BackgroundElevated high‐sensitivity C‐reactive protein (hsCRP) has been associated with increased risks of adverse outcomes of various cardiovascular diseases. The relationship between hsCRP and the prognosis of hypertrophic cardiomyopathy remains to be evaluated.Methods and ResultsThe study used an observational cohort methodology. A total of 490 patients were enrolled in the Fuwai Hospital from 2001 to 2011 and were followed for 3.7±2.0 years. According to the risk category of hsCRP, subjects in the high hsCRP group (>3.0 mg/L) had a higher risk of developing adverse events than the low hsCRP group (<1.0 mg/L): cardiovascular death (adjusted hazard ratios[HR] 5.41, 95% CI 1.96–14.93, P=0.001), all‐cause mortality (adjusted HR 4.78, 95% CI 1.99–11.47, P<0.001), sudden cardiac death (adjusted HR 11.29, 95% CI 1.38–92.20, P=0.024), and heart failure–related death (adjusted HR 4.38, 95% CI 1.15–16.60, P=0.030). Similarly, the continuous variable of hsCRP was also an independent predictor for adverse outcomes: cardiovascular death (adjusted HR 1.15, 95% CI 1.06–1.25, P=0.001), all‐cause mortality (adjusted HR 1.17, 95% CI 1.09–1.26, P<0.001), sudden cardiac death (adjusted HR 1.20, 95% CI 1.06–1.36, P=0.003), and heart failure–related death (adjusted HR 1.15, 95% CI 1.02–1.30, P=0.020).ConclusionsOur results indicate that elevated plasma hsCRP is associated with increased risk for adverse outcomes in patients with hypertrophic cardiomyopathy.

The J-Valve system exhibits a convincing midterm performance and is a safe and feasible procedure with low perioperative and postoperative complications.

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Background Obstructive sleep apnea ( OSA ) is common and independently associated with atrial fibrillation ( AF ) in patients with hypertrophic cardiomyopathy ( HCM ). This study aimed to investigate the relationship between apnea‐hypopnea index ( AHI ), a measure of OSA severity, and prevalence of AF in a large series of patients with HCM. Methods and Results A total of 555 patients with HCM who underwent sleep evaluations were retrospectively included. Data from polysomnography studies, echocardiography, and baseline clinical characteristics were collected. OSA was present in 327 patients (58.9%). Patients with OSA or higher AHI quartiles were older, more often male, had a higher body mass index, and more clinical comorbidities. The prevalence of AF increased in patients with OSA (23.9% versus 13.6%, P =0.003) or across AHI quartiles (9.4%, 17.3%, 26.6%, and 25.2%, respectively; P for trend <0.001). After adjustment for age, sex, body mass index, New York Heart Association class, left atrial diameter, hypertension, oxygen desaturation index, and obstructive HCM , highest AHI quartile (odds ratio, 4.42; 95% CI , 1.35–14.52 [ P =0.014]) or moderate to severe OSA (odds ratio, 3.03; 95% CI , 1.28–7.20 [ P =0.012]) but not presence of OSA (odds ratio, 1.58; 95% CI , 0.84–2.97 [ P =0.153]) were significantly associated with AF . Higher AHI levels were also factors associated with persistent or permanent AF (highest AHI quartile with odds ratio, 10.96; 95% CI , 1.07–111.85). Conclusions Severity of AHI level is independently associated with AF in patients with HCM. Clinical trials are required to determine the benefits of OSA treatment on AF in patients with HCM.

Misregulated microRNA network has been emerging as the main regulator in non-alcoholic fatty liver disease (NAFLD). The deregulation of miR-122-5p is associated with the liver disease. However, the specific role and molecular mechanism of miR-122-5p in NAFLD remain unclear. In this study, we have reported that the high-fat diet (HFD) or palmitic acid (PA) significantly upregulated the hepatic miR-122-5p expression in vivo and in vitro. Inhibition of miR-122-5p suppressed accumulation-induced inflammation of lipids and oxidative stress damage in PA-treated L02 cells and HFD-induced fatty liver. The effect of the miR-122-5p inhibitor on NAFLD did not depend on insulin resistance-mediated PI3K/AKT/mammalian target of rapamycin (mTOR) signaling pathway but rather on the upregulation of its downstream FOXO3. Subsequently, we validated that miR-122-5p directly binds to the predicted 3′-UTR of FOXO3 to inhibit its gene expression. Conversely, silencing FOXO3 abolished the hepatic benefits of miR-122-5p inhibition to obese mice by decreasing the activity of antioxidant enzymes of superoxide dismutase (SOD). This study provides a novel finding that FOXO3 was the target gene of miR-122-5p to attenuate inflammatory response and oxidative stress damage in dietary-induced NAFLD. Our study provided evidence to reveal the physiological role of miR-122-5p in dietary-induced NAFLD.