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

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.

Interferencias por contrastes yodados en la electroforesis capilar / Interference due to iodinated contrast media in capillary electrophoresis

Introducción. La administración de contrastes yodados puede interferir en la electroforesis capilar (EFC) de proteínas séricas. El objetivo fue realizar un estudio in vitro para confirmar la presencia de interferencias por Iomeron® en la EFC y otro in vivo en pacientes sometidos a coronariografías, estudiando la cinética de eliminación del contraste yodado. Material y métodos. Se preparó un pool de sueros libres de componente monoclonal (CM), con patrón electroforético anodino, añadiéndose Iomeron® hasta alcanzar una concentración de 5,4g/100ml. Partiendo de esta solución (A) se realizaron cuatro diluciones decrecientes (2,70g/100ml, 1,35g/100ml, 0,67g/100ml y 0,33g/100ml); y se procesaron por EFC para confirmar la interferencia y observar que disminuye proporcionalmente a su concentración. Material y métodos. Se extrajo sangre, pautadamente (5–10min, 1, 3, 5 y 8h postadministración del contraste) a pacientes sometidos a coronariografías. Se procesaron las muestras de plasma por EFC, y se realizó la inmunofijación (IF) de la obtenida entre los 5–10min para demostrar que la imagen electroforética no se correspondía con un CM. Resultados. La EFC reveló picos similares a los observados ante un CM en la fracción β, que desaparecieron en la dilución 0,33g/100ml en el estudio in vitro, y a las 8h postadministración del Iomeron® en el estudio in vivo (una paciente). Por otra parte, en la electroforesis de referencia del gel de agarosa empleado en la IF no se detectó imagen sugerente de CM. Conclusiones. Se demuestra que los picos observados correspondían a una interferencia producida por el Iomeron® en la fracción β de la EFC, no observada en la electroforesis en gel de agarosa (AU)

Introduction. The administration of iodinated contrast media may interfere with the capillary electrophoresis (CE) of serum proteins. The aim of the study was to perform an in vitro study to confirm the interference caused by lomeron® administration followed by an in vivo study in patients undergoing coronary angiographies, evaluating the kinetics of iodinated contrast elimination. Material and methods. A serum pool free from monoclonal component (MC) and with an anodyne electrophoretic pattern was prepared. lomeron® up to a concentration of 5.4g/100mL was added to this pool and afterwards, four decreasing dilutions were prepared (2.70g/100mL, 1.35g/100mL, 0.67g/100mL and 0.33g/100mL); all of them were processed by CE to confirm the interference and its decreasing effect as the concentration diminishes. Material and methods. Blood was drawn from patients undergoing coronary angiographies, at several time intervals (5–10min, 1, 3, 5 and 8h post-administration of contrast). Plasma samples were processed by CE, and immunofixation (IFx) of the first sample (5–10min) was performed in order to show that the electrophoretic image did not correspond to a MC. Results. In the in vitro study, CE revealed β fraction-MC peaks, which disappeared at the 0.33g/100mL dilution, and 8h after lomeron® administration in the in vivo study (one patient). On the other hand, no image suggestive of MC was detected on the reference agarose gel electrophoresis (AGE) used for the IFx. Conclusions. Peaks were observed that corresponded to an interference produced by lomeron® in the β fraction of CE, which was not found in AGE (AU)