The response of the heart to a continued demand upon its working capacity will, as already indicated, lead to increased muscle bulk or to larger chamber size. Whether hypertrophy be purely the building of a bigger engine or be accompanied by, or due to, muscular disease as had been suggested by certain authors, was a question to which an answer was hoped, but it would seem that the solution is no nearer than can be obtained in human pathology. Fifteen of the 34 cases showed some degree of myocardial damage. Some of the other cases may have been instances of so-called essential hypertrophy, enlargements due to hard work or to low grade hidden infection. Aubertin[8] ascribes such cardiac muscle increase to overwork under the stimulus of intoxication from intestinal sources or from irregular constitutional functions. For information concerning this and pathological enlargements one may consult the Table (2) of Hypertrophies and Dilatations; in advance the method of charting must be known. Since it is usually impossible to decide what may be the single important factor in the cardiac disease, all of the accredited factors have been listed with the hope that the resulting figures would be significant. Thus an animal may have recorded pericarditis, nephritis and arteriosclerosis—who shall say which was primary or most potent in the cardiac change. Essential hypertrophy is limited to those cases for which there was no concomitant pathology that might have been responsible for the overgrowth. There was one in a carnivore (fox) and one in a raptatory bird (buzzard). Idiopathic dilatations on the other hand are much more common, but they still bear a relation to the apparent vulnerability of the heart. Their distribution is as follows: Primates 1, Carnivora 1, Pinnipedia 1, Ungulata 1, Marsupialia 4, Anseres 1. These may be cases such as Plimmer described, of cardiac failure, indicated by dilatation, the result of inactivity. Besides these special instances and the ones accounted for in the list, there were three acute dilatations apparently due to shock, two ungulates and one marsupial, probably incidental to fright when being caught by the keepers. The association of secondary dilatation with hypertrophy is only evident in three instances. One case and perhaps the most interesting, is that in which the principal antecedent pathology was thyroid hyperplasia and nephritis; the dilatation was perhaps agonal or shortly before the last struggles. It would seem that all of the dilatations occurred shortly before death because long standing passive congestions and dropsies of cardiac origin are exceedingly rare; only one certain case is recorded (carnivore).