scholarly journals Biventricular pacemaker therapy improves exercise capacity in patients with non‐obstructive hypertrophic cardiomyopathy via augmented diastolic filling on exercise

2020 ◽  
Vol 22 (7) ◽  
pp. 1263-1272 ◽  
Author(s):  
Ibrar Ahmed ◽  
Brodie L. Loudon ◽  
Khalid Abozguia ◽  
Donnie Cameron ◽  
Ganesh N. Shivu ◽  
...  
Keyword(s):  
Hypertrophic Cardiomyopathy ◽  
Exercise Capacity ◽  
Diastolic Filling ◽  
Pacemaker Therapy ◽  
Biventricular Pacemaker ◽  
Obstructive Hypertrophic Cardiomyopathy

Abstract 4344: Biventricular Pacemaker Therapy Corrects Dyssynchrony in Non-Obstructive Hypertrophic Cardiomyopathy

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Ibrar Ahmed ◽  
Khalid Abozguia ◽  
Ganesh Nallur-Shivu ◽  
Thanh T Phan ◽  
Abdul Maher ◽  
...  
Keyword(s):  
Hypertrophic Cardiomyopathy ◽  
Biventricular Pacing ◽  
Cardiac Resynchronisation Therapy ◽  
Tissue Doppler ◽  
Left Ventricular ◽  
Control Group ◽  
Pacemaker Therapy ◽  
Time To Peak ◽  
Obstructive Hypertrophic Cardiomyopathy ◽  
Peak Longitudinal Strain

Background. Previous studies have reported dyssynchrony using Tissue Doppler in patients with hypertrophic cardiomyopathy (HCM). In this study we assessed dyssynchrony using speckle tracking echocardiography (STE) in patients with non-obstructive hypertrophic cardiomyopathy vs a healthy control group and in a subgroup of highly symptomatic patients evaluated the acute effects of biventricular pacing on STE and Tissue Doppler (TDI) derived measures of dyssynchrony. Methods. We studied 48 healthy controls (age 48 ±18yrs, 22 males, LVEF 63 ±5%, QRS 86 ±7ms) and 57 patients with HCM (age 54 ±11yrs, 38 males, LVEF 61 ±7%, QRS 110 ±36ms). A subgroup of 15 symptomatic patients with HCM (Peak VO2<60% predicted) underwent biventricular pacing (age 53 ±12yrs, 12 males, LVEF 61 ±7%, QRS 110 ±32ms). Echocardiography was performed with the pacemaker off (VVi30) and on (DDDR, AV delay 90ms, LV-RV delay 0 – 4ms). Using STE, the standard deviation (SD) in time to peak longitudinal strain (Tϵ-SD), the time to peak longitudinal systolic velocity (Ts) for each of 18 left ventricular segments and the SD of this timing (Ts-SD) was derived. Using TDI dyssynchrony was assessed from the SD of Ts for the basal six segments and the maximum difference in Ts between any two basal segments (Ts-peak[basal]). Results. Using STE, Tϵ-SD (54.99 ±33.61ms vs 24.55 ±21.18ms p<0.001), Ts-SD (71.06 ±32.32ms vs 46.17 ±21.50ms p<0.001) and Ts (155.74 ±23.14ms vs 123.71 ±11.25ms p<0.001) were greater in HCM than in controls. Using STE we demonstrated that biventricular pacing significantly reduced Tϵ-SD and Ts-SD to values similar to those observed in controls (Ts-SD p=0.13). Using TDI we demonstrated that biventricular pacing significantly reduced Ts, Ts-SD, and Ts-peak[basal]. See Table . (All values expressed as mean ±SD) Conclusion. Cardiac resynchronisation therapy significantly reduced dyssynchrony in symptomatic patients with non-obstructive HCM as demonstrated using STE and TDI. Table

Abstract 17141: Mavacamten Improves Left Ventricular Relaxation and Compliance in Obstructive Hypertrophic Cardiomyopathy Through Direct Myosin Modulation

Circulation ◽  
2018 ◽  
Vol 138 (Suppl_1) ◽  
Author(s):  
Stephen Heitner ◽  
Daniel Jacoby ◽  
Steven Lester ◽  
Anjali T Owens ◽  
Andrew Wang ◽  
...  
Keyword(s):  
Hypertrophic Cardiomyopathy ◽  
Exercise Capacity ◽  
Left Ventricular ◽  
Open Label ◽  
End Diastolic Volume ◽  
Concomitant Reduction ◽  
Obstructive Hypertrophic Cardiomyopathy ◽  
Healthy Dogs ◽  
Cross Bridges ◽  
Doppler Indices

Introduction: Obstructive hypertrophic cardiomyopathy (oHCM) consists of a constellation of LV hypercontractility, LV outflow tract obstruction (LVOTO), and impaired relaxation, often resulting in dyspnea and reduced exercise capacity. In healthy dogs, the novel myosin modulator mavacamten (MAVA), decreased LV hypercontractility and improved compliance. In the PIONEER-HCM clinical study, improvements in post-exercise LVOT gradient, exercise capacity, and symptoms were reported. To examine whether MAVA could also limit residual myosin-actin cross-bridges during diastole, and improve LV compliance, its effects on diastolic indices were evaluated. Methods: In PIONEER-HCM, an open-label, multi-site, prospective study, oHCM subjects received MAVA for 12 weeks at either 10-20 mg/d (n = 11, Cohort A; 10 completed) or at 2-5 mg/d (n = 10, Cohort B). Echo-Doppler indices of LV filling and relaxation were compared at baseline to week 12. The p-values are from Wilcoxon signed rank tests, evaluating the distribution of within-subject 12-wk changes from baseline around a null of zero. Results: MAVA reduced hypercontractility in a dose-dependent fashion, with relief of LVOTO in all subjects achieving plasma MAVA concentration >350 ng/ml (data previously reported). There was also an increase in mitral annular velocity during early diastole (e’ lat ). There was a concomitant reduction in E/e’ lat and increase in LV end-diastolic volume (LVEDV) consistent with improved LV compliance (Table). MAVA improved dyspnea score with a trend towards reduction in NT-proBNP. Conclusions: Administration of MAVA is associated with improvement in measures of myocardial relaxation (e’ lat ) and compliance in parallel with reduction in LVOT gradient. These findings are consistent with preclinical findings reported in healthy dogs and support additional evaluation of MAVA in patients with obstructive or non-obstructive HCM.

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