Fig 1-Mean changes in blood flow, diastolic diameter, and distensibility ofbrachial artery in 12 diabetic subjects and 12 controls during reactive hyperaemia, 1Oug glyceryl trinitrate, and 400 ,ug glyceryl trinitrate. Bars show 95% confidence intervals (9) mm Hg; blood flow 45 (28) v 49 (41) m/min; diastolic diameter 482 (0 60) v 4-47 (1P05) mm; distensibility 4-8 (1-4) v 5 9 (1-6) per kPa). During reactive hyperaemia, heart rate, blood pressure, and the increase in brachial artery blood flow (5548% (99 5%) v 590% (106&6%)) were similar in diabetic and normal subjects (figure 1) but the increases in brachial artery diastolic diameter (1 2% (2-7%) v 9-1% (4-4%); difference 6-9% (95% confidence interval 4.9% to 11%)) and distensibility (-15-3% (10-4%) v 31% (31-7%); difference 46-3% (25-5% to 67<1%)) were significantly less in diabetic subjects (both P < 0-00 1). After 10 ,ug glyceryl trinitrate or 400 ,ug glyceryl trinitrate the increase in flow, diameter, and distensibility was similar in diabetic and normal subjects (figure 1). 700-Comment Endothelium dependent, flow related dilatation and increase in distensibility of the brachial artery are greatly impaired in patients with non-insulin dependent diabetes, but endothelium independent responses induced by glyceryl trinitrate are similar to those in normal subjects. Loss of flow related increase in arterial distensibility will augment systolic pressure, myocardial wall stress, and heart work relative to stroke output, potentially promoting left ventricular hypertrophy and lowering ischaemic threshold. Late systolic pressure will be further augmented by early wave reflection from the periphery3 because pulse wave velocity is increased when distensibility is reduced. Loss of flow mediated vasodilatation reflects endothelial dysfunction and may thus also provide a marker of atherogenetic susceptibility. Our data provide evidence ofvascular dysfunction in non-insulin dependent diabetes before the appearance of microalbuminuria, previously regarded as its earliest marker.4We thank Dr J R Peters for allowing us to study patients under his care and Wendy Simons and Julie-Ann Davies for their secretarial assistance.Funding: British Heart Foundation. Conflict of interest: None.

Some studies suggest that patients with hepatitis C virus (HCV) infection have an increased risk of deep venous thrombosis (DVT) and pulmonary embolism (PE). Unfortunately, available data on this association are contrasting. A systematic review and meta-analysis of literature studies was performed to evaluate the risk of venous thromboembolism (VTE) associated with HCV. Studies reporting on VTE risk associated with HCV were systematically searched in the PubMed, Web of Science, Scopus and EMBASE databases. Six studies (10 data-sets) showed a significantly increased VTE risk in 100,364 HCV patients as compared with 8,471,176 uninfected controls (odds ratio [OR]: 1.900; 95 % confidence interval [CI]: 1.406, 2.570; p<0.0001). These results were confirmed when specifically considering the risk of DVT (6 studies, OR: 1.918; 95 %CI: 1.351, 2.723; p<0.0001), whereas a trend towards an increased risk of PE was documented in HCV patients (4 studies, OR: 1.811; 95 %CI: 0.895, 3.663; p=0.099). The increased VTE risk associated with HCV infection was consistently confirmed when analysing four studies reporting adjusted risk estimates (OR: 1.876; 95 %CI: 1.326, 2.654; P<0.0001), and after excluding studies specifically enrolling populations exposed to transient risk factors for VTE (4 studies, OR: 1.493; 95 %CI: 1.167, 1.910; p=0.001). Meta-regression models suggested that age and male gender may significantly impact on the risk of VTE associated with HCV-positivity. Results of our meta-analysis suggest that HCV-infected subjects may exhibit an increased risk of VTE. However, further high quality studies are needed to extend and confirm our findings.

Psoriatic arthritis appeared significantly associated with subclinical atherosclerosis and endothelial dysfunction and, in turn, with an increased cardiovascular risk. Thus, patients with psoriatic arthritis may benefit from a periodic assessment of surrogate markers of cardiovascular risk. This could help to establish more specific cardiovascular prevention strategies for these patients.

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Since the first identification in December of 2019 and the fast spread of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, it has represented a dramatic global public health concern. Though affecting mainly the respiratory system, SARS-CoV-2 disease, defined as coronavirus disease 2019 (COVID-19), may have a systemic involvement leading to multiple organ dysfunction. Experimental evidence about the SARS-CoV-2 tropism for the liver and the increasing of hepatic cytolysis enzymes during infection support the presence of a pathophysiological relationship between liver and SARS-CoV-2. On the other side, patients with chronic liver disease have been demonstrated to have a poor prognosis with COVID-19. In particular, patients with liver cirrhosis appear extremely vulnerable to infection. Moreover, the etiology of liver disease and the vaccination status could affect the COVID-19 outcomes. This review analyzes the impact of the disease stage and the related causes on morbidity and mortality, clinical outcomes during SARS-CoV-2 infection, as well as the efficacy of vaccination in patients with chronic liver disease.