At the organ level, affected individuals may have concentric remodeling with or without hypertrophy, although many people have normal ventricular geometry. Recent histologic studies have shown reductions in myocardial capillary density that may contribute. PathophysiologyĪt a cellular level, cardiac myocytes in patients with HFpEF are thicker and shorter than normal myocytes, and collagen content is increased. Frequently, these abnormalities are noted only when the circulatory system is stressed. Ventricular diastolic and systolic reserve abnormalities, chronotropic incompetence, stiffening of ventricular tissue, atrial dysfunction, pulmonary hypertension, impaired vasodilation, and endothelial dysfunction are all implicated. Historically, HFpEF was termed diastolic heart failure however, recent investigations suggest a more complex and heterogeneous pathophysiology. Hypertension in particular is a strong risk factor 80 to 90 percent of patients with HFpEF are hypertensive. The interaction between risk factors, cardiac aging and loss of cardiovascular reserve, which results in the development of symptomatic HFpEF. Interaction of factors resulting in symptomatic HFpEF
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