Arterial Wall Thickness: Marker of Atherosclerosis or Risk Factor for Thrombosis

Abstract

Several studies have established that increased intimal-media thickness (IMT) is strongly related to coronary artery disease, ischemic stroke, peripheral vascular disease, and hypertension. The formation of neointimal lesions modifies vessel wall geometry, intramural elasticity, areas of the lumen, and viability, and plays a critical role for a transition from quiescent state to proliferating phenotype; it involves vascular smooth muscle cells (VSMC) and the associated proteolytic system (serine and cysteine proteinase, catepsin, MMP-2 and MPP-9), VEGF, PDGF and fibroblastic growth factor. We used B-mode ultrasonography to quantify early atherosclerotic vessels wall change, IMT of the carotid artery (CIMT) ranged from 0.48 mm to 1.82 mm, and of the femoral artery (FIMT) ranged from 0.44 mm to 3.48 mm; intramural elasticity ranged from 7 to 125 KPa in normal subject. Wall shear stress was 26.38 +/− 7.34 dyne/cmq in individual without atherosclerosis, and 14.36 +/− 6.36 dyne/cmq in those with atherosclerosis, PWv (pulse wave velocity) were respectively 8.6 +/− 1.8 m/sec., and 7.8 +/− 1.6m/sec., IMT and peak shear stress were inversely correlated. High expression of IMT (>2.24 mm by the carotid artery and > 3.86 mm by the femoral artery) showed a tight correlation of VEGF levels 148.38 +/− 64.30 pg/ml, and an increased inflammatory biomarkers of atherosclerosis like CRP 9.8 +/− 3.6mg/l, and CD40L 5.4 +/− 2.2mg/l dangerous co-workers of thrombotic damage. We have studied 64 patients (aged from 54 to 68) Patients (32) Control (32) CIMT > 2.24 from 0.48 to 1.82 mm FIMT > 3.86 from 0.44 to 3.48mm VEGF 148.38 +/− 64.30pg/ml 84.36 +/− 24.58pg/ml CRP 9.8 +/− 3.6mg/l <2.8 +/− 0.4mg/l CD40L 5.4 +/− 2..2mg/l 2.2 +/− 0.8mg/l The degree of IMT, the plaque morphology, and the levels of inflammatory markers showed a direct relationship in atherosclerosis being significantly correlated with thrombotic risk. Among our 32 patients with high degree of IMT: 18 patients with high expression of CIMT from 2.24 to 3.22 have CAD compared with 2 controls (p<0.0001); 8 patients of CIMT from 2.24 to 3.48 have ischemic stroke compared with 1 control (p<0.0001); 6 patients with FIMT from 3.86 to 4.28 have PAD compared with 1 control (p<0.0001). The level of CRP plays a key role in CAD, as it increases the risk of CAD by 30% over 5 years; the cut points of high risk is >3.5 mg/l and could be enhanced IMT, the CRP increased IMT to 3.5 by 9.5% in carotid plaque and change plaque component. The high level of CD40L > 3.2 mg/l is intimately linked with a strong risk of CAD >24% and ischemic stroke >18% within 12–16 month. Although our present study is limited it shows a clear difference between the groups studied an demonstrated a strong evidence of direct endothelial cells damage and abnormal plasma levels of inflammatory markers as predictors of adverse outcome, IMT is a measure of the degree of atheroma progression, reflects generalized disease and predicts strokes, PAD, and myocardial infarction, although the relationship to disease severity is still subject to debate.

Valorization of Chicken Slaughterhouse Byproducts to Obtain Antihypertensive Peptides

“…In addition to ACEi activity, the chicken bone hydrolysate also attenuated the development of age-induced HTN and heart and vascular hypertrophy, when it was administered daily during 8 weeks [ 92 , 93 ]. This is of relevance as HTN was associated with the presence of cardiac hypertrophy (one of the main causes of cardiovascular mortality and morbidity), stretching of smooth muscle cells, and thickening of the vascular wall (present in several cardiovascular diseases) [ 94 , 95 , 96 ].…”

Mechanisms of angioregression of the corpus luteum

“…The diameter of these vessels was demonstrated to be smaller compared to fully functional mid-cycle corpora lutea ( Lei et al, 1991 ; Nio-Kobayashi et al, 2016 ), indicating that vasoconstriction may be occurring in luteal regression. Similarly, arterial wall thickening is associated with various cardiovascular diseases including atherosclerosis, thrombosis, and hypertension ( Burke et al, 1995 ; Corinaldesi and Corinaldesi, 2008 ). Changes in blood flow during luteal regression as a result of vasoactive factors are illustrated in Figure 1 .…”