Whether impaired arterial elasticity in stage 1 hypertension can be brought back to normal by antihypertensive treatment is unknown. Aim of this study was to evaluate the impact of long-term well-controlled blood pressure (BP) on carotid artery elasticity and endothelial function in stage 1 hypertensive patients. We studied 40 middle-age hypertensives (mean age 49.7 years) whose BP had been kept at target by pharmacological treatment and/or lifestyle modifications for a mean of 7.5 years. Carotid compliance coefficient (CC) and distensibility coefficient (DC) were measured by B-mode ultrasound system. Measurement of carotid intima-media thickness (IMT) was performed in each carotid artery segment, bilaterally. Endothelial function was evaluated by post-occlusion flow mediated dilation (FMD). Forty normotensive subjects matched for age and sex served as controls. In the hypertensive subjects, BP levels were well controlled throughout the study period (mean office BP 133.7 ± 9.0/81.27 ± 7.0 mmHg). However, compared to controls, significantly higher office BP levels and waist circumference were present. Compared to normotensives, carotid elasticity (DC 24.5 ± 9.0 vs 37.0 ± 8.5 10 −3 /kPa, and CC 0.92 ± 0.34 vs 1.28 ± 0.36 mm 2 /kPa, p < 0.0005 for both) as well as endothelial function (FMD 5.7 ± 2.4% vs 9.2 ± 2.9%, p < 0.0005) were significantly impaired in hypertensives. In a logistic regression, hypertensive patients had increased risk of impaired carotid vascular stiffness (odds ratio, 95% CI: 13.04 (2.27−74.96), p = 0.004). Despite the “pseudo-normalization” of BP levels, hypertensive patients with long-term well-controlled BP according to current standards exhibited increased local arterial stiffness and endothelial dysfunction suggesting that lower BP targets should be sought.

Background and Aims . A relevant role is emerging for functional foods in cardiovascular prevention. The aim of this study was to assess the effect of a nutraceutical multitargeted approach on lipid profile and inflammatory markers along with vascular remodelling in a cohort of dyslipidemic subjects without history of cardiovascular (CV) disease. Methods and Results . We enrolled 25 subjects (mean age 48.2 years) with low to moderate CV risk profile and total cholesterol (TC) levels between 150 and 250 mg/dl. The patients were assigned to receive for one year a tablet/die of a nutraceutical combination containing red yeast rice (RYR) extract (Monacolin 3 mg/tablet) and coenzyme Q10 (30 mg/tablet). Treatment with the nutraceutical compounds led to a significant reduction of TC (from 227 to 201 mg/dl, p < 0.001), LDL-c (from 150 to 130 mg/dl, p = 0.001), triglycerides (from 121 to 109 mg/dl, p = 0.013), non-HDL-cholesterol (from 168 to 141 mg/dl, p < 0.001), hs-CRP (from 1.74 to 1.20 mg/l, p = 0.015), and osteoprotegerin (from 1488 to 1328 pg/ml, p = 0.045). Levels of HDL-c, Lp(a), glucose, liver enzyme, CPK, or creatinine did not change over time. An ultrasound study was performed to assess changes in mean carotid intima-media thickness (IMT) and maximum IMT (M-MAX) as well as modification in local carotid stiffness by means of determining the carotid compliance coefficient (CC) and distensibility coefficient (DC). At the end of the treatment, we observed small but significant reductions in both mean-IMT (from 0.62 to 0.57 mm, p = 0.022) and M-MAX (from 0.79 to 0.73 mm, p = 0.002), and an improvement in carotid elasticity (DC from 22.4 to 24.3 × 10 −3 /kPa, p = 0.006 and CC from 0.77 to 0.85 mm 2 /kPa, p = 0.019). Conclusions . A long-term treatment with a combination of RYR and coenzyme Q10 showed lipid-lowering activity along with a reduction of inflammatory mediators and an improvement of vascular properties in young subjects with a low-to-moderate CV risk profile.

