Longitudinal Strain Reflects Ventriculoarterial Coupling Rather Than Mere Contractility in Rat Models of Hemodynamic Overload–Induced Heart Failure

Abstract

Background: 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). Methods: 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 [E a ]), and VAC (E a /ESPVR). Preload was evaluated by meridional end-diastolic wall stress. Speckle-tracking echocardiography was performed to assess LS. Results: The TAC group presented with maintained ESPVR, increased E a , and enhanced meridional enddiastolic wall stress. In contrast, the ACF group was characterized by reduced ESPVR, decreased E a , and enhanced meridional end-diastolic wall stress. VAC increased in both HF groups. Furthermore, LS was also impaired in both HF models (À5.9 6 0.6% vs À12.9 6 0.5%, TAC vs Sham t [P < .001], and À11.7 6 0.7% vs À13.5 6 0.4%, ACF vs Sham a [P = .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). Conclusions: Under pathophysiologic conditions when both contractility and afterload become altered, LS reflects VAC rather than mere contractility.

Myocardial work index: a marker of left ventricular contractility in pressure‐ or volume overload‐induced heart failure

“…In a recent publication of our research group, we have demonstrated that GLS does not correlate with LV contractility indices in rat models of VO-induced and PO-induced HF, rather reflecting VAC. 9 Therefore, GLS carries similar shortcomings to the conventional measures of LV function with its considerable load sensitivity.…”

“…However, several studies have demonstrated that STE‐derived strain parameters are significantly influenced by loading conditions 7,8 . In a recent study by our research group using rat models of pressure (PO)‐induced and volume overload (VO)‐induced heart failure (HF), GLS did not show a relationship with LV contractility, rather reflecting ventriculo‐arterial coupling (VAC) 9 . These observations substantially affect the interpretation of deformation parameters in haemodynamic overload states of the LV.…”

Left Ventricular SGLT1 Protein Expression Correlates with the Extent of Myocardial Nitro-Oxidative Stress in Rats with Pressure and Volume Overload-Induced Heart Failure

“…Six-week-old (150–200 g) male Wistar rats underwent shunting of the abdominal aorta and the inferior vena cava to induce chronic progressive volume overload for 24 weeks resulting in HF, as described earlier [ 10 , 11 ]. Briefly, anesthesia was induced by placing the animals in a chamber filled with 5% isoflurane.…”

“…The Vivid I (GE Healthcare, Waukesha, WI, USA) echocardiographic imaging system equipped with the GE 12L-RS linear transducer (13 MHz) was used to non-invasively assess the temporal alterations in LV structure and function [ 10 , 11 ]. Prior to measurements, rats were anesthetized in a chamber with 5% isoflurane, then anesthesia was maintained by inhalation of 2% isoflurane (mixed in pure oxygen) from an insulated facemask, while placing the rats in a supine position on a controlled heating pad (maintaining core temperature at 37 ± 0.5 °C throughout the measurements).…”

Geometrical remodeling of the mitral and tricuspid annuli in response to exercise training: a 3-D echocardiographic study in elite athletes

“…Athletes with MR showed tendentially higher LV volumes; significantly higher LV GLS, LAVi max , and RAVi max ; and significantly lower RA total emptying fraction than athletes with no MR. Although such mild MR (assessed during resting conditions) certainly cannot be considered a hemodynamically relevant stimulus, these observations refer to what can be seen in the case of pathological LV volume overload (18,19). These findings can originate in two ways: 1) an athlete with a predisposition to a more pronounced exercise-induced chamber dilation may also be more prone to higher MA dimensions and a consequential MR, and 2) there is an inherent anatomical cause of the MR that may significantly increase during exercise, resulting in more excessive cardiac remodeling.…”