Hypertrophy of the heart directly consecutive to toxic nephritis noted in two experiments undertaken to in vestigate the pathology of cancer. Two rabbits were inoculated with an aqueous extract of macerated human cancer, after being previously treated by sub cutaneous injections of cantharidin in oil, in order to determine the localiza tion of the malignant growth by means of a renal lesion. In neither ease was any malignant growth found post mortem, but in both distinct nephritis as well as marked hypertrophy of the left ventricle was seen. The first rabbit, which weighed ISS5 grammes, received in five doses milligrammes (V„ grain) of cantharidin between May 19 and June 1, 1S95. Albumin was found in the urine soon after the first injec tion. but disappeared again after the third. After a transitory loss of weight the animal throve until December, when it showed signs of spasmodic paraplegia (due to myelitis caused by cancerous toxins) and died in January, 1896. On examination the kidneys were found in creased in size and showed a uniform gray surface on section. there being no sharp distinction between cortex and medulla. The wall of the left ventricle was much thicker than normal, being twice the normal size as seen in other rabbits of similar weight. In the second case the rabbit was much larger, weigh big kilogrammes. The same dose of cantharidin, milligrammes, was administered in three injections. The urine contained albumin after the first dose, but not after the third. The ani mal wasted rapidly and died in a state of profound caehexia. The kidneys were found in the same condition as those of the first animal, and the left ventricular wall was noticeably thick ened, though not so much so as in the first case. Thus a diffuse nephritis of toxic origin produced marked enlarge should be of about the same bulk as the closed fist of the subject. The wall of the normal left ventricle is about inch in thickness, and of the right 1/4 inch, or a little less. The left ventricle seldom attains the thickness of 1 inch; the right may reach inch, and it has been re ported as being even more than an inch in thickness. The auricles are never very thick. The left in health is about inch and may become inch when meat of the left ventricle within a few mouths in both instances, the duration in the second case being the shorter of the two. Mayet (Lyon Wilicale. Jan. , 19, 1902).
Pathology.—The muscular fibres of an hypertrophied heart are increased in size somewhat, but mainly increased in number. Macroscopically, the cut sur face is red and firm. The extent of the hypertrophy can be determined by the size of the organ. the thickness of its walls, and its weight. A normal heart hypertrophied. The right auricle is still thinner, and shows its tendency to hy pertrophy by changes in its auricular appendix rather than in the rest of its cavity. Before measuring the walls, rigor mortis should be relaxed, as already advised, by soaking in water. Mere in spection may prove deceptive as to the existence or not of hypertrophy in cases of eccentric hypertrophy, because the walls may look relatively thin and yet be absolutely hypertrophied. Weighing is a valuable procedure. The normal
heart weighs 8 or 9 ounces. In disease the organ may weigh 1 pound or 1 7, pounds, and exceptionally 3 pounds, i.e., as much as the liver ! [Description of cuts: Fig. 1. Excen tric hypertrophy as a result of chronic adhesive pericarditis in a man aged 20 years. Weight of heart with pericar dium, 1328 grammes (44 ounces). Valves competent. Wall of left ventricle 2 centimetres thick; of right ventricle 5 millimetres. Patient of Dr. F. C. Shat tuck, at one time under the care of the writer. Specimen due to the courtesy of Dr. J. H. Wright.
Fig. 2. Boy, aged 6 years. in the writer's wards with exeentric hypertrophy due to mitral regurgitation. The black line indicates the extent of cardiac dullness. Two attempts to obtain a radiograph were unsuccessful. HERMAN F. VICK ERY.] Results of the autopsy on a child that died during birth. Both of the patients were healthy, and the child itself did not appear to be abnormal in any way, except that the heart, after evacuation of the blood, weighed 44 grammes: more than twice the normal weight. The wall of the right ventricle varied from 0.75 to 1 centimetre in thickness; the left from 1 to 1.25 centimetres. The septum was 0.75 centimetre wide. Microscopically, the muscle-valves and vessels appeared to be normal. The case is, therefore, one of uncomplicated, primary, congen ital hypertrophy of the heart. Sim monds (Mfinchener med. Woch., Jan. 24, '99).
Of course, the immediate effect of any of the causes of hypertrophy is manifest in the corresponding portion of the heart, and not in the whole organ. Aortic stenosis and regurgitation en large the left ventricle. In time, how ever, stasis is produced in the pulmonary circulation, and the right ventricle also hypertrophies. Valvular lesions, whether regurgitant or obstructive, cause an ap propriate part of the heart to hyper trophy, and then, sooner or later, more or less directly (with one exception) en tails increased labor upon all the other portions of the heart. The exception is mitral stenosis, which affects the left auricle, the right ventricle, and the right auricle, and then tends to cause stasis in the general venous return, with con sequent obstruction to the outflow of blood from the left ventricle and aorta into the arterial capillaries; but this ob struction to the expulsive efforts of the left ventricle does not result in hyper trophy of that portion of the heart, be cause so little blood is admitted into it through the stenosed mitral valve.
The greatest hypertrophy occurs in aortic regurgitation (cor bovinum). There is first eccentric hypertrophy of the left ventricle. When this reaches sufficient size, there arises relative insufficiency of the mitral valves, and thereupon hyper trophy of the left auricle and the right side of the heart.
The inevitable result of hypertrophy is eventual debility and failure. By the time of death dilatation may far surpass hypertrophy; or the hypertrophied mus cle may be more or less changed by fatty degeneration. In some cases the muscu lar condition is apparently so good that the pathologist surmises failure of the nervous mechanism to be the terminal ' factor in the case.