Wound Care During the COVID-19 Emergency in Padua Hospital, Italy.

Chronic vascular wounds have a significant economic and social impact on our society, calling for the allocation of a great deal of attention and resources. The coronavirus disease (COVID-19) outbreak has represented a difficult challenge to face for health care providers and fragile patients, such as for outpatients and Day-Hospital patients needing continuous care at the Angiology Unit of the University Hospital of Padova in Italy, one of the most crucial areas worldwide. The project consisted of a critical revision of all the procedures from the patients' arrivals to their discharge after completing the entire course of treatment. The previous standard of practice was modified according to the current evidence-based guidelines and the national and local government's indications. The new standard of practice allowed our unit to protect every patient and staff member from the coronavirus infection, providing the same high standard of care as before the COVID-19 outbreak.

Potential Association between Distal Deep Vein Thrombosis and Asymptomatic Atherosclerosis.

Background Several studies have previously reported an association between idiopathic proximal deep vein thrombosis (DVT) and atherosclerosis, but whether spontaneous distal DVT is associated with asymptomatic atherosclerosis is still unknown. Methods Ultrasonography of the carotid arteries was done for plaque detection and intima-media thickness (IMT) evaluation, and the ankle-brachial index (ABI) in 116 patients with spontaneous DVT and without symptomatic atherosclerosis. Fifty-seven patients (M/F 19/38, age range 54-78 years) had distal DVT and 59 (M/F 24/35, age range 51-73 years) had proximal DVT. A group of 57 (M/F 21/36, age range 64-70 years) matched subjects acted as controls. Results No significant difference was found in carotid plaques between patients with distal or proximal DVT versus controls ( p > 0.05 in all comparisons). Carotid IMT (mean ± SD) was significantly increased in patients with distal (1.00 ± 0.20 mm) and proximal (0.98 ± 0.16 mm) DVT versus controls (0.88 ± 0.15 mm, p <0.01 in both comparisons). An ABI £ 0.9 was found in 3/57 (5.3%) and 5/59 (8.5%) patients with distal and proximal DVT, respectively versus no controls with abnormal ABI. Conclusion Our results revealed that there may be an association between spontaneous distal DVT and asymptomatic atherosclerosis, and confirmed the known association between idiopathic proximal DVT and asymptomatic atherosclerosis. Larger studies are needed to confirm our results and to evaluate their clinical implications.

Thrombophilia, risk factors and prevention.

INTRODUCTION: Fifty-three years after the first description of an inherited prothrombotic condition (antithrombin deficiency), our knowledge on hereditary and acquired causes of hypercoagulability that can predispose carriers to venous thromboembolism (VTE) has greatly improved. Areas covered: Main causes of hereditary thrombophilia are summarized alongside new prothrombotic mutations recently discovered. The main causes of acquired thrombophilia, and namely, antiphospholipid antibody syndrome and hyperhomocysteinemia, are also discussed together with other common acquired prothrombotic states characterized by an increase of procoagulant factors and/or a decrease of natural anticoagulants. Finally, suggestions for thromboprophylaxis in carriers of hereditary thrombophilia according to current guidelines/evidence are made for the most challenging high-risk situations (i.e. surgery, pregnancy, contraception, cancer, economy class syndrome) as well as for the prevention of post-thrombotic syndrome. Expert opinion: A carrier of inherited thrombophilia should be evaluated in the framework of other (genetic and/or acquired) coexisting risk factors for first or recurrent VTE when assessing the need and duration of prevention (primary prophylaxis). Prevention strategies should be tailored to each patient and every situational risk factor. The knowledge of the carriership status of severe thrombophilia in the proband can be important to provide asymptomatic relatives with adequate counseling on thrombophilia screening or primary thromboprophylaxis.

Failure of old and new anticoagulants to prevent ischemic stroke in high-risk atrial fibrillation: a case report.

Rivaroxaban is an oral anticoagulant that acts as a direct, competitive factor Xa inhibitor. Large randomized clinical trials have shown that, at a daily dose of 20 mg, Rivaroxaban is at least as effective as dose-adjusted warfarin for the prevention of stroke or other embolic complications in patients with nonvalvular atrial fibrillation (AF). The safety and efficacy of combining Rivaroxaban with an antiplatelet agent for secondary stroke prevention has not been established. We report the case of an elderly patient with permanent AF and coronary heart disease, who had already suffered an ischemic stroke while on warfarin treatment, and was consequently switched to treatment with an association of Rivaroxaban and Aspirin. Her CHA2DS2-VASc score was 9. The patient developed a severe recurrent disabling ischemic stroke. This case goes to show that the novel direct anticoagulants may fail to prevent recurrent stroke in patients at particularly high risk, even when associated with antiplatelet drugs.

