Abstract
Background and aimsWith the intention to gain support for the hypothesis that incident ischemic complications of atherosclerotic disease involve a stochastic aspect, we performed a histological, qualitative evaluation of the epidemiology of coronary atherosclerotic disease in a cohort of aortic valve donors.Patients and methodsDonors (n = 695, median age 54, range 11–65 years) were dichotomized into a non-cardiovascular (non-CVD) and a cardiovascular disease death (CVD) group. Consecutive 5 mm proximal left coronary artery segments were Movat stained, and the atherosclerotic burden for each segment was graded (revised AHA-classification).ResultsNon-CVD and CVD groups showed steep increase of atherosclerosis severity beyond the age of 40, resulting in an endemic presence of advanced atherosclerosis in men over 40 and women over 50 years. In fact, only 19% of the non-CVD and 6% of the CVD donors over 40 years were classified with a normal LCA or a so called non-progressive lesion type. Fibrous calcified plaques (FCP), the consolidated remnants of earlier ruptured lesions, dominated in both non-CVD and CVD donors. Estimates of the atherosclerosis burden (i.e. average lesion grade, proportion of FCPs, and average number of FCPs per cross-section) were all higher in the CVD group (p<1.10−16, p<0.0001, and p<0.05, respectively).ConclusionsDominance of consolidated FCP lesions in males over 40 and females over 50 years, show that plaque ruptures in the left coronary artery are common. However, the majority of these ruptures remain asymptomatic. This implies that the atherosclerotic process is repetitive. A relative difference in disease burden between CVD and non-CVD donors supports the concept that complications of atherosclerotic disease involve a stochastic element.
Highlights
Ischemic heart disease remains the leading cause of death worldwide.[1]
Only 19% of the non-cardiovascular disease death (CVD) and 6% of the CVD donors over 40 years were classified with a normal left coronary artery (LCA) or a so called non-progressive lesion type
It has been pointed out that the majority of ischemic events occur in persons currently not identified by risk profiling. [3,4] these reservations may imply shortcomings in current risk profiling models and management strategies, the high prevalence of residual disease may reflect a degree of randomness in the development of the thrombo-embolic complications of coronary atherosclerosis.[5,6]
Summary
Ischemic heart disease remains the leading cause of death worldwide.[1]. While the successes of preventive life-style and medical interventions for ischemic heart disease are almost unprecedented, achievable risk reductions remain below 40%.[2]. [3,4] these reservations may imply shortcomings in current risk profiling models and management strategies, the high prevalence of residual disease may reflect a degree of randomness in the development of the thrombo-embolic complications of coronary atherosclerosis Development of thrombo-embolic complications and its clinical consequences reflect a complex interplay of pro- and anti-thrombotic factors, the fibrinolytic system, ischemia times, (residual) coronary lumen size, tissue oxygen demand, pre-existing collateral vascular networks etc.[10,11,12] In this context, we hypothesized that thrombo-embolic complications of coronary atherosclerosis are stochastically determined, and that human coronary atherosclerotic disease is a repetitive process that proceeds through multi-focal and asynchronous cycles of plaque initiation, -progression, and -destabilization. With the intention to gain support for the hypothesis that incident ischemic complications of atherosclerotic disease involve a stochastic aspect, we performed a histological, qualitative evaluation of the epidemiology of coronary atherosclerotic disease in a cohort of aortic valve donors
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