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      Cardiac Resynchronization Pacing Therapy

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          Approximately one third of patients with congestive heart failure and systolic dysfunction have an intraventricular conduction delay that is manifested as a QRS duration >120 ms. An intraventricular conduction delay adversely affects ventricular performance by causing dyssynchrony in ventricular activation. When ventricular dyssynchrony is present, simultaneous left and right ventricular pacing or cardiac resynchronization therapy can improve ventricular synchrony. This can lead to an improvement in hemodynamics, ventricular remodeling, mitral regurgitation, exercise capacity and quality of life. Candidates for cardiac resynchronization therapy include patients with advanced congestive heart failure that is refractory to medical therapy, a QRS duration >130 ms, left ventricular ejection fraction <0.35 and sinus rhythm. Because patients who are candidates for biventricular pacing are at high risk of sudden death, they should be considered for implantation of a biventricular pacing device that also provides defibrillation therapy. This paper reviews biventricular pacing for congestive heart failure, including results of acute hemodynamic studies and randomized clinical trials, patient and device selection, and procedural issues.

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          Most cited references 8

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          A dose-dependent increase in mortality with vesnarinone among patients with severe heart failure. Vesnarinone Trial Investigators.

          Vesnarinone, an inotropic drug, was shown in a short-term placebo-controlled trial to improve survival markedly in patients with severe heart failure when given at a dose of 60 mg per day, but there was a trend toward an adverse effect on survival when the dose was 120 mg per day. In a longer-term study, we evaluated the effects of daily doses of 60 mg or 30 mg of vesnarinone, as compared with placebo, on mortality and morbidity. We enrolled 3833 patients who had symptoms of New York Heart Association class III or IV heart failure and a left ventricular ejection fraction of 30 percent or less despite optimal treatment. The mean follow-up was 286 days. There were significantly fewer deaths in the placebo group (242 deaths, or 18.9 percent) than in the 60-mg vesnarinone group (292 deaths, or 22.9 percent) and longer survival (P=0.02). The increase in mortality with vesnarinone was attributed to an increase in sudden death, presumed to be due to arrhythmia. The quality of life had improved significantly more in the 60-mg vesnarinone group than in the placebo group at 8 weeks (P<0.001) and 16 weeks (P=0.003) after randomization. Trends in mortality and in measures of the quality of life in the 30-mg vesnarinone group were similar to those in the 60-mg group but not significantly different from those in the placebo group. Agranulocytosis occurred in 1.2 percent of the patients given 60 mg of vesnarinone per day and 0.2 percent of those given 30 mg of vesnarinone. Vesnarinone is associated with a dose-dependent increase in mortality among patients with severe heart failure, an increase that is probably related to an increase in deaths due to arrhythmia. A short-term benefit in terms of the quality of life raises issues about the appropriate therapeutic goal in treating heart failure.
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            Effects of dual-chamber pacing with short atrioventricular delay in dilated cardiomyopathy.

            Mitral or tricuspid regurgitation of long duration may so shorten the ventricular filling time in dilated cardiomyopathy that stroke volume is limited. We assessed the effects of changing the atrioventricular interval during temporary or permanent dual-chamber DDD pacing in twelve dilated cardiomyopathy patients with short ventricular filling times due to regurgitation. We measured ventricular filling time and cardiac output with doppler echocardiography and exercise capacity on a treadmill, at baseline and with the best atrioventricular delay during pacing. The durations of both mitral and tricuspid regurgitation were significantly shorter at the shorter atrioventricular interval (mean reductions 85 [95% CI 60-110] ms and 110 [75-150] ms, respectively; p < 0.001 for both). There were consequent increases in left-ventricular and right-ventricular filling times (65 [35-95] ms and 90 [60-120] ms, p < 0.001). For each 50 ms reduction in atrioventricular delay, left-ventricular filling time increased by 35 ms in six subjects with presystolic mitral regurgitation and right-ventricular filling time by 30 ms in nine subjects with presystolic tricuspid regurgitation. At the short atrioventricular interval, cardiac output was greater than baseline (by 1.1 [0.8-1.4] l/min, p < 0.01) and there were rises in exercise duration (104 [45-165] s, p < 0.05) and maximum oxygen consumption (2.1 [1.5-2.7] ml kg-1 min-1, p < 0.05). There was a decrease in the Likert visual analogue score of breathlessness at peak exercise (8.6 [SD 2.1] vs 4.9 [3.1], p < 0.01). Although from a small sample, these findings suggest that DDD pacing with a short atrioventricular delay may have therapeutic potential in patients with dilated cardiomyopathy, even in the absence of conventional indications for pacemaker implantation.
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              Acute hemodynamic effects of atrio-biventricular pacing in humans.

              Standard postoperative dual-chamber pacing uses ventricular leads placed on the right ventricle that produce dysynchronous ventricular activation and contraction. The hypothesis that simultaneous stimulation of both ventricles by atrio-biventricular pacing improves hemodynamic performance compared with that observed with standard atrio-monoventricular pacing was tested in 18 patients 12 to 36 hours after elective coronary artery revascularization. Temporary epicardial pacing electrodes were placed on the right atrium and into anterior paraseptal sites on the right and left ventricle. Simultaneous biventricular activation was documented by fusion morphology of surface electrocardiograms and by isochronal epicardial activation mapping during biventricular pacing. Hemodynamic data were acquired after 10 minutes of pacing at a fixed overdrive rate during atrial pacing and during dual-chamber pacing using unipolar right ventricular, unipolar left ventricular, and bipolar biventricular (left ventricular cathode) leads. Atrio-biventricular pacing increased cardiac index and decreased systemic vascular resistance compared with atrial pacing and with atrio-right ventricular and atrio-left ventricular dual-chamber pacing (p < 0.05). These data support the use of atrio-biventricular pacing employing paraseptal electrodes to optimize hemodynamic performance.

                Author and article information

                S. Karger AG
                February 2004
                27 February 2004
                : 101
                : 1-3
                : 72-78
                Division of Cardiology, Department of Internal Medicine, University of Chicago, Chicago, Ill., USA
                75987 Cardiology 2004;101:72–78
                © 2004 S. Karger AG, Basel

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                Page count
                Figures: 2, Tables: 1, References: 28, Pages: 7


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