The Deleterious Effect of Right Ventricular Apical Pacing on Atrial Function in Patients with Preserved Systolic Function.

摘要

Cardiac pacing has been the only effective treatment in the management of patients with symptomatic bradycardia caused by sinus node dysfunction or atrioventricular block for decades. Conventional dual-chamber pacing is performed by implanting two leads in right atrial (RA) appendage and right ventricular (RV) apex separately. RV apex is the most commonly applied pacing site because it can be easily reached and allows a chronically stable position and stimulation thresholds. However, large randomized clinical trials have suggested that right ventricular apical (RVA) pacing may cause abnormal ventricular contraction and reduce pump function and lead to myocardial hypertrophy, in particular in patients with impaired left ventricular (LV) function. Recent studies have also reported a reduced LV systolic function in patients with pacing indications and preserved ejection fraction. The deleterious effects of RVA pacing on LV function may be related to the abnormal electrical and mechanical activation pattern or ventricular dyssynchrony. During RVA pacing, conduction of the electrical wave front propagates slowly through ventricular myocardium rather than through the His-Purkinje conduction system, comparable to left bundle branch block (LBBB). In addition, RVA pacing alters ventricular synchrony and loading conditions which may result in diastolic heart failure with abnormal LV relaxation, high filling pressure and low cardiac output state. Furthermore, it is possible that left atrial (LA) remodeling and reduction of atrial function may occur during RVA pacing. However, it is not been carefully studied.;Echocardiography is a convenient, non-invasive and established tool to assess cardiac function in clinical practice. Conventional two-dimensional echocardiography is useful to assess cardiac chamber size, volume and function. With the development of real time three-dimensional echocardiography (RT3DE) and color tissue Doppler imaging (TDI), echocardiography provides further valuable information and more accurate measurements which include myocardial velocity and parameters of dyssynchrony. In the present study, the main echocardiographic parameters including the maximal left atrial volume (LAVmax), pre-atrial contraction volume (LAVpre) and the minimal left atrial volume (LAVmin) were assessed by two-dimensional echocardiography. Peak systolic (Sm-la), peak early diastolic (Em-la), peak late diastolic (Am-la) velocities of left atrium (LA) and atrial conduction time (from onset of P wave on electrocardiogram to onset of atrial velocity) were measured by TDI.;In a cross-sectional study, ninety-eight patients who had been implanted with RVA-based dual-chamber pacemakers were enrolled. Four patients with pacing dependent were excluded. Eventually 94 patients were included in the final analysis. Echocardiography was performed (iE33, Philips) during intrinsic ventricular conduction (V-sense) and RVA pacing (V-pace) modes with 15 minutes between switching modes. We aimed to investigate if RVA pacing has any acute effects on atrial remodeling and function in patients with preserved ejection fraction (LV ejection fraction> 45%). The result showed that during V-pace, LA volumes increased significantly when compared with V-sense (LAVmax: 52.0 +/- 18.8 vs. 55.2 +/- 21.1 ml, p = 0.005; LAVpre: 39.8 +/- 16.4 vs. 41.3 +/- 16.6 ml, p = 0.014; LAVmin: 27.4 +/- 14.0 vs. 29.1 +/- 15.1 ml, p = 0.001). TDI parameters showed significant reduction in Sm-la (3.0 +/- 1.1 vs. 2.7 +/- 0.9 cm/s, p < 0.01), Em-la (2.7 +/- 1.1 vs. 2.4 +/- 1.0 cm/s, p = 0.001). However, there was no change in Am-la.;In a prospective study, patients with symptomatic bradycardia, preserved ejection fraction, and received RVA pacing were recruited. Echocardiography was performed at both baseline and one year follow up through a standard protocol by experienced echocardiographers. LA volumes and velocities as well as intra- and interatrial dyssynchrony were measured offline with the use of dedicated software. The objectives of this study were to investigate: (1) if RVA pacing has any deleterious effects on LA remodeling and function during long-term follow up; (2) if RA appendage pacing has separate effects on atrial pump function, intra- and interatrial dyssynchrony; (3) if atrial dysfunction and dyssynchrony can predict atrial high rate episodes (AHREs) burden in the first year of RVA pacing. The main findings of this study were: (a) at one year follow up, LA volumes and indexes were increased with reduction in passive emptying fraction and total emptying fraction. Atrial velocities showed significant reduction when compared with baseline; (b) in multivariate regression analysis, the ratio of transmitral early diastolic filling velocity to mitral annular early diastolic velocity (E/e') > 15 at one year and reduction of LV ejection fraction ≥ 5% were independent predictors of reduction of Am-la > 30%; (c) high percent of RA appendage pacing prolonged atrial conduction and induced intra- and interatrial dyssynchrony. (d) Am-la < 5.3 cm/s can predict AHREs burden which had a sensitivity of 71% and specificity of 75%.;In conclusion, our studies suggest even short-term RVA pacing induces LA dilatation and impaired passive atrial function, though it did not have direct effect on active atrial contractility. However, chronic RVA pacing results in LA remodeling and reduces atrial function with decreased contractility. This was more likely to occur in those with impaired LV ejection fraction and evidence of diastolic dysfunction. Atrial dysfunction and interatrial dyssynchrony can predict AHREs burden after chronic RVA pacing. Therefore, measures that may minimize such adverse effect of pacing on atrial function need to considered for patients receiving RVA pacing, such as the use of new pacing modalities.