Lower Left Ventricular Ejection Time in MYBPC3 Variant Carriers with Overt or Subclinical Hypertrophic Cardiomyopathy

Figures

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  Figure 1. Graphic overview of the cohorts. Control group = healthy controls of the Hamburg cohort from the MOVE Study 15 ; pathogenic variant Class 4 or 5 = according to the American College of Medical Genetics and Genomics 18 standards and guidelines. LVH−, septum thickness <13 mm; LVH+, septum thickness ≥13 mm.

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  Figure 2. Left ventricular ejection time index (LVETI) in healthy controls and hypertrophic cardiomyopathy (HCM) patients in the discovery cohort. The patients were separated in groups with overt HCM [LVH+, interventricular septal diameter in diastole (IVSd) ≥13 mm] or subclinical HCM (LVH−, IVSd < 13 mm). The statistical significance was assessed by multivariate analysis of variance. A linear model was used for comparison between groups, adjusted for age, sex, left ventricular ejection fraction, IVSd and gradient at rest. Data are shown as median and 1.5 inter‐quartile range. LVH, left ventricular hypertrophy; MYBPC3, myosin‐binding protein C3 gene; MYH7, myosin heavy chain 7 gene; n, number of individuals. A P value <0.05 was considered statistically significant.

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  Figure 3. Left ventricular ejection time index (LVETI) in healthy controls and hypertrophic cardiomyopathy (HCM) patients in the validation cohort. The participants of the VANISH trial were separated in groups with overt HCM [LVH+, interventricular septal diameter in diastole (IVSd) ≥13 mm] or subclinical HCM (LVH−, IVSd < 13 mm). The statistical significance was assessed by multivariate analysis of variance. A linear model was used for comparison between groups, adjusted for age, sex, left ventricular ejection fraction, IVSd and gradient at rest. Data are shown as median and 1.5 inter‐quartile range. LVH, left ventricular hypertrophy; MYBPC3, myosin‐binding protein C3 gene; MYH7, myosin heavy chain 7 gene; n, number of individuals. A P value <0.05 was considered statistically significant.

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  Figure 4. Left ventricular ejection time index (LVETI) in healthy controls and hypertrophic cardiomyopathy (HCM) patients in the pooled cohort. The patients were separated in groups with overt HCM [LVH+, interventricular septal diameter in diastole (IVSd) ≥13 mm] or subclinical HCM (LVH−, IVSd < 13 mm). The statistical significance was assessed by multivariate analysis of variance. A linear model was used for comparison between groups, adjusted for age, sex, left ventricular ejection fraction, IVSd and gradient at rest. Data are shown as median and 1.5 inter‐quartile range. LVH, left ventricular hypertrophy; MYBPC3, myosin‐binding protein C3 gene; MYH7, myosin heavy chain 7 gene; n, number of individuals. A P value <0.05 was considered statistically significant.

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  Figure 5. Left ventricular ejection time index (LVETI) in healthy controls and patients with truncating and non‐truncating myosin‐binding protein C3 gene (MYBPC3) variants in pooled cohort. The patients were separated in groups with truncating and non‐truncating variants. The statistical significance was assessed by multivariate analysis of variance. A linear model was used for comparison between groups, adjusted for age, sex, left ventricular ejection fraction, interventricular septal diameter in diastole and gradient at rest. Data are shown as median and 1.5 inter‐quartile range. LVH, left ventricular hypertrophy; MYH7, myosin heavy chain 7 gene; n, number of individuals. A P value <0.05 was considered statistically significant.