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The pathophysiology of hypertensive acute heart failure
  1. David M Viau1,2,
  2. Javier A Sala-Mercado2,3,
  3. Marty D Spranger2,3,
  4. Donal S O'Leary2,3,
  5. Phillip D Levy1,2,3
  1. 1Department of Emergency Medicine, Wayne State University School of Medicine, Detroit, Michigan, USA
  2. 2Department of Physiology, Wayne State University School of Medicine, Detroit, Michigan, USA
  3. 3Cardiovascular Research Institute, Wayne State University School of Medicine, Detroit, Michigan, USA
  1. Correspondence to Dr David Viau, Department of Emergency Medicine, Wayne State University School of Medicine, 4201 St. Antoine, Detroit, MI 48201, USA; dviau{at}med.wayne.edu

Abstract

While acute heart failure (AHF) is often regarded as a single disorder, an evolving understanding recognises the existence of multiple phenotypes with varied pathophysiological alterations. Herein we discuss hypertensive AHF and provide insight into a mechanism where acute fluid redistribution is caused by a disturbance in the ventricular–vascular coupling relationship. In this relationship, acute alterations in vascular elasticity, vasoconstriction and reflected pulse waves lead to increases in cardiac work and contribute to decompensated LV function with associated subendocardial ischaemia and end-organ damage. Chronic predisposing factors (neurohormonal activity, nitric oxide insensitivity, arterial stiffening) and physiological stressors (sympathetic surge, volume overload, physical exertion) that are causally linked to acute symptom onset are discussed. Lastly, we review treatment options including both nitrovasodilators and promising novel therapeutics, and discuss future directions in the management of this phenotypic variant.

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