Abstract
The 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. The 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. SExc, 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. In 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.
Highlights
Hypertrophic cardiomyopathy (HCM) is a heritable heart disease, in which the classical phenotype is of myocardial hypertrophy occurring independently of an increase in afterload [1]
systolic excursion (SExc), EDExc and e‘were all lower, and early diastolic duration (EDDur) was longer in the HCM group compared to the control group for both left ventricular (LV) walls (p
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‘
Summary
Hypertrophic cardiomyopathy (HCM) is a heritable heart disease, in which the classical phenotype is of myocardial hypertrophy occurring independently of an increase in afterload [1]. A lower systolic peak velocity of mitral annular motion (s‘) using tissue Doppler imaging (TDI) in HCM subjects with the classical phenotype was first described in 2001 [3], and confirmed in subsequent studies [4,5,6]. Other abnormalities of systolic long-axis function reported in HCM include reduced mitral annular systolic excursion (SExc) [7] and prolonged systolic time intervals [5]. The 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. 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
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.