Objectives. Our aim was to evaluate subclinical atherosclerosis progression during 5 years of anti-tumour necrosis factor (TNF)-alpha treatment in psoriatic arthritis (PsA) patients. Methods. Thirty-two consecutive PsA patients starting TNF-alpha inhibitors were enrolled and evaluated at baseline (T0), 2 years (FU1) and 5 years (FU2) of treatment. Arterial structural properties were evaluated by B-mode ultrasound of mean carotid intima-media thickness (mean-IMT) and maximum IMT (M-MAX) in each segment (common, bulb, internal), bilaterally. Endothelial function was assessed by post-occlusion flow-mediated dilation (FMD) of the brachial artery using high-sensitivity ultrasonography. Treatment response was studied through DAS28 (disease activity score) and inflammatory biomarkers (C-reactive protein, TNF-alpha, osteoprotegerin). Metrologic and metabolic data were collected. Results. At T1, a significant decrease of DAS28 (4.2 +/- 0.7 vs. 2.3 +/- 0.8, p<0.001) and CRP (11.25 +/- 9.16 vs. 2.91 +/- 1.72, p<0.01) was observed. Efficacy was preserved at FU2 (DAS28 2.4 +/- 0.9, CRP 2.73 +/- 2.51; p=ns vs. FU1). Systolic blood pressure and BMI remained stable throughout the follow-up, while diastolic blood pressure decreased significantly from FU1 to FU2 (80 +/- 10 vs. 74 +/- 7 mmHg, p=0.001). From T0 to FU1 there was an increase of IMT-mean and M-MAX (0.7 +/- 0.1 vs. 0.9 +/- 0.4 and 0.9 +/- 0.2 vs. 1.1 +/- 0.4, p<0.01). At FU2, IMT-mean and M-max did not change significantly (0.9 +/- 0.3 and 1.1 +/- 0.3, p=ns vs. FU1). No significant variation in FMD values was observed during the study period. Conclusions. A slight progression of subclinical atherosclerosis in PsA was observed in the first 2 years of anti-TNF-alpha treatment. This process seemed to decelerate in follow-up extension to 5 years.

Background and Aims: To date, no pharmacological therapy has proven to slow down the progression of calcific aortic valve disease (CAVD). Our specific aim is to study the effects of acetylsalicylic acid (ASA) and ASA-triggered lipoxins (ATL) on valvular interstitial cells (VIC) calcification.

We aimed to investigate whether the expression of the OPG/RANK/RANKL triad in peripheral blood mononuclear cells (PBMC) and circulating levels of markers of ectopic mineralization (OPG, FGF-23, PPi) are modified in patients with calcific aortic valve disease (CAVD). We found that patients affected by CAVD (n = 50) had significantly higher circulating levels of OPG as compared to control individuals (p = 0.003). No differences between the two groups were found in FGF-23 and PPi levels. RANKL expression was higher in the PBMC from CAVD patients (p = 0.018) and was directly correlated with the amount of valve calcification (p = 0.032). In vitro studies showed that treatment of valve interstitial cells (VIC) with RANKL plus phosphate was followed by increase in matrix mineralization (p = 0.001). In conclusion, RANKL expression is increased in PBMC of patients with CAVD, is directly correlated with the degree of valve calcification, and promotes pro-calcific differentiation of VIC.

Therapeutic Apheresis and DialysisVolume 22, Issue 2 p. 207-208 Letter to the Editor Acute Splenic Sequestration Crisis After Red Blood Cell Exchange for Acute Chest Syndrome in an Adult With Sickle β-Thalassemia: What Went Wrong? Angelo Di Vincenzo, Corresponding Author Angelo Di Vincenzo divincenzoang@gmail.com orcid.org/0000-0002-7678-5671 Internal Medicine 3, Department of Medicine, Padua, ItalyEmail: divincenzoang@gmail.comSearch for more papers by this authorPiero Marson, Piero Marson Blood Transfusion Unit, Department of Transfusion Medicine, Hospital of Padua, Padua, ItalySearch for more papers by this authorMassimo Puato, Massimo Puato Internal Medicine 3, Department of Medicine, Padua, ItalySearch for more papers by this author Angelo Di Vincenzo, Corresponding Author Angelo Di Vincenzo divincenzoang@gmail.com orcid.org/0000-0002-7678-5671 Internal Medicine 3, Department of Medicine, Padua, ItalyEmail: divincenzoang@gmail.comSearch for more papers by this authorPiero Marson, Piero Marson Blood Transfusion Unit, Department of Transfusion Medicine, Hospital of Padua, Padua, ItalySearch for more papers by this authorMassimo Puato, Massimo Puato Internal Medicine 3, Department of Medicine, Padua, ItalySearch for more papers by this author First published: 04 December 2017 https://doi.org/10.1111/1744-9987.12638Citations: 1Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat No abstract is available for this article.Citing Literature Volume22, Issue2April 2018Pages 207-208 RelatedInformation

