Fig 1.
Movat staining of a coronary artery cross section illustrating the foot prints of consolidated calcified lesions (purple-brown demarcations indicated by the arrow in the enlarged insert), and the presence of multiple lesions within a single cross section.
I: late fibro-atheroma (LFA) lesion (necrotic core covered by a fibrous cap). II-V: indicating consolidated former lesions (fibrotic calcified plaque (FCP)) [15].
Fig 2.
Adapted AHA (Virmani) classification of coronary atherosclerotic lesions [15] (Movat stained coronary artery segments).
(2-A) Normal and non-progressive (reversible) lesions [15] Adaptive intimal thickening (AIT) is characterized by hyperplasia of the tunica intima (blue); intimal infiltration of macrophages (black arrows) and presence of foam cells characterize intimal xanthoma (IX). (2-B) Progressive atherosclerotic lesions.[15] Pathological intimal thickening (PIT) is hallmarked by a pre-necrotic lipid core, with or without surrounding infiltrated foam cells (black arrows). Early and late fibro-atheroma (EFA and LFA) are characterized by a necrotic lipid core, cholesterol crystals, and an overlying thick collagen-rich (yellow/green) fibrous cap. Thin cap fibro-atheroma (TCFA) is characterized by a thin fibrous cap, which precedes rupture (plaque rupture (PR)). Rupture is followed by a healing process with formation of a new proteoglycan/cell rich cap (healed rupture (HR)). (2-C) Stabilized atherosclerotic lesions and acute total occlusion.[15,16] The healed rupture ultimately transforms into a scar, the fibrotic calcified plaque (FCP) contains calcified remnants of the necrotic core. New lesions can develop on top of FCPs (neo-intima, blue), which can ultimately result in stacked lesions. This may eventually cause accumulation of multiple lesions within one cross section (red arrows) and formation of a neo-intima overlying the consolidated earlier lesions. Acute occlusion represents an example of a (fatal) thrombo-embolic acute full occlusion of the LCA.
Table 1.
Adapted AHA classification schema for human atherosclerosis [15].
Table 2.
Donor characteristics for the full cohort (A)).
(mean [sd] or absolute number (proportion)). P-values are for the non-CVD† vs. CVD cohorts.
Table 3.
Donor characteristics for the individuals† over 40 years of age.
(mean [sd] or absolute number (proportion)). P-values are for the non-CVD vs. CVD cohorts.
Fig 3.
Age distribution for the most advanced lesion type present in the proximal left coronary artery .segment studied.
Fig 3A: non-cardiovascular death donors. Fig 3B: cardiovascular death donors. ‘+’ represent females and ‘o’ represent males. Data points have been jittered [17] in order to avoid overlap.