right auricle. Stenosis of mitral and tricuspid orifices. The auricles are shown in transverse section, the right above much dilated. The contracted orifices are also shown.
The total Increase in weight in hypertrophy of the heart is greatest in cases where both ventricles are enlarged, and the weight of the heart in such cases not uncommonly reaches from 27 to 30 ounces-. It is least where the right ventricle alone is enlarged, because this ventricle, as a whole, weighs much less than the left, but in pure right ventricular hypertrophy a weight up to 17 ounces is not infrequent. In hypertrophy of the left ventricle, as in Bright's disease, the weight is frequently over 20 ounces.
The hypertrophied heart often presents a peculiarly firm condition of its wall, and this has been ascribed by Sir William Jenner to a Passive congestion of the heart. Cases of cardiac hypertrophy are very frequently such as to lead to a general venous engorgement, in which the heart itself, being related to the general venous system, partakes. Now, prolonged venous hyperremia produces in organs, as we have seen already, a certain hypertrophy and increased density of the connective tissue. Some part of the hypertrophy in such cases may even be due to increase of the interstitial connective tissue. Hence the result is that the walls of the heart are more rigid than normal, and when the cavities are laid open they do not collapse, but stand out with their outline retained, the walls having a tough leathery character. The muscular substance also is frequently of a very red colour, this being largely due to the excess of blood in the vessels.
Gairdnek (causes of dilatation), Brit, and For. Med. Chir. Review, 1853; Peacock, On some of the causes and effects of valv. dis. of heart, 1865; Leitz, Deutsch. Arch. f. klin. Med., xi. and xii.; Munzinger, do., xix.; Maclean, Brit. Med. Jour., Feb. 16, 1867, etc.; Myers, On diseases of the heart among soldiers, 1870; Fraentzel, Virchow's Arch., lvii., 215; Clifford Allbutt, St. George's Hosp. Rep., 1870, v., 23, and System of medicine, 1898, vol. v.; Da Costa, Am. Journ. of Med. Sc, 1871; Roy and Adami, Brit. Med. Jour., 1888, ii., 1321; Laache (Athletics), Internat. |Med. Congress, 1894, Brit. Med. Jour., 1894, i., 738; Jenner (Congested heart), Med. Chr. trans., 1860, p. 199; Middleton, Clinical Records, 1894.