Clinical cardiology · 2020
Burden of premature ventricular contractions beyond nonsustained ventricular tachycardia is related to the myocardial extracellular space expansion in patients with hypertrophic-cardiomyopathy.
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Chung Hyemoon, Park Chul-Hwan, Kim Yoonjung, Kim Jong-Youn, Min Pil-Ki, Yoon Young Won, Lee Kyung-A, Lee Byoung Kwon, Hong Bum-Kee, Kim Tae Hoon, Rim Se-Joong, Kwon Hyuck Moon, Choi Eui-Young
Аннотация
BACKGROUND: Although nonsustained ventricular tachycardia (NSVT) is a risk factor for sudden cardiac death in hypertrophic-cardiomyopathy (HCM), the impact of premature ventricular contraction (PVC) burden, in the absence of NSVT, is not well-known.
HYPOTHESIS: PVC burden may be associated with myocardial fibrosis and genetic mutations in patients with HCM.
METHODS: Of the 212 patients prospectively enrolled to the HCM registry of genetics, 84 were evaluated with both cardiac magnetic resonance, 24-hour Holter monitoring and genetic analysis. Among them, 71 patients have not been diagnosed with NSVT.
RESULTS: Patients with NSVT (n = 13) had a higher late gadolinium enhancement (LGE) amount, extracellular volume fraction (ECV), and prevalence of sarcomere mutations compared with patients without NSVT. Among patients without NSVT, those with LGE (n = 46) had a higher total PVC (109 ± 332 vs 7 ± 13, P = .003) and PVC burden (0.114 ± 0.225 vs 0.008 ± 0.014%, P = .003) during 24-hour Holter monitoring compared with others. The %LGE and global ECV were correlated with PVC burden (r = 0.377, P = .001; r = 0.401, P = .001). The optimal cutoff value for PVC number for LGE was 45 (37.0% and 100% sensitivity and specificity, respectively) with 0.733 of the area under the receiver operating characteristic-curve (P < .001). Thick filament gene mutation was more prevalent in the higher PVC burden group (41.2% vs 16.7%, P = .048).
CONCLUSION: Total PVC burden is significantly related to increase in myocardial fibrosis in HCM patients without NSVT.
HYPOTHESIS: PVC burden may be associated with myocardial fibrosis and genetic mutations in patients with HCM.
METHODS: Of the 212 patients prospectively enrolled to the HCM registry of genetics, 84 were evaluated with both cardiac magnetic resonance, 24-hour Holter monitoring and genetic analysis. Among them, 71 patients have not been diagnosed with NSVT.
RESULTS: Patients with NSVT (n = 13) had a higher late gadolinium enhancement (LGE) amount, extracellular volume fraction (ECV), and prevalence of sarcomere mutations compared with patients without NSVT. Among patients without NSVT, those with LGE (n = 46) had a higher total PVC (109 ± 332 vs 7 ± 13, P = .003) and PVC burden (0.114 ± 0.225 vs 0.008 ± 0.014%, P = .003) during 24-hour Holter monitoring compared with others. The %LGE and global ECV were correlated with PVC burden (r = 0.377, P = .001; r = 0.401, P = .001). The optimal cutoff value for PVC number for LGE was 45 (37.0% and 100% sensitivity and specificity, respectively) with 0.733 of the area under the receiver operating characteristic-curve (P < .001). Thick filament gene mutation was more prevalent in the higher PVC burden group (41.2% vs 16.7%, P = .048).
CONCLUSION: Total PVC burden is significantly related to increase in myocardial fibrosis in HCM patients without NSVT.