Mechanisms and Models in Heart Failure

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Abstract
The people who bind themselves to systems are those who are unable to encompass the whole truth and try to catch it by the tail; a system is like the tail of truth, but the truth is like a lizard; it leaves its tail in your fingers and runs away knowing full well that it will grow a new one in a twinkling. –Ivan Turgenev to Leo Tolstoy Despite repeated attempts to develop a unifying hypothesis that explains the clinical syndrome of heart failure, no single conceptual paradigm for heart failure has withstood the test of time. One logical explanation for our inability to define the syndrome of heart failure in precise mechanistic and/or clinical terms is that the clinical syndrome of heart failure almost certainly represents the summation of multiple anatomic, functional, and biological alterations that interact together in an exceedingly complex manner and in different genetic and environmental backgrounds over a sustained (but variable) period of time. Thus, it is not surprising that clinicians and investigators have used a variety of increasingly complex model systems in an attempt to describe the syndrome of heart failure. Whereas clinicians initially viewed heart failure as a problem of excessive salt and water retention that was caused by abnormalities of renal blood flow (the “cardiorenal model”1 ), as physicians began to perform careful hemodynamic measurements, it also became apparent that heart failure was associated with a reduced cardiac output and excessive peripheral vasoconstriction. This latter realization led to the development of the cardiocirculatory or hemodynamic model for heart failure,1 wherein heart failure was thought to arise largely as a result of abnormalities of the pumping capacity of the heart and excessive peripheral vasoconstriction. However, although both the cardiorenal and cardiocirculatory models for heart failure explained the excessive salt and water …