Evolving concepts of heart failure: cooling furnace, malfunctioning pump, enlarging muscle--Part I.
Understanding of the causes of dyspnea and anasarca, the cardinal features of heart failure, has changed dramatically since Greco-Roman times, when sputum and pleural effusions were thought to originate in the brain, and the heart was believed to heat and distribute the vital spirit. It was not until the seventeenth century, when Harvey demonstrated that the heart was a pump and autopsy descriptions revealed valve abnormalities that interfered with the circulation, that it became possible to identify the role of heart disease in causing shortness of breath and edema. Morgagni's recognition, toward the end of the eighteenth century, that overload caused the heart to enlarge was followed less than 50 years later by Corvisart's distinction between hypertrophy and dilation. Differences in the architecture of failing hearts focused attention of nineteenth-century clinical scientists on the myocardial response to overload, and by the end of this century overload-induced hypertrophy was recognized not only to have immediate adaptive effects, but also to cause progressive degeneration of the heart muscle. This focus on the failing myocardium ended in the early years of the twentieth century, when new discoveries in hemodynamic physiology shifted attention to pressure and flow abnormalities caused by the then prevalent rheumatic valvular heart disease. During the past decade, new emphasis on prognosis, along with realization that drugs intended to correct hemodynamic abnormalities often had adverse effects on survival, has led to a reexamination of the biology of the failing heart. As a result, the focus in heart failure research has returned to the myocardium. This article reviews some of the misconceptions and errors of early physicians, who, while often careful and intelligent observers, lacked the means to explain and treat heart failure. It is hoped an appreciation of the evolving concepts of heart failure will help the reader meet today's challenge of incorporating new information from molecular biology that holds the key to further progress in understanding the causes and therapy of this syndrome.
Katz
A M
AM
Cardiology Division, University of Connecticut School of Medicine, Farmington 06030-1305, USA.
D002309:Cardiology / Q000266:history*; D006333:Heart Failure / Q000266:history*; D049668:History, 15th Century; D049669:History, 16th Century; D049670:History, 17th Century; D049671:History, 18th Century; D049690:History, Ancient; D049691:History, Medieval; D006801:Humans