The COURSE of a case of ordinary hypertrophy may be divided into three stages: 1st. The period of development, which varies much with the nature of the primary disease. Thus in rupture of an aortic cusp or in sudden overstrain from exertion it may require months, or even years, before the hypertrophy becomes fully developed. In these cases it may never do so, and then death results. On the other hand, in sclerotic affections of the valves with stenosis or incompetence the hypertrophy develops pari passu with the lesion, and may continue to counterbalance a progressive impairment of the valves. 2d. The period of full compensation, the latent stage, during which the heart's vigor meets all the requirements of the circulation. There may be no signs whatever of heart weakness, but the hypertrophied muscle completely equalizes the valvular or other defects. It may last an indefinite period of years. In some cases this fortunate period is never fully attained, and indications of incomplete compensation remind the individual that he has a heart affection. 3d. The period of disturbed compensation, which sooner or later awaits all victims of hypertrophy. It may come suddenly during an extra exertion, and death follow from acute dilatation; or more commonly it takes place slowly, and results from degeneration and weakening of the heart-muscle, with consequent dilatation and all its evils. There may be repeated failures before the end is reached, represented clinically by attacks of cardiac dyspnoea and dropsy.
The breaking, as it is called, of a compensatory hypertrophy may be induced by many causes. Among the most important is failure of general or local (cardiac) nutrition. In many a chronic heart case readmitted to hospital, perhaps for the third or fourth time, with dyspnoea and dropsy, exposure, poor food, and whiskey are responsible for the failure. Gradual sclerosis of the coronary arteries leading to fatty or fibroid changes is a fruitful source of disturbed compensation. It is well known that during or after an acute illness, pneumonia, fever, or a bronchial attack the first symptoms of heart disease may be manifested. Mental emotions, severe grief, or fright have been known to bring on symptoms of heart failure in hypertrophy. One of the most frequent causes is sudden or prolonged muscular exertion, which may disturb a compensation perfect for years, and induce death in a few days.59 The intimate pathology of broken compensation is not always clear. It certainly does not always depend on degeneration of the muscle-fibres, so far as microscopical examination can tell, and in many cases we are forced to conclude that the ganglia are at fault and the breakdown is nervous, not muscular.
59 Traube, Gesammelte Beiträge, Bd. iii.
The PROGNOSIS depends entirely upon the nature of the cause which has induced the hypertrophy. When remediable or removable, the heart may return to its normal size, as after pregnancy, acute Bright's disease, and some cases of hypertrophy from deranged innervation and muscular exertion. When the cause is irremediable, as in chronic valve disease, sclerosis of the arteries, or obliteration of pulmonary capillaries, the case is quite different. Here the prognosis depends largely on the capability of maintaining in its integrity a sufficient hypertrophy to compensate for the obstruction: so long as this keeps up all is well; the evils come with failure of the hypertrophy and increase of the dilatation. Conditions of general and local nutrition are all-important factors, and when these can be supported to the highest possible degree the prognosis is favorable. Ill-health may be indicated at once by the onset of cardiac symptoms, pointing to disturbed compensation. Much depends on the seat of the original disease. Mitral stenosis carries with it as good prognosis, quo ad longevity, as aortic stenosis,60 and the latter much better than aortic insufficiency. The nutrition of the muscle of the heart demands a full and constant supply of blood, but in aortic incompetency the rapid regurgitation does not permit of the complete distension of the coronary vessels,61 and the strain is such that atheroma of these arteries is very apt to follow and still further diminish the blood-supply. Hence the prognosis in aortic insufficiency for enduring hypertrophy is bad. The hypertrophy which accompanies general arterial degeneration, though compensating for peripheral obstruction, carries with it certain dangers, as already indicated, in the liability to cause rupture. With care such patients may survive for years, though exposed to risks other than cardiac.
60 Brückes held that the coronary vessels were filled in diastole alone, but there can be no question that blood also enters during the systole. The sigmoid valves certainly do not in the majority of cases cover the orifices of these arteries during this act. Undoubtedly, however, the heart-vessels are more distended in diastole. The pallor of the muscle in systole is a proof that the coronary vessels are not well filled at this period.
61 This is not the usual statement, but my experience—limited, it is true—seems to point to the conclusion that mitral stenosis may also exist for many years without exciting symptoms of heart disease. It may, I think, be safely affirmed that a larger number of persons with mitral valve disease live in blissful ignorance of the existence of serious heart lesion than any other group of cardiac cases. Particularly is this the case in women. Two points have attracted my attention in this connection: the frequency with which we find evidence of stenosis—as shown by the presystolic thrill and rough murmur—in women complaining, perhaps, of shortness of breath on exertion and slight cardiac distress—symptoms which are readily relieved—and the discovery post-mortem of stenosis of the mitral orifice in cases of sudden death by embolism or from some intercurrent disease occurring in persons in whom heart disease had never been suspected. The narrowing may be extreme—an orifice only 13 millimeters in width in one case in which a woman was stricken with hemiplegia while attending to her household duties. Such cases, and they are not very uncommon, teach us how perfect compensation may be in this lesion.
The TREATMENT of hypertrophy consists largely of measures directed toward its maintenance in a degree proportionate to the extra work which the heart has to do. In organic disease the well-being of the patient depends on this: we cannot remove the cause, but we can by careful hygienic and dietetic regulations maintain the balance between the defect and the compensation. The original lesion is usually beyond control, and the special indications are to moderate certain dangers associated with hypertrophy, and to promptly meet the earliest symptoms of heart failure. The utmost moderation in food, drink, and exercise must be enjoined. Quiet, regular habits are all important; excesses of all kind quickly lead to impairment of the heart's action. In the hypertrophy associated with arterial and renal disease a special danger exists in the tendency to rupture of vessels. In these cases vigorous heart-beat, with very high tension in the peripheral arteries, indicates mischief which may be met by taking prompt measures for the reduction of the high pressure. A brisk cathartic may avert an apoplectic attack, and there are cases in which the old practice of bleeding—formerly so much in vogue for hypertrophy—is justifiable. Palpitation and shortness of breath are among the earliest signs of failing compensation, and call for the treatment to be considered under Dilatation. The condition of hypertrophy from organic disease is not directly amenable to treatment; we cannot diminish the size of the organ, but we can regulate its action by measures which control the contractions when from any cause they become too forcible or irregular. More particularly is this the case in hypertrophy due to disturbed innervation. When vigorous, rest and the administration of cardiac sedatives, such as aconite or veratrum viride, will generally suffice to reduce the force of the contractions. The palpitation and irregular action in cases of irritable heart from over-exertion, the abuse of tobacco, or sexual excesses may subside with the removal of the cause. The steadying action of small doses of digitalis is often well seen in these cases.
Dilatation of the Heart.
DEFINITION.—An increase in the size of one or more of the chambers, with or without thickening of the walls.
VARIETIES.—Two varieties may be recognized: (1) dilatation with thickening, and (2) dilatation with thinning. Dilatation with thickening is the most common, and corresponds with the dilated or eccentric hypertrophy and the active dilatation of some writers. Those cases of dilatation with walls of apparently normal thickness—simple dilatation of authors—also belong to this category, for if the chamber is distended, and yet the walls maintain their normal diameter, they must of course be hypertrophied. The dilatation with thinning—passive dilatation—is specially met with in the auricles, and is characterized by increase in the size of the chamber and attenuation of the walls.