Update on the Pharmacological Actions of Enoxaparin in Nonsurgical Patients.

Low-molecular-weight heparins are a class of drugs derived from the enzymatic depolymerization of unfractionated heparin that includes enoxaparin. Several studies have been performed on enoxaparin in recent years, in particular for the prevention and treatment of venous thromboembolism and for the treatment of acute coronary syndrome. Furthermore, the use of enoxaparin has been extended to other clinical situations that require antithrombotic pharmacological prevention, such as hemodialysis and recurrent abortion. In this review, we report the main clinical experiences of using enoxaparin in the prevention of VTE in nonsurgical patients.

Thromboembolism in COVID-19: the unsolved problem.

INTRODUCTION: The recent Sars-CoV-2 pandemic (COVID-19) has led to growing research to explain the poor clinical prognosis in some patients. While early observational studies highlighted the role of the virus in lung failure, in a second moment thrombosis emerged as a possible explanation of the worse clinical course in some patients. Despite initial difficulties in management of such patients, the constant increase of literature in the field is to date clarifying some questions from clinicians. However, several other questions need answer. EVIDENCE ACQUISITION: We performed systematic research using Embase and PubMed, inserting the keywords and mesh terms relative to the new coronavirus and to VTE: "COVID-19," "SARS," "MERS," "coronavirus," "2019 n-CoV," venous thromboembolism," "pulmonary embolism," "deep vein thrombosis," "thromboembolism," "thrombosis." Boolean operators "AND," "OR," "NOT" were used where appropriate. We found 133 articles of interest but only 20 were selected, providing the most representative information. EVIDENCE SYNTHESIS: A novel disease (COVID-19) due to severe acute respiratory syndrome coronavirus 2 (Sars-CoV-2) infection was responsible for thousands of hospitalizations for severe acute respiratory syndrome, with several cases of thrombotic complications due to excessive inflammation, platelet activation, endothelial dysfunction, and stasis. COVID-19 and hospitalizations for COVID-19 may carry several potential risk factors for thrombosis. Severe coagulation abnormalities may occur in almost all the severe and critical ill COVID-19 cases. CONCLUSIONS: Despite a strong pathophysiological rationale, the evidence in literature is not enough to recommend an aggressive antithrombotic therapy in COVID-19. However, it is our opinion that an early use, even at home at the beginning of the disease, could improve the clinical course.

Alarmins as a Possible Target of Future Therapies for Atrial Fibrillation.

To date, worldwide, atrial fibrillation is the most common cardiovascular disease in adults, with a prevalence of 2% to 4%. The trigger of the pathophysiological mechanism of arrhythmia includes several factors that sustain and exacerbate the disease. Ectopic electrical conductivity, associated with the resulting atrial mechanical dysfunction, atrial remodeling, and fibrosis, promotes hypo-contractility and blood stasis, involving micro endothelial damage. This causes a significant local inflammatory reaction that feeds and sustains the arrhythmia. In our literature review, we evaluate the role of HMGB1 proteins, heat shock proteins, and S100 in the pathophysiology of atrial fibrillation, offering suggestions for possible new therapeutic strategies. We selected scientific publications on the specific topics "alarmins" and "atrial fibrillation" from PubMed. The nonsystematic review confirms the pivotal role of molecules such as S100 proteins, high-mobility group box-1, and heat shock proteins in the molecular pattern of atrial fibrillation. These results could be considered for new therapeutic opportunities, including inhibition of oxidative stress, evaluation of new anticoagulant drugs with novel therapeutic targets, molecular and genetic studies, and consideration of these alarmins as predictive or prognostic biomarkers of disease onset and severity.

Novel active fixation lead guided by electrical delay can improve response to cardiac resynchronization therapy in heart failure.

AIMS: Cardiac resynchronization therapy (CRT) for heart failure (HF) recently has shown optimal results by targeting electrically delayed sites in coronary sinus (CS) branches. However this purpose often cannot be reached because of unstable left ventricular (LV) lead position. In current study were assessed the long-term effects of the novel active fixation LV lead in CS, guided by electrical delay (QLV), in patients with HF due to coronary artery disease. METHODS: One hundred eighty-five consecutive patients underwent CRT with intraoperative evaluation of QLV in the target position of the LV lead. When the novel active fixation LV lead was available, 98 consecutive patients received it, composing the Fix group. They were compared with 87 patients with a conventional passive fixation lead (No Fix group). The final LV lead position was assessed by fluoroscopy. Clinical response to CRT was assessed within a period of about 3 years: patients experiencing HF rehospitalization and death due to HF were defined as non-responders. RESULTS: There were no significant differences between groups in the final position of LV lead in left anterior oblique view (Pearson χ2  = 0.12; P = 0.73). In right anterior oblique view, a basal position was reached more in the Fix group (38%) than in the No Fix group (6.5%) (Pearson χ2  = 23.095; P < 0.001). QLV was significantly greater in the Fix group (122.6 ± 33.2 ms; SE = 3.6) than in the No Fix group (97.5 ± 37.8 ms; SE = 4.9) (t = 4.17; P < 0.001). Rehospitalizations for HF were 37 in the No Fix group and 14 in the Fix group. Deaths due to HF were 49 in the No Fix group and 18 in the Fix group. Survival analysis, assessed by Cox regression, showed that the Fix group had a better outcome both for HF rehospitalizations [hazard ratio (HR) = 0.48; 95% confidence interval (CI) = 0.25-0.9; P = 0.023] and death due to HF (HR = 0.55; 95% CI = 0.31-0.97; P = 0.04) in comparison with the No Fix group. Adjustment for baseline characteristics by multivariate analysis showed that an active fixation lead in CS, as a covariate, was still significant both for HF rehospitalizations (HR 0.46; 95% CI = 0.24-0.88; P = 0.019) and for death due to HF (HR 0.5; 95% CI = 0.28-0.9; P = 0.021). CONCLUSIONS: The novel active fixation LV lead allowed to target sites with greater QLV. Often maximum QLV was documented in basal segments, were stability of conventional passive fixation leads is not enough. Patients receiving it experienced less HF rehospitalizations and less death due to HF. Active fixation lead in CS guided by QLV can improve long-term prognosis in patients with HF due to coronary artery disease undergoing to CRT.