Acute mesenteric ischemia: which predictive factors of delayed diagnosis at emergency unit?

PURPOSE: Acute mesenteric ischemia (AMI) is frequently diagnosed late, leading to a poor prognosis. Our aims were to identify predictive factors of delayed diagnosis and to analyze the outcomes of patients with AMI admitted in emergency units. METHODS: All the patients with AMI (2015-2020), in two Emergency units, were retrospectively included. Two groups were defined according to the time of diagnosis between the arrival at emergency unit and the CT scan: ≤ 6 h (early), > 6 h (delayed). RESULTS: 119 patients (mean age = 71 ± 7 years) were included. The patients with a delayed diagnosis (n = 33, 28%) were significantly associated with atypical presentation, including lower rates of abdominal pain (73 vs 89%, p = 0.003), abdominal tenderness (33 vs 43%, p = 0.03), and plasma lactate (4 ± 2 vs 6 ± 7 mmol/l, p = 0.03) when compared with early diagnosis. After multivariate analysis, the absence of abdominal pain was the only independent predictive factor of delayed diagnosis (Odd Ratio = 0.17; 95% CI = 0.03-0.88, p = 0.03). Patients with delayed diagnosis tended to be associated to lower rates of revascularization (9 vs 17%, p = 0.4), higher rates of major surgical morbidity (90 vs 57%, p = 0.1), longer length of stay (16 ± 23 vs 13 ± 15 days, p = 0.4) and, at the end of follow-up, higher rate of short small bowel syndrome (18 vs 7%, p = 0.095). CONCLUSION: AMI is a challenge for emergency physicians. History of patient, physical exam, biological data are not sufficient to diagnose AMI. New biomarkers, and awareness of emergency physicians should improve and accelerate the diagnosis of AMI.

Adenosine and Adenosine Receptors: Advances in Atrial Fibrillation.

Atrial fibrillation (AF) is the most common arrhythmia in the world. Because the key to developing innovative therapies that limit the onset and the progression of AF is to fully understand the underlying molecular mechanisms of AF, the aim of the present narrative review is to report the most recent advances in the potential role of the adenosinergic system in the pathophysiology of AF. After a comprehensive approach describing adenosinergic system signaling and the mechanisms of the initiation and maintenance of AF, we address the interactions of the adenosinergic system's signaling with AF. Indeed, adenosine release can activate four G-coupled membrane receptors, named A1, A2A, A2B and A3. Activation of the A2A receptors can promote the occurrence of delayed depolarization, while activation of the A1 receptors can shorten the action potential's duration and induce the resting membrane's potential hyperpolarization, which promote pulmonary vein firing, stabilize the AF rotors and allow for functional reentry. Moreover, the A2B receptors have been associated with atrial fibrosis homeostasis. Finally, the adenosinergic system can modulate the autonomous nervous system and is associated with AF risk factors. A question remains regarding adenosine release and the adenosine receptors' activation and whether this would be a cause or consequence of AF.

Adenosine, Adenosine Receptors and Neurohumoral Syncope: From Molecular Basis to Personalized Treatment.

Adenosine is a ubiquitous nucleoside that is implicated in the occurrence of clinical manifestations of neuro-humoral syncope (NHS). NHS is characterized by a drop in blood pressure due to vasodepression together with cardio inhibition. These manifestations are often preceded by prodromes such as headaches, abdominal pain, feeling of discomfort or sweating. There is evidence that adenosine is implicated in NHS. Adenosine acts via four subtypes of receptors, named A1 (A1R), A2A (A2AR), A2B (A2BR) and A3 (A3R) receptors, with all subtypes belonging to G protein membrane receptors. The main effects of adenosine on the cardiovascular system occurs via the modulation of potassium ion channels (IK Ado, K ATP), voltage-gate calcium channels and via cAMP production inhibition (A1R and A3R) or, conversely, through the increased production of cAMP (A2A/BR) in target cells. However, it turns out that adenosine, via the activation of A1R, leads to bradycardia, sinus arrest or atrioventricular block, while the activation of A2AR leads to vasodilation; these same manifestations are found during episodes of syncope. The use of adenosine receptor antagonists, such as theophylline or caffeine, should be useful in the treatment of some forms of NHS. The aim of this review was to summarize the main data regarding the link between the adenosinergic system and NHS and the possible consequences on NHS treatment by means of adenosine receptor antagonists.