Assessment of QT Dispersion in Prediction of Life-threatening Ventricular Arrythmias in Recipients of Implantable Cardioverter Defibrillator (original) (raw)
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Electrophysiologic study: its predictive value for ventricular arrhythmias
Texas Heart Institute journal / from the Texas Heart Institute of St. Luke's Episcopal Hospital, Texas Children's Hospital, 2010
Studies have shown the predictive value of inducible ventricular tachycardia and clinical arrhythmia in patients who have structural heart disease. We examined the possible predictive value of electrophysiologic study before the placement of an implantable cardioverter-defibrillator. Our retrospective study group comprised 315 patients who had ventricular tachycardia that was inducible during electrophysiologic study and who had undergone at least 1 month of follow-up (247 men; mean age, 66.9 +/- 13.5 yr; mean follow-up, 24.9 +/- 14.8 mo). Recorded characteristics included induced ventricular tachycardia cycle length, atrio-His and His-ventricular electrograms, PR and QT intervals, QRS duration, and drug therapy. Of the 315 patients, 97 experienced ventricular arrhythmia during the follow-up period, as registered by 184 of more than 400 interrogations. There were 187 episodes of ventricular arrhythmia (tachycardia, 178; fibrillation, 9) during 652.5 person-years of follow-up. Subjec...
Journal of the American Heart Association, 2020
Background Short‐term variability of the QT interval (STV QT ) has been proposed as a novel electrophysiological marker for the prediction of imminent ventricular arrhythmias in animal models. Our aim is to study whether STV QT can predict imminent ventricular arrhythmias in patients. Methods and Results In 2331 patients with primary prophylactic implantable cardioverter defibrillators, 24‐hour ECG Holter recordings were obtained as part of the EU‐CERT‐ICD (European Comparative Effectiveness Research to Assess the Use of Primary Prophylactic Implantable Cardioverter Defibrillators) study. ECG Holter recordings showing ventricular arrhythmias of >4 consecutive complexes were selected for the arrhythmic groups (n=170), whereas a control group was randomly selected from the remaining Holter recordings (n=37). STV QT was determined from 31 beats with fiducial segment averaging and calculated as , where D n represents the QT interval. STV QT was determined before the ventricular arrhy...
Medical Journal of Indonesia, 2005
Beberapa penelitian terdahulu menunjukkan kontradiksi hubungan antara dispersi QT dengan kejadian takiaritmia ventrikel dan atau kematian jantung mendadak. Penelitian-penelitian itu tidak mengeluarkan pengguna obat penghambat reseptor beta, bahkan pengguna obat tersebut merupakan mayoritas pada sampel mereka. Karena penggunaan penghambat reseptor beta sebagai pencegahan sekunder yang masih rendah di Pusat Jantung Nasional Harapan Kita, maka penelitian ini dilakukan untuk mengetahui hubungan antara dispersi QT dengan kejadian takiaritmia ventrikel dan atau kematian jantung mendadak pada pasien pascainfark. Interval QT, dispersi QT dan variabel klinis dibandingkan antara 36 orang pasien pascainfark yang mengalami takiaritmia ventrikel dan atau kematian jantung mendadak (kelompok kasus), dengan 75 pasien pascainfark yang tidak mengalami kedua kejadian tersebut (kelompok kelola). Dispersi QT yang lebih panjang (115 + 41 msec vs 81 + 25 msec, p < 0.001). Interval QT maksimal terkoreksi juga lebih panjang pada kelompok kasus (534 + 56 vs 501 + 35 msec, p < 0.001). Analisa regresi logistik menunjukkan adanya hubungan antara pemanjangan dispersi QT dengan kejadian takiaritmia ventrikel dan atau kematian jantung mendadak dengan RO 3,2, 4, dan 5,8 masing-masing untuk nilai potong 80, 90, dan 100 mdet. Dispersi QT dapat memprediksi kejadian takiaritmia ventrikel dan atau kematian jantung mendadak pada pasien infark miokard akut. Hasil ini menunjukkan bahwa dispersi QT tetap bermanfaat pada kondisi bebas pengaruh obat penghambat reseptor beta. (Med J Indones 2005; 14: 230-6)
Heart Rhythm, 2013
BACKGROUND As left ventricular ejection fraction (LVEF) may improve, worsen, or remain the same over time, patients' prognosis may also be expected to change because of the change in LVEF, among other factors. OBJECTIVE To evaluate the effect of LVEF change on outcome in the Defibrillators in Non-Ischemic Cardiomyopathy Treatment Evaluation (DEFINITE) trial. METHODS Patients with nonischemic cardiomyopathy with LVEF o36%, history of symptomatic heart failure, and the presence of significant ventricular ectopic activity were enrolled in the DEFINITE trial. Follow-up LVEF measurements were obtained annually in only a minority (17%) of trial participants. This study therefore evaluated survival and arrhythmic end points in patients whose LVEF was reassessed between 90 and 730 days after enrollment. RESULTS During the 90-730-day postrandomization period, 187 of 449 (42%) enrolled patients who survived at least 90 days had at least 1 follow-up LVEF measurement; these patients were younger and white; had diabetes, better 6-minute walk test results, and higher BMI; were more likely to have appropriate shocks; and had fewer deaths compared to those without follow-up LVEF measurements. Patients whose LVEF improved had reduced mortality compared to patients whose LVEF decreased (hazard ratio 0.09; 95% confidence interval 0.02-0.39; P ¼ .001). Survival free of appropriate shocks was not significantly related to LVEF improvement during follow-up. CONCLUSIONS LVEF improvement was associated with improved survival, but not with a significant decrease in appropriate shocks. These data highlight that appropriate caution should be exercised not to extrapolate the positive effect of improved LVEF to the elimination of arrhythmic events.
