Background: Stress hyperglycemia is a strong predictor of adverse outcomes in patients with acute myocardial infarction (AMI). Recently, the stress hyperglycemia ratio (SHR) has been designed as an index to identify acute hyperglycemia with true risk; however, data regarding the impact of SHR on the prognosis of ST-segment elevation myocardial infarction (STEMI) remains limited. This study aimed to evaluate the predictive value of the SHR in patients with acute STEMI and to assess whether it can improve the predictive efficiency of the Thrombolysis in Myocardial Infarction (TIMI) risk score. Methods: This study included 7476 consecutive patients diagnosed with acute STEMI across 274 emergency centers. After excluding 2052 patients due to incomplete data, 5417 patients were included in the final analysis. Patients were divided into three groups according to SHR tertiles (SHR1, SHR2, and SHR3) and were further categorized based on diabetes status. All patients were followed up for major cardiovascular adverse events (MACEs) and all-cause mortality. Results: After 30 days of follow-up, 1547 MACEs (28.6%) and 789 all-cause deaths (14.6%) occurred. The incidence of MACEs was highest among patients in the SHR3 group with diabetes mellitus (DM) (42.6%). Kaplan–Meier curves demonstrated that patients with SHR3 and DM also had the highest risk for MACEs when compared with other groups (p < 0.001). Moreover, C-statistics improved significantly when SHR3 was added into the original model: the ΔC-statistics (95% confidence interval) were 0.008 (0.000–0.013) in the total population, 0.010 (0.003–0.017) in the DM group, and 0.007 (0.002–0.013) in the non-DM group (all p < 0.05). In the receiver operating characteristic analysis, the area under the curve (AUC) for the original TIMI risk score for all-cause death was 0.760. When an SHR3 value of 1 point was used to replace the history of DM, hypertension, or angina in the original TIMI risk score, the Delong test revealed significant improvements in the AUC value (∆AUC of 0.009, p < 0.05), especially in the DM group (∆AUC of 0.010, p < 0.05). Conclusion: The current results suggest that SHR is independently related to the risks of MACEs and mortality in patients with STEMI. Furthermore, SHR may aid in improving the predictive efficiency of the TIMI risk score in patients with STEMI, especially those with DM.

Background: Renin–angiotensin–aldosterone-system inhibitors markedly play an active role in the primary prevention of atrial fibrillation (AF), but the impact of angiotensin-converting enzyme inhibitors (ACEIs) or angiotensin receptor blockers (ARBs) on the mortality of patients with AF remains unclear. This study aimed to examine the relationship between treatment with ACEIs or ARBs and mortality in emergency department (ED) patients with AF and hypertension. Methods: This multicenter study enrolled 2016 ED patients from September 2008 to April 2011; 1110 patients with AF and hypertension were analyzed. Patients were grouped according to whether they were treated with ACEI/ARB or not and completed a 1-year follow-up to evaluate outcomes including all-cause death, cardiovascular death, stroke, and major adverse events (MAEs). Results: Among the 1110 patients with AF and hypertension, 574 (51.7%) received ACEI/ARB treatment. During the 1-year follow-up, 169 all-cause deaths (15.2%) and 100 cardiovascular deaths (9.0%) occurred, while 98 strokes (8.8%) and 255 MAEs (23.0%) occurred. According to the multivariate Cox regression analysis, ACEI/ARB therapy was significantly associated with a reduced risk of all-cause death (HR, 0.605; 95% CI 0.431–0.849; P = 0.004). Moreover, ACEI/ARB therapy was independently associated with a reduced risk of cardiovascular death (HR 0.585; 95% CI 0.372–0.921; P = 0.020) and MAEs (HR 0.651, 95% CI 0.496–0.855, P = 0.002) after adjusting for other risk factors. Conclusions: Our results revealed that ACEI/ARB therapy was independently associated with a reduced risk of all-cause death, cardiovascular death, and MAEs in ED patients with AF and hypertension. These results provide evidence for a tertiary preventive treatment for patients with AF and hypertension.

Patients with pulmonary arterial hypertension (PAH) exhibit a distinct gut microbiota profile; however, the causal association between gut microbiota, associated metabolites, and PAH remains elusive. We aimed to investigate this causal association and to explore whether dietary patterns play a role in its regulation. Summary statistics of gut microbiota, associated metabolites, diet, and PAH were obtained from genome-wide association studies. The inverse variance weighted method was primarily used to measure the causal effect, with sensitivity analyses using the weighted median, weighted mode, simple mode, MR pleiotropy residual sum and outlier (MR-PRESSO), and MR-Egger methods. A reverse Mendelian randomisation analysis was also performed. Alistipes (odds ratio [OR] = 2.269, 95% confidence interval [CI] 1.100–4.679, P = 0.027) and Victivallis (OR = 1.558, 95% CI 1.019–2.380, P = 0.040) were associated with an increased risk of PAH, while Coprobacter (OR = 0.585, 95% CI 0.358–0.956, P = 0.032), Erysipelotrichaceae (UCG003) (OR = 0.494, 95% CI 0.245–0.996, P = 0.049), Lachnospiraceae (UCG008) (OR = 0.596, 95% CI 0.367–0.968, P = 0.036), and Ruminococcaceae (UCG005) (OR = 0.472, 95% CI 0.231–0.962, P = 0.039) protected against PAH. No associations were observed between PAH and gut microbiota-derived metabolites (trimethylamine N-oxide [TMAO] and its precursors betaine, carnitine, and choline), short-chain fatty acids (SCFAs), or diet. Although inverse variance-weighted analysis demonstrated that elevated choline levels were correlated with an increased risk of PAH, the results were not consistent with the sensitivity analysis. Therefore, the association was considered insignificant. Reverse Mendelian randomisation analysis demonstrated that PAH had no causal impact on gut microbiota-derived metabolites but could contribute to increased the levels of Butyricicoccus and Holdemania, while decreasing the levels of Clostridium innocuum, Defluviitaleaceae UCG011, Eisenbergiella, and Ruminiclostridium 5. Gut microbiota were discovered suggestive evidence of the impacts of genetically predicted abundancy of certain microbial genera on PAH. Results of our study point that the production of SCFAs or TMAO does not mediate this association, which remains to be explained mechanistically.

