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  • Title: Pacemaker-induced mitral regurgitation: prominent role of abnormal ventricular activation sequence versus altered atrioventricular synchrony.
    Author: Sassone B, De Simone N, Parlangeli G, Tortorici R, Biancoli S, Di Pasquale G.
    Journal: Ital Heart J; 2001 Jun; 2(6):441-8. PubMed ID: 11453581.
    Abstract:
    BACKGROUND: Functional mitral regurgitation is a hemodynamic adverse consequence of right ventricular apical pacing that profoundly modifies the contraction and relaxation of the left ventricle by inverting and delaying its activation sequence. The aim of this study was to analyze by Doppler echocardiography in the acute setting the true incidence and the mechanism responsible for the right ventricular apical pacing-induced mitral regurgitation. METHODS: We studied 27 consecutive patients submitted to pacemaker implantation (VVI n = 9; DDD n = 18) because of bradyarrhythmias. The exclusion criteria were structural cardiac disease and permanent atrioventricular block. Patients underwent Doppler echocardiographic examination during both spontaneous rhythm (pacemaker off) as well as during programmed pacing at a rate of 70 b/min. In case of a double chamber pacemaker, a non-optimized atrioventricular delay of 150 ms was chosen. RESULTS: Two groups were identified: 11 patients with (Group 1, mean age 71 +/- 7 years) and 16 patients without (Group 2, mean age 71 +/- 4 years) new-onset pacing-induced mitral regurgitation. The incidence of mitral regurgitation was found to be higher during DDD (33%) than during VVI (24%) pacing mode. The relationship between gender and the occurrence of pacing-induced mitral regurgitation was striking: 10/13 women (77%) presented with mitral regurgitation during acute right ventricular apical pacing while this complication occurred in only 1/14 men (7%). Moreover, analysis of variance (ANOVA) and post-hoc pairwise multiple comparison showed an increased size of the mitral apparatus, as defined by the enlargement of the annulus (long axis 28 +/- 3 vs 23 +/- 2 mm; short axis 25 +/- 3 vs 20 +/- 3 mm, p = 0.05) and the lengthening of the anterior mitral leaflet (23 +/- 4 vs 18 +/- 2 mm, p = 0.05) and chordae tendineae (16 +/- 3 vs 13 +/- 2 mm, p = 0.05). This was probably related to the high female prevalence (91%) in Group 1 as compared to the control group (50 healthy subjects; 17 men, 33 women; mean age 71 +/- 8 years). No significant differences were observed between Group 2 and controls. CONCLUSIONS: Our study confirmed that functional mitral regurgitation is a frequent consequence of right ventricular apical pacing. Despite the maintenance of normal atrioventricular synchrony, we found that the pathway for ventricular depolarization was the critical determinant of normal mitral valve function. Such data show the importance of the preservation of a normal ventricular activation sequence during permanent cardiac pacing where it is technically feasible. Female patients seemed to be exposed to a higher risk of pacing-induced mitral regurgitation due to an anatomic predisposing condition of the mitral apparatus and to the left ventricular dyssynchronous contraction secondary to right ventricular apical pacing.
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