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“It is generally established that the normal heart may become incapable of maintaining an adequate cardiac output or preventing venous engorgement whenever it is presented acutely with an overwhelming load beyond its pumping capacity. This state is not failure of a diseased heart, but it has been designated `failure' by many. It is more difficult to define the situation where such an overload sets up a vicious cycle which progressively potentiates the load upon the heart for hours or days. After a lapse of time, this load strains the mechanisms available for compensation to the point where venous congestion or reduced cardiac output becomes evident. Does this turning point mean that the heart has become abnormal, in a functional sense, and, therefore, is it now to be a case of heart failure in the accepted sense? . . . How much of the circulatory change is due to the load and how much to mechanisms called upon to meet the load? When does myocardial deterioration begin, and when does myocardial failure start? . . . How can one determine whether it is cardiac loading or myocardial failure whch is responsible for invoking the compensatory mechanisms?”1

Biochemical "Defect" in the Hypertrophied and Failing Heart