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Introduction: Numerous reports suggest, among HIV+ patients (pts), an increased rate of acute coronary syndrome and cardiac death. Several data suggest that endothelial dysfunction is a major mechanisms in the development of coronary atherosclerosis in non-HIV infected patients. Hypothesis: The aim of our study is to assess coronary microvascular function using Doppler-flow wire in HIV+ patients in therapy with HAART. Methods: Thirteen HIV-infected patients were enrolled from the Department of Cardiovascular, Respiratory, Nephrology, Anesthesiology and Geriatric Sciences of the “Sapienza” University of Rome (Italy). The main inclusion criteria were: Framingham risk score Diagnostic coronary angiography was performed via percutaneous radial approach. Microvascular function was assessed by measuring coronary flow velocity reserve (CFR). Intracoronary functional tests were performed to evaluate both endothelium-dependent microvascular function [via intracoronary (IC) infusion of acetylcholine (2.5[[Unable to Display Character: –]]10 μg)] and non-endothelium-dependent microvascular function [via IC infusion of adenosine (5 μg) ]. Results: All the patients presented a Framingham risk score Conclusion: Microvascular function is not compromised in HIV + pts who presented coronary atherosclerotic plaque. Microvascular dysfunction, involved in pathophysiology of coronary artery disease in general population, seems to be not implicated in coronary atherosclerosis in HIV + pts. These data suggest a peculiar pathophysiological mechanisms for HIV related atherosclerosis.

Background: According to guidelines, implantable cardioverter defibrillator (ICD) is recommended in prevention of sudden cardiac death (SCD) in heart failure (HF) patients (pts). Guidelines have several limitations because ICD indication is based mainly on left ventricular ejection fraction (EF). Recent data showed that, independently from EF, 123-iodine metaiodobenzylguanidine imaging (123-I MIBG) could help to identify HF pts at high risk of SCD [heart/ mediastinum (H/M) ratio ≤1.6 and a summed score (SS) > 26], who may benefit of ICD. Aim: Our aim is to assess, in a real world registry, the role of 123-I MIBG for the prediction of ventricular tachyarrhythmia (VT) causing appropriate ICD therapy in HF pts. Methods: We consecutively enrolled 97 patients admitted to our hospital with diagnosis of HF, left ventricular ejection fraction (LVEF) ≤35% and indication to ICD. All patients underwent MIBG imaging. The patients were classified into two groups: Group 1 with H/M≤1.6 , SS> 26; Group2 with H/M>1.6, SS Results: 65 pts were included in group 1 and 32 pts in group 2. All baseline characteristics were similar in 2 groups apart from the etiology (table 1). In group 1, H/M ratio was 1.37±0.3 vs 1.8 ± 0.2 in group 2 (p=0.0002); SS was 37.5± 9.7 vs 16 ±6 in group 2 (p = 0.0001). At 1 year follow-up VTs causing appropriate ICD therapy in group 1 were 13.4% vs 1.28% in group 2(p=0.02); overall cardiac events were in group 1 16.4 % vs 1.92% in group 2 (p=0.02). Conclusion: Our results suggest that 123 I-MIBG can identify patients at increased risk for arrhythmic death and can be useful in the decision-making of ICD implantation independently from ejection fraction.