In this real-life study, 32% of patients received an inappropriate dose of DOAC. Several clinical factors can identify patients at risk of this situation.

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ObjectiveTo study the relationship between antiretroviral (ARV) treatment and abnormal ankle-branch index (ABI) and to compare the risk factors for altered ABI. MethodsPatients coming to the office from April 2007 until July 2007 were offered the chance to take part in the study. ABI was obtained by the standard technique. Those 0.9 or 1.3 were considered altered ABI. Clinical reports were reviewed to examine traditional vascular risk factors, coinfection with hepatitis C virus and/or hepatitis B virus, tobacco use, highly active antiretroviral therapy use and its components and length of use of each ARV drug.Results ABI was measured in 147 patients, 82.3% males. Thirty-three patients (22.45%) had an altered ABI, and it was related to CD4 cell nadir, dyslipidaemia and protease inhibitor (PI) use. When logistic regression was carried out, only dyslipidaemia (OR 2.68, CI 95%: 1.06-6.91) and PI use (OR 2.79, CI 95%: 1.15-6.54) remained in the model. ConclusionsAltered ABI is associated with PI use independently of dyslipidaemia. Probably, it marks patients with high vascular risk not identified with traditional scales.Keywords: ankle-branch index, HAART, HIV, protease inhibitors, vascular risk IntroductionSince the introduction of highly active antiretroviral therapy (HAART) in the management of infection by HIV, patients' life expectancy has increased spectacularly [1,2]. Some cohort studies even compare the survival rates of lesser immunosuppressed HIV patients with those of the general population [3].However, some observational studies published over the last few years support the idea that HIV, and above all HAART, increase the risk of major vascular events [4,5]. Clinical evidence suggests that protease inhibitors (PIs) are mainly responsible for most of these events [6]. PI implication in changes to the lipid profile [7,8] [decreasing high-density lipoproteins (HDL) and increasing low-density lipoproteins (LDL) as well as triglycerides], insulin resistance [9,10] and lowering of the peripheral arterial vasodilation response [11] have been proved.In addition, hepatitis C virus (HCV) co-infection increases insulin resistance [12,13], and HIV infection chronic immune activation causes deterioration in the lipid profile [14,15]. Patients' mean age has also increased. All these factors make an early diagnosis and treatment of vascular disease necessary.Because there are no reliable scores to evaluate the vascular risk of the HIV-infected population other than clinical history (past medical history and family history), physical exploration and blood tests (renal function, lipid profile, glycaemia, etc) it would be most desirable to have a test to determine early vascular risk in HIV patients that is simple, affordable and easy to perform.Ankle-brachial index (ABI) meets these criteria. It is a non-invasive diagnostic test of peripheral arterial disease and a marker of vascular morbimortality. An altered ABI is associated with cardiovascular and cerebrovascular disease. If lower than 0.9, ABI has been related to hi...

Prognosis for patients with the human immunodeficiency virus (HIV) has improved with the introduction of highly active antiretroviral therapy (HAART). Evidence over recent years suggests that the incidence of cardiovascular disease is increasing in HIV patients. The ankle-brachial index (ABI) is a cheap and easy test that has been validated in the general population. Abnormal ABI values are associated with increased cardiovascular mortality. To date, six series of ABI values in persons with HIV have been published, but none was a prospective study. No agreement exists concerning the risk factors for an abnormal ABI, though its prevalence is clearly higher in these patients than in the general population. Whether this higher prevalence of an abnormal ABI is associated with a higher incidence of vascular events remains to be determined.

Background: Sudden death (SD) constitutes one of the principal causes of death and is an important problem in healthcare provision. Cardiovascular diseases have a high prevalence in dialysis patients and constitute the principal cause of death. We sought to analyze retrospectively the incidence of SD in patients commencing dialysis and the factors related to its presence. Methods: We evaluated all the patients who began dialysis in our center between 1/11/2003 and 15/9/2007, and who were followed up until death, transplant, or study completion on 31/12/2012. We determined the presence of SD according to the following criteria: SD at 24 h (SD 24H): unexpected death occurring in the 24 h following the start of symptoms, or when the patient was found dead and had been seen alive 24 h earlier; SD at 1 h (SD 1H): death witnessed as occurring in the first hour following the start of symptoms. Results: We evaluated 285 patients, mean age 65.67 ± 15.7 years. In a follow-up of 39.9 ± 34.2 months (947.6 patient-years of follow-up) 168 died (59%), 28 (10%) patients presented SD 24H (2.9/100 patient-years), and 16 (6%) patients presented SD 1H (1.7/100 patient-years). In the multivariate analysis, having had a myocardial infarction or having had electrocardiographic abnormalities (Q wave, negative T wave, subendocardial lesion or QRS >120 ms) were the principal independent predictors of SD 24H (OR 7.83; 95% CI 2.20-27.86; p = 0.001) and of SD 1H (OR 13.43; 95% CI 1.56-115.42; p = 0.018). Conclusions: SD on dialysis is very frequent. Two groups can be identified easily, with risk profiles clearly differentiated.