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Pathophysiology of intraventricular electrical activation and its relation to cardiac resynchronization therapy
Sedláček, Kamil ; Wichterle, Dan (advisor) ; Linhart, Aleš (referee) ; Čurila, Karol (referee)
The QRS complex shortening by cardiac resynchronization therapy (CRT) has been associated with improved outcomes. We hypothesized that (1) the absence of QRS duration (QRSd) prolongation by right ventricular septal pacing may indicate a complete left bundle branch block (cLBBB), and (2) that the interval between the right-ventricular pacing stimulus and left-ventricular lead electrogram (RVP-LV) is a better predictor of the electrocardiographic effect of CRT than the interval Q-LV. We prospectively collected 12-lead surface ECG and intracardiac electrograms during CRT implant procedures. Digital ECG and intracardiac recordings were edited and manually measured. The outcome measure was the QRS duration change induced by CRT (deltaCRT). Several outcome predictors were investigated: native QRS duration (QRSd), cLBBB (as defined by Strauss), Q-LV and RVP-LV intervals, and a newly proposed index defined by the difference between the right-ventricle-paced QRSd and native QRSd (deltaRVP). We included 133 consecutive patients in the study and found that the baseline QRSd, deltaRVP, and Q-LV represent strong independent predictors of electrocardiographic response to CRT (deltaCRT). DeltaRVP correlates tightly with the CRT effect on QRSd and outperforms predictive value of the ECG-based cLBBB. Strong...
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Physiological Mechanisms of Heart Rate Turbulence
Wichterle, Dan ; Kautzner, Josef (advisor) ; Kvasnička, Jiří (referee) ; Táborský, Miloš (referee)
Our papers on HRT physiology covered several electrophysiological phenomena associated with turbulent behaviour of sinus nodal discharge after isolated premature beat. Some observations were fairly novel (AV nodal turbulence, QT-turbulence, and HRT after atrial premature complexes), others were confirmative or complementary to the findings of other authors (impact of left ventricular ejection fraction and coupling interval). All of them were helpful for even deeper understanding the fundamental principles involved in HRT that, consequently, may offer an explanation of why HRT is such a potent postinfarction risk stratifier. From the very beginning we tried to suggest that late deceleration phase of HRT does not simply reflect the vagal function but originates from a complex interplay of both sympathetic and parasympathetic systems. Our paper on HRT hemodynamics (Wichterle et al. 2006) together with the article by Segersen et al. (2007) added perhaps "the last piece to the heart turbulence puzzle", as appreciated in Heart Rhythm editorial by Munich working group (Bauer et al. 2007).
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