Elsevier

Heart Rhythm

Volume 11, Issue 2, February 2014, Pages 299-306
Heart Rhythm

Ventricular premature depolarization QRS duration as a new marker of risk for the development of ventricular premature depolarization–induced cardiomyopathy

https://doi.org/10.1016/j.hrthm.2013.10.055Get rights and content

Background

Frequent ventricular premature depolarizations (VPDs) can cause cardiomyopathy (CMP). The mechanisms underlying its development remain unclear, with VPD burden being only a weak predictor of risk.

Objective

To determine whether VPD QRS duration at the time of initial presentation could predict risk for the subsequent development of CMP in patients with normal left ventricular ejection fraction (LVEF).

Methods

From consecutive patients referred for ablation between January 1, 2006, and April 2, 2013, with ≥10% VPDs on 24-hour Holter monitoring, we identified 45 patients with normal LVEF and an electrocardiogram of the targeted VPD, who were then followed for at least 6 months (median 14 months; interquartile range [IQR] 8–32 months) before intervention. We excluded patients with structural or genetic heart disease.

Results

Of the 45 patients, 28 (62%) maintained normal LVEF and 17(38%) developed VPD-induced CMP. VPD burden was similar (26.5% [IQR 19.3%–39.5%] vs 26.0% [IQR 16.4%–41.0%]; P = 0.4) between the 2 groups. Patients who developed VPD-induced CMP had significantly longer VPD QRS duration (159 ms vs 142 ms; P < .001) and a longer sinus QRS duration (97 ms vs 89 ms; P = .04). A VPD QRS duration of ≥153 ms best predicted development of VPD CMP (82% sensitivity and 75% specificity). Longer VPD QRS duration and a non–outflow tract site of VPD origin were independent risk factors for left ventricular dysfunction after multivariate analysis.

Conclusion

VPD QRS duration longer than 153 ms and a non–outflow tract site of origin might be useful predictors of the subsequent development of VPD-induced CMP.

Introduction

Ventricular premature depolarizations (VPDs) are usually regarded as benign in the absence of structural heart disease. However, a subset of patients with frequent VPDs develop a cardiomyopathy (CMP) that usually reverses after successful ablation.1, 2, 3, 4, 5, 6 The spectrum of dysfunction that can occur with frequent VPDs is wide, ranging from severe CMP to more frequent and subtle forms of biventricular impairment.7 Currently, the mechanisms underlying the development of VPD-induced CMP remain unclear. Although it seems that a critical VPD burden is required, VPD burden remains a weak predictor of the development of CMP.2, 3, 8, 9, 10, 11 A longer VPD QRS duration has been associated with the presence of CMP in previous cross-sectional studies.11, 12 We have previously shown that shorter VPD QRS duration is associated with the recovery of left ventricular (LV) function after successful ablation, but the temporal relationship of VPD QRS duration to CMP is unknown.13 We therefore sought to determine whether VPD QRS duration measured before the onset of CMP would be a useful predictor of the subsequent development of CMP.

Section snippets

Study population

We identified all patients who underwent VPD ablation at the Hospital of the University of Pennsylvania between January 1, 2006, and April 2, 2013. As previous data suggested that a significant VPD burden is required for the development of VPD-induced CMP, we restricted our study to patients with ≥10% VPDs on preprocedural 24-hour Holter monitoring.9 We further identified for inclusion those patients with an electrocardiogram (ECG) of the targeted VPD obtained at least 6 months before ablation.

Results

During the study period, a total of 605 VPD ablations were performed on 540 patients. One hundred twenty (22%) patients were excluded owing to the presence of structural or inherited heart disease (Figure 1). From the remainder, only 110 (20%) patients had a documented VPD burden of ≥10% VPDs on preprocedural 24-hour Holter monitoring along with a baseline echocardiogram and ECG at least 6 months before ablation. Forty-five (8%) of these patients had a normal baseline LVEF and are the focus of

Discussion

This longitudinal study is the first to evaluate systematically the risk factors implicated in the development of VPD-induced CMP rather than to associate risk factors in a cross-sectional fashion. In our population, with a preset inclusion threshold of ≥10% daily VPD, the arrhythmia burden was not associated with the development of LV dysfunction. This contrasts with the observations of previous cross-sectional studies.8, 11 For example, Baman et al9 found that >24% daily VPD burden

Conclusions

This study sheds light on the temporal association between VPD widening and development of CMP. We found that VPD QRS duration longer than 153 ms and non–outflow tract sites of VPD origin were associated with greater risk of developing VPD-induced CMP, above and beyond VPD burden. This is the first prospective study of risk factors for the development of VPD-induced CMP. By improving our ability to define risk of development of CMP, more informed decisions regarding VPD ablation can be made.

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    This work was supported in part by the Mark S. Marchlinski Research Fund at the University of Pennsylvania. Dr Carballeira Pol has received a research grant from the Sociedad Española de Cardiología. Dr Squara is supported by a research grant from the Fédération Française de Cardiologie.

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