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CHAPTER 22 - Pathophysiology of Heart Failure from Libby: Braunwald...

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Libby: Braunwald's Heart Disease: A Textbook of Cardiovascular Medicine, 8th ed. Copyright © 2007 Saunders, An Imprint of Elsevier

CHAPTER 22 – Pathophysiology of Heart Failure Douglas L. Mann Overview, 541 Pathogenesis, 541 Heart Failure as a Progressive Model, 541 Neurohormonal Mechanisms, 541 Activation of the Sympathetic Nervous System, 542 Activation of the Renin-Angiotensin System, 542 Neurohormonal Alterations of Renal Function, 544 Neurohormonal Alterations in the Peripheral Vasculature, 547 Left Ventricular Remodeling, 549 Alterations in Cardiac Myocyte Biology, 549 Alterations in the Myocardium, 553 Alterations in the Left Ventricular Structure, 557 Reversibility of Left Ventricular Remodeling (Myocardial Recovery), 559 Future Directions, 559 References, 560

OVERVIEW Despite repeated attempts to develop a unifying hypothesis that describes the clinical syndrome of heart failure (HF), no single conceptual paradigm has withstood the test 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 HF. Although clinicians initially viewed HF as a problem of excessive salt and water retention that was caused by abnormalities of renal blood flow (the “cardiorenal model” [1] ), as they began to perform careful hemodynamic measurements, it also became apparent that HF 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 HF, [1] wherein HF 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 HF explained the excessive salt and water retention that HF patients experience, neither of these models explained the relentless “disease progression” that occurs in this syndrome. Indeed, although the cardiorenal models provided the rational basis for the use of diuretics to control the volume status of patients with HF, and the cardiocirculatory model provided the rational basis for the use of inotropes and intravenous vasodilators to augment cardiac output, these therapeutic strategies have not prevented HF from progressing, nor have they led to prolonged life for patients with moderate to severe HF. On the basis of these arguments, it has become increasingly apparent that HF can no longer be defined in simple hemodynamic terms. Accordingly, in this chapter we focus on the molecular and cellular changes that underlie HF with depressed systolic function, with an emphasis on the role of neurohormonal activation and left ventricular (LV) remodeling as the primary determinants for disease progression in HF. The hemodynamic, contractile, and wall motion disorders in systolic HF are discussed in the chapters on echocardiography (see Chap 14 ), cardiac catheterization (see Chap 19 ), radionuclide imaging (see Chap 16 ), and the clinical assessment of the patients with HF (see Chap 23 ). The pathogenesis of HF with a normal ejection fraction is discussed elsewhere (see Chap 26 ).

21/10/2008 11:41 a.m.

CHAPTER 22 - Pathophysiology of Heart Failure from Libby: Braunwald...

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21/10/2008 11:41 a.m.