Abstract
In this work we present a one-dimensional (1D) mathematical model of the coronary circulation and use it to study the effects of arrhythmias on coronary blood flow (CBF). Hydrodynamical models are rarely used to study arrhythmias’ effects on CBF. Our model accounts for action potential duration, which updates the length of systole depending on the heart rate. It also includes dependency of stroke volume on heart rate, which is based on clinical data. We apply the new methodology to the computational evaluation of CBF during interventricular asynchrony due to cardiac pacing and some types of arrhythmias including tachycardia, bradycardia, long QT syndrome and premature ventricular contraction (bigeminy, trigeminy, quadrigeminy). We find that CBF can be significantly affected by arrhythmias. CBF at rest (60 bpm) is 26% lower in LCA and 22% lower in RCA for long QT syndrome. During bigeminy, trigeminy and quadrigeminy, respectively, CBF decreases by 28%, 19% and 14% with respect to a healthy case.
Highlights
Coronary blood flow (CBF) supplies the myocardium tissue with oxygen and other essential nutrients
We calculate the ratios of the average blood flow in the left coronary artery (LCA) and right coronary artery (RCA) in the asynchronous and normal pacing conditions at different heart rate (HR)
The relative change in the average blood flow in LCA is less than 0.5% in all cases because resistance functions (14) for the left coronary arteries (CA) are always synchronous to the heart outflow (7) and, blood flow in LCA is synchronised to the contractions of the left ventricle
Summary
Coronary blood flow (CBF) supplies the myocardium tissue with oxygen and other essential nutrients. The distal coronary vessels are immersed in the myocardium. Myocardium contractions produce external pressure to the immersed blood vessels and substantially elevate the terminal hydraulic resistance. The dependence of the blood flow in coronary arteries (CA) on the characteristics of the heart cycle is an essential feature of CBF. The characteristics of the heart cycle are controlled by the electrical activity of the sinoatrial node (SAN). The SAN activity is modified by a variety of factors: signals from the sympathetic and the parasympathetic nervous system and humoral factors. Some pathological processes and artificial electric stimulation of the myocardium are among the factors, which can modify the heart activity
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