High triglycerides (TG) and low high-density lipoprotein cholesterol (HDL-C) are cardiovascular risk factors. A positive correlation between elevated TG/HDL-C ratio and all-cause mortality and cardiovascular events exists in women. However, utility of TG to HDL-C ratio for prediction is unknown among acute coronary syndrome (ACS). Fasting lipid profiles, detailed demographic data, and clinical data were obtained at baseline from 416 patients with ACS after coronary revascularization. Subjects were stratified into three levels of TG/HDL-C. We constructed multivariate Cox-proportional hazard models for all-cause mortality over a median follow-up of 3 years using log TG to HDL-C ratio as a predictor variable and analyzing traditional cardiovascular risk factors. We constructed a logistic regression model for major adverse cardiovascular events (MACEs) to prove that the TG/HDL-C ratio is a risk factor. The subject’s mean age was 64 ± 11 years; 54.5% were hypertensive, 21.8% diabetic, and 61.0% current or prior smokers. TG/HDL-C ratio ranged from 0.27 to 14.33. During the follow-up period, there were 43 deaths. In multivariate Cox models after adjusting for age, smoking, hypertension, diabetes, and severity of angiographic coronary disease, patients in the highest tertile of ACS had a 5.32-fold increased risk of mortality compared with the lowest tertile. After adjusting for conventional coronary heart disease risk factors by the logistic regression model, the TG/HDL-C ratio was associated with MACEs. The TG to HDL-C ratio is a powerful independent predictor of all-cause mortality and is a risk factor of cardiovascular events.

Background: The causal relationship between childhood adiposity and adult risk of heart diseases has not been clearly demonstrated. This study aims to ascertain whether genetically predicted childhood body mass index (BMI) and childhood obesity are causally associated with adult coronary heart disease, myocardial infarction, heart failure, atrial fibrillation, hypertrophic cardiomyopathy, and pulmonary heart disease. Methods and Results: To investigate the causative relationships and underlying mechanisms between childhood adiposity and adult heart diseases, 3 main methods of Mendelian randomization were used: 2‐sample Mendelian randomization, multivariable Mendelian randomization with controlling for several cardiometabolic risk variables, and mediation analysis. Every 1‐SD rise in genetically predicted childhood body mass index was associated with 24% (odds ratio [OR], 1.24 [95% CI, 1.12–1.37]), 28% (OR, 1.28 [95% CI, 1.14–1.42]), 28% (OR, 1.28 [95% CI, 1.14–1.42]), and 27% (OR, 1.27 [95% CI, 1.04–1.49]) higher risk of coronary heart disease, myocardial infarction, heart failure, and atrial fibrillation, respectively. Every 1‐unit increase in log‐odds in childhood obesity was associated with 11% (OR, 1.11 [95% CI, 1.06–1.16]), 14% (OR, 1.14 [95% CI, 1.04–1.23]), 10% (OR, 1.10 [95% CI, 1.03–1.18]), and 20% (OR, 1.20 [95% CI, 1.08–1.32]) higher risk of coronary heart disease, myocardial infarction, heart failure, and atrial fibrillation, respectively. The link between childhood adiposity and adult heart diseases was found to be mediated by high‐density lipoprotein cholesterol, triglyceride, hypertension, and type 2 diabetes. Conclusions: Our findings support the causal relationships between childhood adiposity and risk of adult coronary heart disease, myocardial infarction, heart failure, and atrial fibrillation. Blood lipids, hypertension, and type 2 diabetes are factors that mediate the aforementioned associations.

Objectives: Previously, a genome-wide scan has identified a nonsynonymous single nucleotide polymorphism (rs3812316, G771C, Gln241His) in the MLXIPL gene that is associated with the level of plasma triglycerides. However, no data are available on the association of this polymorphism with coronary artery disease (CAD) in the Chinese population. The aim of this study was to evaluate the association between a gene polymorphism related to triglyceride metabolism and CAD. Methods: The genotype of the polymorphism in the MLXIPL gene was determined in 352 CAD patients and 152 CAD-free subjects. All of the participants were selected to study the MLXIPL gene rs3812316 polymorphism using the polymerase chain reaction restriction fragment length polymorphism method. Results: In Chinese participants, we observed that there was a significant difference in genotype between the cases and controls (p = 0.002). After allowance for potential confounders, unconditional logistic analysis revealed that the SNP was significantly related to a risk in CAD patients (adjusted OR 2.96, 95% CI 1.30–5.08; p =0.004). We also found that there was a significant association between the single nucleotide polymorphism and plasma triglyceride levels (OR 1.28, 95% CI 1.061–1.542; p < 0.05). Conclusion: The gene sequence variation in the MLXIPL gene may serve as a novel genetic marker for the risk of significant CAD.