Non‐invasive Evaluation of Ventricular Function and Volumes During Atrioventricular Sequential and Ventricular Pacing

The aim of this clinical crossover study was to elucidate the effects of atrioventricular (AV) synchronous pacing on cardiac function in patients with sick sinus syndrome (SSS). Thirty SSS patients, each with dual chamber pacemaker (DDD), were enrolled and divided into two groups based on echocardiographic findings. Group A (n = 16) had hypertensive heart disease (wall thickness 11 approximately 12 mm) or mitral or aortic regurgitation (Grade I or II). Group B (n = 14) had no organic heart disease. Three successive 3-month pacing periods were tested. For the first 3 months, long AV delay that achieved > 80% ventricular sensing was chosen. For the next 3 months, AV delay was abbreviated to achieve > 80% ventricular pacing at an optimal AV interval. For the final 3 months, the first setting was resumed. At the end of each period, M mode echocardiography, pulsed-Doppler study, and measurement of plasma brain natriuretic peptide (BNP) level were conducted. In both groups, echocardiographic parameters were not significantly changed during the evaluation. In group A, plasma BNP level was significantly higher at the end of the short AV delay period than at the long AV delay period (P = 0.009), while in group B it did not differ during each period. AV synchronous pacing (> 80% ventricular pacing) in the SSS patients with a DDD pacemaker implanted could increase the ventricular load, and it is better to preserve the spontaneous QRS with the DDD mode with prolonged AV delay in patients with mild hypertensive or valvular disease.

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Clinical Significance of Preserving Spontaneous QRS Wave in the Therapy of DDD Pacing for Sick Sinus Syndrome

Mani¹,

Shirayama

Suzaki

et al. 2004

“…The importance of LA con- tribution to LV performance during ventricular pacing was previously shown in dogs 8 and humans. 6,9,10 Padeletti et al 19 demonstrated that optimal AV delay was longer in patients with the atrial lead located in the RAA versus intraatrial septum. LV function was also related to ventricular pacing lead location in dogs 20 and humans.…”

Section: Discussionmentioning

confidence: 99%

“…Previous investigations have evaluated the dependence of ventricular performance on AV coupling. [6][7][8][9][10] In addition, the increased clinical use of active-fixation atrial pacing leads has stimulated exploration of alternative atrial lead locations to prevent atrial arrhythmias. [11][12][13][14][15] The present investigation tested the hypothesis that atrial pacing lead location can change the dependence of left atrial (LA) and left ventricular (LV) hemodynamics on AV timing in dogs.…”

Section: Introductionmentioning

confidence: 99%

Atrial Pacing Lead Location Alters the Effects of Atrioventricular Delay on Atrial and Ventricular Hemodynamics

Hettrick

Euler

Pagel

et al. 2002

The combined role of atrial pacing lead location and AV timing on cardiovascular performance has not been defined. This study tested the hypothesis that atrial pacing lead location can change the dependence of LA and LV hemodynamics on AV timing in vivo. Dogs anesthetized with isoflurane (n = 8) were instrumented for measurement of hemodynamics including LA pressure, LA volume, and pulmonary venous bloodflow. Data were recorded during normal sinus rhythm, and atrial overdrive pacing from the right atrial appendage (RAA), proximal coronary sinus (CS), and LA lateral wall (LAW). The AV node was then ablated and measurements repeated during synchronous ventricular pacing and during dual chamber pacing from each atrial lead location at various AV delays (20, 60, 120, 180, 240, and 350 ms). Hemodynamics during intrinsic sinus rhythm and overdrive atrial pacing from different sites were similar. In contrast, ventricular or dual chamber pacing caused significant (P < 0.05) changes in cardiac output with different AV timing during RAA (3.5 +/- 0.2 vs 2.9 +/- 0.2 L/min at 120 and 350 ms, respectively) and LAW pacing but not CS pacing. A significant interaction between atrial lead location and AV delay was observed for changes in stroke volume, pulmonary venous blood transport, LA volume, and LV preload. The results indicate that the atrial contribution to cardiac output depends on AV timing and atrial lead location in isoflurane-anesthetized dogs with AV nodal conduction block.

“…Hemodynamic benefits of dual chamber pacing including adaptation to sinus rhythm and maintenance of AV synchrony, [24][25][26][27][28] have been demonstrated by Doppler, 10,14,15,29,30 radionuclide, 31 and invasive 32 studies in patients with diverse underlying pathologies. 9,10,[33][34][35][36][37][38][39][40] Cardiac output may increase by nearly 30% in AV synchronous pacing compared to ventricular inhibited single chamber pacing.…”

Section: Discussionmentioning

confidence: 99%

Atrioventricular Interval Optimization and Exercise Tolerance

Khairy

Talajic

Domínguez

et al. 2001

Modern pacemakers offer many programming options regarding the AV interval including the ability to vary AV intervals depending on whether atrial activity is paced or spontaneous and to shorten AV intervals with increasing rates. To determine if optimization of these features improves exercise tolerance, 14 patients with intact sinus node function and AV block treated with dual chamber pacemakers were enrolled in a randomized double-blind crossover trial. Doppler echocardiographic measurements of cardiac index and mitral flow were assessed over a range of programmable AV intervals at rest to determine each patient's optimal AV interval. Eleven patients completed serial graded exercise tests with spiroergometry after randomly programming the AV interval three ways in a crossover manner: fixed AV interval = 150 ms without rate adaptation (150/Fixed), fixed AVinterval = 150 ms with rate adaptation (150/R), or optimized AV interval with rate adaptive AV interval shortening (optimized/R). Exercise capacity was determined by maximum oxygen uptake. Ten men and four women, age 64 +/- 8 years, were enrolled. At rest, optimization of the AVintervalimproved the cardiac index by 21% (P < 0.001) and mitral flow by 13.4% (P < 0.001) when compared to least-favorable AV intervals. During exercise, no differences in maximum heart rates were noted. Maximum oxygen uptake was increased in both groups with rate adaptive AVinterval shortening when compared tofixed AVinterval without rate adaptation: 13.9% (adjusted P < 0.04) and 14.6% (adjusted P < 0.02) in optimized/R and 150/R, respectively. No differences were noted between optimized/R and 150/R. In conclusion, rate adaptive AV interval shortening improved exercise tolerance independent of changes in heart rate. However, optimization of the AV interval with Doppler echocardiography at rest did not further improve exercise capacity.