Background: The ideal blood pressure (BP) target for patients with atrial fibrillation (AF) is still unclear. The present study aimed to assess the effect of the baseline BP on all-cause mortality in patients with AF. Methods: This registry study included 20 emergency centers across China and consecutively enrolled patients with AF from 2008 to 2011. All participants were followed for 1 year ± 1 month. The primary endpoint was all-cause mortality. Results: During the follow-up, 276 (13.9%) all-cause deaths occurred. Kaplan–Meier curves showed that a systolic blood pressure (SBP) ≤110 mmHg or >160 mmHg was associated with a higher risk of all-cause mortality (log-rank test, P = 0.014), and a diastolic blood pressure (DBP) <70 mmHg was associated with the highest risk of all-cause mortality (log-rank test, P = 0.002). After adjusting for confounders, the multivariable Cox regression model suggested that the risk of all-cause mortality was increased in the group with SBP ≤110 mmHg (hazard ratio [HR], 1.963; 95% confidence interval [CI], 1.306–2.951), and DBP <70 mmHg (HR, 1.628; 95% CI, 1.163–2.281). In the restricted cubic splines, relations between baseline SBP or DBP and all-cause mortality showed J-shaped associations (non-linear P <0.001 and P = 0.010, respectively). The risk of all-cause mortality notably increased at a lower baseline SBP and DBP. Conclusions: Having a baseline SBP ≤110 mmHg or DBP <70 mmHg was associated with a significantly higher risk of all-cause mortality in patients with AF. An excessively low BP may not be an optimal target for patients with AF.

Background: Many studies have revealed the observational associations between lipoprotein(a) (Lp(a)) concentrations and the incidence of cardiovascular diseases (CVDs). However, the causal associations remain unclear. Methods: Public summary data were analyzed using a Mendelian randomization (MR) design to assess the causal associations between Lp(a) levels and risks of nine CVDs and evaluate the potential impact of aspirin on Lp(a) levels. The principal analysis was conducted employing the random-effects inverse-variance weighted (IVW) method. Furthermore, the weighted median and MR-Egger approaches were used as the sensitivity analysis. Additionally, the significantly associated single nucleotide polymorphisms (SNPs) in salicylic acid (INTERVAL and EPIC-Norfolk, n = 14,149) were chosen to assess the potential effects of aspirin on lowering Lp(a) levels. Results: The IVW analysis showed that the per standard deviation (SD) increment in Lp(a) level was causally associated with a higher risk of coronary artery disease (odds ratio (OR), 1.237; 95% confidence interval (CI), 1.173–1.303), atrial fibrillation (OR, 1.030; 95% CI, 1.011–1.050), heart failure (OR, 1.074; 95% CI, 1.053–1.096), hypertension (OR, 1.006; 95% CI, 1.004–1.008), and peripheral artery disease (OR, 1.001; 95% CI, 1.001–1.001) (all p < 0.001). The investigation did not reveal any significant heterogeneities or instances of horizontal pleiotropy. Furthermore, for each SD increase in salicylic acid concentration, there was a corresponding 5.4% reduction in Lp(a) levels (OR: 0.946, 95% CI: 0.900–0.993; p = 0.022). Conclusions: A causal nexus was discerned between Lp(a) levels and an increased risk of conditions including coronary artery disease, atrial fibrillation, heart failure, hypertension, and peripheral artery disease. Furthermore, administering aspirin may be a potential therapeutic to reduce these CVD risks among individuals with elevated Lp(a) levels.

Background: Sleep apnea is a risk factor for atrial fibrillation (AF) but it is underdiagnosed. Whether obstructive sleep apnea (OSA) is correlated with thrombotic risk in AF remains unclear. The aim of the present study was to analyze the clinical characteristics and assess the thrombotic risk of AF with OSA. Methods: In the present registry study,1990 consecutive patients with AF from 20 centers were enrolled. The patients were divided into 2 groups depending on whether they presented with both AF and OSA. All the patients were followed up for 1 year to evaluate the incidences of stroke and non-central nervous system (CNS) embolism. Results: Of the 1990 AF patients, 70 (3.5%) and 1920 (96.5%) patients were in the OSA group and non-OSA group, respectively. The results of the multivariate logistic model analysis showed that male sex, body mass index (BMI), smoking, and major bleeding history were independent risk factors for patients with AF and OSA. The comparison of the Kaplan–Meier curves using the log-rank test revealed that AF with OSA was correlated with an increased risk of non-CNS embolism (p < 0.01). After multivariate adjustments were performed, OSA remained an independent risk factor for non-CNS embolism (HR 5.42, 95% CI 1.34–22.01, p = 0.02), but was not correlated with the risk of stroke in patients with AF. Conclusions: The present study revealed that male sex, high BMI values, smoking, and major bleeding history were independent risk factors for patients with AF and OSA. Moreover, OSA was an independent risk factor for non-CNS embolism in AF. Our results indicate that non-CNS embolism requires focus in patients with AF and OSA.