: OBJECTIVES: We investigated the anatomical evolution of residual aortic dissection after type A repair and factors associated with poor prognosis at a high-volume aortic centre. METHODS: Between 2017 and 2019, all type A aortic dissections were included for prospective follow-up. Patients without follow-up computed tomography (CT) scan available for radiological analysis and patients without residual aortic dissection were excluded from this study. The primary end point was a composite end point defined as dissection-related events including aneurysmal evolution (increased diameter > 5 mm/year), aortic reintervention for malperfusion syndrome, aortic diameter >55 mm, rapid aortic growth >10 mm/year or aortic rupture and death. The secondary end points were risk factors for dissection-related events and reintervention analysis. All immediate and last postoperative CT scans were analysed. RESULTS: Among 104 patients, after a mean follow-up of 20.4 months (8–41), the risk of dissection-related events was 46.1% (48/104) and the risk of distal reintervention was 17.3% (18/104). Marfan syndrome (P < 0.01), aortic bicuspid valve (P = 0.038), innominate artery debranching (P = 0.025), short aortic cross-clamp time (P = 0.011), initial aortic diameter >40 mm (P < 0.01) and absence of resection of the primary entry tear (P = 0.015) were associated with an increased risk of dissection-related events or reintervention during follow-up. CONCLUSIONS: Residual aortic dissection is a serious disease requiring close follow-up at an expert centre. This study shows higher reintervention and aneurysmal development rates than currently published. To improve long-term outcomes, the early demographic and anatomic poor prognostic factors identified may be used for more aggressive treatment at an early phase.

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, down-regulation 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 modelling of spare A2AR, based upon a new concept allowing for a new and non-invasive CAD management.

Background After a type A aortic dissection repair, a patent false lumen in the descending aorta is the most common situation encountered, and is a well-known risk factor for aortic growth, reinterventions and mortality. The aim of this study was to analyze the long-term results of residual aortic dissection (RAD) at a high-volume aortic center with prospective follow-up. Methods In this prospective single-center study, all patients operated for type A aortic dissection between January 2017 and December 2022 were included. Patients without postoperative computed tomography scans or during follow-up at our center, and patients without RAD were excluded. The primary endpoint was all-cause mortality during follow-up for patients with RAD. The secondary endpoints were perioperative mortality, rate of distal aneurysmal evolution, location of distal aneurysmal evolution, rate of distal reinterventions, outcomes of distal reinterventions, and aortic-related death during follow-up. Results In total, 200 survivors of RAD comprised the study group. After a mean follow-up of 27.2 months (1–66), eight patients (4.0%) died and 107 (53.5%) had an aneurysmal progression. The rate of distal reintervention was 19.5% (39/200), for malperfusion syndrome in seven cases (3.5%) and aneurysmal evolution in 32 cases (16.0%). Most reinterventions occurred during the first 2 years (82.1%). Twenty-seven patients were treated for an aneurysmal evolution of RAD including aortic arch with hybrid repair in 21 cases and branched aortic arch endoprosthesis in six cases. In the hybrid repair group, there was no death, and the rate of morbidity was 28.6% (6/21) (one minor stroke, one pulmonary complication, one recurrent paralysis with complete recovery and three major bleeding events). In the branched endograft group, there was no death, no stroke, and no paraplegia. There was one case (16.7%) of carotid dissection. Complete aortic remodeling or complete FL thrombosis on the thoracic aorta was found in 18 cases (85.7%) and in five cases (83.3%) in the hybrid and branched endograft groups, respectively. Conclusions: Despite a critical course in most cases of RAD, with a high rate of aneurysmal evolution and reintervention, the long-term mortality rate remains low with a close follow-up and a multidisciplinary management in an expert center.

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, A_2AR, A_2BR, 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. A_2A 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 A_2A receptor subtypes. This review aims to focus on the specific exploration of the adenosine plasma level and its relationship with the A_2A 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 A_2A receptor agonists/antagonists are useful tools to improve the management of patients suffering from coronary artery disease.