Strength-duration curves for left bundle branch area pacing.

BACKGROUND: Despite growing clinical use of left bundle branch pacing (LBBP), data regarding the fundamentals of this pacing modality, including chronaxie and rheobase, are scarce. OBJECTIVE: The purpose of this study was to calculate strength-duration curves with chronaxie and rheobase values for LBBP and left ventricular septal pacing (LVSP), and to analyze battery current drain and presence of selective LBBP at very short pulse duration (PD). METHODS: A group of 141 patients with permanent LBBP were studied. LBBP and LVSP capture thresholds were assessed at 6 different PDs to calculate the strength-duration curves. Battery current drain at these PDs and presence of selective LBBP were determined. For comparison of strength-duration curves between His-bundle pacing (HBP) and LBBP, source data from our previous work based on 127 patients with HBP were obtained. RESULTS: The chronaxies for LBBP and LVSP were very similar (0.38 vs 0.39 ms), and the rheobases were identical (0.27 V). The chronaxie for LBBP was lower than for HBP (0.38 vs 0.53 ms; P <.001), whereas rheobases were similar (0.27 vs 0.26 V). A narrow zone of selective capture was present in 19% and 41% of patients at PD of 0.06 and 0.03 ms, respectively. When pacing with the safety margin of +1 V, the lowest battery current drain was achieved with PD of 0.2 ms. CONCLUSION: The obtained strength-duration curves for LBBP and LVSP provide insights to optimal programming of left bundle branch area pacing devices with regard to PD, voltage amplitude, battery longevity, and selective capture.

Link between fibrosis-specific biomarkers and interstitial fibrosis in hypertrophic cardiomyopathy.

BACKGROUND: Cardiac fibrosis is a hallmark of hypertrophic cardiomyopathy (HCM) and has confirmed unfavorable clinical significance. Replacement fibrosis is better known and has already been studied on a larger scale, whereas interstitial fibrosis is less explored. AIMS: We aimed to analyze the relationship between serum biomarkers and interstitial fibrosis, as assessed with cardiac magnetic resonance (CMR) in HCM patients. METHODS: We performed 3T CMR scans in 50 HCM patients to assess interstitial fibrosis as expressed by extracellular volume (ECV). In all patients, we determined levels of serum cardiac-specific (troponin T [TnT], N-terminal prohormone of brain natriuretic peptide [NT-proBNP]) and fibrosis-specific (procollagen I C-terminal propeptide, procollagen III N-terminal propeptide, transforming growth factor ß1, galectin-3) biomarkers. Patients were divided based on their median value of ECV. RESULTS: The final study population included 49 patients. The median value of ECV in our cohort was 28.1%. Patients stratified according to median ECV differed in terms of several variables: body mass index, late gadolinium extent, NT-proBNP, and galectin-3 levels (all P <0.05). Cardiac biomarkers (TnT and NT-proBNP) and galectin-3 were significantly correlated with ECV (rS = 0.34; P = 0.02; rS = 0.39; P = 0.006; rS = 0.43; P = 0.002, respectively). Galectin-3 and body mass index were found to be independent predictors of ECV (odds ratio [OR], 2.29 [1.07-4.91]; P = 0.03; OR, 0.81 [0.68-0.97]; P = 0.02, respectively). CONCLUSIONS: Galectin-3 was an independent predictor of interstitial fibrosis in HCM patients expressed as elevated ECV values. The other measured fibrosis-specific biomarkers were not useful in detecting interstitial fibrosis in HCM. In addition, there was a positive correlation between classical cardiac biomarkers and interstitial fibrosis in HCM patients.

The Relationship between Cardiac Magnetic Resonance-Assessed Replacement and Interstitial Fibrosis and Ventricular Arrhythmias in Hypertrophic Cardiomyopathy.

Non-sustained ventricular tachycardia (nsVT) creates the electrical basis for sudden cardiac death (SCD) in hypertrophic cardiomyopathy (HCM). We aimed to evaluate the relationship between interstitial fibrosis on cardiac magnetic resonance (CMR) and nsVT in HCM. A total of 50 HCM patients underwent CMR with a 3 T scanner to determine the presence of replacement fibrosis expressed by late gadolinium enhancement (LGE), and interstitial fibrosis expressed by native T1, post-contrast T1, and extracellular volume (ECV). The incidence of nsVT was assessed by Holter monitoring. We detected nsVT in 14 (28%) out of 50 HCM patients. Replacement fibrosis expressed by LGE was present in 37 (74%) patients and only showed a trend towards a differentiation between the groups with and without nsVT (p = 0.07). However, the extent of LGE was clearly higher in the nsVT group (3.8 ± 4.9% vs. 7.94 ± 4.5%, p = 0.002) and was an independent predictor of nsVT in a multivariable regression analysis (OR 1.2; 95%CI 1.02-1.4; p = 0.02). No relationship was observed between interstitial fibrosis and nsVT. To conclude, it was found that it is not the mere presence but the actual extent of LGE that determines the occurrence of nsVT in HCM patients; the role of interstitial fibrosis remains unclear.