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MICHAEL J. DOMANSKI DOUGLAS P. ZIPES DAVID G. BENDITT A. JOHN CAMM DEREK V. EXNER MICHAEL D. EZEKOWITZ H. LEON GREENE MICHAEL D. LESH JOHN M. MILLER CRAIG M. PRATT SANJEEV SAKSENA MELVIN M. SCHEINMAN BRAMAH N. SINGH CYNTHIA M. TRACY ALBERT L. WALDO 《Pacing and clinical electrophysiology : PACE》2001,24(4):526-534
DOMANSKI, M.J., et al. : Central Clinical Research Issues in Electrophysiology: Report of the NASPE Committee. This article contains the results of an attempt by appointed members of the North American Society of Pacing and Electrophysiology to define the research frontier in electrophysiology and suggest areas of study as an aid in setting the research agenda. 相似文献
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LAUREN JOHNSON B.S.E. MARC A. SIMON M.D. † MICHAEL R. PINSKY M.D. ‡ SANJEEV G. SHROFF Ph .D. 《Pacing and clinical electrophysiology : PACE》2009,32(2):224-233
Background: The effects of dyssynchrony on global left ventricular (LV) mechanics have been well documented; however, its impact on LV energetics has received less attention. Objective: To assess the effects of LV contraction dyssynchrony on global LV mechano‐energetic function in a pacing‐induced acute model of dyssynchrony. Methods: Using blood‐perfused isolated rabbit heart preparations (n = 11), LV pressure, coronary flow, and arteriovenous oxygen content difference were recorded for isovolumic contractions under right atrial (RA) pacing (control) and simultaneous RA and right ventricular outflow tract (RVOT) pacing (dyssynchrony). LV mechanical function was quantified by the end‐systolic pressure‐volume relationship (ESPVR). Myocardial oxygen consumption‐pressure‐volume area (MVO2‐PVA) relationship quantified LV energetic function. Internal PVA for MVO2 RVOT was calculated based on the MVO2‐PVA relationship for RA pacing. Thus, lost PVA (internal PVA–PVARVOT) represents the mechanical energy not observable at the global level. Results: Compared to RA pacing, RVOT pacing depressed LV mechanics as indicated by a rightward shift of ESPVR (i.e., increase in Vd from 0.58 ± 0.10 to 0.67 ± 0.10 mL, P < 0.05). Despite depressed mechanics, RVOT pacing was associated with greater MVO2 such that the MVO2‐PVA relationship intercept was markedly increased from 0.025 ± 0.003 to 0.029 ± 0.003 mL?O2/beat/100gLV (P < 0.05). Excess MVO2 (i.e., MVO2 RVOT– MVO2 RA) significantly correlated with lost PVA (R2= 0.54, P < 0.001). Conclusion: A potential mechanism explaining the observed increase in MVO2 with dyssynchrony may be that the measured PVA at the global level underestimates the internal PVA at the cellular level, which is likely to be the true determinant of MVO2. 相似文献
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ASHISH SHUKLA M.D. M.P.H. ANNE B. CURTIS M.D. MANDEEP R. MEHRA M.B.B.S. NANCY M. ALBERT Ph.D. R.N. MIHAI GHEORGHIADE M.D. J. THOMAS HEYWOOD M.D. YANG LIU M.S. CHRISTOPHER M. O'CONNOR M.D. DWIGHT REYNOLDS M.D. MARY NORINE WALSH M.D. CLYDE W. YANCY M.D. GREGG C. FONAROW M.D. 《Pacing and clinical electrophysiology : PACE》2013,36(4):433-443
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SANJEEV SAKSENA RICARDO A. CALVO DEMETRIS PANTOPOULOS ARUN GADHOKE STEPHEN T. ROTHBART 《Pacing and clinical electrophysiology : PACE》1987,10(5):1130-1141
By using a prospective randomized study design, we compared the clinical efficacy and safety of single unidirectional and bidirectional transvenous cardioversion shocks for termination of rapid ventricular tachycardia (VT) having cycle lengths less than 300 ms. A Medtronic 6880 catheter was placed in the right ventricular apex and an R2 skin patch electrode was placed over the left scapula. Patients were randomized into two groups. Group A patients received unidirectional transvenous shocks using the two catheter electrodes (right ventricular apical cathode and superior vena caval anode) which resulted in a single current pathway. Group B patients received bidirectional transvenous shocks using a common cathode (right ventricular apex) and two separate anodes (superior vena caval and R2 patch) resulting in two current pathways. Identical shocks with total energies of 2.7, 5.0 and 10.0 J and waveform tilt of 27% were delivered to Groups A and B. In selected Group B patients, delivered shock currents through the right ventricular apex/superior vena caval and right ventricular apex/R2 patch electrode pairs were measured. We analyzed the initial episode of VT with a cycle length less than 300 ms in 33 patients with organic heart disease (mean age, 64 +/- 9 years; mean VT cycle length, 248 +/- 37 ms) who underwent programmed electrical stimulation. Transvenous cardioversion shocks terminated 31% of 16 VT episodes in Group A and 41% of 17 VT episodes in Group B (p greater than .2). The mean successful shock energy was 6.1 +/- 3.7 J in Group A and 3.0 +/- 0.9 J in Group B (p less than .05). Forty percent of all successfully cardioverted episodes in Group A and 86% of all successfully cardioverted VT episodes in Group B were terminated at an energy of 2.7 J (p = .09). Analysis of shock waveforms in Group B revealed 47 to 74% of the total current was transmitted through the right ventricular apex/superior vena caval electrodes and 26 to 53% through the right ventricular apex/R2 electrodes. We conclude that single bidirectional transvenous shocks are effective for rapid VT termination in selected patients. Dual current pathways decrease energies needed for successful transvenous cardioversion in this patient population. 相似文献