Ventricular late potentials and myocardial fibrosis in hypertrophic cardiomyopathy

• Published in: Journal of electrocardiology Vol. 58; pp. 87 - 91
• Main Authors: Matsuki, Ayumi, Kawasaki, Tatsuya, Kawamata, Hirofumi, Sakai, Chieko, Harimoto, Kuniyasu, Kamitani, Tadaaki, Yamano, Michiyo, Matoba, Satoaki
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 01.01.2020; Elsevier Science Ltd
• Subjects: Cardiac arrhythmia; Electrocardiography; Heart attacks; Heart failure; Hypertrophic cardiomyopathy; Late gadolinium enhancement; Late potentials; Myocardial fibrosis; Strength training; Studies; Hypertrophic cardiomyopathy; Myocardial fibrosis; Late potentials; Late gadolinium enhancement
• ISSN: 0022-0736; 1532-8430
• DOI: 10.1016/j.jelectrocard.2019.10.003

Ventricular late potentials (VLPs) represent delayed conduction due in part to myocardial fibrosis. We sought to examine the relationship of signal-averaged electrocardiography findings with myocardial fibrosis as assessed by cardiac magnetic resonance (CMR) in patients with hypertrophic cardiomyopathy (HCM). This study consisted of 41 HCM patients with sinus rhythm who had undergone risk assessment including CMR and signal-averaged electrocardiography such as VLPs, filtered QRS duration, low amplitude signal duration of the terminal filtered QRS below 40 μV (LAS), and root mean square voltage of the late 40 ms of the filtered QRS (RMS). The concordance rate between VLPs and myocardial fibrosis as assessed by CMR was examined. Late gadolinium enhancement (LGE) on CMR was detected in 13 patients, and VLPs were detected in 14. Filtered QRS duration, LAS, RMS, and VLPs were not associated with LGE. The results of LGE and VLPs were concordant in 26 patients, whereas 15 exhibited discordance. Patients with discordance had a higher maximum wall thickness (24.1 ± 4.0 mm versus 21.0 ± 5.9 mm, p < 0.05), higher LGE volume (2.3 ± 1.2 g/cm versus 0.0 ± 0.8 g/cm, p < 0.01), lower LGE volume/the total number of sites with LGE (1.5 ± 0.7 versus 3.1 ± 2.8, p < 0.01), and predominant LGE location of the interventricular septum and anterior wall (60% versus 8%, p < 0.01) than patients with concordance. VLPs were not a reliable marker for the detection of myocardial fibrosis as assessed by LGE on CMR in our cohort of patients with HCM. Ventricular late potentials on signal-averaged electrocardiography represent delayed conduction due in part to myocardial fibrosis but were not an alternative to cardiac magnetic resonance for detecting myocardial fibrosis in patients with hypertrophic cardiomyopathy.