Heart Failure With Preserved Ejection Fraction: Is it Due to Contractile Dysfunction?

MacIver, David H.

doi:10.1253/circj.cj-09-0190

Cited by 1 publication

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References 10 publications

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“…In clinical conditions, several factors contribute to the development of HFpEF (Bench et al, 2009; Shah and Solomon, 2012; Sengupta and Marwick, 2018). These factors include abnormalities in both the systolic and the diastolic mechanics of the LV (MacIver and Townsend, 2008; MacIver, 2009; Shah and Solomon, 2012), the LV hypertrophy and geometric changes (Aurigemma et al, 1995; Vasan et al, 1999; Adeniran et al, 2015) and material properties of the LV (stiffness). A recent study employed computational models with heterogeneous transmural distributions of T max (Wang et al, 2016).…”

Section: Discussionmentioning

confidence: 99%

Relationship of Transmural Variations in Myofiber Contractility to Left Ventricular Ejection Fraction: Implications for Modeling Heart Failure Phenotype With Preserved Ejection Fraction

et al. 2018

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The pathophysiological mechanisms underlying preserved left ventricular (LV) ejection fraction (EF) in patients with heart failure and preserved ejection fraction (HFpEF) remain incompletely understood. We hypothesized that transmural variations in myofiber contractility with existence of subendocardial dysfunction and compensatory increased subepicardial contractility may underlie preservation of LVEF in patients with HFpEF. We quantified alterations in myocardial function in a mathematical model of the human LV that is based on the finite element method. The fiber-reinforced material formulation of the myocardium included passive and active properties. The passive material properties were determined such that the diastolic pressure-volume behavior of the LV was similar to that shown in published clinical studies of pressure-volume curves. To examine changes in active properties, we considered six scenarios: (1) normal properties throughout the LV wall; (2) decreased myocardial contractility in the subendocardium; (3) increased myocardial contractility in the subepicardium; (4) myocardial contractility decreased equally in all layers, (5) myocardial contractility decreased in the midmyocardium and subepicardium, (6) myocardial contractility decreased in the subepicardium. Our results indicate that decreased subendocardial contractility reduced LVEF from 53.2 to 40.5%. Increased contractility in the subepicardium recovered LVEF from 40.5 to 53.2%. Decreased contractility transmurally reduced LVEF and could not be recovered if subepicardial and midmyocardial contractility remained depressed. The computational results simulating the effects of transmural alterations in the ventricular tissue replicate the phenotypic patterns of LV dysfunction observed in clinical practice. In particular, data for LVEF, strain and displacement are consistent with previous clinical observations in patients with HFpEF, and substantiate the hypothesis that increased subepicardial contractility may compensate for subendocardial dysfunction and play a vital role in maintaining LVEF.

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