Clinical features and prognosis of cardiac metastatic tumors.

BACKGROUND: This study aimed to explore the clinical features and prognosis of cardiac metastatic tumors. In addition, whether continuing antitumor therapy after the development of cardiac metastases can benefit patients and the response of cardiac metastases were investigated. METHODS: A retrospective analysis was conducted on patients with malignancies who were admitted to Fujian Cancer Hospital and Fujian Provincial Hospital from January 2007 to September 2022, and the follow-up period ended in March 2023. Clinical data were gathered, treatment efficacy was evaluated, and survival analysis was performed. RESULTS: After the patients developed cardiac metastasis, the overall 30-day, 3-month, 6-month, and 12-month survival rates were 85.00%, 59.00%, 51.00% and 38.00%, respectively. With continued treatment, the average survival time was 27.33 months (95% confidence interval [CI]: 16.88-37.79), which exceeded the 6.6 months (95% confidence interval [CI]: 0.03-13.69) observed for patients who withdrew from treatment (P < 0.001). The responses of cardiac metastases corresponded to the responses of the primary tumors. Patients with a cardiac response had a median survival time of 55.60 months, which exceeded the 13.40 months observed for those without a cardiac response. However, there was no significant difference (P = 0.375). CONCLUSIONS: In conclusion, continuing antitumor therapy after the development of cardiac metastases can significantly prolong patient survival. Cardiac metastases and primary tumors respond consistently to antitumor treatment. The risk of death due to heart failure in cancer patients with cardiac metastases needs to be further investigated.

Association of ambient PM10 and PM2.5 with coronary stenosis measured using selective coronary angiography.

BACKGROUND: Long-term ambient particulate matter (PM) exposure exerts detrimental effects on cardiovascular health. Evidence on the relation of chronically exposed ambient PM10 and PM2.5 with coronary stenosis remains lacking. Our aim was to investigate the association of PM10 and PM2.5 with coronary stenosis in patients undergoing coronary angiography. METHODS: We performed a retrospective cohort study consisting of 7513 individuals who underwent coronary angiography in Fujian Province, China, from January 2019 to December 2021. We calculated a modified Gensini score (GS) to represent the degree of stenosis in coronary arteries by selective coronary angiography. We fitted linear regressions and logistic models to assess the association of PM10 and PM2.5 with coronary stenosis. We employed restricted cubic splines to describe the exposure-response curves. We performed mediation analyses to assess the potential mediators. RESULTS: Long-term ambient PM10 and PM2.5 (prior three years average) exposure was significantly associated with the GS, with a breakpoint concentration of 47.5 µg/m3 and 25.8 µg/m3 for PM10 and PM2.5, respectively, above which we found a linear positive exposure-response relationship of ambient PM with GS. Each 10 µg /m3 increase in PM10 exposure (ß: 4.81, 95 % CI: 0.44-9.19) and PM2.5 exposure [ß: 10.50, 95 % CI: 3.14-17.86] were positively related to the GS. The adjusted odds ratio (OR) for each 10 µg/m3 increment in PM10 exposure on severe coronary stenosis was 1.33 (95 % CI: 1.04-1.76). Correspondingly, the adjusted OR for PM2.5 was 1.87 (95 % CI: 1.24-2.99). The mediation analysis indicated that the effect of PM10 on coronary stenosis may be partially mediated through total cholesterol, low-density lipoprotein cholesterol, apolipoprotein B, serum creatinine and blood urea nitrogen, and the effect of PM2.5 may be mediated in part by hemoglobin A1c. CONCLUSION: Our study provides the first evidence that chronic ambient PM10 and PM2.5 exposure was associated with coronary stenosis assessed by GS in patients with suspected coronary artery disease and reveals its potential mediators.

[Cardiovascular disease risk and vascular damage status in pre- and hypertension population in coastal areas of Fujian province].

OBJECTIVE: To observe the cardiovascular risk factors and vascular damage status of pre- and hypertensive population in the coastal areas of Fujian province. METHODS: This cross-sectional study surved 3344 Fujian coastal people aged older than 30 years. Glycolipids, uric acid, urine, microalbumin, brachial-ankle pulse wave velocity(baPWV) and central retinal arteriolar equivalent(CRAE) measurements were performed. Variance analysis and binary logistic regression were applied to evaluate cardiovascular risk factors and vascular damage of prehypertensive as well as hypertensive population. RESULTS: (1) The morbidity of prehypertension as well as hypertension was 30.0% in coastal population of Fujian Province, there were more than 3 cardiovascular risk factors in 65.5% (909/1388) of the hypertensive population and 37.5% of the prehypertensive population.(2) The abnormal rates of creatinine ratio(UACR), baPWV, and CRAE in hypertensive [25.7% (357/1388) , 84.2% (1169/1388) , 29.5% (409/1388) ] and prehypertensive population [20.0% (176/880) , 29.1% (256/880) , 25.6% (225/880)] were significantly higher than those of normotensive individuals [8.5% (91/1076), 8.9% (96/1076), 18.8% (202/1076), all P < 0.05].(3) Prehypertension and hypertension served as independent risk factors of UACR, baPWV and CRAE according to logistic regression analysis. The odds ratios (OR) value and 95% confidence intervals were 1.496 (1.095-2.044) , 2.477 (1.815-3.381) , 0.700 (0.549-0.891) in prehypertensive population, and 1.976 (1.454-2.686) , 7.707 (12.938-24.235) , 0.591 (0.474-0.736) in hypertensive population. CONCLUSION: Multiple cardiovascular risk factors coexist in prehypertensive and hypertensive population in the coastal area of coastal areas of Fujian province and there is more morbidity of vascular damage in prehypertensive and hypertensive individuals compared to normotensive subjects in these areas.

A Pilot Study About the Role of PANoptosis-Based Genes in Atherosclerosis Development.

Background: As a chronic inflammatory disease, atherosclerosis (AS) and ischemia events are primarily affected by inflammation in AS. PANoptosis has been implicated in many human systemic disorders, including infection, cancer, neurodegeneration, and inflammation. On the other hand, little is understood about PANoptosis's function in AS. Methods: We used consensus clustering to divide the GSE100927 dataset into two panoptosis-related subgroups. PANoptosis-associated genes were screened by differential analysis and weighted gene co-expression network analysis (WGCNA) and enriched by ClueGO software. Investigating LASSO regression and MCODE to identify AS Diagnostic Markers. Immunoinfiltration analysis and single-cell analysis were used to search for cell types associated with the diagnostic genes. Final validation was performed by polymerase chain reaction (PCR). Results: We classified the GSE100927 dataset into two PANoptosis-related subtypes based on the expression of PANoptosis-related genes (PRGs) using consensus clustering. A total of 36 PANoptosis-associated genes were screened in the differentially expressed genes and WGCNA-related module. 4 hub genes were identified by MCODE and LASSO regression, and 3 AS diagnostic markers (ACP5, CCL3, HMOX1) were screened by external validation set. Immunoinfiltration analysis and single-cell analysis showed that the three diagnostic markers were associated with macrophages, and PCR results demonstrated that ACP5 and HMOX1 could be used as AS diagnostic markers. Conclusion: Our study identified ACP5 and HMOX1 as diagnostic genes for AS that may be associated with PANoptosis. ACP5 and HMOX1 may be involved in the pathogenesis of AS by regulating macrophage PANoptosis.