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Left ventricular simulation of cardiac compression: Hemodynamics and regional mechanics.

ABSTRACT: Heart failure is a global epidemic. Left ventricular assist devices provide added cardiac output for severe cases but cause infection and thromboembolism. Proposed direct cardiac compression devices eliminate blood contacting surfaces, but no group has optimized the balance between hemodynamic benefit and excessive ventricular wall strains and stresses. Here, we use left ventricular simulations to apply compressions and analyze hemodynamics as well as regional wall mechanics. This axisymmetric model corresponds with current symmetric bench prototypes. At nominal pressures of 3.1 kPa applied over the epicardial compression zone, hemodynamics improved substantially. Ejection fraction changed from 17.6% at baseline to 30.3% with compression and stroke work nearly doubled. Parametric studies were conducted by increasing and decreasing applied pressures; ejection fraction, peak pressure, and stroke work increased linearly with changes in applied compression. End-systolic volume decreased substantially. Regional mechanics analysis showed principal stress increases at the endocardium, in the middle of the compression region. Principal strains remained unchanged or increased moderately with nominal compression. However, at maximum applied compression, stresses and strains increased substantially providing potential constraints on allowable compressions. These results demonstrate a framework for analysis and optimization of cardiac compression as a prelude to biventricular simulations and subsequent animal experiments.

SUBMITTER: Aranda-Michel E

PROVIDER: S-EPMC6822737 | biostudies-literature | 2019

REPOSITORIES: biostudies-literature

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Left ventricular simulation of cardiac compression: Hemodynamics and regional mechanics.

Aranda-Michel Edgar E Waldman Lewis K LK Trumble Dennis R DR

PloS one 20191031 10

Heart failure is a global epidemic. Left ventricular assist devices provide added cardiac output for severe cases but cause infection and thromboembolism. Proposed direct cardiac compression devices eliminate blood contacting surfaces, but no group has optimized the balance between hemodynamic benefit and excessive ventricular wall strains and stresses. Here, we use left ventricular simulations to apply compressions and analyze hemodynamics as well as regional wall mechanics. This axisymmetric m ...[more]

PMID: 31671155

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Project description:Left ventricular (LV) twist mechanics differ between men and women during acute physiological stress, which may be partly mediated by sex differences in autonomic control. While men appear to have greater adrenergic control of LV twist, the potential contribution of vagal modulation to sex differences in LV twist remains unknown. Therefore, the present study examined the role of vagal control on sex differences in LV twist during graded lower body negative pressure (LBNP) and supine cycling. On two separate visits, LV mechanics were assessed using two-dimensional speckle-tracking echocardiography in 18 men (22?±?2 yr) and 17 women (21?±?4 yr) during -40- and -60-mmHg LBNP and 25% and 50% of peak supine cycling workload with and without glycopyrrolate (vagal blockade). LV twist was not different at baseline but was greater in women during -60 mmHg in both control (women: 16.0?±?3.4° and men: 12.9?±?2.3°, P = 0.004) and glycopyrrolate trials (women: 17.7?±?5.9° and men: 13.9?±?3.3°, P?< 0.001) due to greater apical rotation during control (women: 11.9?±?3.6° and men: 7.8?±?1.5°, P?< 0.001) and glycopyrrolate (women: 11.6?±?4.9° and men: 7.1?±?3.6°, P = 0.009). These sex differences in LV twist consistently coincided with a greater LV sphericity index (i.e., ellipsoid geometry) in women compared with men. In contrast, LV twist did not differ between the sexes during exercise with or without glycopyrrolate. In conclusion, women have augmented LV twist compared with men during large reductions to preload, even during vagal blockade. As such, differences in vagal control do not appear to contribute to sex differences in the LV twist responses to physiological stress, but they may be related to differences in ventricular geometry. NEW & NOTEWORTHY This is the first study to specifically examine the role of vagal autonomic control on sex-related differences in left ventricular (LV) mechanics. Contrary to our hypothesis, vagal control does not appear to primarily determine sex differences in LV mechanical or hemodynamic responses to acute physiological stress. Instead, differences in LV geometry may be a more important contributor to sex differences in LV mechanics.

Project description:Background Cardiac resynchronization therapy (CRT) restores ventricular synchrony and induces left ventricular (LV) reverse remodeling in patients with heart failure (HF) and dyssynchrony. However, 30% of treated patients are non-responders despite all efforts. Cardiac magnetic resonance imaging (CMR) can be used to quantify regional contributions to stroke volume (SV) as potential CRT predictors. The aim of this study was to determine if LV longitudinal (SVlong%), lateral (SVlat%), and septal (SVsept%) contributions to SV differ from healthy controls and investigate if these parameters can predict CRT response. Methods Sixty-five patients (19 women, 67 ± 9 years) with symptomatic HF (LVEF ≤ 35%) and broadened QRS (≥ 120 ms) underwent CMR. SVlong% was calculated as the volume encompassed by the atrioventricular plane displacement (AVPD) from end diastole (ED) to end systole (ES) divided by total SV. SVlat%, and SVsept% were calculated as the volume encompassed by radial contraction from ED to ES. Twenty age- and sex-matched healthy volunteers were used as controls. The regional measures were compared to outcome response defined as ≥ 15% decrease in echocardiographic LV end-systolic volume (LVESV) from pre- to 6-months post CRT (delta, Δ). Results AVPD and SVlong% were lower in patients compared to controls (8.3 ± 3.2 mm vs 15.3 ± 1.6 mm, P < 0.001; and 53 ± 18% vs 64 ± 8%, P < 0.01). SVsept% was lower (0 ± 15% vs 10 ± 4%, P < 0.01) with a higher SVlat% in the patient group (42 ± 16% vs 29 ± 7%, P < 0.01). There were no differences between responders and non-responders in neither SVlong% (P = 0.87), SVlat% (P = 0.09), nor SVsept% (P = 0.65). In patients with septal net motion towards the right ventricle (n = 28) ΔLVESV was − 18 ± 22% and with septal net motion towards the LV (n = 37) ΔLVESV was − 19 ± 23% (P = 0.96). Conclusions Longitudinal function, expressed as AVPD and longitudinal contribution to SV, is decreased in patients with HF scheduled for CRT. A larger lateral contribution to SV compensates for the abnormal septal systolic net movement. However, LV reverse remodeling could not be predicted by these regional contributors to SV.

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Left ventricular simulation of cardiac compression: Hemodynamics and regional mechanics.

Publications

Left ventricular simulation of cardiac compression: Hemodynamics and regional mechanics.

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