Dysfunction of the endothelial lining of lesion-prone areas of the arterial vasculature is an important contributor to the pathobiology of atherosclerotic cardiovascular disease. Endothelial cell dysfunction, in its broadest sense, encompasses a constellation of various nonadaptive alterations in functional phenotype, which have important implications for the regulation of hemostasis and thrombosis, local vascular tone and redox balance, and the orchestration of acute and chronic inflammatory reactions within the arterial wall. In this review, we trace the evolution of the concept of endothelial cell dysfunction, focusing on recent insights into the cellular and molecular mechanisms that underlie its pivotal roles in atherosclerotic lesion initiation and progression; explore its relationship to classic, as well as more recently defined, clinical risk factors for atherosclerotic cardiovascular disease; consider current approaches to the clinical assessment of endothelial cell dysfunction; and outline some promising new directions for its early detection and treatment.

Endothelial Cell Dysfunction and the Pathobiology of Atherosclerosis

Article types include original clinical and basic research articles, case reports, commentaries, meeting reports, methodology, perspectives. Research into inflammation, atherosclerosis and coronary artery disease, including observational studies, clinical trials, epidemiology, and advances in applied (translational) research. The supplement is intended to include overviews of new concepts in pathophysiology, natural history, diagnostic strategies, and treatment approaches.

https://journals.sagepub.com/doi/pdf/10.4137/CMC.S39423

Inflammation, Atherosclerosis and Coronary Artery Disease.

Background Experimental and clinical evidence supports the role of inflammation in atherosclerosis and its complications. Colchicine is an orally administered, potent antiinflammatory medi...

https://www.nejm.org/doi/pdf/10.1056/NEJMoa1912388?articleTools=true

Efficacy and Safety of Low-Dose Colchicine after Myocardial Infarction

2010 ACCF/AHA/AATS/ACR/ASA/SCA/SCAI/SIR/STS/SVM guidelines for the diagnosis and management of patients with thoracic aortic disease: Executive summary: A report of the american college of cardiology foundation/american heart association task force on practice guidelines, american association for thoracic surgery, american college of radiology, american stroke association

Tea is the most consumed drink in the world after water. Green tea is a 'non-fermented' tea, and contains more catechins, than black tea or oolong tea. Catechins are in vitro and in vivo strong antioxidants. In addition, its content of certain minerals and vitamins increases the antioxidant potential of this type of tea. Since ancient times, green tea has been considered by the traditional Chinese medicine as a healthful beverage. Recent human studies suggest that green tea may contribute to a reduction in the risk of cardiovascular disease and some forms of cancer, as well as to the promotion of oral health and other physiological functions such as anti-hypertensive effect, body weight control, antibacterial and antivirasic activity, solar ultraviolet protection, bone mineral density increase, anti-fibrotic properties, and neuroprotective power. Increasing interest in its health benefits has led to the inclusion of green tea in the group of beverages with functional properties. However, although all the evidence from research on green tea is very promising, future studies are necessary to fully understand its contributions to human health, and advise its regular consumption in Western diets, in which green tea consumption is nowadays limited and sporadic.

Beneficial Effects of Green Tea—A Review

LDL fractions assessed by anion-exchange high-performance liquid chromatography in patients with coronary artery disease.

Excessive apoptosis is known to be a common feature of atherosclerotic lesions. Fortilin is recognized to have potent antiapoptotic properties. An increased fortilin expression was demonstrated in atherosclerotic lesions, and fortilin knockout mice developed less atherosclerosis. However, no study has reported blood fortilin levels in patients with coronary artery disease (CAD). We investigated plasma fortilin levels in 384 patients undergoing coronary angiography. CAD severity was evaluated as the numbers of stenotic vessels and segments. CAD was found in 208 patients (one-vessel (1VD), n = 86; two-vessel (2VD), n = 68; and three-vessel disease (3VD), n = 53). Plasma C-reactive protein (CRP) levels were higher in patients with CAD than without CAD (median 0.60 vs. 0.45 mg/L, p < 0.01). Notably, fortilin levels were higher in patients with CAD than without CAD (75.1 vs. 69.7 pg/mL, p < 0.02). A stepwise increase in fortilin was found according to the number of stenotic vessels: 69.7 in CAD(−), 71.1 in 1VD, 75.7 in 2VD, and 84.7 pg/mL in 3VD (p < 0.01). Fortilin levels also correlated with the number of stenotic segments (r = 0.16) and CRP levels (r = 0.24) (p < 0.01). In a multivariate analysis, fortilin levels were independently associated with 3VD. The odds ratio for 3VD was 1.93 (95%CI = 1.01–3.71) for a high fortilin level (>70.0 pg/mL). Thus, plasma fortilin levels in patients with CAD, especially those with 3VD, were found to be high and to be associated with the severity of CAD.

/pdf/high-plasma-levels-of-fortilin-in-patients-with-coronary-30mhxjfk.pdf

High Plasma Levels of Fortilin in Patients with Coronary Artery Disease

High plasma concentrations of vanin-1 in patients with coronary artery disease.

Vinculin and talin-1, which are cytoskeletal proteins affecting focal adhesions, were reported to be down-expressed in atherosclerotic lesions. Recently, we reported high concentrations of plasma talin-1 in patients with coronary artery disease (CAD). However, blood vinculin concentrations in CAD patients have not been clarified. Plasma vinculin concentrations as well as talin-1 were studied in 327 patients in whom coronary angiography was performed. CAD was proven in 177 patients (1-vessel, n = 79; 2-vessel, n = 57; 3-vessel disease, n = 41). However, vinculin concentrations were not markedly different between the CAD(-) and CAD groups (median 122.5 vs. 119.6 pg/mL, p = 0.325) or among patients with CAD(-), 1-, 2-, and 3-vessel diseases (122.5, 112.8, 107.9, and 137.2 pg/mL, p = 0.202). In contrast, talin-1 concentrations were higher in CAD than the CAD(-) group (0.29 vs. 0.23 ng/mL, p = 0.006) and increased stepwise in the number of stenotic vessels: 0.23 in CAD(-), 0.28 in 1-vessel, 0.29 in 2-vessel, and 0.33 ng/mL in 3-vessel disease (p = 0.043). No correlation was observed between vinculin and talin-1 concentrations. In multivariate analysis, vinculin concentrations were not a factor for CAD. In conclusion, plasma vinculin concentrations in patients with CAD were not high and were not associated with the presence or severity of CAD.

/pdf/plasma-concentrations-of-vinculin-versus-talin-1-in-coronary-1uzow0cl.pdf

Plasma Concentrations of Vinculin versus Talin-1 in Coronary Artery Disease

Exercise-induced T-wave altemans as a marker of high-risk patients with hypertrophic cardiomyopathy

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