Background: Soluble suppression of tumorigenicity (sST2) has been proposed to be a marker for biomechanical strain and a possible predictor of mortality in patients with chronic heart failure. The use of sST2 in pulmonary arterial hypertension (PAH) has not been well defined.Hypothesis: Plasma sST2 levels may correlate with the disease severity and predict clinical worsening in PAH.Methods: We performed a cohort study of 40 idiopathic PAH patients with data on demographics, exercise capacity, echocardiographic parameters, laboratory tests, hemodynamics, and medications. Plasma sST2 was assessed with the high‐sensitivity ST2 ELISA kit at diagnostic catheterization. All patients were followed up from the date of blood sampling. The endpoint was clinical worsening.Results: sST2 was significantly elevated in patients with idiopathic PAH compared with control subjects (28.9 ± 13.9 vs 20.7 ± 7.5 ng/mL, P = 0.003). Pearson correlation analysis revealed that sST2 levels correlated with cardiac index (r = −0.534, P = 0.000) and pulmonary vascular resistance (r = 0.350, P = 0.027), and could reflect disease severity of PAH. After a mean follow‐up of 14 ± 5 months, 12 patients showed clinical worsening. Receiver operating characteristic analysis suggested that sST2 levels >31.4 ng/mL discriminated clinical worsening with a sensitivity and specificity of 83.3% and 78.6%, respectively. Kaplan‐Meier analysis showed that higher sST2 levels (>31.4 ng/mL) were associated with poor clinical outcomes (P = 0.008). Multivariate Cox regression analysis showed that sST2 was an independent predictor of clinical worsening (hazard ratio: 6.067, 95% confidence interval: 1.317–27.948, P = 0.021).Conclusions: sST2 correlates with disease severity and is a significant predictor of clinical worsening in patients with PAH.

Myocardial injury induced by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is reportedly related to disease severity and mortality, attracting attention to exploring relevant pathogenic mechanisms. Limited by insufficient evidence, myocardial injury caused by direct viral invasion of cardiomyocytes (CMs) is not fully understood. Based on recent studies, endosomal dependence can compensate for S protein priming to mediate SARS-CoV-2 infection of CMs, damage the contractile function of CMs, trigger electrical dysfunction, and tip the balance of the renin–angiotensin–aldosterone system to exert a myocardial injury effect. In this review, we shed light on the direct injury caused by SARS-CoV-2 to provide a comprehensive understanding of the cardiac manifestations of coronavirus disease 2019 (COVID-19).

The gut microbiota is a complex community of microorganisms inhabiting the intestinal tract, which plays a vital role in human health. It is intricately involved in the metabolism, and it also affects diverse physiological processes. The gut–lung axis is a bidirectional pathway between the gastrointestinal tract and the lungs. Recent research has shown that the gut microbiome plays a crucial role in immune response regulation in the lungs and the development of lung diseases. In this review, we present the interrelated factors concerning gut microbiota and the associated metabolites in pulmonary hypertension (PH), a lethal disease characterized by elevated pulmonary vascular pressure and resistance. Our research team explored the role of gut‐microbiota‐derived metabolites in cardiovascular diseases and established the correlation between metabolites such as putrescine, succinate, trimethylamine N‐oxide (TMAO), and N, N, N‐trimethyl‐5‐aminovaleric acid with the diseases. Furthermore, we found that specific metabolites, such as TMAO and betaine, have significant clinical value in PH, suggesting their potential as biomarkers in disease management. In detailing the interplay between the gut microbiota, their metabolites, and PH, we underscored the potential therapeutic approaches modulating this microbiota. Ultimately, we endeavor to alleviate the substantial socioeconomic burden associated with this disease. This review presents a unique exploratory analysis of the link between gut microbiota and PH, intending to propel further investigations in the gut–lung axis.

Aims: To assess the trends in calcific aortic valve disease (CAVD) epidemiology, with an emphasis on CAVD mortality, leading risk factors, and their associations with age, period, and birth cohort. Methods and results: Prevalence, disability-adjusted life years, and mortality were derived from the Global Burden of Disease Study 2019. The age–period–cohort model was employed to study the detailed trends of CAVD mortality and its leading risk factors. Globally, CAVD showed unsatisfactory results from 1990 to 2019, with the CAVD deaths of 127 000 in 2019. CAVD mortality was substantially reduced in high socio-demographic index (SDI) countries [−1.45%, 95% confidence interval (CI) (−1.61 to −1.30)], mildly increased in high-middle SDI countries [0.22%, 95% CI (0.06–0.37)], and unchanged in other SDI quintiles. There was a noticeable transition in CAVD deaths from younger to older populations globally. The CAVD mortality increased exponentially with age, and the male had higher mortality than the female before 80 years old. Favourable period [0.69, 95% CI (0.66–0.72)] and birth effects [0.30, 95% CI (0.22–0.43)] were mainly observed in high SDI countries, while unfavourable effects were mostly noticed in high-middle SDI countries. High systolic blood pressure was the leading risk factor of CAVD deaths globally, and it showed favourable trends in high SDI regions. Conclusion: Although CAVD mortality reduction was observed globally, unfavourable period, and cohort effects were found in many countries. Increase of mortality rate among the population ≥85 years was the common challenge across all SDI quintiles, stressing the necessity to further improve health care for CAVD patients worldwide.