Abstract

Patients with atrial fibrillation (AF) may present ischemic chest pain in the absence of classical obstructive coronary disease. Among the possible causes, the direct hemodynamic effect exerted by the irregular arrhythmia has not been studied in detail. We performed a computational fluid dynamics analysis by means of a 1D-0D multiscale model of the entire human cardiovascular system, enriched by a detailed mathematical modeling of the coronary arteries and their downstream distal microcirculatory districts (subepicardial, midwall and subendocardial layers). Three mean ventricular rates were simulated (75, 100, 125 bpm) in both sinus rhythm (SR) and atrial fibrillation, and an inter-layer and inter-frequency analysis was conducted focusing on the ratio between mean beat-to-beat blood flow in AF compared to SR. Our results show that AF exerts direct hemodynamic consequences on the coronary microcirculation, causing a reduction in microvascular coronary flow particularly at higher ventricular rates; the most prominent reduction was seen in the subendocardial layers perfused by left coronary arteries (left anterior descending and left circumflex arteries).

Highlights

  • Patients with atrial fibrillation (AF) may present ischemic chest pain in the absence of classical obstructive coronary disease

  • At each simulated ventricular rate, independently from the myocardial layer, QAF was significantly reduced compared to QSR (p-values for all QAF vs QSR comparisons < 0.001)

  • Inter-layer analysis showed that, for each simulated ventricular rate, QAF/QSR progressively decreased from the epicardial to the endocardial layer in the distal left coronary artery districts (p-values < 0.001 for both Left Anterior Descending Artery (LAD) and Left Circumflex Artery (LCx)), while this was not the case for the distal Right Coronary Artery (RCA) district (p-value 0.669, 0.409, 0.186 for 75 bpm, 100 bpm and 125 bpm simulations, respectively)

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Summary

Introduction

Patients with atrial fibrillation (AF) may present ischemic chest pain in the absence of classical obstructive coronary disease. Its prevalence has constantly grown during the last decades, reaching a threefold increase over the last 50 ­years[2], and recent epidemiological predictions foresee a further increase, with an estimation of 16–17 million prevalent cases by 2050 in US and Europe, ­respectively[3] Given this important epidemiological burden, detailed comprehension of the physiopathology of this arrhythmia is warranted. Mathematical modeling is a powerful tool to study the complex process of fluid dynamics, complementing empirical findings and providing quantitative insights into physiological and pathophysiological aspects of the cardiovascular system. In this respect, a recent computational multiscale model of the coronary circulation has demonstrated that AF exerts, especially at higher ventricular rates, direct epicardial coronary flow impairment, as well as an imbalance of the oxygen supply–demand ­ratio[18]. By the use of an advanced computational model of the human cardiovascular system, including both arterial and venous vascular compartments, cardio-pulmonary circulation and short-term autoregulation mechanisms, Scientific Reports | (2022) 12:841

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