The constricting effect of reduced coronary artery compliance on the left ventricle is an important cause of reduced diastolic function in patients with coronary heart disease

Abstract

Abstract Background Previous studies of left ventricular diastolic function (LVDF) have focused on the decrease in active and passive diastolic function due to ischemic factors but have not investigated if the decrease in compliance of the coronary arteries that bypass the surface of the heart and travel between the myocardium could cause a constricting effect on the ventricular wall like that caused by myocardial fibrosis. Methods and Results 581 patients diagnosed with coronary heart disease (CHD) were divided into A group (patients are the control group), B group (patients with less than 50% coronary artery stenosis), C group (patients with coronary artery stenosis between 50 and 75%), D group (patients with coronary artery stenosis greater than 75%) according to the degree of coronary stenosis. The diastolic function of the ventricle is reflected by applying the relaxation time constant T value, which refers to the time between peak dp/dt and end-diastolic pressure in the left ventricle. It was concluded that there was a statistical difference in Gensini scores between patients in groups B, C and D (P < 0.001). And multiple linear regression analysis showed that T was correlated with Gensini score and C-dp/dtmax (R = 0.711, P < 0.001). Grouping according to the site of stent implantation and the number of stents implanted, it was found out that the changes in T values before and after left anterior descending artery (LAD) stent implantation were greater than left circumflex artery (LCX) and right coronary artery (RCA) (P < 0.001). And multiple linear regression revealed a correlation between T values and stent length, ventricular stiffness, and C-dp/dtmax (P = 0.001). Conclusions The decrease in compliance of the coronary arteries bypassing the surface of the heart and travelling between the myocardium would cause a constricting effect on the ventricular wall like that caused by myocardial fibrosis.