Expression of AR on PBMC correlated with those measured in coronary artery and aortic tissues in CAD patients, AR activity of PBMC matched that observed in aorta, and AR expression and activity in PBMC were found reduced as compared to controls. Measuring the expression level of AR on PBMC represents a good tool to address in situ expression in coronary tissues of CAD patients.

Adenosine is an endogenous nucleoside that plays a major role in the physiology and physiopathology of the coronary artery system, mainly by activating its A2A receptors (A2AR). Adenosine is released by myocardial, endothelial and immune cells during hypoxia, ischaemia or inflammation, each condition being present in coronary artery disease (CAD). While activation of A2AR improves coronary blood circulation and leads to anti-inflammatory effects, downregulation of A2AR has many deleterious effects during CAD. A decrease in the level and/or activity of A2AR leads to: i) lack of vasodilation, which decreases blood flow, leading to a decrease in myocardial oxygenation and tissue hypoxia; ii) an increase in the immune response, favouring inflammation; and iii) platelet aggregation, which therefore participates, in part, in the formation of a fibrin-platelet thrombus after the rupture or erosion of the plaque, leading to the occurrence of acute coronary syndrome. Inflammation contributes to the development of atherosclerosis, leading to myocardial ischaemia, which in turn leads to tissue hypoxia. Therefore, a vicious circle is created that maintains and aggravates CAD. In some cases, studying the adenosinergic profile can help assess the severity of CAD. In fact, inducible ischaemia in CAD patients, as assessed by exercise stress test or fractional flow reserve, is associated with the presence of a reserve of A2AR called spare receptors. The purpose of this review is to present emerging experimental evidence supporting the existence of this adaptive adenosinergic response to ischaemia or inflammation in CAD. We believe that we have achieved a breakthrough in the understanding and modeling of spare A2AR, based upon a new concept allowing for a new and non–invasive CAD management.

The mechanism of atrial fibrillation (AF) in patients with normal heart remains unclear. While exogenous adenosine can trigger AF, nothing is known about the behavior of endogenous adenosine plasma level (APL) at the onset of AF and during ablation procedure. Ninety-one patients (68 with paroxysmal AF: 40 males, 66 ± 16 years; 23 with persistent AF: 14 males, 69 ± 11 years) and 18 controls were included. Among paroxysmal patients: i) medical therapy alone was performed in 45 cases and ablation procedure in 23. AF was spontaneously resolutive in 6 cases; ii) 23 underwent ablation procedure and blood was collected simultaneously in a brachial vein and in the left atrium; 17 were spontaneously in sinus rhythm while 6 were in sinus rhythm after direct current cardioversion. Among persistent patients: i) in 17 patients, blood samples were collected in a brachial vein before and after direct current cardioversion; ii) in 6 patients, blood samples were collected simultaneously in a brachial vein and in left atrium before and after cardioversion during ablation procedure. CV-APL was higher in patients with persistent AF vs patients with paroxysmal AF (median [

BackgroundAltered blood flow occurs in patients with low extremity peripheral artery disease (LE-PAD). LE-PAD is mostly associated with coronary artery disease (CAD). Adenosine is an endogenous nucleoside that affects both coronary and limb artery blood flow, mostly via the adenosine A2A receptor (A2AR). We evaluated A2AR expression and function in peripheral blood mononuclear cells (PBMCs) and the femoral artery tissues of patients with LE-PAD. MethodsArtery tissues and PBMCs were sampled in 24 patients with intermittent claudication, and compared with PBMCs in 24 healthy subjects. Expression and function of A2AR was studied, using a A2AR antibody with agonist properties, allowing determination of A2AR affinity (KD) and cAMP production (ie.EC50). Results A2AR expression onPBMCs was lower in patients than controls (median1.3 [range 0.6-1.8]vs1.75 [1.45-2.1] arbitrary units; P<0.01), and correlated with A2AR expression in artery tissues (Pearson's r=0.71; P<0.01). Basal and maximally stimulated cAMP production of PBMCs was lower in patients vs controls: 172 [90-310]vs244 [110-380]pg/10 6 cells (P<0.05) and 375 [160-659]vs670 [410-980]pg/10 6 cells (P<0.05), respectively. A high KD/EC50 ratio, characteristic of spare receptors, was observed in CAD with inducible-myocardial-ischemia. ConclusionA2AR expression in the arteries of patients, correlated with their expression in PBMCs. A2AR expression was lower in patients than in controls. A single blood sample (for measurement of A2AR expression on PBMCs) may help to screen patients with LE-PAD, whereas the presence of spare receptors may help with risk stratification before vascular surgery in CAD patients with high risk of myocardial ischemia.

