RT Journal Article
SR Electronic
T1 The pathophysiology of hypertensive acute heart failure
JF Heart
JO Heart
FD BMJ Publishing Group Ltd and British Cardiovascular Society
SP 1861
OP 1867
DO 10.1136/heartjnl-2015-307461
VO 101
IS 23
A1 David M Viau
A1 Javier A Sala-Mercado
A1 Marty D Spranger
A1 Donal S O'Leary
A1 Phillip D Levy
YR 2015
UL http://heart.bmj.com/content/101/23/1861.abstract
AB 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.