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In recent years there has been a tendency to minimize the effects of valvular lesions and to regard infection of the myocardium as almost the sole determining factor in the course of rheumatic heart disease. This point of view1represents a reaction to the older, purely mechanical conception of valvular disease, and it may have been carried too far by some. The truth rests between the two extremes. As White2has pointed out: With chronic healed valvular disease there need not be any trace of previous infection in the perfectly healthy muscle. Eventually the myocardium may become exhausted and fail . . . . In other words, it is the valve lesion, if well marked, and not the myocardial disease that eventually causes failure and death. This profound effect of valvular lesions on the dynamics of the circulation is demonstrated in many ways. Fluoroscopic examination, for instance, shows significant changes in the
Kurt Berliner (1938) studied this question.