INTRODUCTION:Vitamin K antagonists, such as warfarin, are known to promote arterial calcification through blockade of gamma-carboxylation of Matrix-Gla-Protein. It is currently unknown whether other oral anticoagulants such as direct inhibitors of Factor Xa can have protective effects on the progression of aortic valve calcification.AIMS:To compare the effect of warfarin and rivaroxaban on the progression of aortic valve calcification in atherosclerotic mice.RESULTS:42 ApoE-/- mice fed with Western-type Diet (WTD) were randomized to treatment with warfarin (n = 14), rivaroxaban (n = 14) or control (n = 14) for 8 weeks. Histological analyses were performed to quantify the calcification of aortic valve leaflets and the development of atherosclerosis. The analyses showed a significant increase in valve calcification in mice treated with warfarin as compared to WTD alone (P = .025) or rivaroxaban (P = .005), whereas no significant differences were found between rivaroxaban and WTD (P = .35). Quantification of atherosclerosis and intimal calcification was performed on the innominate artery of the mice and no differences were found between the 3 treatments as far as atherogenesis and calcium deposition is concerned. In vitro experiments performed using bovine interstitial valve cells (VIC) showed that treatment with rivaroxaban did not prevent the osteogenic conversion of the cells but reduce the over-expression of COX-2 induced by inflammatory mediators.CONCLUSION:We showed that warfarin, but not rivaroxaban, could induce calcific valve degeneration in a mouse model of atherosclerosis. Both the treatments did not significantly affect the progression of atherosclerosis. Overall, these data suggest a safer profile of rivaroxaban on the risk of cardiovascular disease progression.

Background: Residual cardiovascular risk (RCVR) is an emerging issue in the clinical and therapeutic management of patients affected by hypertension. In fact, a number of clinical studies showed that even in case of optimal blood pressure (BP) control, the hypertensive patients still carry a sizeable increase in the CV risk as compared to normotensive individuals.Methods: We will review the clinical evidence about the determinants and the impact of RCVR on hypertension, with a specific focus on the progression of vascular damage.Results: The presence of RCVR in hypertensive patients is a significant phenomenon which challenges our clinical effort far beyond the reaching of BP targets. Although major determinants of RCVR are still undefined, there is a clear indication about the importance of an early and sustained control of BP values, so as to prevent the onset of target organ damage. In fact, our data and findings from the literature indicate that the "pseudo-normalization" of BP is not sufficient to abolish the risk of pro-atherogenic remodeling of arterial vessels.Conclusion: Additional studies are needed to establish whether the intervention on specific BP profiles and inflammatory mechanisms can have some clinical relevance in the management of RCVR. In the meanwhile, the precise phenotyping of the CV risk profile of each patient, coupled with a tailored pharmacological approach, represents the most effective strategy to hinder the progression of vascular damage and reduce the RCVR.

Objective: Aim of the study was to evaluate the impact of long-term well-controlled blood pressure (BP) on local arterial stiffness in hypertensives. Arterial stiffness increases with age and this process can be exacerbated by the presence of cardiovascular risk factors such as hypertension. Carotid distensibility evaluation is a reliable method that could reflect the stiffness of arteries. Design and method: We studied 40 young hypertensives (mean age 49.7 years) that had been kept on pharmacological treatment and/or on lifestyle modification for at least 12 months (mean 38 months) to maintain target BP. Follow-up visit were scheduled every 6-month. Carotid compliance coefficient (CC) and distensibility coefficient (DC) were measured by B-mode based system coupled with dedicated software. We assessed mean carotid intima-media thickness (IMT) and maximum IMT in each carotid artery segment, bilaterally. Endothelial function was evaluated by post-occlusion flow mediated dilation (FMD). Forty normotensive subjects paired for age and sex served as controls. Results: In the hypertensives, BP levels were well controlled (office BP 131/79 mmHg). Compared to controls, significantly higher BP levels and BMI were present in hypertensives, whereas age and metabolic parameters were similar. Compared to normotensives, carotid elasticity was significantly impaired in hypertensives (DC 24.5 ± 8.9 vs 36.9 ± 8.5 10–3/kPa, and CC 0.92 ± 0.34 vs 1.28 ± 0.36 mm2/kPa). Local stiffness parameters were inversely related to age, BP, and LDL-cholesterol. Moreover, DC and CC were inversely related to IMT measurements and directly with FMD values. Conclusions: In hypertensives with long term well-controlled BP, it is evident an increase in arterial local stiffness respect normotensive controls.

