Myocardial Constructive Work Research Articles

Myocardial constructive work is impaired in hypertrophic cardiomyopathy and predicts left ventricular fibrosis.

The estimation of myocardial work by pressure strain loops (PSLs) is a totally new non-invasive approach to assess myocardial performance, and its role in patients with hypertrophic cardiomyopathy is unknown. The aims of the present study are therefore: (a) to compare myocardial work in patients with non-obstructive hypertrophic cardiomyopathy (HCM) and in a subset of age-matched healthy controls and (b) to assess the correlation between myocardial work and left ventricular (LV) fibrosis. Eighty-two patients with non-obstructive HCM (58±14years) and 20 age-matched healthy subjects (58±7years, P=0.99) underwent standard and speckle-tracking echocardiography to assess myocardial dimensions and deformation parameters. PSLs analysis was used to estimate global myocardial constructive work (GCW) and wasted work (GWW). LV fibrosis was estimated at cardiac magnetic resonance (CMR) by qualitative assessment of late gadolinium enhancement (LGE), and significant fibrosis was defined as LGE in ≥2 LV segments. Global constructive work (1599±423 vs 2248±249mmHg%, P<0.0001) was significantly reduced in HCM compared to the control group. No difference was observed in GWW (141±125 vs 101±88mmHg%, P=0.18) and LV ejection fraction (LVEF) (63±13 vs 66±4% P=0.17) between the two groups. In HCM, GCW was the only predictor of LV fibrosis at multivariable analysis (OR 1.01, 95% CI: 0.99-1.08, P=0.04). A cutoff value of 1623mmHg% (AUC 0.80, 95% CI: 0.66-0.93, P<0.0001) was able to predict myocardial fibrosis with a good sensitivity and fair specificity (82% and 67%, respectively). Global constructive work is significantly reduced in HCM despite normal LVEF and is associated with the LV fibrosis as assessed by LGE.

Role of myocardial constructive work in the identification of responders to CRT.

Cardiac resynchronization therapy (CRT) plays a pivotal role in the management of patients with heart failure (HF) and wide QRS complex. However, the treatment is plagued by numerous non-responders. Aim of the study is to evaluate the role myocardial work estimated by pressure-strain loops (PSLs) in the comprehension of physiological mechanisms associated with CRT and in the prediction of CRT response. Ninety-seven patients with symptomatic HF (ejection fraction: 27 ± 6%, QRS duration 164 ± 18 ms) undergoing CRT implantation according to current recommendations were retrospectively included in the study. Standard 2D and speckle tracking echocardiography were performed before CRT and at the 6-month follow-up (FU). PSL analysis allowed the calculation of global and regional myocardial constructive work (CW) and wasted work (WW). A > 15% reduction in left ventricular (LV) end-systolic volume at FU defined CRT-positive response (CRT-PR). At FU, 63 (65%) patients responded to CRT. Global CW (CWtot) was significantly increased in CRT-responders. At multivariate analysis, CWtot > 1057 mmHg% (OR 14.69, P = 0.005) and septal flash (OR 8.05, P = 0.004) were the only significant predictors of CRT-PR. CWtot was associated with the entity of CRT-induced myocardial remodelling in both ischaemic (r = -0.55, P < 0.0001) and non-ischaemic patients (r = 0.65, P < 0.0001). A CWtot < 1057 mmHg% identified 85% of non-responders with a positive predictive value of 88%. Patients with higher CWtot exhibit a favourable response to CRT. These data encourage further studies for the assessment of the myocardial substrate related to the functional response to CRT.