QT variability paradox after premature ventricular contraction in patients with structural heart disease and ventricular arrhythmias☆,☆☆
Introduction
Sudden cardiac death (SCD) is responsible for approximately 50% of deaths from cardiovascular disease in the United States and other developed countries. In the United States alone, it accounts for between 300,000 and 400,000 deaths.1 Implantable cardioverter defibrillators (ICD) have been shown to be the most effective therapy for patients with ventricular tachycardia (VT)/ventricular fibrillation (VF). Among patients in the Multicenter Automatic Defibrillator Implantation Trial (MADIT) who were given ICD devices or conventional medical therapy, after a 27-month follow-up implanted patients had a 54% decreased rate of mortality.2 It is known that the ICD is an effective therapy. However, a method to identify patients at high risk of SCD has yet to be fully developed. Guidelines of the American College of Cardiology and the American Heart Association3 recognize a low left ventricular ejection fraction (LVEF) as a significant predictor of SCD. At the same time low specificity of LVEF has instigated a search for additional predictive markers to use for risk stratification of VT/VF.
It was previously shown that increased temporal variability of QT interval duration (QT variability) is associated with life-threatening ventricular arrhythmias.4, 5, 6 It is known that premature ventricular contractions (PVC) can alter the QT interval within several consecutive cardiac cycles.7 QT variability analysis requires exclusion of one sinus beat immediately after PVC. However, the effect of PVC on QT variability has not been systematically studied. The goal of our study was to compare QT variability during 15 consecutive sinus beats before and after single PVC in patients with structural heart disease with and without VT/VF during follow-up.
Section snippets
Study patients population
We retrospectively analyzed the prospectively collected data of 33 patients enrolled in the ICD-EGM study4 (NCT00916435). The study enrolled patients with structural heart disease who have been implanted with Medtronic (Minneapolis, MN, USA) or Boston Scientific Corporation (Natick, MA, USA) ICD device for primary or secondary prevention of SCD. The design and selection criteria of the original cohort have been previously described.4 Briefly, the study included patients with approved
Results
Study population comprised patients with ICD implanted for primary prevention of SCD (85%) and secondary prevention (15%). Majority of patients had ischemic cardiomyopathy (67%) with mild heart failure (mean ejection fraction 33.9 ± 10.0), predominantly NYHA class II. Mean age was 60.5 ± 12.2 years (range 33–81 years), 73% were men. Mean heart rate was 83.6 ± 13.7 bpm. On average patients had 1.3 ± 0.9 PVCs per minute. There were no statistically significant differences in baseline clinical characteristics
Discussion
In the present study we described QT variability paradox after PVC. We showed that QTVI elevated at baseline is decreased during the first 15 beats after PVC in patients at risk for VT/VF. The steeper decrease of QTVI after PCV the higher the odds of having VT/VF. At the same time, patients with ICD who did not have VT/VF during follow-up were characterized by increased QTVI immediately after PCV. Difference in QTVI before and after PVC was strongly associated with sustained VT/VF with
Conclusion
In patients with structural heart disease, those that show sustained VT/VF are characterized by decreased QTVI over a 15-beat interval following a PVC compared to an increased QTVI in similar patients with structural heart disease who do not experience VT/VF.
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Cited by (9)
QT instability, an indicator of augmented arrhythmogenesis, increases with the progression of myxomatous mitral valve disease in dogs
2018, Journal of Veterinary CardiologyCitation Excerpt :Although premature ventricular contractions were excluded from the analysis of QT variability, QT dynamics after these contractions is poorly understood. It is speculated, however, that premature complexes can alter the QT interval within several consecutive cardiac cycles [34]. It can also be argued that formulas that correct the QT for heart rate are not sensitive or accurate enough to clarify abnormal repolarization [35].
QT variability index
2013, Progress in Cardiovascular DiseasesA new ECG sign for sudden death: Transient prolonged QT interval following premature contraction
2021, Journal of Central South University (Medical Sciences)Measurement of autonomic tone in cardiac implantable electronic devices
2019, Remote Monitoring: Implantable Devices and Ambulatory ECGA novel technique for analysing beat-to-beat dynamical changes of QT-RR distribution for arrhythmia prediction
2015, Computing in Cardiology
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Registration identification number: NCT00916435.
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Financial support: The study was partially supported by Medtronic as an investigator-initiated research project (awarded to Dr. Tereshchenko).