Introduction: It is currently unclear whether chronic kidney disease (CKD) and the decrease in renal function can influence the risk of venous thromboembolism (VTE) recurrence. Materials and methods: We performed an ambispective observational study on 409 patients with a previous episode of VTE. All the patients were included in the retrospective analysis whereas a subgroup of 260 individuals, without history of recurrence and that stopped oral anticoagulation, were then followed-up for a mean of 52.3 +/- 20.7 months. Results: At the enrollment, subjects with history of recurrent VTE were prevalently male with higher blood pressure and lower eGFR. Prevalence of CKD (defined as eGFR < 60 ml/min/1.73 m(2)) was higher in patients with previous VTE recurrence with an adjusted OR of 5.69 (IC95% 2.17-14.90, p < 0.001) compared to patients with normal eGFR. Similar findings were obtained from the prospective study where an adjusted 5.32 HR for VTE recurrence was seen in patients with CKD compared to subjects with normal renal function (IC95% 1.49-18.95, p = 0.010). An increase in the risk of recurrent VTE was also observed in patients with mild decrease in renal function (eGFR 60-90 vs = 90 ml/min/1.73 m(2) adjusted HR 2.84, IC95% 1.13-7.11, p = 0.025). Moreover, a multivariate Cox regression analysis including eGFR as continuous variable showed that renal function decrease was independently associated with the risk of VTE recurrence (p = 0.001). Conclusions: CKD and mild decrease in renal function are associated with a significant increase in the risk of recurrent VTE.

Objective: The aim of this study was to evaluate the effect of 5 years of anti-TNFalpha treatment on subclinical atherosclerosis progression. Psoriatic Arthritis (PsA) is associated with accelerated atherosclerosis and increased cardiovascular mortality. Influence of anti-TNFalpha treatment of PsA in subclinical atherosclerosis is still unclear. Design and method: Twenty-seven consecutive PsA patients were evaluated before TNF blockers therapy (T0), after 2 years (T1) and after 5 years (T2) of treatment. Subclinical atherosclerosis was evaluated through carotid duplex scanning, analyzing intima-media thickness (IMT) and flow-mediated dilation (FMD). IMT values were expressed as IMT mean (cumulative mean of all the IMT mean in every analyzed carotid segment) and M-MAX (cumulative mean of all the higher IMT in every analyzed carotid segment). Response to therapy was studied by the evaluation of DAS 28 (disease activity score), and C-reactive protein (CRP). Results: A good response to treatment was evident already at T1, with a significant decrease of DAS 28 (4.16 vs 2.30, p < 0.01) and CRP (11.25 vs 2.91, p < 0.01). The efficacy was preserved from T1 to T2 in terms of DAS 28 (2.30 vs 2.40, p = ns), CRP (2.91 vs 2.73, p = ns). From T0 to T1 there was a significant increment in both IMT-mean and M-MAX (0.72 vs 0.91 and 0.89 vs 1.06, respectively, p < 0.01). At T2 IMT-mean did not change significantly (0.91 vs 0.92, p = ns), while M-MAX worsened further (1.10 vs 1.06, p < 0.05). No significant variation in FMD values was observed during the 5-year follow up (T0 5.40%, T1 5.37%, T2 5.40%, p = ns). Noteworthy, systolic blood pressure and BMI remained stable from T0 to T2 (132 vs 131 mmHg, p = ns, and BMI 26 vs 25, p = ns), while diastolic blood pressure decreased significantly (79 vs 74 mmHg, p = 0.001). Conclusions: Our data revealed that in patients with PsA, despite treatment with TNF blockers, there is still a gradual, albeit slight progression of subclinical atherosclerosis assessed by ultrasonography. Other inflammatory mechanisms not related to TNF may be responsible of the progression of the atherosclerotic disease.