An unusual finding of massive pulmonary embolism in a patient during treatment with high-dose ibuprofen.

Non-steroidal anti-inflammatory drugs have been associated with an increased risk of venous thromboembolism. We report for the first time, the case of a patient who developed massive pulmonary embolism after a long period of treatment with high doses of ibuprofen. A 65-year-old woman was admitted with severe dyspnea while on treatment with high doses of ibuprofen for diffuse spine pain due to arthrosis. A spiral computed tomography showed a massive pulmonary embolism. No other explanation for the thromboembolic disorder was found. She was successfully treated with therapeutic doses of low-molecular-weight heparin followed by rivaroxaban. Ibuprofen was discontinued and replaced by tramadol. High-dose ibuprofen is likely to have accounted for the life-threatening thromboembolic disorder.

Effects of GLP-1 on forearm vasodilator function and glucose disposal during hyperinsulinemia in the metabolic syndrome.

OBJECTIVE: Patients with the metabolic syndrome (MetS) have impaired insulin-induced enhancement of vasodilator responses. The incretin hormone glucagon-like peptide 1 (GLP-1), beyond its effects on blood glucose, has beneficial actions on vascular function. This study, therefore, aimed to assess whether GLP-1 affects insulin-stimulated vasodilator reactivity in patients with the MetS. RESEARCH DESIGN AND METHODS: Forearm blood flow responses to acetylcholine (ACh) and sodium nitroprusside (SNP) were assessed in MetS patients before and after the addition of GLP-1 to an intra-arterial infusion of saline (n = 5) or insulin (n = 5). The possible involvement of oxidative stress in the vascular effects of GLP-1 in this setting was investigated by infusion of vitamin C (n = 5). The receptor specificity of GLP-1 effect during hyperinsulinemia was assessed by infusing its metabolite GLP-1(9-36) (n = 5). The metabolic actions of GLP-1 were also tested by analyzing forearm glucose disposal during hyperinsulinemia (n = 5). RESULTS: In MetS patients, GLP-1 enhanced endothelium-dependent and -independent responses to ACh and SNP, respectively, during hyperinsulinemia (P < 0.001 for both), but not during saline (P > 0.05 for both). No changes in vasodilator reactivity to ACh and SNP were seen after GLP-1 was added to insulin and vitamin C (P > 0.05 for both) and after GLP-1(9-36) was given during hyperinsulinemia (P > 0.05 for both). Also, GLP-1 did not affect forearm glucose extraction and uptake during hyperinsulinemia (P > 0.05 for both). CONCLUSIONS: In patients with the MetS, GLP-1 improves insulin-mediated enhancement of endothelium-dependent and -independent vascular reactivity. This effect may be influenced by vascular oxidative stress and is possibly exerted through a receptor-mediated mechanism.

Coexistence of functional angiotensin II type 2 receptors mediating both vasoconstriction and vasodilation in humans.

OBJECTIVES: Angiotensin (Ang) II type 1 (AT1) receptors mediate the majority of cardiovascular effects of Ang II, whereas the role of type 2 (AT2) receptors is still controversial. The present study, therefore, investigated regional hemodynamic responses mediated by AT2 receptors in humans. METHODS: Studies were performed in 20 healthy individuals (eight men; mean age 37 ± 3 years) through intra-arterial infusion of agonists and antagonists of Ang II receptors by use of strain-gauge plethysmography. RESULTS: Selective blockade of either AT1 or AT2 receptors by telmisartan or PD 123319, respectively, resulted in mild forearm blood flow increase (15 ± 5% and 10 ± 4, respectively; both P > 0.05); combined AT1 and AT2 receptor antagonism, however, was associated with greater vasodilator response (25 ± 5%; P = 0.02). This effect was unrelated to increased nitric oxide activity, being unaffected (27 ± 5%; P = 0.65) by a ' nitric oxide clamp' (coinfusion of the nitric oxide synthase inhibitor L-NMMA and the nitric oxide donor sodium nitroprusside). Graded doses of Ang II induced a progressive vasoconstrictor response that was blunted not only by telmisartan, but also by PD 123319 and by the combination of PD 123319 and telmisartan (all P < 0.001 vs. Ang II alone). AT2 receptor stimulation by CGP 42112A resulted in a dose-dependent vasodilation (P < 0.001 vs. baseline), that was abolished by the nitric oxide clamp and by PD 123319 (both P < 0.001 vs. CGP 42112A alone). CONCLUSION: In the human forearm, vasoconstrictor AT2 receptors coexist with AT2 receptors mediating nitric oxide-dependent vasodilation. These findings suggest that imbalance between these opposing hemodynamic actions may affect vascular homeostasis and foster further investigation about the role of AT2 receptors in human disease.