Literature Review: Pathophysiology of Heart Failure with Preserved Ejection Fraction.

Heart failure with preserved ejection fraction is a growing public health concern, a disease with poor health outcomes, and is showing increased prevalence globally. This review paper explores the literature with a focus on the pathophysiology and microbiology of preserved ejection fraction heart failure while drawing connections between preserved and reduced ejection fraction states. The discussion teases out the cellular level changes that affect the overall dysfunction of the cardiac tissue, including the clinical manifestations, microbiological changes (endothelial cells, fibroblasts, cardiomyocytes, and excitation-contraction coupling), and the burden of structural diastolic dysfunction. The goal of this review is to summarize the pathophysiological disease state of heart failure with preserved ejection fraction to enhance understanding, knowledge, current treatment models of this pathology.

Calculation of Mitral Valve Area by Continuity Equation Using Velocity-Time Integral From Mitral Valve Orifices After Mitral Clip.

BACKGROUND: This study investigates the hemodynamics of a dual-orifice mitral valve after mitral valve clip closure (MVCC) in patients with functional and nonfunctional mitral regurgitation (MR). If inflow velocity-time integral (VTi) of both orifices is equal, then the standard continuity equation can be applied to calculate the total mitral valve area (MVA). METHODS AND RESULTS: Adults undergoing MVCC placement were prospectively enrolled. With transesophageal echocardiography (TEE), the vena contracta (VC) of the medial and lateral mitral valve (MV) orifices were determined using color-flow Doppler and dual MV orifice areas were calculated. Valve orifices were classified as large vs small based on VC diameters. Continuous-wave Doppler measurements from both orifices were obtained. Forty-nine patients with severe MR (functional, n = 18) were enrolled. The VTi, mean gradient, peak gradient, and mean velocity of the larger vs smaller orifice were not significantly different, irrespective of MR etiology (P=nonsignificant). There was no difference in these parameters between large and small orifice regardless of MR mechanism (P=nonsignificant). There were no differences in the means of MVA as derived from either large or small VTi-derived and VC-derived areas (P=nonsignificant). CONCLUSIONS: Mitral valve inflow hemodynamics were the same regardless of the size differences between the large and small orifices. Therefore, total MVA can be calculated using the continuity equation in patients irrespective of MR mechanism. This allows for a derivation of total MVA at the time of MVCC placement to evaluate for mitral stenosis.