Janiuary 10th, 1931, p. 8) remarks that estimation of the myocardial in-tegrity is difficult w}ien obvious defects such as valvular disease are absent. All valvular lesions except the congeniital forms are associated with myocardial defect, but the onset is obscure and the symptoms are indefinite. The recognized terminations of myocardial disease are (1) congestive failure, (2) angina, (3) coronary thrombosis, (4) the Stokes-Adams syndrome, (5) ventricular fibrillation, and (6) myocardial

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... e; two or more of-these may be associated. Ventricular fibrillation aInd ventricular rupture are most rapidly fatal, and couigestive failure is the slowest. Chloroform anaesthesia may produice fatal ventricular fibrillation in a healthy myocardium, as a terininal phenomenon fibrillation connotes a final effortof dying muscle. Rupture is rare, but it may result-from an infarction or from fibrosis due to a gumma. The Stokes--Adams -syncdrome may terminate in deat-h du-ring asystole. Congestive failure commences clinically with dyspnoea, but this is not pathognomonic. Cvanosis may occur, and a history of rheumatism or syphilis may assist diagnosis. Rh-eumatic mvocarditis is associated generally with valvular lesions, usually mitral stenosis; it is seldom cured. Acute congestive failure, due to a transient condition.such as severe tachycardia-for example, in sea-sickness-may subbside completely, or remissions may occur. Congestive failure may be due to hyperpiesia, chronic nephritis,' cardio-vascular syphilis, or acute inifective carditis. Acutefailure may ensue in the exanthemata. Angina may be fatal in a case which has shown no previous physical signs or symptoms. The quality of the heart sounds is often