Longitudinal strain correlated with ventriculoarterial coupling (R=0.654, P<0.001) but not with contractility (R=0.058, P=0.668) in rat models of overload-induced heart failure.
Does longitudinal strain reflect ventriculoarterial coupling rather than mere contractility in rat models of hemodynamic overload-induced heart failure?
In rat models of hemodynamic overload-induced heart failure, longitudinal strain reflects ventriculoarterial coupling rather than isolated myocardial contractility.
Tasa de eventos absoluta: 0% vs 0%
•LV contractility and afterload are both major determinants of LS and LSSr.•In hemodynamic overload–induced HF, contractility and afterload are both altered.•Thus, under these conditions, LS and LSSr reflect VAC rather than mere contractility. BackgroundLongitudinal strain (LS) is a sensitive marker of systolic function. Recent findings suggest that both myocardial contractility and loading conditions determine LS. The aim of this study was to investigate whether LS reflects the connection of cardiac contractility to afterload (termed ventriculoarterial coupling VAC) rather than mere contractility in rat models of hemodynamic overload–induced heart failure (HF).MethodsPressure overload–induced HF was evoked by transverse aortic constriction (TAC; n = 14). Volume overload–induced HF was established by an aortocaval fistula (ACF; n = 12). Age-matched sham-operated animals served as controls for TAC (n = 14) and ACF (n = 12), respectively. Pressure-volume analysis was carried out to compute contractility (slope of end-systolic pressure-volume relationship ESPVR), afterload (arterial elastance Ea), and VAC (Ea/ESPVR). Preload was evaluated by meridional end-diastolic wall stress. Speckle-tracking echocardiography was performed to assess LS.ResultsThe TAC group presented with maintained ESPVR, increased Ea, and enhanced meridional end-diastolic wall stress. In contrast, the ACF group was characterized by reduced ESPVR, decreased Ea, and enhanced meridional end-diastolic wall stress. VAC increased in both HF groups. Furthermore, LS was also impaired in both HF models (−5.9 ± 0.6% vs −12.9 ± 0.5%, TAC vs Shamt P < .001, and −11.7 ± 0.7% vs −13.5 ± 0.4%, ACF vs ShamaP = .048). Statistical analysis revealed that strain parameters were determined predominantly by afterload in the TAC group and by contractility in the ACF group, while preload had a minor effect. In the entire study population, LS showed a correlation with VAC (R = 0.654, P < .001) but not with ESPVR (R = 0.058, P = .668).ConclusionsUnder pathophysiologic conditions when both contractility and afterload become altered, LS reflects VAC rather than mere contractility. Longitudinal strain (LS) is a sensitive marker of systolic function. Recent findings suggest that both myocardial contractility and loading conditions determine LS. The aim of this study was to investigate whether LS reflects the connection of cardiac contractility to afterload (termed ventriculoarterial coupling VAC) rather than mere contractility in rat models of hemodynamic overload–induced heart failure (HF). Pressure overload–induced HF was evoked by transverse aortic constriction (TAC; n = 14). Volume overload–induced HF was established by an aortocaval fistula (ACF; n = 12). Age-matched sham-operated animals served as controls for TAC (n = 14) and ACF (n = 12), respectively. Pressure-volume analysis was carried out to compute contractility (slope of end-systolic pressure-volume relationship ESPVR), afterload (arterial elastance Ea), and VAC (Ea/ESPVR). Preload was evaluated by meridional end-diastolic wall stress. Speckle-tracking echocardiography was performed to assess LS. The TAC group presented with maintained ESPVR, increased Ea, and enhanced meridional end-diastolic wall stress. In contrast, the ACF group was characterized by reduced ESPVR, decreased Ea, and enhanced meridional end-diastolic wall stress. VAC increased in both HF groups. Furthermore, LS was also impaired in both HF models (−5.9 ± 0.6% vs −12.9 ± 0.5%, TAC vs Shamt P < .001, and −11.7 ± 0.7% vs −13.5 ± 0.4%, ACF vs ShamaP = .048). Statistical analysis revealed that strain parameters were determined predominantly by afterload in the TAC group and by contractility in the ACF group, while preload had a minor effect. In the entire study population, LS showed a correlation with VAC (R = 0.654, P < .001) but not with ESPVR (R = 0.058, P = .668). Under pathophysiologic conditions when both contractility and afterload become altered, LS reflects VAC rather than mere contractility.
Ruppert et al. (Fri,) reported a other. Longitudinal strain correlated with ventriculoarterial coupling (R=0.654, P<0.001) but not with contractility (R=0.058, P=0.668) in rat models of overload-induced heart failure.