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Left Ventricular Pacing (leave + ventricular_pacing)

Distribution by Scientific Domains
Medical Sciences100%

Selected Abstracts

Two Different Cycle Lengths During Left Ventricular Pacing: What Is the Mechanism?

JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 6 2006
JOSEPH Y. CHAN M.R.C.P.
[source]

Biventricular Pacing and Left Ventricular Pacing in Heart Failure:

JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 12 2004
Similar Hemodynamic Improvement Despite Marked Electromechanical Differences
Introduction: We conducted an acute echocardiographic study comparing hemodynamic and ventricular dyssynchrony parameters during left ventricular pacing (LVP) and biventricular pacing (BVP). We sought to clarify the mechanisms responsible for similar hemodynamic improvement despite differences in electrical activation. Methods and Results: Thirty-three patients underwent echocardiography prior to implantation with a multisite pacing device (spontaneous rhythm [SR]) and 2 days after implantation (BVP and LVP). Interventricular dyssynchrony (pulsed-wave Doppler), extent of myocardium displaying delayed longitudinal contraction (%DLC; tissue tracking), and index of LV dyssynchrony (pulsed-wave tissue Doppler imaging) were assessed. Compared to SR, BVP and LVP caused similar significant improvement of cardiac output (LVP: 3.2 ± 0.5, BVP: 3.1 ± 0.7, SR: 2.3 ± 0.6 L/min; P < 0.01) and mitral regurgitation (LVP: 25.1 ± 10, BVP: 24.7 ± 11, baseline: 37.9 ± 14% jet area/left atria area; P < 0.01). LVP resulted in a smaller index of LV dyssynchrony than BVP (29 ± 10 vs 34 ± 14; P < 0.05). However, LVP exhibited a longer aortic preejection delay (220 ± 34 vs 186 ± 28 msec; P < 0.01), longer LV electromechanical delays (244.5 ± 39 vs 209.5 ± 47 msec; P < 0.05), greater interventricular dyssynchrony (56.6 ± 18 vs 31.4 ± 18; P < 0.01), and higher%DLC (40.1 ± 08 vs 30.3 ± 09; P < 0.05), leading to shorter LV filling time (387 ± 54 vs 348 ± 44 msec; P < 0.05) compared to BVP. Conclusion: Although LVP and BVP provide similar hemodynamic improvement, LVP results in more homogeneous but substantially delayed LV contraction, leading to shortened filling time and less reduction in postsystolic contraction. These data may influence the choice of individual optimal pacing configuration. [source]

Simple Access to the Coronary Venous System for Left Ventricular Pacing

PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 9 2003
DANY E. SAYAD
Implantation of the LV lead for biventricular pacing can be challenging, time consuming, and often requires extensive fluoroscopy time. A conventional diagnostic 5 Fr left Amplatz catheter was used to cannulate the coronary sinus in 15 consecutive patients undergoing implantation of a biventricular pacemaker. When the coronary sinus was cannulated, the proximal end of the Amplatz catheter was cut and the coronary sinus sheath was passed over the Amplatz catheter that was then removed. Coronary sinus cannulation was achieved in all 15 patients with a mean fluoroscopy time of3.34 ± 1.9 minutes. Subsequent implantation of a biventricular pacemaker was successful and free of complications in all the 15 patients. (PACE 2003; 26:1856,1858) [source]

Biventricular Pacing and Left Ventricular Pacing in Heart Failure:

JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 12 2004
Similar Hemodynamic Improvement Despite Marked Electromechanical Differences
Introduction: We conducted an acute echocardiographic study comparing hemodynamic and ventricular dyssynchrony parameters during left ventricular pacing (LVP) and biventricular pacing (BVP). We sought to clarify the mechanisms responsible for similar hemodynamic improvement despite differences in electrical activation. Methods and Results: Thirty-three patients underwent echocardiography prior to implantation with a multisite pacing device (spontaneous rhythm [SR]) and 2 days after implantation (BVP and LVP). Interventricular dyssynchrony (pulsed-wave Doppler), extent of myocardium displaying delayed longitudinal contraction (%DLC; tissue tracking), and index of LV dyssynchrony (pulsed-wave tissue Doppler imaging) were assessed. Compared to SR, BVP and LVP caused similar significant improvement of cardiac output (LVP: 3.2 ± 0.5, BVP: 3.1 ± 0.7, SR: 2.3 ± 0.6 L/min; P < 0.01) and mitral regurgitation (LVP: 25.1 ± 10, BVP: 24.7 ± 11, baseline: 37.9 ± 14% jet area/left atria area; P < 0.01). LVP resulted in a smaller index of LV dyssynchrony than BVP (29 ± 10 vs 34 ± 14; P < 0.05). However, LVP exhibited a longer aortic preejection delay (220 ± 34 vs 186 ± 28 msec; P < 0.01), longer LV electromechanical delays (244.5 ± 39 vs 209.5 ± 47 msec; P < 0.05), greater interventricular dyssynchrony (56.6 ± 18 vs 31.4 ± 18; P < 0.01), and higher%DLC (40.1 ± 08 vs 30.3 ± 09; P < 0.05), leading to shorter LV filling time (387 ± 54 vs 348 ± 44 msec; P < 0.05) compared to BVP. Conclusion: Although LVP and BVP provide similar hemodynamic improvement, LVP results in more homogeneous but substantially delayed LV contraction, leading to shortened filling time and less reduction in postsystolic contraction. These data may influence the choice of individual optimal pacing configuration. [source]

Changes in Left Ventricular Repolarization and Ion Channel Currents Following a Transient Rate Increase Superimposed on Bradycardia in Anesthetized Dogs

JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 6 2000
MICHAEL RUBART M.D.
Electrical Remodeling of the Heart due to Rate. Introduction: We previously demonstrated in dogs that a transient rate increase superimposed on bradycardia causes prolongation of ventricular refractoriness that persists for hours after resumption of bradycardia. In this study, we examined changes in membrane currents that are associated with this phenomenon. Methods and Results: The whole cell, patch clamp technique was used to record transmembrane voltages and currents, respectively, in single mid-myocardial left ventricular myocytes from dogs with 1 week of complete AV block; dogs either underwent 1 hour of left ventricular pacing at 120 beats/min or did not undergo pacing. Pacing significantly heightened mean phase 1 and peak plateau amplitudes by ,6 and ,3 mV, respectively (P < 0.02). and prolonged action potential duration at 90% repolarization from 235 ± 8 msec to 278 ± 8 msec (1 Hz; P = 0.02). Rapid pacing-induced changes in transmembrane ionic currents included (1) a more pronounced cumulative inactivation of the 4-aminopyridine-sensitive transient outward K+ current, I to over the range of physiologic frequencies, resulting from a ,30% decrease in the population of quickly reactivating channels; (2) increases in peak density of L-type Ca2+ currents, Ica.I.' by 15% to 35% between +10 and +60 mV; and (3) increases in peak density of the Ca2+ -activated chloride current, ICl.Ca' by 30% to 120% between +30 and +50 mV. Conclusion: Frequency-dependent reduction in Ito combined with enhanced ICa.I. causes an increase in net inward current that may he responsible for the observed changes in ventricular repolarization. This augmentation of net cation influx is partially antagonized by an increase in outward ICa.Cl. [source]