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Summary: Background: The Transient Perivascular Inflammation of the Carotid artery (TIPIC) syndrome is presumably a very rare disease characterized by a local transient inflammation of the tissue around the carotid artery. Its pathophysiology remains unknown. We performed an updated study of TIPIC syndrome cases in the setting of a multinational collaborative study. Methods: This study was conducted as an observational multinational retrospective individual patient level cohort study. Information from all known cases diagnosed with TIPIC syndrome in the literature (2005–2020) was collected after a semi-structured literature search of PubMed and Web of Science. We also collected unpublished information of patients from French, Swiss, and Italian vascular medicine or radiology departments. Results: A total of 72 patients were included and served for data analysis: 42 (58.3%) were women; the mean age was 47.9 (SD=11.4) years. Symptoms were unilateral in 92% of patients and 81.4% required pain killers. At baseline, irrespective of the imaging method used, the median thickness of the carotid lesions was 5 (Q1–Q3: 4–7; range: 2–11) mm and the median length of the lesion was 20 (Q1–Q3: 10–30; range: 3–50) mm. We found a positive linear correlation between thickness and length. At follow-up, the thickness of the carotid lesions decreased to a median of 2 (Q1–Q3: 1–3; range: 0–6) mm; the length decreased to a median 10 (Q1–Q3: 5–15; range: 0–41) mm. A linear correlation between baseline and follow-up values was observed for both thickness and length measurements. Symptoms disappeared after a median of 14 (Q1–Q3: 10–15) days. Thirteen patients experienced a recurrence after a median follow-up of 6 (Q1–Q3: 2–12) months. Conclusions: The present analysis elucidates clinical and sonographic characteristics of TIPIC syndrome, indicating the benign nature of this condition. A future international registry will study the long-term course of the disease.

Introduction: Venous thromboembolism (VTE) is a leading cause of cardiovascular morbidity and mortality. The majority of VTE events are hospital-associated. In 2008, the Epidemiologic International Day for the Evaluation of Patients at Risk for Venous Thromboembolism in the Acute Hospital Care Setting (ENDORSE) multinational

Thromboembolic complications in HIV-infected patients have been reported. To our knowledge, no case-control studies have compared the prevalence of thromboembolic events between HIV-positive and HIV-negative individuals. One hundred and sixty-nine HIV-infected patients and 180 randomly selected blood donors were enrolled. Selected patients completed a specific questionnaire and were subsequently interviewed. Information was collected on family and personal history of cardiovascular disorders and the presence of personal risk factors for venous and arterial thrombosis. All reported events were adjudicated only if adequate documentation of objective tests was available. Mean age and sex were similar in the two groups. A vascular event was documented in six HIV-infected patients (3.55%) and in none of the controls (P=0.0108). Family history of cardiovascular disorders, cigarette smoking and hypertriglyceridemia were more prevalent in HIV patients than in controls. In multivariate analysis, neither family traditional cardiovascular risk factors nor HIV infection were independently associated with the presence of thromboembolic events. The results confirm the hypothesis that HIV-positive patients have an increased risk of thromboembolic disorders. Whether this increased risk has been provoked by HIV infection itself or by other associated risk factors for cardiovascular events, such as cigarette smoking and hypertriglyceridemia, remain to be clarified.

SummaryOptimal timing for restarting anticoagulant therapy after intracranial bleeding is a critical issue. The purpose of this systematic review is to summarize published studies on the management of oral anticoagulant therapy after intracranial bleeding secondary to the use of vitamin K antagonists in patients with a mechanical heart valve. A computer-assisted search of the MEDLINE and EMBASE electronic databases till January 2008 was performed. Two investigators independently performed study selection and completed a predefined quality assessment and data extraction form. Main inclusion criterion was the enrolment of patients with a mechanical heart valve and intracranial haemorrhage during oral anticoagulant treatment. Any randomised controlled trial, observational cohort study, case series and reports was included. No randomised controlled trials were identified. Six observational cohort studies were included in the final analysis. All studies were of low quality. A total of 120 patients were enrolled. Anticoagulation was restarted within a broad time range (2 days to 3 months). Four ischaemic strokes and two recurrent cerebral haemorrhages occurred after anticoagulation was restarted after a mean follow-up of 7.9 months. Eighteen patients were described in the selected case reports. Anticoagulant therapy was restarted within four days to eight weeks. Two patients had a recurrent haemorrhagic event, and no ischaemic events were reported. In conclusion, restarting oral anticoagulant therapy few days and, indirectly, stopping anticoagulant therapy for a few days (even for 7–14 days) after the occurrence of cerebral haemorrhage are both safe. However, well-designed studies are strongly recommended to provide better evidence.