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(Circulation. 2000;102:IV-14.)
© 2000 American Heart Association, Inc.

Special Anniversary Issue

Congestive Heart Failure: Fifty Years of Progress

Eugene Braunwald, MD; Michael R. Bristow, MD, PhD

From the Department of Medicine, Harvard Medical School and Brigham and Women’s Hospital, Boston, Mass, and the Division of Cardiology, Department of Medicine, University of Colorado Health Sciences Center, Denver.

Correspondence to Eugene Braunwald, MD, Brigham and Women’s Hospital, 75 Francis St, Boston, MA 02115.

Key Words: angiotensin • cardiomyopathy • edema • endothelin • heart failure

Volume 1 of Circulation provides an excellent snapshot of the understanding of the mechanisms and treatment of heart failure a half century ago. During that era, circulatory pathophysiology was at the center of investigative attention. For example, Tinsley Harrison and his group divided heart failure into "primary disorders of filling and primary disorders of emptying,"¹ a forerunner of our current terms diastolic and systolic heart failure. The great Swedish clinical physiologist Gustav Nylin used ³²P-labeled red blood cells for measuring cardiac output and cardiothoracic blood volume by the indicator-dilution method in normal subjects and in patients with heart failure.² Andre Cournand’s group defined the pathophysiology of heart failure secondary to cor pulmonale, distinguished it from left ventricular failure, and compared the acute hemodynamic effects of digoxin in these 2 conditions.³ In a seminal paper, Raab and Lepeschkin extracted sympathin from the heart and established norepinephrine as the cardiac adrenergic neurotransmitter.⁴ In one of the earliest efforts to manage patients with chronic congestive heart failure on an outpatient basis, Vander Veer and colleagues demonstrated the effectiveness and tolerability of an oral form of the widely used parenteral diuretic mercuhydrin.⁵

Myocardial Function

In the 1950s, the role of hypertrophy in the heart’s adaptation to hemodynamic overload was examined. After Laplace’s law was applied to the heart and permitted the calculation of wall stress in the human heart,⁶ it became clear that myocardial hypertrophy prevents excessive elevation of wall stress consequent to hemodynamic overload.^{7 8} In the 1960s, there was a lively debate about the mechanism . . . [Full Text of this Article]