During the last 50 years, physicians have developed three distinct conceptual models of heart failure that have provided a rational basis for the treatment of the disease. In the 1940s through the 1960s, physicians regarded heart failure principally as an edematous disorder and formulated a cardioorenal model of the disease in an attempt to explain the sodium retention of these patients. This model led to the widespread use of digitalis and diuretics. In the 1970s and 1980s, physicians viewed heart failure principally as a hemodynamic disorder and formulated a cardiocirulatory model of the disease in an attempt to explain patients' symptoms and disability. This model ted to the widespread use of peripheral vasodilators and the development of novel positive inotropic agents. Now, in the 1990s, physicians are beginning to think about heart failure as a neurohormonal disorder in an attempt to explain the progression of the disease and its poor long-term survival. This new conceptual framework has ted to the widespread use of converting-enzyme inhibitors and the development of β bockers for the treatment of heart failure. Which conceptual model most accurately describes the syndrome of heart failure and leads physicians to utilize the most effective treatment? This paper critically reviews the available evidence supporting and refuting the validity of all three models of heart failure. We conclude that, to varying degrees, all three approaches provide useful, but incomplete, insights into this physiologically complex and therapeutically challenging disease.
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine