Cardiovascular disease remains the leading cause of mortality in women, yet it has not raised the awareness from the public. The pathogenesis of cardiovascular disease differs significantly between females and males concerning the effect of sex hormones. Estrogen and progestogen impact cardiovascular system through genomic and non-genomic effects. Before menopause, cardiovascular protective effects of estrogens have been well described. Progestogens were often used in combination with estrogens in hormone therapy. Fluctuations in sex hormone levels, particularly estrogen deficiency, were considered the specific risk factor in women’s cardiovascular disease. However, considerable heterogeneity in the impact of hormone therapy was observed in clinical trials. The heterogeneity is likely closely associated with factors such as the initial time, administration route, dosage, and formulation of hormone therapy. This review will delve into the pathogenesis and hormone therapy, summarizing the effect of female sex hormones on hypertension, pre-eclampsia, coronary heart disease, heart failure with preserved ejection fraction, and cardiovascular risk factors specific to women.

Coronary artery disease (CAD) is showing an increasing trend in young adults. Cigarette smoking has been shown to be a major cause of premature CAD. Previous studies have also shown that hyperuricemia (HUA) is associated with CAD; however, the interaction effect between HUA and smoking on CAD is uncertain. Therefore, this study was designed to determine the relationship and interactive effects of HUA and smoking on the risk of CAD in young adults ≤ 35 years of age. In this observational study we consecutively included adults (18–35 years of age) with suspected CAD who underwent coronary angiography for the first time in our institution from January 2005 to December 2015. Patients with stenosis affecting ≥50% of the luminal diameter and acute myocardial infarction were considered to have CAD. A serum uric acid (SUA) level ≥ 7.0 mg / dl (420 mmol / L) in males and ≥ 6.0 mg / dl (357 mmol / L) in females was defined as hyperuricemia. We tested for an interaction between HUA and cigarrete smoking on CAD. The relationship between HUA, cigarrete smoking, and CAD was assessed by multivariate logistic regression analysis. A total of 1113 participants were included in this study; 771 participants were confirmed to have CAD. HUA was present in 34.8% of the participants. HUA was significantly higher in the CAD group (odds ratio [OR], 1.34; 95% confidence interval [CI], 1.02–1.76; p = 0.035). More smokers were in the CAD group (OR, 1.59; 95% CI, 1.22–2.07; p = 0.001). Based on multivariate regression analysis and after adjustment for age, BMI, high LDL-C level, low HDL-C level, hypercholesterolemia, hypertriglyceridemia, metabolic syndrome, diabetes mellitus, and hypertension, HUA was shown to be strongly associated with the presence of CAD in non-smokers (OR, 1.84; 95% CI, 1.03–3.29; p = 0.039). We further demonstrated that the interaction between HUA and cigarrete smoking achieved statistical significance for the presence of CAD (p = 0.008). In the current study, HUA was shown to be associated with the presence of CAD in non-smokers ≤ 35 years of age.

(1) Background: The aim of this study was to investigate whether the prognostic value of the atherogenic index of plasma (AIP) for adverse cardiovascular events in acute coronary syndrome (ACS) patients undergoing percutaneous coronary intervention (PCI) varied across different BMI groups. (2) Methods: This study was a retrospective analysis of a prospective registry involving 1725 ACS patients undergoing PCI. The primary endpoint was a composite of all-cause death, non-fatal ischemic stroke, non-fatal spontaneous myocardial infarction (MI), and unplanned repeat revascularization. (3) Results: The study population finally consisted of 526 patients with BMI < 24 kg/m² (age 62 ± 10 years; male 64.3%), 827 patients with 24 kg/m² ≤ BMI < 28 kg/m² (age 60 ± 10 years; male 81.8%), and 372 patients with BMI ≥ 28 kg/m² (age 57 ± 11 years; male 81.2%). The AIP as a continuous variable increased the risk for the primary endpoint in ACS patients undergoing PCI with BMI < 24 kg/m² (HR 2.506; 95% CI 1.285–4.885; p = 0.007), while it did not increase the risk in patients with BMI ≥ 24 kg/m² (hazard ratio [HR]: 1.747; 95% CI 0.921–3.316; p = 0.088 for patients with 24 kg/m² ≤ BMI < 28 kg/m²; and HR: 2.096; 95% CI 0.835–5.261; p = 0.115 for patients with BMI ≥ 28 kg/m², respectively). Compared with the lowest AIP tertile, the top AIP tertile was associated with a significantly increased risk of the primary endpoint in BMI < 24 kg/m² group (HR: 1.772, 95% CI: 1.110 to 2.828, p = 0.016). (4) Conclusions: The AIP was significantly associated with an increased risk of adverse cardiovascular events in ACS patients undergoing PCI with BMI < 24 kg/m², but not in the patients with BMI ≥ 24 kg/m².

Central hemodynamic indices have been demonstrated to correlate with coronary artery disease (CAD). However, in the context of type 2 diabetes mellitus (DM), this correlation has not been fully illustrated. Therefore, this study was employed to investigate the impact of DM on the correlation between aortic augmentation index and the severity of coronary artery disease. In this study, we analyzed 197 patients who underwent coronary angiography at Anzhen Hospital from September 2015 to January 2016. Central hemodynamics were non-invasively measured with BPro® device (Health STATS, Singapore). The severity of CAD was defined according to SYNTAX scores. Type 2 diabetes was defined according to ADA guidelines. AIx@75 was defined as AIx normalized to a heart rate of 75 bpm. Receiver operating characteristics (ROC) determined the optimal cut-off value of AIx@75 to predict moderate to severe CAD. Multivariate logistic regression analysis evaluated the correlation between central hemodynamic parameters and CAD severity. Eighty-four (42.6 %) of the studied subjects were diabetic patients. Our findings were that (1) AIx@75 was significantly correlated with SYNTAX. (ROC analyzed AUC: 0.638, 95 % CI 0.555–0.721, p < 0.05). The cut-off value of AIx@75 to predict moderate-to-severe CAD as SYNTAX score more than 22 was 71.45. (2) In non-diabetic patients, correlation analysis revealed that AIx@75, augmentation pressure and peak relative time were significantly correlated with CAD severity (p < 0.05). After adjustment, AIx@75 remained as the only independent predictor of moderate-to-severe CAD (odds ratio 1.099, 95 % CI 1.028–1.176, p < 0.05). (3) In diabetic patients, the correlation between central hemodynamic parameters and the severity of CAD did not exist. Aortic augmentation index was significantly related to the severity of CAD and was an independent predictor of severe CAD. However, clinical practitioners should note that its value in DM populations was compromised.