کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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2923678 | 1175883 | 2011 | 6 صفحه PDF | دانلود رایگان |

BackgroundAbnormalities of ventricular repolarization as well as depolarization have been associated with increased risk of ventricular arrhythmias.ObjectiveTo evaluate the relative contribution of these predictors to risk of sudden cardiac death (SCD) in patients with coronary artery disease (CAD).MethodsIn the ongoing Oregon Sudden Unexpected Death Study, adult residents from the Portland, Oregon, metropolitan area (population ∼1 million) who suffered SCD were identified prospectively (2002–2007). Of these, we analyzed the subgroup of SCDs that had a resting 12-lead ECG prior to SCD and also had associated CAD. Comparisons were conducted with a control group of subjects with known CAD but no history of SCD from the same geographic region. Corrected QT interval (QTc), JT interval (JTc), QRS duration (QRSd), and other parameters were measured from ECG prior and unrelated to SCD. Analysis of left ventricular function was limited to those subjects who had undergone echocardiography prior to and remote from SCD.ResultsA total of 642 SCD cases (71 ± 13 years, 62% male) were compared to 450 controls (66 ± 12 years, 64% male). SCD cases had significantly longer QRSd (102 ± 25 ms vs 97 ± 20 ms, P = .0008) as well as JTc (348 ± 44 ms vs 339 ± 34 ms, P = .0006) vs controls. In cases with prolonged QRSd, 38% had severe left ventricular systolic dysfunction and 62% had normal, mild, or moderately decreased left ventricular systolic function. In a multivariable model, QRSd, JTc, age, and severe left ventricular systolic dysfunction were independent predictors. There was minimal overlap between prolonged QRSd and JTc in both case and control groups (3% and 4%, respectively).ConclusionProlonged QRSd, JTc, and severe left ventricular systolic dysfunction had independent contributions to risk of SCD in coronary disease, in this community-based setting.
Journal: Heart Rhythm - Volume 8, Issue 10, October 2011, Pages 1562–1567