Heart rhythm · 2013
Ventricular premature depolarization QRS duration as a new marker of risk for the development of ventricular premature depolarization-induced cardiomyopathy.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Carballeira Pol Lidia, Deyell Marc W, Frankel David S, Benhayon Daniel, Squara Fabien, Chik William, Kohari Maria, Deo Rajat, Marchlinski Francis E
Аннотация
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.
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.