TY - JOUR
T1 - New concepts in the pathophysiology of heart failure
T2 - Beneficial and deleterious interaction of endogenous haemodynamic and neurohormonal mechanisms
AU - Packer, M.
PY - 1996
Y1 - 1996
N2 - During most of the last 50 years, physicians have viewed heart failure primarily as an oedematous disorder, in which fluid retention occurs because the heart cannot pump adequate quantities of blood to the kidneys, This conceptual model led to the successful utilization of diuretics for heart failure, but it failed to permit physicians to recognize that heart failure is a chronic progressive disorder that impairs both the quality and quantity of life, even when oedema is adequately controlled. To accommodate this new understanding, a new model has been developed, in which the development and progression of heart failure is viewed as resulting from the interplay of haemodynamic and neurohormonal mechanisms. Both mechanisms support the inotropic state of the heart following an injury to the myocardium, but when sustained for long periods, their ability to augment cardiac contractility wanes, and, instead, these same mechanisms act to enhance ventricular wall stress, thereby impairing ventricular performance. As the heart-failure state evolves, endogenous mechanisms that are normally activated to control wall stress become exhausted, and peripheral vasoconstriction and sodium retention develop. Unopposed activation of haemodynamic stresses and neurohormonal systems leads to further destruction of the myocardium and progression of the underlying disease. The acceptance of this haemodynamic-neurohormonal model has led to the development of vasodilators and neurohormonal antagonists that have been shown to be useful alone, or when added to diuretics, in the treatment of heart failure.
AB - During most of the last 50 years, physicians have viewed heart failure primarily as an oedematous disorder, in which fluid retention occurs because the heart cannot pump adequate quantities of blood to the kidneys, This conceptual model led to the successful utilization of diuretics for heart failure, but it failed to permit physicians to recognize that heart failure is a chronic progressive disorder that impairs both the quality and quantity of life, even when oedema is adequately controlled. To accommodate this new understanding, a new model has been developed, in which the development and progression of heart failure is viewed as resulting from the interplay of haemodynamic and neurohormonal mechanisms. Both mechanisms support the inotropic state of the heart following an injury to the myocardium, but when sustained for long periods, their ability to augment cardiac contractility wanes, and, instead, these same mechanisms act to enhance ventricular wall stress, thereby impairing ventricular performance. As the heart-failure state evolves, endogenous mechanisms that are normally activated to control wall stress become exhausted, and peripheral vasoconstriction and sodium retention develop. Unopposed activation of haemodynamic stresses and neurohormonal systems leads to further destruction of the myocardium and progression of the underlying disease. The acceptance of this haemodynamic-neurohormonal model has led to the development of vasodilators and neurohormonal antagonists that have been shown to be useful alone, or when added to diuretics, in the treatment of heart failure.
KW - Heart failure
KW - Neurohormonal activation
KW - Wall stress
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U2 - 10.1046/j.1365-2796.1996.463796000.x
DO - 10.1046/j.1365-2796.1996.463796000.x
M3 - Article
C2 - 8774387
AN - SCOPUS:0029984396
SN - 0954-6820
VL - 239
SP - 327
EP - 333
JO - Journal of Internal Medicine
JF - Journal of Internal Medicine
IS - 4
ER -