European Heart Journal, 2007
Aims The most widely accepted marker for stratifying the risk of sudden cardiac death (SCD) in post myocardial infarction patients is a depressed left ventricular function. Left ventricular ejection fractions (EF) of 35% or less increase the risk of sudden death but values between 35 and 40% raise concern. The underlying pathophysiological mechanism is sustained ventricular tachycardia or fibrillation, both associated with increased cardiac repolarization variability. We assessed whether the indices of QT variability from a short-term electrocardiographic (ECG) recording predict sudden death. Methods and results A total of 396 subjects with chronic heart failure (CHF) due to post-ischaemic cardiomyopathy, with an EF between 35 and 40% and in NYHA class I, underwent a 5 min ECG recording to calculate the following variables: QT variance (QT v ), QT normalized for the square of the mean QT (QTVN), and QT variability index (QTVI). Corrected QT (QT c ) was calculated from a 12-lead ECG recording. All participants were followed for 5 years. A multivariable survival model indicated that a QTVI greater than or equal to the 80th percentile indicated a high risk of SCD [hazards ratio (HR) 4.6, 95% confidence interval (CI) 1.5-13.4, P ¼ 0.006] and, though to a lesser extent, a high risk of total mortality (HR 2.4, 95% CI 1.2-4.9, P ¼ 0.017). The model including QTVI as a continuous variable confirmed a similar high risk for SCD (HR 2.9, 95% CI 1.3-6.5, P ¼ 0.01) and for total mortality (HR 2.6, 95% CI 1.3-5.2, P ¼ 0.008). Conclusion Although asymptomatic patients with CHF who have a slightly depressed EF are at low risk of sudden death, the category is extraordinarily numerous. The QTVI could be helpful in stratifying the risk of sudden death in this otherwise undertreated population.
Background Despite identifying several risk factors for sudden cardiac death, our ability to predict arrhythmic events in patients with an implantable cardioverter defibrillator (ICD) remains poor. The purpose of this study was to determine if patients who received appropriate ICD shocks had a higher degree of right ventricular (RV) dysfunction at baseline when compared to patients who did not receive ICD shocks. Methods We conducted a 1:2 case-control, retrospective study comparing RV end-diastolic and end-systolic areas (RV ED and RV ES areas, respectively), fractional RV area change, and RV wall thickness in 19 consecutive patients who received appropriate ICD shocks (shock group) with another group of 38 patients who did not receive ICD shocks (no-shock group). Results There was no significant difference in the RV end-diastolic areas between the groups. However, patients who experienced ICD shocks had a higher RV end-systolic area and a lower RV fractional area change when compared to patients without ICD shocks, 16.3± 4.9 cm 2 and 27.7±9.0% in the shock group versus 14.2± 4.4 cm 2 and 35.8±10.3% in the no-shock group; (p=0.08 and 0.004, respectively). Furthermore, the RV wall thickness was greater in patients with ICD shocks when compared to patients without ICD shocks, 0.49±0.05 cm and 0.44±0.04 cm, respectively (p=0.001). Utilizing a logistic regression analysis and after controlling for variables with univariate significance (p<0.1), RV wall thickness independently predicted ICD shocks (OR 13.9 mm −1 change of RV thickness, p=0.004). Conclusion Our findings suggest that some measurements of RV function might prove to be useful in predicting future arrhythmic events. Additional prospective studies are needed to test this hypothesis.
Annals of Noninvasive Electrocardiology, 2009
Background: Increased QT Variability (QTVI) is predictive of life threatening arrhythmias in vulnerable patients. The predictive value of QTVI is based on resting ECGs, and little is known about the effect of acute exercise on QTVI. The relation between QTVI and arrhythmic vulnerability markers such as T-wave alternans (TWA) has also not been studied. This study examined the effects of exercise on QTVI and TWA in patients with arrhythmic vulnerability. Methods: Digitized ECGs were obtained from 47 ICD patients (43 males; age 60.9 ± 10.1) and 23 healthy controls (18 males; age 59.7 ± 9.5) during rest and bicycle exercise. QTVI was assessed using a previously validated algorithm and TWA was measured as both a continuous and a categorical variable based on a priori diagnostic criteria. Results: QTVI increased with exercise in ICD patients (−0.79 ± 0.11 to 0.36 ± 0.08, P < 0.001) and controls (−1.50 ± 0.07 to −0.19 ± 0.12, P < 0.001), and QTVI levels were consistently higher in ICD patients than controls during rest and exercise (P < 0.001). The magnitude of QTVI increase from baseline levels was not larger among ICD patients versus controls (P > 0.20). Among ICD patients, elevated exercise QTVI was related to lower LV ejection fraction and inducibility of ischemia (P < 0.05). QTVI at rest correlated with exercise TWA (r = 0.54, P = 0.0004). Conclusions: QT variability increases significantly with exercise, and exercise QTVI is related to other well-documented markers of arrhythmic vulnerability, including low ejection fraction, inducible ischemia, and TWA. Resting QTVI may be useful in the risk stratification of individuals incapable of performing standard exercise protocols.