Volume-weighted unipolar endocardial voltage: An excellent, novel parameter for predicting cardiac mortality in patients with dilated cardiomyopathy and ventricular arrhythmias
Authors: Kimura Y , Beukers HKC , Ebert M , Wijnmaalen AP , De Riva M , Zeppenfeld K 
Published: May 2021

Funding Acknowledgements

Type of funding sources: None.

Background

Patients with dilated cardiomyopathy (DCM) and ventricular tachyarrhythmias (VT) are at risk for heart failure (HF) death. Global left ventricular endocardial voltage may reflect the amount of excitable viable myocardium and identify patients at risk for rapid progression to end-stage HF. 

Aim

To determine if volume-weighted endocardial voltage, as a surrogate for the total excitable viable myocardium, predicts mortality in patients with DCM and VT. 

Methods

Consecutive patients with DCM, who underwent high-density endocardial voltage mapping for VT or PVC ablation (2012-2018), were included. Mapping data were transferred from CARTO to ParaView after excluding valve areas. The volume-weighted UV and BV (vwUV, vwBW) were calculated by mathematically integrating the UV and BV over the whole LV (thereby correcting for mapping density heterogeneity) divided by the endocardial LV surface area and corrected for LV wall thickness determined by echocardiography. The prognostic values of vwUV and vwBV for cardiac function and cardiac death were evaluated.

Results

One hundred three patients (VT, n = 83 and PVC, n = 20; age, 57 ± 14yrs; LVEF, 39 ± 13%; [likely] pathogenic genetic variants 33 [32%]; amiodarone use 36 [35%]) were included. VwUV and vwBV were 9.94 ± 3.42 and 4.70 ± 1.46. During a median follow-up of 24 months, cardiac mortality was 18% (end-stage HF 16/19, the median time to death 5.7 months). Patients who died had a significantly lower vwUV and vwBV (vwUV 5.62 ± 0.93 vs. 10.91 ± 3.10, P &lt; 0.001; vwBV 2.99 ± 0.70 vs. 5.04 ± 1.28, P &lt; 0.001). The optimal cutoff of vwUV for predicting HF-related death was 6.64 (AUC, 0.98; Sensitivity, 94%; Specificity, 95%), superior to LVEF or vwBV (AUC, 0.77, 0.92, respectively, Figure A). In multivariable analysis, vwUV remained the only significant predictor for cardiac death (for one decrease, HR 2.66, CI 1.41-5.00, P = 0.002), independently of LVEF, NT-proBNP, vwBV, genetic variants, and amiodarone use. In a subanalysis, the correlations between vwUV and changes of LVEF over time after voltage mapping were analyzed in patients with mid-range (HFmrEF, EF40-49%, n = 27) and reduced (HFrEF, EF &lt; 40%, n = 53) LVEF, respectively. In patients with HFmrEF, a significant LVEF deterioration (defined as an EF decrease &gt;5% and transition to HFrEF) occurred in 22% and was strongly related with a low vwUV (6.65 ± 1.15 vs. 10.08 ± 2.92, P = 0.02, Figure B left). Furthermore, in patients with HFrEF, a significant LVEF improvement (defined as an EF increase &gt;5% and transition to HFmrEF) was noted in 32% and was correlated with a high vwUV (11.68 ± 2.70 vs. 8.62 ± 2.69, P = 0.002, Figure B right).

Conclusion

VwUV is a newly proposed surrogate for the amount of LV viable myocardium, available from routine endocardial mapping and an excellent parameter to identify patients with DCM at high risk for rapid progression to HF-related death. Abstract Figure. vwUV and outcomes