BackgroundRisk factors for embolism and recurrence of primary cardiac myxoma are not well established. This study aimed to assess the risk factors for embolism and recurrence of cardiac myxoma, as well as the survival of the patients.MethodsThe medical records of 207 consecutive patients treated for primary cardiac myxoma between September 1988 and October 2014 were retrospectively analyzed. All diagnoses were pathologically confirmed. Data were collected to identify the risk factors influencing the prognosis.ResultsMean age at surgery was 44.2 ± 15.8 years. Operative mortality (within 30 days of the surgery) occurred in seven patients. Mean follow-up was 9.35 ± 6.55 years. Embolism occurred in 32 (15.5 %) patients before surgery. Multivariate analysis indicated that small (≤4.5 cm) myxoma (OR = 5.14; 95 % CI, 2.30–11.94; P < 0.0001) and soft, gelatinous myxoma (OR = 5.84; 95 % CI, 1.91–25.61; P = 0.001) were independently associated with the occurrence of embolism. Ten patients experienced recurrences. After excluding the patients who died within 30 days of surgery, survival was 92.7 % at 10 years. Age, sex, tumor size, cardiopulmonary bypass duration, aortic cross clamp duration, tumor appearance, and pre-operative embolism were not associated with early mortality. Multivariate analysis showed that multicentric myxomas were independently associated with recurrence (OR = 9.45, 95 % CI, 2.15–41.3, P = 0.004).ConclusionsThe surgical resection of primary cardiac myxoma is associated with excellent long-term survival. Tumors ≤4.5 cm and soft tumors were independent risk factors for embolism. Multicentric cardiac myxoma was an independent risk factors for recurrence of myxoma.

Background/Aims: Previous studies have examined the associations between the single nucleotide polymorphism in the Paraoxonase 1 (PON1) gene and development of calcific aortic valve stenosis (CAVS). The association between functional SNP in 3’UTR of PON1 and the risk of CAVS, however, is unclear. In this study, we investigated the role of SNP in the regulation of PON1 expression via miR-616, as well as the association of SNP with the risk of CAVS. Methods: Two hundred and sixteen patients with CAVS and 243 CAVS-free participants were recruited in this study.They all obtained transthoracic echocardiogram and the ejection fraction (EF) and aortic valve area were recorded and analyzed. The PON1 expression were measured by western blot, Quantitative Real-Time Polymerase Chain Reaction were used to examine the transcriptional activity of miR-616 and PON1. Differences between CVAS patients and controls in terms of genotype frequency distribution and the estimates of Hardy-Weinberg equilibrium were evaluated using chi-square tests. Logistic regression modeling was used to determine the association between the independent effect of rs3735590 SNP and the interaction between genotype, PON1 activity, and other covariates on lipids and CAVS risk. All statistical analyses were performed using SPSS, version 17.0.1 for Windows (SPSS Inc., Chicago, IL). A p value of < 0 .05 was considered significant for all analyses. Results: This study confirmed that PON1 is a validated target gene of miR-616 in liver cells. The relative quantification representing the expression of PON1 mRNA and the serum level of PON1 protein was decreased in the TT genotype. Moreover, the expression of PON1 had a negative regulatory relationship with the expression of miR-616(r=-0.3959, P<0.05) in human tissues. The patients with CT OR TT genotype at loci rs3735590 had a lower risk of CAVS than patients with the CC genotype. Conclusions: Our results suggest that functional SNP in the 3’UTR of PON1 regulates the expression of PON1 via miR-616, and such SNP is associated with the risk of CAVS in human.

IntroductionTranscatheter aortic valve replacement (TAVR) is the first-line treatment for patients with moderate-to-high surgical risk of severe aortic stenosis. Paravalvular leakage (PVL) is a serious complication of TAVR, and aortic valve calcification contributes to the occurrence of PVL. This study aimed to investigate the effect of location and quantity of calcification in the aortic valve complex (AVC) and left ventricular outflow tract (LVOT) on PVL after TAVR.MethodWe performed a systematic review and meta-analysis to evaluate the effect of quantity and location of aortic valve calcification on PVL after TAVR using observational studies from PubMed and EMBASE databases from inception to February 16, 2022.ResultsTwenty-four observational studies with 6,846 patients were included in the analysis. A high quantity of calcium was observed in 29.6% of the patients; they showed a higher risk of significant PVL. There was heterogeneity between studies (I2 = 15%). In the subgroup analysis, PVL after TAVR was associated with the quantity of aortic valve calcification, especially those located in the LVOT, valve leaflets, and the device landing zone. A high quantity of calcium was associated with PVL, regardless of expandable types or MDCT thresholds used. However, for valves with sealing skirt, the amount of calcium has no significant effect on the incidence of PVL.ConclusionOur study elucidated the effect of aortic valve calcification on PVL and showed that the quantity and location of aortic valve calcification can help predict PVL. Furthermore, our results provide a reference for the selection of MDCT thresholds before TAVR. We also showed that balloon-expandable valves may not be effective in patients with high calcification, and valves with sealing skirts instead of those without sealing skirts should be applied more to prevent PVL from happening.Systematic Review Registrationhttps://www.crd.york.ac.uk/PROSPERO/display_record.php?RecordID=354630, identifier: CRD42022354630.