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[Dual-chamber DDD pacing in NYHA III-IV functional class dilated cardiomyopathy: short and middle-term evaluation]
E Occhetta1, M Bortnik, G Francalacci
1Cattedra e Divisione Clinicizzata di Cardiologia, Università degli Studi di Torino, Sede di Novara.
Insights
Dual-chamber pacing (DDD) in dilated cardiomyopathy patients yielded disappointing results, with no significant long-term improvements. Further research into patient selection and alternative pacing methods is warranted.
Area of Science:
- Cardiology
- Biomedical Engineering
Background:
- Dual-chamber pacing (DDD) effectiveness in dilated cardiomyopathy (DCM) remains controversial.
- Optimizing atrioventricular (AV) delay is crucial for pacing efficacy.
Purpose of the Study:
- To determine the optimal atrioventricular (AV) delay for DDD pacing in DCM patients.
- To compare short-term and long-term hemodynamic effects of DDD pacing versus sinus rhythm.
- To assess the overall effectiveness of DDD pacing in improving clinical outcomes for DCM patients.
Main Methods:
- Nineteen patients with DCM (NYHA class III-IV, EF < 30%) received DDD pacemakers.
- Hemodynamic parameters, clinical status, exercise tolerance, and neurohormonal activity were monitored.
- Patients underwent randomized periods of VVI and DDD pacing with optimized AV delay.
Main Results:
- No significant long-term improvements in clinical or laboratory parameters were observed after 1 year of DDD pacing.
- Three patients died due to refractory heart failure, and one patient discontinued due to intolerance.
- Individualized AV delay optimization did not yield significant benefits in this cohort.
Conclusions:
- DDD pacing in selected DCM patients showed disappointing long-term results.
- Patient selection based on Doppler mitral flow patterns may identify potential responders.
- Biatrial and biventricular pacing strategies warrant further investigation for DCM.
Abstract:
Effectiveness of dual-chamber pacing in patients with dilated cardiomyopathy is still controversial. Our study was performed: to select the most favorable individual atrioventricular (AV) delay; to compare hemodynamic short-term effects in each patient after 2 periods of DDD pacing and sinus rhythm (AV spontaneous); to assess hemodynamic long-term (1 year) effects after DDD pacing at optimum AV delay. In 1996, 9 patients (7 men, 2 women; mean age 69 +/- 5 years) with dilated cardiomyopathy (5 idiopathic, 4 ischemic), NYHA functional class III-IV, ejection fraction < 30%, end-diastolic volume > 60 ml/m2, mitral regurgitation +2/+3, PR interval > or = 200 ms, were enrolled. All patients were implanted with DDD pacemakers and monitored for: ejection fraction and end-diastolic volume (measured by echocardiography and radionuclide angiography); clinical conditions; exercise tolerance and maximum oxygen consumption (by Weber exercise protocol); neurohormonal activity (plasma renin, aldosterone, atrial natriuretic factor). Data were recorded: before DDD implantation; after 2 randomized, single-blind periods of 3 months in VVI mode (at ventricular "sentinel" rate of 50 b/min) and in DDD mode with the optimum AV delay, corresponding for each patient to the minimum end-diastolic volume measured by radionuclide angiography and to the highest cardiac output recorded by echocardiography; after 6 months of DDD pacing with most favorable AV delay. Three more patients died 6 months after (between sixth and twelfth month of follow-up), due to refractory heart failure; 1 patient dropped out because his pacemaker was programmed in VVI mode at low rate, due to intolerance of DDD pacing. Among the other 4 patients no clinical and laboratory parameters were significantly different after 1 year of follow-up. In conclusion, DDD pacing in selected patients with dilated cardiomyopathy showed disappointing results, despite a strict and laboratory monitoring; DDD pacing could be of major benefit in larger populations, according to Doppler mitral flow pattern: those patients with a larger A-wave amplitude could be more sensitive to DDD pacing than those with evidence of poor atrial systole. Moreover, biatral and/or biventricular pacing could also play a significant role.