BackgroundPsoriatic arthritis (PsA) is associated with increased morbility and mortality and an accelerated atherosclerosis. Influence of anti-TNFalpha treatment (a widely used therapy in PsA) in subclinical atherosclerosis is still unclear.ObjectivesThe aim of this study was to evaluate subclinical atherosclerosis progression before, during and after 5 years of anti-TNFalpha treatment.MethodsTwenty-seven consecutive PsA patients were evaluated before TNF blockers therapy (T0), after 2 years (T1) and after 5 years (T2) of treatment. Subclinical atherosclerosis was evaluated through carotid duplex scanning, analyzing intima-media thickness (IMT) and flow-mediated dilation (FMD). IMT values were expressed as IMT mean (cumulative mean of all the IMT mean in every analyzed carotid segment) and M-MAX (cumulative mean of all the higher IMT in every analyzed carotid segment). Response to therapy was studied by the evaluation of tender and swollen joints (Tj and Sj), DAS 28 (disease activity score), erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP). Metrologic and metabolic data were collected. For the statistical evaluation of parameters over time (T0 vs T1, T1 vs T2) Student9s T test for paired data was used.ResultsFrom T0 to T1 a deterioration in IMT-mean and M-MAX (p<0.01) was noted. At T2 IMT-mean remained stable, M-MAX worsened further (p<0.05). No significant variation in FMD was observed (Table). Noteworthy, from T0 to T2 systolic blood pressure and Body Mass Index remained stable (p=ns), while diastolic blood pressure decreased (p=0,001). A good response to PsA treatment was confirmed by a significant decrease (T0 vs T1) in Tj, Sj, DAS 28 and CRP (p<0.01); treatment efficacy was preserved from T1 to T2 (p=ns) (Table).ConclusionsOur data revealed that in patients with PsA, despite treatment with TNF blockers, there is still a gradual, albeit slight progression of subclinical atherosclerosis assessed by ultrasonography. Other inflammatory mechanisms not related to TNF may be responsible of the progression in atherosclerotic disease.Disclosure of InterestNone declared

AIM:Circulating osteoprogenitors and receptor activator of nuclear factor kappa-B ligand (RANKL) expression in immune cells have been implicated in the pathogenesis of osteoporosis and vascular calcification. The role played by statin therapy in the bone-vascular axis is unknown.METHODS:Twenty naïve postmenopausal osteoporotic hypercholesterolemic women were treated with Atorvastatin 40 mg/day for 3 months. Gene expression analysis was performed to assess modification in osteoprotegerin (OPG)/RANK/RANKL expression in isolated T cells and monocytes. A flow cytometry analysis was used to study changes in the levels of circulating osteoprogenitor cells.RESULTS:After 3 months of treatment, Atorvastatin significantly reduced total cholesterol and LDL-C, without affecting HDL-C and triglycerides. Among circulating bone and phosphocalcium homeostasis markers, we found a significant increase in OPG levels (P < 0.01) and a modest reduction in osteocalcin (OCN) (P < 0.05). We also observed a significant reduction in RANKL expression in T cells (P < 0.05). No differences were found in the expression of RANK in T cells and RANKL and RANK in monocytes. OPG expression was low in both immune cell types and was not affected by the treatment. As for circulating osteoprogenitors, we found a significant reduction of CD34(+) BAP(+) (P < 0.05) and CD34(+) OCN(+) BAP(+) (P < 0.05) cells. In vitro studies showed that Atorvastatin reduced RANKL expression in activated human T-lymphoblastoid cells (Jurkat cell line).CONCLUSIONS:Three-month Atorvastatin treatment leads to a reduction in circulating osteoprogenitor cells and RANKL expression in T cells, as well as increase in OPG serum levels. These data suggest that statins could have protective effects in the bone-vascular axis.

