Background: Apolipoproteins (Apo) are known atherogenic factors that play important roles in many mechanisms related to coronary heart disease (CHD). However, it is unclear whether the apoB/apoA1 ratio is an equal or a better predictor than the Framingham Risk Score or TC/HDL-c for predicting clinical outcomes in patients undergoing percutaneous coronary intervention. Methods: We investigated the association between Apolipoprotein B/A1 ratio and cardiovascular risk factors as well as the severity of CHD in 2256 Han Chinese patients. The potential of Apolipoprotein B/A1 ratio, Framingham Risk Score and TC/HDL-c were assessed as a marker to predict cardiovascular adverse events in a prospective subgroup of 1639 CHD patients during a 5-year follow-up. Results: In the multivariate model, adjusted odds ratios (ORs) were significant for 3-VD vs. 1-VD (OR = 2.36; 95% CI: 1.65–3.38, for the fourth vs. first quartile; P_trend < 0.001). The subgroup analysis showed that patients with a higher ApoB/ApoA1 ratio had an increased risk of developing multi-branch lesions and potentially suffer more cardiovascular adverse events (anginas, myocardial infarctions, heart failures, strokes, and cardiac deaths) in the future (adjusted HR =1.92; 95% CI: 1.10–3.13, for the fourth vs. first quartile). In the ROC analysis, the AUC for ApoB/A1 ratio was larger than that of Framingham Risk Score (0.604 vs. 0.543, p = 0.01) and TC/HDL-c (0.604 vs. 0.525, p < 0.01). Conclusion: Our results suggest a significant association between ApoB/ApoA1 ratio and CHD severity and cardiovascular outcomes among patients with existing CHD and ApoB/A1 ratio demonstrated a better predictive accuracy for clinical outcomes compared with Framingham Risk Score and TC/HDL-c.

Background: We sought to describe the tendency and extent of high-sensitivity cardiac troponin I (hs-cTnI) changes in patients with fulminant myocarditis (FM) after admission and to explore the relationship between the in-hospital mortality of FM and the absolute and relative changes in hs-cTnI within 24 h and 48 h after admission. Methods: In the retrospective study, the object are patients diagnosed with FM in our single centre. The value of cardiac troponin was recorded after patients admitted to hospital in succession. The absolute and relative changes in hs-cTnI within 24 h and 48 h were described as range distributions. Receiver operating characteristic (ROC) curve and Cox analyses were performed to determine the relationship between in-hospital mortality of FM and hs-cTnI changes. Results: A total of 83 FM patients admitted to our centre from January 1, 2010 to December 31, 2019 were included; 69 patients survived and 14 patients died. In the survival group, 78% of patients experienced a decline in hs-cTnI within 24 h, while 36% of the mortality group exhibited a declining tendency in hs-cTnI (P = 0.003). Nearly 60% of survival group had a 0–2000 ng/l reduction in troponin from baseline within 24 h of admission. However, troponin levels of 50% of patients in the mortality group were 0–10,000 ng/ L higher than baseline 24 h after admission. Multivariable logistic analysis revealed that the declining tendency of hs-cTnI within 24 h, in addition to time from onset to admittance to hospital, intravenous immunoglobulin treatment and the abnormal level of creatinine, were associated with the in-hospital mortality of FM (for the declining tendency of hs-cTnI within 24 h, OR = 0.10, 95% CI 0.02–0.68, P = 0.018). The ROC curve revealed optimal cut-off values of − 618 ng/l for absolute change within 24 h (AUC = 0.800, P < 0.01), − 4389 ng/l for absolute change within 48 h (area under the curve = 0.711, P < 0.01), − 28.46% for relative change within 24 h (AUC = 0.810, P < 0.01), and − 52.23% for relative change within 48 h (AUC = 0.795, P < 0.01). Absolute changes and relative changes in hs-cTnI within 24 h and 48 h were strong predictors of in-hospital mortality by Cox regression analysis after adjustment for sex, time from onset to admission, and occurrence of ventricular tachycardia or ventricular fibrillation. Conclusion: Most FM patients who survived experienced a decline in hs-cTnI within 24 h. The absolute and relative changes in hs-cTnI within 24 h and 48 h were strong predictors of in-hospital mortality.

Aims: Numerous observational studies have indicated a potential association between the consumption of processed and red meat and an increased risk of cardiovascular disease and Type 2 diabetes mellitus (T2DM). However, the presence of a causal relationship remains uncertain. Therefore, the purpose of this study was to evaluate the impact of processed meat and red meat (pork, lamb, and beef) on the risk of cardiovascular disease, including coronary artery disease (CAD), hypertension, and stroke, and T2DM, using a two-sample Mendelian randomization (MR) analysis. Methods and results: An MR analysis was conducted using the inverse-variance weighted, weighted median, and MR-Egger methods. To identify heterogeneity and pleiotropy, Cochrane’s Q test and MR-Egger test were employed. Additionally, the stability of the MR results was assessed using the leave-one-out method. Inverse-variance weighted analyses reveal no causal association between the consumption of processed and red meat and the incidence of CAD, hypertension, stroke, and T2DM (P > 0.05). When considering processed meat intake, heterogeneity is observed in hypertension and stroke outcomes (P < 0.05). For pork intake, heterogeneity is seen in hypertension, stroke, and T2DM (P < 0.05). Lamb intake shows heterogeneity in hypertension and T2DM (P < 0.05). However, other exposures and outcomes examined show no heterogeneity (P > 0.05). No significant pleiotropy is detected for all exposures through an MR-Egger test (P > 0.05). Furthermore, the leave-one-out test demonstrates the robustness of the results. Conclusion: The study discerned no observable impact of red and processed meat consumption on CAD, hypertension, stroke, and T2DM. The findings of this study challenge the prevailing conventional perspective in the field.