Comparison of acute changes in left ventricular volume, systolic and diastolic functions, and intraventricular synchronicity after biventricular and right ventricular pacing for heart failure
ABSTRACT Biventricular pacing (BiV) therapy has recently been shown to improve systolic function and cause reverse remodeling in patients with advanced heart failure with electromechanical delay. In these patients, the benefit of right ventricular (RV)-based pacing was controversial. We compared the acute changes in systolic and diastolic function, left ventricular (LV) volume, and intraventricular synchronicity in BiV pacing, RV pacing, and without pacing (No) by means of echocardiography and tissue Doppler imaging (TDI).
TDI was performed in 33 patients with heart failure after undergoing pacemaker implantation, when the device was randomized to BiV, RV, and no pacing modes.
Systolic function was only improved during BiV pacing, but not during RV pacing. This included ejection fraction (No vs RV vs BiV = 24% +/- 12% vs 25% +/- 10% vs 30% +/- 14%, P =.02 vs No), +dp/dt (P =.01), myocardial performance index (P =.01), and isovolumic contraction time (P =.03). Mitral regurgitation was only reduced during BiV pacing (P =.02). LV early diastolic function was depressed in both RV and BiV pacing, as detected by transmitral flow (97 +/- 34 vs 80 +/- 34 vs 82 +/- 32 cm/s, both P < or =.005) and TDI (mean myocardial early diastolic velocity of 6 basal segments, 3.3 +/- 1.7 vs 2.6 +/- 1.0 vs 2.6 +/- 1.0 cm/s, both P =.01). The LV end-diastolic (187 +/- 86 vs 177 +/- 84 vs 166 +/- 79, P =.003) and end-systolic (146 +/- 77 vs 138 +/- 79 vs 122 +/- 69, P =.003) volumes were only decreased during BiV pacing. For systolic synchronicity, a significant delay in peak systolic contraction in the lateral over the septal wall (171 +/- 37 vs 217 +/- 46 ms, P =.004) was revealed by TDI when there was no pacing. This was abolished by BiV pacing, in which septal contraction was delayed (195 +/- 38 vs 201 +/- 53 ms, P = not significant). However, RV pacing restored the lateral wall delay, and systolic asynchrony reappeared (190 +/- 40 vs 227 +/- 56 ms, P =.01). Diastolic asynchrony between the septal and lateral walls was not evident in these patients and was not affected by either pacing mode.
Only BiV pacing, but not RV pacing, improves systolic function, and reduces mitral regurgitation and LV volumes in patients with heart failure and electromechanical delay. This is attributed to the improvement of systolic synchronicity. Diastolic synchronicity was unaffected, whereas early diastolic function could be jeopardized, by either pacing mode.
- SourceAvailable from: Xiu-Xia Luo
[Show abstract] [Hide abstract]
- "If there was Doppler angle between ultrasound beam and color signal, an angle correction was performed without exceeding 30°. Peak diastolic velocity, diastolic duration and velocity-time integral (VTI) were calculated   . "
ABSTRACT: Introduction: Right ventricular (RV) pacing may affect myocardial perfusion and coronary blood flow; however, it remains unknown whether this is related to systolic dyssynchrony induced by RV pacing. This prospective study was aimed to assess the relationship between dyssynchrony and the changes of coronary blood flow. Methods: Seventy patients with sinus node dysfunction were prospectively enrolled. Coronary flow was evaluated by measuring diastolic velocity time integral (VTI) and duration at the distal-portion of left anterior descending coronary artery (LAD) with transthoracic echocardiography at baseline and follow-up. Systolic dyssynchrony was assessed with tissue Doppler imaging by time standard deviation to peak systolic velocity of 12 left ventricular segments (Ts-SD, cutoff value ≥ 33 ms). Results: Adequate data for analysis was available from 65 patients. At follow-up (mean follow up time: 127 ± 45 days), LAD velocity-time integral (LAD-VTI: 12.1 ± 4.2 vs. 10.7 ± 4.6 cm, p<0.001) was decreased and there was deterioration of left ventricular systolic function (left ventricular ejection fraction: 65 ± 7% vs. 62 ± 7%). However, these changes were only detected in those with RV pacing induced systolic dyssynchrony. Significant reduction of LAD-VTI (defined as ≥ 5%) occurred in 34 (52%) patients which was more prevalent in those with pacing-induced systolic dyssynchrony than those without (85.3% versus 16.1%, χ(2)=31.1, p<0.001). Though similar at baseline, LAD-VTI was significantly lower in the dyssynchrony group at follow up (p<0.001). Cox-regression analysis showed that pacing-inducing systolic dyssynchrony [hazard ratio (HR): 3.62, p=0.009] and higher accumulative pacing percentage (HR: 1.02, p=0.002) were independently associated with reduction of LAD-VTI. ROC curve demonstrated that accumulative pacing percentage ≥ 35% was 97% sensitive and 84% specific in revealing significant reduction (area under the curve: 0.961, p<0.001). Conclusions: RV pacing induced dyssynchrony is associated with reduced coronary flow and this may account for, in part, the deleterious effect of RV pacing on ventricular function over time.International Journal of Cardiology 07/2014; 176(1). DOI:10.1016/j.ijcard.2014.06.037 · 4.04 Impact Factor
- [Show abstract] [Hide abstract]
ABSTRACT: Heart failure is a major epidemic. Many people with heart failure struggle with refractory symptoms despite optimal medical therapy. Those with severe left ventricular dysfunction and ventricular conduction delay are at significant risk from either dying suddenly or dying from progression of their heart failure. Cardiac resynchronization therapy (CRT) improves hemodynamics and symptoms of heart failure and has recently been shown to improve survival. One problem facing the use of CRT is that 30% of patients fail to respond. The dominant theory is that QRS duration (electrical dyssynchrony) does not accurately reflect mechanical dyssynchrony. Echocardiographic tools have recently been developed that enable clinicians to assess the degree of mechanical dyssynchrony in patients being considered for CRT. These tools are able to predict with a significant amount of accuracy whether a patient will respond to CRT. This allows for a more refined approach to evaluating patients for CRT and optimizing the treatment of congestive heart failure.Congestive Heart Failure 07/2005; 11(4):199-206. DOI:10.1111/j.1527-5299.2005.04408.x