Coronary atherosclerosis: Un-altered physiology

Background End-stage coronary artery atherosclerosis has been studied extensively but the exact mechanisms of initiation and progression have not been defined fully. The aim of this study was to mathematically describe luminal change in relation to coronary vessel wall thickness in its progression from normal to atherosclerotic to establish whether these explain the pathophysiology. Methods One hundred coronary artery sections were graded histologically as ‘normal’ to ‘highly atherosclerotic’. Random systemic sampling by image analysis yielded 32 measurements (lumen radius and intima, medial, and adventitial thickness) from each section along 32 evenly spaced radii. Results The raw data follow an undulating course in relation to successive segments in all sections analyzed, pointing to a dynamic and well-ordered system. The calculated values, studied in triplets, followed a non-synchronized parabolic course, which was converted to linearity by taking the change in numbers (n-(n-1)=Δ) into account. The course and sign of ‘Δvessel wall’ (resulting from summed Δintima, Δmedia, Δadventitia) and ‘Δlumen radius’ values were unique for each triplet. Triplets order according to ‘Δlumen radius minus Δvessel wall’ and its course given by the trendline a-value presented stages in which increased Δvessel wall resulted in increased Δlumen radius in stages 1 and 3 and decreased Δlumen radius in stage 2. This phenomenon was found in all sections regardless of histological indication and independent of vessel wall constituent parts (intima, media, adventitia). Conclusions Similar basic processes are defined in all sections regardless of histological rating, indicating un-altered physiology. As such, coronary atherosclerosis can only be defined by a large to small shift of the triplets Δvessel wall trendline a-value. Consequently, no parameter of vessel wall pathology exists in absolute terms. Vessel wall composition has no importance for Δlumen radius.