LV cathode position in CRT recipients: How can we benefit from CMR?

BACKGROUND: Left ventricular lead positioning represents a key step in CRT optimization. However, evidence for its guidance based on specific topographical factors and related imaging techniques is sparse. OBJECTIVE: To analyze reverse remodeling (RR) and clinical events in CRT recipients based on LV cathode (LVC) position relative to latest mechanical activation (LMA) and scar as determined by cardiac magnetic resonance (CMR). METHODS: This is a retrospective single-center study of 68 consecutive Q-LV-guided CRT-D and CRT-P recipients. Through CMR-based 3D reconstructions overlayed on fluoroscopy images, LVCs were stratified as concordant, adjacent, or discordant to LMA (3 segments with latest and greatest radial strain) and scar (segments with >50% scar transmurality). The primary endpoint of RR (expressed as percentage ESV change) and secondary composite endpoint of HF hospitalizations, LVAD/heart transplant, or cardiovascular death were compared across categories. RESULTS: LVC proximity to LMA was associated with a progressive increase in RR (percentage ESV change: concordant -47.0 ± 5.9%, adjacent -31.4 ± 3.1%, discordant +0.4 ± 3.7%), while proximity to scar was associated with sharply decreasing RR (concordant +10.7 ± 12.9%, adjacent +0.3 ± 5.3%, discordant -31.3 ± 4.4%, no scar -35.4 ± 4.8%). 4 integrated classes of LVC position demonstrated a significant positive RR gradient the more optimal the category (class I -47.0 ± 5.9%, class II -34.9 ± 2.8%, class III -5.5 ± 4.3%, class IV + 3.4 ± 5.2%). Freedom from composite secondary endpoint of HF hospitalization, LVAD/heart transplant, or cardiovascular death confirmed these trends demonstrating significant differences across both integrated as well as individual LMA and scar categories. CONCLUSION: Integrated CMR-determined LVC position relative to LMA and scar stratifies response to CRT.

Stimulus-effect relations for left ventricular growth obtained with a simple multi-scale model: the influence of hemodynamic feedback.

Cardiac growth is an important mechanism for the human body to respond to changes in blood flow demand. Being able to predict the development of chronic growth is clinically relevant, but so far models to predict growth have not reached consensus on the stimulus-effect relation. In a previously published study, we modeled cardiac and hemodynamic function through a lumped parameter approach. We evaluated cardiac growth in response to valve disease using various stimulus-effect relations and observed an unphysiological decline pump function. Here we extend that model with a model of hemodynamic feedback that maintains mean arterial pressure and cardiac output through adaptation of peripheral resistance and circulatory unstressed volume. With the combined model, we obtain stable growth and restoration of pump function for most growth laws. We conclude that a mixed combination of stress and strain stimuli to drive cardiac growth is most promising since it (1) reproduces clinical observations on cardiac growth well, (2) requires only a small, clinically realistic adaptation of the properties of the circulatory system and (3) is robust in the sense that results were fairly insensitive to the exact choice of the chosen mechanics loading measure. This finding may be used to guide the choice of growth laws in more complex finite element models of cardiac growth, suitable for predicting the response to spatially varying changes in tissue load. Eventually, the current model may form a basis for a tool to predict patient-specific growth in response to spatially homogeneous changes in tissue load, since it is computationally inexpensive.

Evaluation of stimulus-effect relations in left ventricular growth using a simple multiscale model.

Cardiac growth is the natural capability of the heart to change size in response to changes in blood flow demand of the growing body. Cardiac diseases can trigger the same process leading to an abnormal type of growth. Prediction of cardiac growth would be clinically valuable, but so far published models on cardiac growth differ with respect to the stimulus-effect relation and constraints used for maximum growth. In this study, we use a zero-dimensional, multiscale model of the left ventricle to evaluate cardiac growth in response to three valve diseases, aortic and mitral regurgitation along with aortic stenosis. We investigate how different combinations of stress- and strain-based stimuli affect growth in terms of cavity volume and wall volume and hemodynamic performance. All of our simulations are able to reach a converged state without any growth constraint, with the most promising results obtained while considering at least one stress-based stimulus. With this study, we demonstrate how a simple model of left ventricular mechanics can be used to have a first evaluation on a designed growth law.