Background & Aims Hepatitis C virus (HCV)‐related mixed cryoglobulinaemia vasculitis (MCV) is characterized by the expansion of rheumatoid factor‐producing B‐cell clones. The aim of this study was to assess whether B‐cell clones may persist in these patients after the clearance of the virus with antiviral therapy, and whether their persistence influences clinical outcomes. Methods Forty‐five HCV‐cured MCV patients were followed up for a median of 18.5 (range 9‐38) months after the clearance of HCV. Circulating B‐cell clones were detected using flow cytometry either by the skewing of kappa/lambda ratio or by the expression of a VH1‐69‐encoded idiotype. Results The clinical response of vasculitis was 78% complete, 18% partial and 4% null. However, cryoglobulins remained detectable in 42% of patients for more than 12 months. Circulating B‐cell clones were detected in 18 of 45 patients, and in 17 of them persisted through the follow‐up; nine of the latter patients cleared cryoglobulins and had complete response of vasculitis. Several months later, two of these patients had relapse of MCV. Conclusions B‐cell clones persist in MCV patients long after HCV infection has been cleared but halt the production of pathogenic antibody. These ‘dormant’ cells may be reactivated by events that perturb B‐cell homeostasis and can give rise to the relapse of cryoglobulinaemic vasculitis.

Using bio-impedance to deduce some hemodynamic parameters combined with some short-term ECG temporal dispersion intervals, and measuring myocardial depolarization, intraventricular conduction, and repolarization. A total of 65 in-hospital patients (M/F:35/30) were enrolled, 39 with HFrEF and 26 HFpEF, in New York Heart Association (NYHA) class IV. Stroke volume (SVI), cardiac indexes (CI), left ventricular ejection fraction (LVEFBIO), end diastolic volume (LV-EDV), and other systolic and diastolic parameters were noninvasively obtained at enrollment and at hospital discharge. At the same time, QR, QRS, QT, ST, Tpeak-Tend (Te) interval mean, and standard deviation (SD) from 5 min ECG recordings were obtained. At baseline, HFrEF patients reported significantly lower SVI (p < 0.05), CI (p < 0.05), and LVEF (p < 0.001) than HFpEF patients; moreover, HFrEF patients also showed increased LV-EDV (p < 0.05), QR, QRS, QT, ST, and Te means (p < 0.05) and standard deviations (p < 0.05) in comparison to HFpEF subjects. Multivariable logistic regression analysis reported a significant correlation between hospital mortality and Te mean (odds ratio: 1.03, 95% confidence limit: 1.01–1.06, p: 0.01). Fifty-seven percent of patients were considered responders to optimal medical therapy and, at discharge, they had significantly reduced NT-proBNP, (p < 0.001), heart rate (p < 0.05), and TeSD (p < 0.001). LVEF, obtained by transthoracic echocardiography, and LVEFBIO were significantly related (r: 0.781, p < 0.001), but these two parameters showed a low agreement limit. Noninvasive hemodynamic and ECG-derived parameters were useful to highlight the difference between HFrEF and HFpEF and between responders and nonresponders to the optimal medical therapy. Short-period bioimpedance and electrocardiographic data should be deeply evaluated to determine possible advantages in the therapeutic and prognostic approach in severe CHF.

Objective As recently reported, elevated fasting glucose plasma level constitutes a risk factor for 30-day total mortality in acutely decompensated chronic heart failure (CHF). Aim of this study was to evaluate the 30-day mortality risk in decompensated CHF patients by fasting glucose plasma level and some repolarization ECG markers. Method A total of 164 decompensated CHF patients (M/F: 94/71; mean age, 83 ± 10 years) were studied; Tend (Te), QT interval (QT) and 5 min of ECG recordings were obtained, studying mean, SD and normalized index of the abovementioned ECG intervals. These repolarization variables and fasting glucose were analyzed to assess the 30-day mortality risk among these patients. Results Thirty-day mortality rate was 21%, deceased subjects showed a significant increase in N terminal-pro-brain natriuretic peptide (P < 0.001), higher sensitivity cardiac troponin, fasting glucose, creatinine clearance, QTSD, QTVN, Te mean, TeSD and TeVN than the survivals. Multivariable regression analysis reported that fasting glucose (hazard ratio, 1.59; 95% confidence interval, 1.09–2.10; P < 0.01), Te mean (hazard ratio, 1.03; 95% confidence interval, 1.01–1.05; P < 0.01) and QTSD (hazard ratio, 1.17; 95% confidence interval, 1.01–1.36; P < 0.05) were significantly related to higher mortality risk, whereas only fasting glucose (hazard ratio, 1.84; 95% confidence interval, 1.12–3.02; P < 0.05) and Te mean (hazard ratio, 1.07; 95% confidence interval, 1.02–1.11; P < 0.01) were associated to cardiovascular mortality. Conclusion Data suggest that two simple, inexpensive, noninvasive markers, as fasting glucose and Te, were capable to stratify the short-term total and cardiovascular mortality risk in acutely decompensated CHF.