Adenosine is an endogenous nucleoside which strongly impacts the cardiovascular system. Adenosine is released mostly by endothelial cells and myocytes during ischemia or hypoxia and greatly regulates the cardiovascular system via four specific G-protein-coupled receptors named A1R, A2AR, A2BR, and A3R. Among them, A2 subtypes are strongly expressed in coronary tissues, and their activation increases coronary blood flow via the production of cAMP in smooth muscle cells. A2A receptor modulators are an opportunity for intense research by the pharmaceutical industry to develop new cardiovascular therapies. Most innovative therapies are mediated by the modulation of adenosine release and/or the activation of the A2A receptor subtypes. This review aims to focus on the specific exploration of the adenosine plasma level and its relationship with the A2A receptor, which seems a promising biomarker for a diagnostic and/or a therapeutic tool for the screening and management of coronary artery disease. Finally, a recent class of selective adenosine receptor ligands has emerged, and A2A receptor agonists/antagonists are useful tools to improve the management of patients suffering from coronary artery disease.

A bdominal aortic aneurysm (AAA) is a serious and common pathologic abnormality that accompanies aging. Among men older than 65 years, the prevalence of AAA reaches 7.7%, increasing from 5.7% in ages 64-69 years to 8.9% in individuals older than 74 years (1). The high overall mortality from ruptured AAAs makes growth and subsequent rupture risk assessment crucial for AAA management.Since the 1970s, many studies (2) have demonstrated that AAA diameter correlates with rupture rate. Accordingly, AAA maximum diameter, effectively measured by using diagnostic US, has been the primary prognostic variable used to determine patient care (3,4). Current guidelines dictate elective repair to be appropriate at a diameter threshold of 50-55 mm or for AAA exhibiting growth greater than 1 cm per year (5,6).However, whereas some AAAs smaller than 55 mm do not grow more than 1 cm per year (7), other AAAs that are too small to trigger intervention grow rapidly. The sole use of maximal diameter measurement may be insufficient to

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BackgroundCarotid artery stenting (CAS) has been advocated as an alternative to redo surgery for the treatment of post-carotid endarterectomy (CEA) stenosis. This study analyzed the efficacy of CAS for post-CEA restenosis, focusing on an analysis of technical and anatomical predictive factors for in-stent restenosis.MethodsWe performed a retrospective monocentric study. We included all patients who underwent CAS for post-CEA restenosis at our institution from July 1997 to November 2013. The primary endpoints were the technical success, the presence of in-stent restenosis >50% or occlusion, either symptomatic or asymptomatic, during the follow-up period, and risk factors for restenosis. The secondary endpoints were early and late morbidity and mortality (TIA, stroke, myocardial infarction, or death).ResultsA total of 153 CAS procedures were performed for post-CEA restenosis, primarily because of asymptomatic lesions (137/153). The technical success rate was 98%. The 30-day perioperative stroke and death rate was 2.6% (two TIAs and two minor strokes), and rates of 2.2% (3/137) and 6.2% (1/16) were recorded for asymptomatic and symptomatic patients, respectively. The average follow-up time was 36 months (range, 6–171 months). In-stent restenosis or occlusion was observed in 16 patients (10.6%). Symptomatic restenosis was observed in only one patient. We found that young age (P = 0.002), stenosis > 85% (P = 0.018), and a lack of stent coverage of the common carotid artery (P = 0.006) were independent predictors of in-stent restenosis.ConclusionWe identified new risk factors for in-stent restenosis that were specific to this population, and we propose a technical approach that may reduce this risk.