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

Abstract

Aims While global longitudinal strain (GLS) is considered to be a sensitive marker of left ventricular (LV) function, it is significantly influenced by loading conditions. We hypothesized that global myocardial work index (GMWI), a novel marker of LV function, may show better correlation with load-independent markers of LV contractility in rat models of pressure-induced or volume overload-induced heart failure. Methods and results Male Wistar rats underwent either transverse aortic constriction (TAC; n = 12) or aortocaval fistula creation (ACF; n = 12), inducing LV pressure or volume overload, respectively. Sham procedures were performed to establish control groups (n = 12/12). Echocardiographic loops were obtained to determine GLS and GMWI. Pressure-volume analysis with transient occlusion of the inferior caval vein was carried out to calculate preload recruitable stroke work (PRSW), a load-independent 'gold-standard' parameter of LV contractility. Myocardial samples were collected to assess interstitial and perivascular fibrosis area and also myocardial atrial-type natriuretic peptide (ANP) and brain-type natriuretic peptide (BNP) relative mRNA expression. Compared with controls, GLS was substantially lower in the TAC group (À7.0 ± 2.8 vs. À14.5 ± 2.5%; P < 0.001) and was only mildly reduced in the ACF group (À13.2 ± 2.4 vs. À15.4 ± 2.0%, P < 0.05). In contrast with these findings,

Regional Myocardial Work Measured by Echocardiography for the Detection of Myocardial Ischemic Segments: A Comparative Study With Invasive Fractional Flow Reserve

“…In contrast, MWI and MCW showed relatively good specificities (63.6–72.7%) in single-vessel stenosis group for identifying LV segments perfused by vessels with an FFR ≤ 0.75. This may partly be due to MW being used to assess the myocardial contraction in the context of afterload, which makes it less load-dependent ( 34 ).…”

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).…”

Ca2+/calmodulin‐dependent protein kinase II and protein kinase G oxidation contributes to impaired sarcomeric proteins in hypertrophy model

“…Pathological and pathophysiological alterations have been reported in VO models. 1 , 31 Earlier, in compensated stages, alterations in myofilament Ca 2+ sensitivity, cross‐bridge cycling, and electromechanical coupling across the intercalated disc have been documented, 32 in addition to alterations in Ca 2+ cycling at the late stages of VO induced HF progression in rats, dogs, and humans. 32 , 33 , 34 , 35 However, the changes of sarcomeric proteins remain at end‐stage heart failure, even without a significant change in the amount of Ca 2+ available for contraction.…”