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Left ventricular systolic function changes in hypertrophic cardiomyopathy patients detected by the strain of different myocardium layers and longitudinal rotation.

ABSTRACT: Impairment of left ventricular (LV) longitudinal function has an important role in hypertrophic cardiomyopathy (HCM). This research investigated an association between the longitudinal strain of different myocardial layers, longitudinal rotation and the LV systolic function of HCM patients.The research was performed on 36 HCM patients and 36 healthy subjects. The peak systolic longitudinal strain of the subendocardial, midmyocardial, and subepicardial layers was measured using 2-dimensional speckle tracking echocardiography (2D-STE). The apical long-axis and 4- and 2- chamber views were acquired via 2D Doppler echocardiography. The curve of the longitudinal rotation was traced at 17 timepoints in the analysis of 2 cardiac cycles.Compared with healthy subjects, in HCM patients regional LV peak systolic longitudinal strain was less, not only in hypertrophied LV myocardium, but also in non-hypertrophied myocardium. The rotational degrees of the midmyocardial-septal, apex, and lateral wall of HCM patients were significantly different from that of normal subjects, as follows. In HCM patients, clockwise longitudinal rotation was found. The interventricular septum thickness at end-diastole positively correlated with the peak longitudinal systolic strain of the subendocardial, the midmyocardial, and the subepicardial layers. The area under ROC curve values for subendocardial, midmyocardial and subepicardial layers in HCM patients were 0.923, 0.938, 0.948.In HCM patients, the longitudinal function was damaged, even with normal LV ejection fraction. The peak longitudinal systolic strain of the subendocardial, midmyocardial, and subepicardial layers, and the longitudinal rotation detected by 2D-STE, are very sensitive predictors of systolic function in patients with HCM.

SUBMITTER: Huang J

PROVIDER: S-EPMC5541417 | biostudies-other | 2017 Aug

REPOSITORIES: biostudies-other

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Project description:BackgroundThe term "end stage" has been used to describe hypertrophic cardiomyopathy (HCM) with left ventricular systolic dysfunction (LVSD), defined as occurring when left ventricular ejection fraction is <50%. The prognosis of HCM-LVSD has reportedly been poor, but because of its relative rarity, the natural history remains incompletely characterized.MethodsData from 11 high-volume HCM specialty centers making up the international SHaRe Registry (Sarcomeric Human Cardiomyopathy Registry) were used to describe the natural history of patients with HCM-LVSD. Cox proportional hazards models were used to identify predictors of prognosis and incident development.ResultsFrom a cohort of 6793 patients with HCM, 553 (8%) met the criteria for HCM-LVSD. Overall, 75% of patients with HCM-LVSD experienced clinically relevant events, and 35% met the composite outcome (all-cause death [n=128], cardiac transplantation [n=55], or left ventricular assist device implantation [n=9]). After recognition of HCM-LVSD, the median time to composite outcome was 8.4 years. However, there was substantial individual variation in natural history. Significant predictors of the composite outcome included the presence of multiple pathogenic/likely pathogenic sarcomeric variants (hazard ratio [HR], 5.6 [95% CI, 2.3-13.5]), atrial fibrillation (HR, 2.6 [95% CI, 1.7-3.5]), and left ventricular ejection fraction <35% (HR, 2.0 [95% CI, 1.3-2.8]). The incidence of new HCM-LVSD was ?7.5% over 15 years. Significant predictors of developing incident HCM-LVSD included greater left ventricular cavity size (HR, 1.1 [95% CI, 1.0-1.3] and wall thickness (HR, 1.3 [95% CI, 1.1-1.4]), left ventricular ejection fraction of 50% to 60% (HR, 1.8 [95% CI, 1.2, 2.8]-2.8 [95% CI, 1.8-4.2]) at baseline evaluation, the presence of late gadolinium enhancement on cardiac magnetic resonance imaging (HR, 2.3 [95% CI, 1.0-4.9]), and the presence of a pathogenic/likely pathogenic sarcomeric variant, particularly in thin filament genes (HR, 1.5 [95% CI, 1.0-2.1] and 2.5 [95% CI, 1.2-5.1], respectively).ConclusionsHCM-LVSD affects ?8% of patients with HCM. Although the natural history of HCM-LVSD was variable, 75% of patients experienced adverse events, including 35% experiencing a death equivalent an estimated median time of 8.4 years after developing systolic dysfunction. In addition to clinical features, genetic substrate appears to play a role in both prognosis (multiple sarcomeric variants) and the risk for incident development of HCM-LVSD (thin filament variants).

Project description:BackgroundThe peak velocity of early diastolic mitral annular motion (e`) is believed to provide sensitive detection of left ventricular (LV) diastolic dysfunction in hypertrophic cardiomyopathy (HCM), but other aspects of LV long-axis function in HCM have received less attention. Systolic mitral annular excursion (SExc) is also reduced in HCM and must be an intrinsic limitation to the extent of the subsequent motion during diastole. However, the effects of HCM on excursion during early diastole (EDExc) and atrial contraction (AExc), the duration of early diastolic motion (EDDur), and the relationships of EDExc with SExc, and of e`with EDExc and EDDur, are all unknown.MethodsThe study group was 22 subjects with HCM and there were 22 age and sex matched control subjects. SExc, EDExc, e`, AExc and EDDur were measured from pulsed wave tissue Doppler signals acquired from the septal and lateral walls. In the combined group of HCM and control subjects, multivariate analyses were performed to identify independent predictors of EDExc and e`for both LV walls.ResultsSExc, EDExc and e`were all lower, and EDDur was longer in the HCM group compared to the control group for both LV walls (p<0.05 for all). In contrast, AExc was lower for the septal wall in the HCM group (p<0.05), but not different between the groups for the lateral wall. In regression analyses of the combined group, EDExc was positively correlated with SExc, and SExc explained 57-86% of the variances in septal and lateral EDExc, e`was positively correlated with EDExc, and EDExc explained 58-68% of the variances of e`, whereas the combination of EDExc with EDDur explained 87-92% of the variances in e`. A diagnosis of HCM was not an independent predictor of EDExc when in combination with SExc, but was a minor contributor to the prediction of e`in combination with EDExc and EDDur.ConclusionIn HCM, the decrease in LV longitudinal contraction is the major mechanism accounting for a lower EDExc, the lower e`is accounted for by contributions from the lower EDExc and prolongation of early diastolic motion, and there is no atrial compensation for the reduction of long-axis contraction.

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Left ventricular systolic function changes in hypertrophic cardiomyopathy patients detected by the strain of different myocardium layers and longitudinal rotation.

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