BackgroundSeptal myectomy (SM) has been the gold standard therapy for most patients with hypertrophic obstructive cardiomyopathy (HOCM). Endocardial radiofrequency ablation of septal hypertrophy (ERASH) is a novel treatment for septal reduction. We aimed to assess the efficacy and safety between two treatment strategies.MethodsWe searched PubMed, Web of Science, Cochrane Library, and Embase databases to identify relevant studies published up to March 2021. Random-effect models were used to calculate standardized mean difference (SMD) and 95% confidence intervals (CIs) for resting left ventricular outflow tract gradient (LVOTG) and septal thickness.ResultsTwenty-five studies are included in this review, eighteen studies for SM and seven studies for ERASH. During follow-up, there were significant reductions of the mean resting LVOTG in adults (SM groups: SMD = −3.03, 95% CI [−3.62 to −2.44]; ERASH groups: SMD = −1.95, 95% CI [−2.45 to −1.45]) and children (SM groups: SMD = −2.67, 95% CI [−3.21 to −2.12]; ERASH groups: SMD= −2.37, 95% CI [−3.02 to −1.73]) after the septal reduction therapies. For adults, SM groups contributed to more obvious reduction than ERASH groups in interventricular septal thickness (SM groups: SMD = −1.82, 95% CI [−2.29 to −1.34]; ERASH groups: SMD = −0.43, 95% CI [−1.00 to 0.13]). The improvement of the New York Heart Association class was similar in the two groups (SM groups: 46.4%; ERASH groups: 46.7%). The periprocedural mortality in SM and ERASH were 1.1 and 1.8%, respectively.ConclusionsThis systematic review suggests that SM is superior to ERASH in the treatment of HOCM. But for the patients who are at risk for open cardiac surgeries or prefer a less invasive approach, ERASH might be an optional approach.

Background Although Lesion size index (LSI) has been reported to highly predict radiofrequency lesion size in vitro, its accuracy in lesion size and steam pop estimation has not been well investigated for every possible scenario. Methods Initially, radiofrequency ablations were performed on porcine myocardial slabs at various power, CF, and time settings with blinded LSI. Subsequently, radiofrequency power at 20, 30, 40, 50, and 60 W was applied at CF values of 5, 10, 20, and 30 g to reach target LSIs of 4, 5, 6, and 7. Lesion size and steam pops were recorded for each ablation. Results Lesion size was positively correlated with LSI regardless of power settings (p < 0.001). The linear correlation coefficients of lesion size and LSI decreased at higher power settings. At high power combined with high CF settings (50 W/20 g), lesion depth and LSI showed an irrelevant correlation (p = 0.7855). High‐power ablation shortened ablation time and increased the effect of resistive heating. LSI could predict the risk of steam pops at high‐power settings with the optimal threshold of 5.65 (sensitivity, 94.1%; specificity, 46.1%). The ablation depth of the heavy heart was shallower than that of the light heart under similar ablation settings. Conclusions LSI could predict radiofrequency lesion size and steam pops at high power settings in vitro, while synchronous high power and high CF should be avoided. Lighter hearts require relatively lower ablation settings to create appropriate ablation depth.

Notopterol is a naturally occurring furanocoumarin compound found in the root of Notopterygium incisum. Hyperuricemia involves the activation of chronic inflammation and leads to cardiac damage. Whether notopterol has cardioprotective potential in hyperuricemia mice remains elusive. The hyperuricemic mouse model was constructed by administration of potassium oxonate and adenine every other day for six weeks. Notopterol (20 mg/kg) and allopurinol (10 mg/kg) were given daily as treatment, respectively. The results showed that hyperuricemia dampened heart function and reduced exercise capacity. Notopterol treatment improved exercise capacity and alleviated cardiac dysfunction in hyperuricemic mice. P2X7R and pyroptosis signals were activated both in hyperuricemic mice and in uric acid-stimulated H9c2 cells. Additionally, it was verified that inhibition of P2X7R alleviated pyroptosis and inflammatory signals in uric acid-treated H9c2 cells. Notopterol administration significantly suppressed expression levels of pyroptosis associated proteins and P2X7R in vivo and in vitro. P2X7R overexpression abolished the inhibition effect of notopterol on pyroptosis. Collectively, our findings suggested that P2X7R played a critical role in uric acid-induced NLRP3 inflammatory signals. Notopterol inhibited pyroptosis via inhibiting the P2X7R/NLRP3 signaling pathway under uric acid stimulation. Notopterol might represent a potential therapeutic strategy against pyroptosis and improve cardiac function in hyperuricemic mice.