Abstract

Coronary wave intensity analysis (cWIA) is a diagnostic technique based on invasive measurement of coronary pressure and velocity waveforms. The theory of WIA allows the forward- and backward-propagating coronary waves to be separated and attributed to their origin and timing, thus serving as a sensitive and specific cardiac functional indicator. In recent years, an increasing number of clinical studies have begun to establish associations between changes in specific waves and various diseases of myocardium and perfusion. These studies are, however, currently confined to a trial-and-error approach and are subject to technological limitations which may confound accurate interpretations. In this work, we have developed a biophysically based cardiac perfusion model which incorporates full ventricular–aortic–coronary coupling. This was achieved by integrating our previous work on one-dimensional modelling of vascular flow and poroelastic perfusion within an active myocardial mechanics framework. Extensive parameterisation was performed, yielding a close agreement with physiological levels of global coronary and myocardial function as well as experimentally observed cumulative wave intensity magnitudes. Results indicate a strong dependence of the backward suction wave on QRS duration and vascular resistance, the forward pushing wave on the rate of myocyte tension development, and the late forward pushing wave on the aortic valve dynamics. These findings are not only consistent with experimental observations, but offer a greater specificity to the wave-originating mechanisms, thus demonstrating the value of the integrated model as a tool for clinical investigation.

Highlights

  • Impaired myocardial blood flow underlies a wide range of cardiac diseases

  • The heart and coronary geometries were obtained from a previous experimental study performed on a 40-kg Danish Landrace pig (Schuster et al 2010)

  • The resulting mesh was truncated to restrict its extent to the upper arterial network, by dividing the myocardium into approximately 0.02 mL volumes and seeking a supplying vessel segment within each, with a target diameter of 200 μm

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Summary

Introduction

Impaired myocardial blood flow underlies a wide range of cardiac diseases. Notably, there are ∼3M coronary angiographies undertaken every year to diagnose coronary artery disease in Europe alone (Cook 2011). Myocardial ischaemia has received attention as a secondary contributor to several other cardiac diseases including hypertrophic cardiomyopathy (Maron et al 2009), aortic stenosis (Rajappan et al 2003) and heart failure (Nakanishi et al 2012). Perfusion deficits can be brought on by disparate causes, including stenotic lesions in large vessels or microvascular dysfunction, as well as the increase in extravascular compression which is known to heighten subendocardial vulnerability to ischaemia (Hittinger et al 1995; Heusch 2008). Due to this physiological complexity, the differential diagnosis and the therapeutic trajectories must be pieced together from additional clinical evidences. There has been much interest in a diagnostic approach which would unite the currently overlooked assessments of coronary microcirculation and perfusion–contraction crosstalk into the existing routine clinical workflow

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