title: The pathophysiology of hypertensive acute heart failure.
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.
authors.affiliation: Department of Emergency Medicine, Wayne State University School of Medicine, Detroit, Michigan, USA Department of Physiology, Wayne State University School of Medicine, Detroit, Michigan, USA.
authors.forename: David M
authors.initials: DM
authors.lastname: Viau
authors.affiliation: Department of Physiology, Wayne State University School of Medicine, Detroit, Michigan, USA Cardiovascular Research Institute, Wayne State University School of Medicine, Detroit, Michigan, USA.
authors.forename: Javier A
authors.initials: JA
authors.lastname: Sala-Mercado
authors.affiliation: Department of Physiology, Wayne State University School of Medicine, Detroit, Michigan, USA Cardiovascular Research Institute, Wayne State University School of Medicine, Detroit, Michigan, USA.
authors.forename: Marty D
authors.initials: MD
authors.lastname: Spranger
authors.affiliation: Department of Physiology, Wayne State University School of Medicine, Detroit, Michigan, USA Cardiovascular Research Institute, Wayne State University School of Medicine, Detroit, Michigan, USA.
authors.forename: Donal S
authors.initials: DS
authors.lastname: O'Leary
authors.affiliation: Department of Emergency Medicine, Wayne State University School of Medicine, Detroit, Michigan, USA Department of Physiology, Wayne State University School of Medicine, Detroit, Michigan, USA Cardiovascular Research Institute, Wayne State University School of Medicine, Detroit, Michigan, USA.
authors.forename: Phillip D
authors.initials: PD
authors.lastname: Levy
mesh_terms: D000208:Acute Disease; D015984:Causality; D006333:Heart Failure / Q000453:epidemiology / Q000209:etiology / Q000503:physiopathology / Q000517:prevention & control; D006439:Hemodynamics / Q000187:drug effects*; D006801:Humans; D006973:Hypertension / Q000150:complications / Q000188:drug therapy / Q000503:physiopathology; D054539:Medication Therapy Management; D018487:Ventricular Dysfunction, Left / Q000503:physiopathology