What causes hypertensive dilated cardiomyopathy?

Updated: Nov 28, 2018
  • Author: Vinh Q Nguyen, MD, FACC; Chief Editor: Gyanendra K Sharma, MD, FACC, FASE  more...
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The classic paradigm of hypertensive heart disease involves concentric left ventricular hypertrophy (LVH) as a mechanism to curtail wall stress, as demonstrated by LaPlace’s Law. As the disease progresses (“transition to failure”), the LV dilates and LVEF declines in what is described as a “burned out” LV (eccentric remodeling). This stepwise evolution of the hypertensive heart has been challenged such that progression to concentric versus eccentric remodeling is not set, and that the tendency toward one or the other remains uncertain. However, certain factors such as ethnicity (African Americans), female sex, and increased age have a disposition for the development of a concentric response, whereas obesity and lower plasma renin activity are predisposed to eccentric response. Furthermore, the “transition to failure” phase in which the concentric myocardium with intact LVEF progresses to eccentric myocardium with impaired LVEF is uncommon in the absence of myocardial infarction. [17]

The development from asymptomatic LV systolic dysfunction to symptomatic heart failure (Stage B to C) is not completely understood. However, a number of factors appear to govern this transition. First, the transition to decompensation is accelerated by degree of depressed ejection fraction. [18]  As cardiac function worsens, compensating mechanisms such as enhanced salt and water retention, increased peripheral vasoconstriction, and increased sympathetic response add further insult and accelerate the development of a decompensated state. The accompanying myocardial remodeling is characterized by fibrosis and LV dilation, with LV geometry taking a less efficient spherical shape, and reduced systolic function is consider to play major roles ushering the development of the symptomatic state.

Also noteworthy is the progression of the hypertensive heart with concentric hypertrophy with normal (preserved) ejection fraction (HFpEF) to a symptomatic state. Although the exact mechanism is not well understood, evidence suggests that collagen deposition and titin impact adverse changes in myocardial compliance. [18, 19]  Other factors that have been postulated to herald the development of clinical heart failure include increased mineralocorticoid receptor activation [20]  and levels of matrix metalloproteinases (MMPs) and tissue inhibitors of MMPs. [21]  Finally, the increased filling pressure is most intertwined with the development of symptomatic HFpEF.

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