Aim of this study was to evaluate in a long follow-up the carotid artery remodelling in a cohort of young hypertensive subjects having good blood pressure (BP) control. We studied 20 grade I hypertensives (HT) by assessing the B-mode ultrasound of mean carotid intima-media thickness (mean-IMT) and maximum IMT (M-MAX) in each carotid artery segment (common, bulb, internal), bilaterally. We compared their ultrasound measurements with those recorded 5 and 10 years earlier. While the first 5-year follow-up was observational, in the second 5-year follow-up, lifestyle modifications and/or pharmacological therapy were started to obtain well-controlled BP levels. Office BP was measured at the time of the ultrasound studies and every 6 months during the follow-up. BP levels were: 10 years 144/91mmHg, 5 years 143/90mmHg and 129 +/- 79mmHg at the time of the study. In the first 5-year observational follow-up, both mean-IMT and M-MAX increased ( 0.116 and 0.165mm, respectively, p<0.0005). In the 5-year intervention follow-up, characterized by well-controlled BP, mean-IMT slightly but significantly increased ( 0.084mm, p=0.004), whereas M-MAX remained stable ( 0.026mm). In our HT, well-controlled BP levels were able to prevent pro-atherogenic remodelling (expressed by M-MAX). Conversely, good BP control slightly decreased but did not stop the progression in mean-IMT, which is likely to reflect some hypertrophy of the arterial media layer.

Objective: The aim of this study was to evaluate the impact of well controlled blood pressure (BP) levels on structural and functional properties of arteries in essential hypertensives. Design and Method: We studied 80 young hypertensives (mean age 49 yo) allocated either to pharmacological treatment (55 of 80) or to lifestyle modifications (25 of 80) for at least 12 months (mean 38 months) to maintain target BP. Follow-up visits were scheduled every 6 months. Office BP was taken three times by the same doctor at the time of the study. We assessed the B-mode ultrasound of mean carotid intima-media thickness (mean-IMT) and maximum IMT (M-MAX) in each carotid artery segment (common, bulb, internal), bilaterally. Endothelial function was evaluated by post-occlusion flow mediated dilation (FMD) of the brachial artery using high-sensitivity ultrasonography. Arterial elastic properties were evaluated by assessing carotid distensibility (DC) and compliance (CC). Forty normotensive subjects paired for age and sex served as controls. Results: Throughout the study, BP levels were well controlled in hypertensives (mean BP levels: 131/79 mmHg). The IMT (mean-IMT 0.65 mm, M-MAX 0.79 mm) was significantly higher in hypertensives than in controls (mean-IMT 0.60 mm, M-MAX 0.70 mm). FMD was impaired in hypertensives (5.7%) compared to controls (9.2%). IMT parameters correlated only to age, while LDL-cholesterol was the only factor related to FMD. Compared to controls, arterial elasticity was significantly impaired in hypertensives (DC 25.6 vs 52.4 10–3/kPa, and CC 0.97 vs 1.40 mm2/kPa). Conclusions: In essential hypertensives, despite long-term well controlled BP, the pro-atherogenic remodelling was still present. IMT was mainly dependent upon age, while FMD was mainly related to cholesterol levels. Moreover, carotid elasticity was impaired. The “pseudo-normalization” of BP levels does not result in normalization of structural and functional properties of the arterial wall.

Objective: Risk of arterial cardiovascular events is increased in patients with history of venous thromboembolism (VTE), although underlying mechanisms are still unclear. We previously found an increase prevalence of metabolic syndrome (MetS) among patients affected by VTE. In the present study we investigated the association between individual components of MetS and the risk of VTE recurrence. Design and method: We enrolled 350 patients who had had at least one objective diagnosed episode of VTE. Data about VTE characteristics were obtained from the medical records of the patients and the presence of MetS was established according to the NCEP ATP III guidelines. Results: We identified 67 (19,1%) subjects with history of VTE recurrence and 283 (80,9%) patients without relapsing VTE. The two groups showed comparable age, BMI, waist circumference and prevalence of smoking habit. Patients with recurrent VTE showed increase systolic blood pressure (p = 0.026), lower HDL-C levels (p = 0.037) and increase in triglycerides (TG) (p = 0.005) as compared to those without recurrence. After adjustment for age and gender, the prevalence of MetS was significantly increased in patients with recurrent VTE (OR 2.25, p = 0.005). Among the individual components of MetS we found a significant increase in the presence of high blood pressure (OR 4.44, p = 0.01), low HDL-C (OR 2.04, p = 0.04) and elevated triglycerides (OR 2.34, p = 0.008) in the patients with recurrent VTE. No differences between the two groups were seen in the prevalence of elevated glycaemia and visceral obesity. Conclusions: The prevalence of MetS, in particular high blood pressure and atherogenic lipid profile (low HDL/high TG), is increased in patients with recurrence of VTE.