Proposal criteria of paradoxical low-flow low-gradient aortic stenosis for predicting prognosis in patients undergoing transcatheter aortic valve implantation.

BACKGROUND: Paradoxical low-flow, low-gradient (PLF-LG) aortic stenosis (AS) is associated with poor prognosis in patients undergoing transcatheter aortic valve implantation (TAVI). This study aimed to verify the conventional criteria of PLF-LG AS (left ventricular ejection fraction [LVEF] > 50%, mean aortic valve pressure gradient [AVPG] < 40 mm Hg and stroke volume index [SVI] < 35 ml/m2 by measuring Doppler method) compatible for predicting prognosis in patients undergoing TAVI. MATERIALS AND METHODS: A total of 128 consecutive patients who underwent TAVI for AS with LVEF > 50% were enrolled. The primary endpoint was the hospital readmission due to heart failure (HRHF) and the secondary endpoint was all-cause mortality after hospital discharge. The patients were classified by both the conventional criteria of PLF-LG AS and the proposal criteria of PLF-LG AS if mean aortic valve pressure gradient (AVPG) < 40 mmHg and SVI by measuring Simpson's method < cut off value based on the ROC curve for predicting HRHF. RESULTS: According to the conventional criteria, only 6 patients were diagnosed with PLF-LG AS. However, according to the proposal criteria, 16 patients were diagnosed with PLF-LG AS. Fourteen patients developed HRHF during the follow-up period after TAVI. Based on the ROC curves, SVI by measuring Simpson's method (cut off value = 25 ml/m2) had higher sensitivity and specificity for predicting HRHF (AUC = 0.74, p = 0.0013) than SVI by measuring Doppler method (AUC = 0.63, p = 0.045). The multivariate analysis revealed that PLF-LG AS defined by the proposal criteria (HR: 5.25; 95% CI: 1.60-17.16; p = 0.0073) but not by the conventional criteria was independently associated with HRHF. PLF-LG AS defined by the conventional criteria and the proposal criteria were not associated with all-cause mortality in the univariate analysis. CONCLUSIONS: Our results demonstrated that new criteria of PLF-LG AS defined as SVI < 25 ml/m2 measured by Simpson's method could predict HRHF in patients with severe AS who underwent TAVI.

Catheter ablation of atrial fibrillation reduces heart failure rehospitalization in patients with heart failure with preserved ejection fraction.

BACKGROUND: Atrial fibrillation (AF) is associated with heart failure (HF) rehospitalization in patients with heart failure with preserved ejection fraction (HFpEF). OBJECTIVE: We tested the hypothesis that catheter ablation of AF could reduce HF rehospitalization compared with conventional pharmacotherapy in patients with HFpEF. METHODS: Eighty-five consecutive HFpEF (EF ≥ 50% and a history of HF hospitalization) patients diagnosed as AF by 12-lead electrocardiogram were retrospectively analyzed. Thirty-five patients who received catheter ablation (ABL group) were compared with 50 patients treated by antiarrhythmic drugs and/or beta-blockers (CNT group). The primary endpoint was rehospitalization due to HF. RESULTS: The patients characteristics did not differ between the two groups including, age (71 ± 8 vs 71 ± 13 years; P = .637), female sex (34% vs 36%; P = .870), mean plasma brain natriuretic peptide (145 ± 112 vs 195 ± 153 pg/mL; P = .111), mean left ventricular ejection fraction (62% ± 8% vs 61% ± 9%; P = .624), and type of AF (nonparoxysmal AF 60% vs 62%; P = .852). Amiodarone was continued 40% (14 out of 35) and 40% (20 out of 70) in ABL and CNT groups, respectively (P = 1.000). Neither major complication nor major side effect was observed during the follow-up period. During a mean follow-up period of 792 ± 485 days, Kaplan-Meier curve analysis showed that significantly more patients in the ABL group were free from HF rehospitalization (log-rank P = .0039). Additionally, multivariate analysis revealed that catheter ablation of AF was the only preventive factor of HF rehospitalization (OR = 0.15; 95% CI: 0.04-0.46; P < .001). CONCLUSIONS: Catheter ablation of AF reduced HF rehospitalization compared with conventional pharmacotherapy in patients with HFpEF in our institute. Multicenter randomized study is warranted to confirm the result.

Interleukin 10 Treatment Ameliorates High-Fat Diet-Induced Inflammatory Atrial Remodeling and Fibrillation.

BACKGROUND: Obesity, characterized by systemic low-grade inflammation, is considered a well-known risk for atrial fibrillation. In fact, IL-10 (interleukin 10), which is a potent anti-inflammatory cytokine, has been reported to decrease in obese and diabetic patients. We tested the hypotheses forwarding that genetic deletion of IL-10 exacerbates high-fat diet (HFD)-induced obesity-caused atrial inflammation, lipidosis, fibrosis, and fibrillation and that IL-10 therapy inhibits this pathology. METHODS: Eight- to 10-week-old male CL57/B6 (wild-type) mice and IL-10 knockout mice were divided into a 12-week HFD group and a 12-week normal-fat diet (NFD) group, respectively. In addition, the effect of IL-10 administration was also investigated. RESULTS: HFD-induced obesity for 12 weeks significantly depressed serum levels of IL-10 but were found to increase several proinflammatory cytokines in wild-type mice. Adverse atrial remodeling, including atrial inflammation, lipidosis, and fibrosis, was induced in both wild-type and IL-10 knockout mice by HFD. Vulnerability to atrial fibrillation was also significantly enhanced by HFD. With regard to epicardial and pericardial adipose tissue, the total amount of epicardial adipose tissue+pericardial adipose tissue volume was increased by HFD. Besides, proinflammatory and profibrotic cytokines of epicardial adipose tissue+pericardial adipose tissue were also upregulated. In contrast, the protein level of adiponectin was downregulated by HFD. These HFD-induced obesity-caused adverse effects were further exaggerated in IL-10 knockout mice in comparison to wild-type mice. Systemic IL-10 administration markedly ameliorated HFD-induced obesity-caused left atrial remodeling and vulnerability to atrial fibrillation, in addition to improving the quality of epicardial adipose tissue+pericardial adipose tissue. CONCLUSIONS: Our results highlight IL-10 treatment as a potential therapeutic approach to limit the progression of HFD-induced obesity-caused atrial fibrillation.