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Efficient preloading of the ventricles by a properly timed atrial contraction underlies stroke work improvement in the acute response to cardiac resynchronization therapy.

ABSTRACT: The acute response to cardiac resynchronization therapy (CRT) has been shown to be due to 3 mechanisms: resynchronization of ventricular contraction, efficient preloading of the ventricles by a properly timed atrial contraction, and mitral regurgitation reduction. However, the contribution of each of the 3 mechanisms to the acute response to CRT, specifically stroke work improvement, has not been quantified.To use a magnetic resonance image-based anatomically accurate 3-dimensional model of failing canine ventricular electromechanics to quantify the contribution of each of the 3 mechanisms to stroke work improvement and identify the predominant mechanisms.An MRI-based electromechanical model of the failing canine ventricles assembled previously by our group was further developed and modified. Three different protocols were used to dissect the contribution of each of the 3 mechanisms to stroke work improvement.Resynchronization of ventricular contraction did not lead to a significant stroke work improvement. Efficient preloading of the ventricles by a properly timed atrial contraction was the predominant mechanism underlying stroke work improvement. Stroke work improvement peaked at an intermediate atrioventricular delay, as it allowed ventricular filling by atrial contraction to occur at a low diastolic left ventricular pressure but also provided adequate time for ventricular filling before ventricular contraction. Reduction of mitral regurgitation by CRT led to stroke work worsening instead of improvement.Efficient preloading of the ventricles by a properly timed atrial contraction is responsible for a significant stroke work improvement in the acute CRT response.

SUBMITTER: Hu Y

PROVIDER: S-EPMC3852188 | biostudies-literature | 2013 Dec

REPOSITORIES: biostudies-literature

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Efficient preloading of the ventricles by a properly timed atrial contraction underlies stroke work improvement in the acute response to cardiac resynchronization therapy.

Hu Yuxuan Y Gurev Viatcheslav V Constantino Jason J Trayanova Natalia N

Heart rhythm 20130806 12

<h4>Background</h4>The acute response to cardiac resynchronization therapy (CRT) has been shown to be due to 3 mechanisms: resynchronization of ventricular contraction, efficient preloading of the ventricles by a properly timed atrial contraction, and mitral regurgitation reduction. However, the contribution of each of the 3 mechanisms to the acute response to CRT, specifically stroke work improvement, has not been quantified.<h4>Objective</h4>To use a magnetic resonance image-based anatomically ...[more]

PMID: 23928177

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Project description:AimsA waiting period of more than 3 months is recommended for patients before undergoing cardiac resynchronization therapy (CRT). However, due to an anticipated high mortality rate, early implementation of CRT might be beneficial for some patients. We aimed to evaluate the rate and the probability of left ventricular (LV) function improvement and their predictors in patients with heart failure (HF) with indications for CRT.Methods and resultsFrom March 2011 to February 2014, a total of 5625 hospitalized patients for acute HF were consecutively enrolled in 10 tertiary hospitals. Among them, we analysed 1792 patients (mean age 63.96 ± 15.42 years, female 63.1%) with left ventricular ejection fraction (LVEF) ≤ 35% at the baseline echocardiography and divided them into three groups: 144 with left bundle branch block (LBBB), 136 with wide QRS complexes without LBBB, and 1512 not having these findings (control). We compared and analysed these three groups for improvement of LV function at follow-up echocardiography. In patients who met CRT indications (patients with LBBB or wide QRS complexes without LBBB), logistic regression was performed to identify risk factors for no improvement of LV. No improvement of LV was defined as LVEF ≤ 35% at follow-up echocardiography or the composite adverse outcomes: death, heart transplantation, extracorporeal membrane oxygenation, or use of a ventricular assist device before follow-up echocardiography. A classification tree was established using the binary recursive partitioning method to predict the outcome of patients who met CRT indications. In a median follow-up of 11 months, LVEF improvement was observed in 24.3%, 15.4%, and 40.5% of patients with LBBB, wide QRS complexes without LBBB, and control, respectively. Patients meeting CRT indications had higher 3 month mortality rates than the control (24.6% vs. 17.7%, P = 0.002). Multivariable logistic regression analysis revealed that large LV end-systolic dimension [odds ratio (OR) 1.10, 95% confidence interval (CI) 1.05-1.15, P < 0.001], low LVEF (OR 0.92, 95% CI 0.87-0.98, P = 0.006), diabetes requiring insulin (OR 6.49, 95% CI 2.53-19.33, P < 0.001), and suboptimal medical therapy (OR 6.85, 95% CI 3.21-15.87, P < 0.001) were significant factors predictive of no improvement. A decision tree analysis was consistent with these results.ConclusionsPatients with CRT indications had higher mortality during their follow-up compared with control. LV function improvement was rare in this population, especially when they had some risk factors. These results suggest that the uniform waiting period before CRT implantation could be reconsidered and individualized.

Project description:Introduction: Timing of atrial, right (RV), and left ventricular (LV) stimulation in cardiac resynchronization therapy (CRT) is known to affect electrical activation and pump function of the LV. In this study, we used computer simulations, with input from animal experiments, to investigate the effect of varying pacing delays on both LV and RV electrical dyssynchrony and contractile function. Methods: A pacing protocol was performed in dogs with atrioventricular block (N = 6), using 100 different combinations of atrial (A)-LV and A-RV pacing delays. Regional LV and RV electrical activation times were measured using 112 electrodes and LV and RV pressures were measured with catheter-tip micromanometers. Contractile response to a pacing delay was defined as relative change of the maximum rate of LV and RV pressure rise (dP/dtmax) compared to RV pacing with an A-RV delay of 125 ms. The pacing protocol was simulated in the CircAdapt model of cardiovascular system dynamics, using the experimentally acquired electrical mapping data as input. Results: Ventricular electrical activation changed with changes in the amount of LV or RV pre-excitation. The resulting changes in dP/dtmax differed markedly between the LV and RV. Pacing the LV 10-50 ms before the RV led to the largest increases in LV dP/dtmax. In contrast, RV dP/dtmax was highest with RV pre-excitation and decreased up to 33% with LV pre-excitation. These opposite patterns of changes in RV and LV dP/dtmax were reproduced by the simulations. The simulations extended these observations by showing that changes in steady-state biventricular cardiac output differed from changes in both LV and RV dP/dtmax. The model allowed to explain the discrepant changes in dP/dtmax and cardiac output by coupling between atria and ventricles as well as between the ventricles. Conclusion: The LV and the RV respond in a opposite manner to variation in the amount of LV or RV pre-excitation. Computer simulations capture LV and RV behavior during pacing delay variation and may be used in the design of new CRT optimization studies.

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Efficient preloading of the ventricles by a properly timed atrial contraction underlies stroke work improvement in the acute response to cardiac resynchronization therapy.

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Efficient preloading of the ventricles by a properly timed atrial contraction underlies stroke work improvement in the acute response to cardiac resynchronization therapy.

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