Strain and strain rate by speckle-tracking echocardiography correlate with pressure-volume loop-derived contractility indices in a rat model of athlete's heart

Abstract

function is considered to be precisely measurable only by invasive hemodynamics. We aimed to correlate strain values measured by speckle-tracking echocardiography (STE) with sensitive contractility parameters of pressure-volume (P-V) analysis in a rat model of exercise-induced left ventricular (LV) hypertrophy. LV hypertrophy was induced in rats by swim training and was compared with untrained controls. Echocardiography was performed using a 13-MHz linear transducer to obtain LV long-and short-axis recordings for STE analysis (GE EchoPAC). Global longitudinal (GLS) and circumferential strain (GCS) and longitudinal (LSr) and circumferential systolic strain rate (CSr) were measured. LV P-V analysis was performed using a pressure-conductance microcatheter, and load-independent contractility indices [slope of the end-systolic P-V relationship (ESPVR), preload recruitable stroke work (PRSW), and maximal dP/dt-enddiastolic volume relationship (dP/dtmax-EDV)] were calculated. Trained rats had increased LV mass index (trained vs. control; 2.76 Ϯ 0.07 vs. 2.14 Ϯ 0.05 g/kg, P Ͻ 0.001). P-V loop-derived contractility parameters were significantly improved in the trained group (ESPVR: 3.58 Ϯ 0.22 vs. 2.51 Ϯ 0.11 mmHg/ l; PRSW: 131 Ϯ 4 vs. 104 Ϯ 2 mmHg, P Ͻ 0.01). Strain and strain rate parameters were also supernormal in trained rats (GLS: Ϫ18.8 Ϯ 0.3 vs. Ϫ15.8 Ϯ 0.4%; LSr: Ϫ5.0 Ϯ 0.2 vs. Ϫ4.1 Ϯ 0.1 Hz; GCS: Ϫ18.9 Ϯ 0.8 vs. Ϫ14.9 Ϯ 0.6%; CSr: Ϫ4.9 Ϯ 0.2 vs. Ϫ3.8 Ϯ 0.2 Hz, P Ͻ 0.01). ESPVR correlated with GLS (r ϭ Ϫ0.71) and LSr (r ϭ Ϫ0.53) and robustly with GCS (r ϭ Ϫ0.83) and CSr (r ϭ Ϫ0.75, all P Ͻ 0.05). PRSW was strongly related to GLS (r ϭ Ϫ0.64) and LSr (r ϭ Ϫ0.71, both P Ͻ 0.01). STE can be a feasible and useful method for animal experiments. In our rat model, strain and strain rate parameters closely reflected the improvement in intrinsic contractile function induced by exercise training. speckle-tracking echocardiography; pressure-volume analysis; athlete's heart; contractility; strain LONG-TERM EXERCISE TRAINING induces physiological left ventricular (LV) hypertrophy, a molecular and cellular growth process of the heart in response to altered loading conditions (6). In contrast to pathological hypertrophy, this adaptation leads to maintained or even enhanced cardiac function (2, 14). Hemodynamic changes of exercise-induced hypertrophy were characterized by our research group in a rat model, focusing also on the improved LV inotropic state (23). Contractility is the intrinsic ability of the myocardium to generate force and to shorten independently of changes in preload or afterload with fixed heart rates. In the past few decades, efforts have been made to transfer the physiological concept of contractility to the intact beating heart (4).Pressure-volume (P-V) analysis recently became the gold standard to investigate in vivo hemodynamics in animal models. During preload reduction maneuvers such as gradual occlusion of vena cava inferior, load-independent indices of myocardial contractility could be obtained (20). Th...

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