Safety of cardioversion in atrial fibrillation lasting less than 48 h without post-procedural anticoagulation in patients at low cardioembolic risk.

Currently, there is no unified consensus on short-term anticoagulation after cardioversion of atrial fibrillation lasting less than 48 h in low-cardioembolic-risk patients. The aim of this study is to evaluate the rate of transient ischemic attacks, stroke and death in this subset of patients after cardioversion without post-procedural anticoagulation. In a prospective observational study, patients with recent-onset AF undergoing cardioversion attempts in the Emergency Department were evaluated over the past 3 years. Inclusion criteria were conversion to sinus rhythm, low thromboembolic risk defined by a CHA2DS2VASc score of 0-1 points for males (0-2 points for females aged over 65 years), and hospital discharge without anticoagulant treatment. Patients with severe valvular heart disease, underlying systemic causes of AF, and those discharged with anticoagulant therapy were excluded. The main outcomes measured were TIA, stroke and death at thirty days' follow-up after discharge. During the study period, 218 successful cardioversions, obtained both electrically and pharmacologically, were performed on 157 patients. One hundred and eleven patients were males (71%), the mean age was 55.2 years (±standard deviation 10.7), 99 patients (63%) reported a CHA2DS2VASc score of 0, and the remaining 58 (37%) had a risk profile of 1 point. Of these, latter 8 were females (5%) older than 65 years (risk score 2 points). At the thirty days outcome, none of the 150 enrolled patients who completed a follow-up visit has reported TIA or stroke, nor died, in the overall 211 successful cardioversions evaluated. In our study, the rate of thromboembolic events after cardioversion of recent-onset AF of less than 48 h duration, in patients with a 0-1 CHA2DS2VASc risk profile (females 0-2), appeared to be extremely low even in absence of post-procedural anticoagulation. These findings seem to confirm data from previous studies, and suggest that routine post-procedural short-term anticoagulation may be considered as an overtreatment in this very low-risk subset of patients.

Redistribution of regulatory T-cells across the evolving stages of chronic hepatitis C.

BACKGROUND: Hepatitis C virus infection frequently leads to chronic hepatitis, possibly evolving to end-stage liver disease and hepatocellular carcinoma. Regulatory T cells can affect antiviral immune response thus influencing the outcome of the disease. AIM: To determine numeric and functional distribution of regulatory T cells expressing CD4+CD25hiFoxp3+ (T-regs) during the different stages of hepatitis C virus-related liver disease. METHODS: 90 hepatitis C viraemic patients and 50 healthy controls were included. Surface and intracellular (Foxp3) T-reg markers were evaluated by flow cytometry. Target cell proliferation and interferon-gamma production were evaluated in 37 HCV patients. In 16 cases intrahepatic distribution of Foxp3 by immuno-histochemistry was assessed. RESULTS: T-regs were increased in hepatitis C virus infected patients and correlated inversely with aminotransferases and directly with MELD score and disease duration. A preserved inhibitory ability of interferon-gamma production was distinctive of patients with normal aminotransferases. Circulating T-regs did not correlate with intrahepatic distribution of Foxp3. CONCLUSIONS: In chronic hepatitis C, selective expansion of peripheral T-regs in patients with normal aminotransferases and advanced disease suggests that, though a continual low level inflammation does not prevent liver disease progression, once cirrhosis has developed it may represent an attempt to prevent immuno-mediated decompensation.