A computational model applied to myocardial perfusion in the human heart: From large coronaries to microvasculature

2021 ◽  
Vol 424 ◽  
pp. 109836
Author(s):  
Simone Di Gregorio ◽  
Marco Fedele ◽  
Gianluca Pontone ◽  
Antonio F. Corno ◽  
Paolo Zunino ◽  
...  
2021 ◽  
Author(s):  
Giulio Del Corso ◽  
Roberto Verzicco ◽  
Francesco Viola

Mathematics ◽  
2021 ◽  
Vol 9 (17) ◽  
pp. 2128
Author(s):  
Xinyang Ge ◽  
Sergey Simakov ◽  
Youjun Liu ◽  
Fuyou Liang

(1) Background: Arrhythmia, which is an umbrella term for various types of abnormal rhythms of heartbeat, has a high prevalence in both the general population and patients with coronary artery disease. So far, it remains unclear how different types of arrhythmia would affect myocardial perfusion and the risk/severity of myocardial ischemia. (2) Methods: A computational model of the coronary circulation coupled to the global cardiovascular system was employed to quantify the impacts of arrhythmia and its combination with coronary artery disease on myocardial perfusion. Furthermore, a myocardial supply–demand balance index (MSDBx) was proposed to quantitatively evaluate the severity of myocardial ischemia under various arrhythmic conditions. (3) Results: Tachycardia and severe irregularity of heart rates (HRs) depressed myocardial perfusion and increased the risk of subendocardial ischemia (evaluated by MSDBx), whereas lowering HR improved myocardial perfusion. The presence of a moderate to severe coronary artery stenosis considerably augmented the sensitivity of MSDBx to arrhythmia. Further data analyses revealed that arrhythmia induced myocardial ischemia mainly via reducing the amount of coronary artery blood flow in each individual cardiac cycle rather than increasing the metabolic demand of the myocardium (measured by the left ventricular pressure-volume area). (4) Conclusions: Both tachycardia and irregular heartbeat tend to increase the risk of myocardial ischemia, especially in the subendocardium, and the effects can be further enhanced by concomitant existence of coronary artery disease. In contrast, properly lowering HR using drugs like β-blockers may improve myocardial perfusion, thereby preventing or relieving myocardial ischemia in patients with coronary artery disease.


2015 ◽  
Vol 14 (4) ◽  
pp. 829-849 ◽  
Author(s):  
Viatcheslav Gurev ◽  
Pras Pathmanathan ◽  
Jean-Luc Fattebert ◽  
Hui-Fang Wen ◽  
John Magerlein ◽  
...  

2021 ◽  
Author(s):  
Karoline Horgmo Jæger ◽  
Andrew G. Edwards ◽  
Wayne R. Giles ◽  
Aslak Tveito

AbstractAtrial fibrillation (AF) is a common health problem with substantial individual and societal costs. The origin of AF has been debated for more than a century, and the precise, biophysical mechanisms that are responsible for the initiation and maintenance of the chaotic electrochemical waves that define AF, remains unclear. It is well accepted that the outlet of the pulmonary veins is the primary anatomical site of AF initiation, and that electrical isolation of these regions remains the most effective treatment for AF. Furthermore, it is well known that certain ion channel or transporter mutations can significantly increase the likelihood of AF. Here, we present a computational model capable of characterizing functionally important features of the microanatomical and electrophysiological substrate that represents the transition from the pulmonary veins (PV) to the left atrium (LA) of the human heart. This model is based on a finite element representation of every myocyte in a segment of this (PV/LA) region. Thus, it allows for investigation a mix of typical PV and LA myocytes. We use the model to investigate the likelihood of ectopic beats and re-entrant waves in a cylindrical geometry representing the transition from PV to LA. In particular, we investigate and illustrate how six different AF- associated mutations can alter the probability of ectopic beats and re-entry in this region.


1999 ◽  
Vol 1 ◽  
pp. S31-S31
Author(s):  
M MORALES ◽  
D ROVAI ◽  
A GIMELLI ◽  
C MARINI ◽  
U STARTARI ◽  
...  

2007 ◽  
Vol 6 (1) ◽  
pp. 3-3
Author(s):  
T THUM ◽  
P GALUPPO ◽  
S KNEITZ ◽  
C WOLF ◽  
L VANLAAKE ◽  
...  
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