Determinants and Prognoses of Visual-Functional Mismatches After Mechanical Reperfusion in ST-Elevation Myocardial Infarction.

Background: Discordance between the anatomy and physiology of the coronary has important implications for managing patients with stable coronary disease, but its significance in ST-elevation myocardial infarction has not been fully elucidated. Methods: The retrospective study involved patients diagnosed with ST-elevation myocardial infarction (STEMI) who underwent percutaneous coronary intervention (PCI), along with quantitative coronary angiography (QCA) and quantitative flow ratio (QFR) assessments. Patients were stratified into four groups regarding the severity of the culprit vessel, both visually and functionally: concordantly negative (QCA-diameter stenosis [DS] ≤ 50% and QFR > 0.80), mismatch (QCA-DS > 50% and QFR > 0.80), reverse mismatch (QCA-DS ≤ 50% and QFR ≤ 0.80), and concordantly positive (QCA-DS > 50% and QFR ≤ 0.80). Multivariable logistic regression analyses were conducted to identify the clinical factors linked to visual-functional mismatches. Kaplan‒Meier analysis was conducted to estimate the 18-month adverse cardiovascular events (MACE)-free survival between the four groups. Results: The study involved 310 patients, with 68 presenting visual-functional mismatch, and 51 exhibiting reverse mismatch. The mismatch was associated with higher angiography-derived microcirculatory resistance (AMR) (adjusted odds ratio [aOR]=1.016, 95% CI: 1.010-1.022, P<0.001). Reverse mismatch was associated with larger area stenosis (aOR=1.044, 95% CI: 1.004-1.086, P=0.032), lower coronary flow velocity (aOR=0.690, 95% CI: 0.567-0.970, P<0.001) and lower AMR (aOR=0.947, 95% CI: 0.924-0.970, P<0.001). Additionally, the mismatch group showed the worst 18-month MACE-free survival among the four groups (Log rank test p = 0.013). Conclusion: AMR plays a significant role in the occurrence of visual-functional mismatches between QCA-DS and QFR, and the mismatch group showed the worst prognosis.

Transition of visceral adiposity index and risk of cardiovascular disease in middle-aged and older Chinese adults.

OBJECTIVE: Visceral obesity and the lifetime risk of cardiovascular disease (CVD) have received increasing attention. However, the relationship between dynamic changes in visceral obesity and CVD has not been studied. We aimed to determine the association of visceral adiposity index (VAI) transition with CVD risk. METHODS: A total of 5395 participants were recruited in 2011-2012 and followed up until 2018 from the China Health and Retirement Longitudinal Study. The cut-off value of the VAI was obtained by the receiver-operating characteristic curve. Participants were grouped based on VAI change patterns during the follow-up period (2011-2015): the low-low group, low-high group, high-low group, and high-high group. CVD was defined as a medical diagnosis of heart disease and/or stroke. A Cox proportional hazards model was used to evaluate the correlation between VAI transition and CVD. RESULTS: Over a median follow-up period of 7 years, 969 participants (17.9 %) developed CVD. VAI change patterns were significantly associated with CVD risk after adjustment for demographic characteristics and risk factors. The high-high group (hazard ratio (HR): 1.65, 95 % confidence interval (CI): 1.39-1.97) and the low-high group (HR: 1.29, 95 % CI: 1.04-1.61) were associated with a higher risk of CVD after adjusting for demographic characteristics and traditional risk factors compared to the low-low group, while the effect in the high-low group was not significant. CONCLUSIONS: VAI transition was significantly associated with the risk of CVD. Monitoring the dynamics of the VAI in public health practice would help prevent CVD.

Lipoprotein(a) as a Higher Residual Risk for Coronary Artery Disease in Patients with Type 2 Diabetes Mellitus than without.

Purpose: Lipoprotein(a) (Lp[a]) is well-known as a residual risk factor for coronary artery disease (CAD). However, the different adverse effects of Lp(a) about CAD in patients with or without type 2 diabetes mellitus (T2DM) are unclear. This study aimed to investigate the Lp(a) thresholds for CAD diagnosis in T2DM and non-T2DM patients, and further compare the Lp(a) alarm values along with optimal low-density lipoprotein cholesterol (LDL-C) level. Methods: This retrospective study consecutively enrolled patients with suspected CAD who underwent coronary angiography in Guangdong Provincial People's Hospital between September 2014 and July 2015. A logistic regression model was established to explore the association of Lp(a) and CAD in patients. Restricted cubic splines were used to compare the threshold values of Lp(a) for CAD in patients with and without T2DM, and further in optimal LDL-C level situation. Results: There were 1522 patients enrolled finally. After multivariable adjustment, Lp(a) was an independent risk factor for CAD in patients with T2DM (odds ratio [OR]: 1.98, 95% CI]: 1.12-3.49, p = 0.019) and without T2DM (OR: 3.42, 95% CI: 2.36-4.95, p < 0.001). In the whole population, the Lp(a) threshold of CAD was 155, while 145 mg/L for T2DM and 162 mg/L for non-T2DM ones, respectively. In patients with LDL-C<1.8 mmol/l, the alarm value of Lp(a) was even lower in T2DM than non-T2DM patients (155 vs 174 mg/L). Conclusion: Lp(a) was a significant residual risk for CAD in patients whether with T2DM or not. And Lp(a) had a lower alarm value in T2DM patients, especially in optimal LDL-C level.

Triglyceride-glucose index is associated with quantitative flow ratio in patients with acute ST-elevation myocardial infarction after percutaneous coronary intervention.

Background: The triglyceride-glucose (TyG) index is a novel marker representing the degree of insulin resistance (IR) and is closely related to cardiovascular diseases. However, the association between the TyG index and vascular function in patients with acute ST-elevation myocardial infarction (STEMI) after percutaneous coronary intervention (PCI) remains unknown. Materials and methods: This study was a post hoc analysis of a multicenter, prospective cohort study. In this study, patients with STEMI who underwent PCI were included, and coronary angiography data were analyzed by Quantitative coronary angiography (QCA) and quantitative flow ratio (QFR). In addition, the TyG index was calculated as follows: Ln [fasting triglyceride (mg/dl) × fasting blood glucose (mg/dl) × 1/2]. According to the post-PCI QFR, patients were divided into two groups: post-PCI QFR ≤ 0.92 group and post-PCI QFR > 0.92 group. Construction of logistic regression model to explore the relationship between the TyG index and post-PCI QFR. Results: A total of 241 STEMI patients were included in this study. Compared with patients in the post-PCI QFR > 0.92 group, the TyG index was higher in the post-PCI QFR ≤ 0.92 group. Logistic regression model showed that after adjusting for other confounding factors, the TyG index was positively correlated with the risk of post-PCI QFR ≤ 0.92 (OR = 1.697, 95% CI 1.171-2.460, P = 0.005). Restricted cubic splines showed the cutoff value of TyG index associated with post-PCI QFR ≤ 0.92 risk was 9.75. Conclusion: The TyG index was associated with the risk of post-PCI QFR ≤ 0.92 in STEMI patients. The risk of post-PCI QFR ≤ 0.92 increased when the TyG index exceeded 9.75.

Elevated serum uric acid was associated with pre-inflammatory state and impacted the role of HDL-C on carotid atherosclerosis.

BACKGROUND AND AIMS: Uric acid (UA) and high-density lipoprotein cholesterol (HDL-C) are positively and negatively associated with atherosclerosis, respectively. UA and HDL-C are involved in the balance of proinflammatory and anti-inflammatory processes in atherosclerosis. However, it is still unclear whether UA affects the effect of HDL-C on atherosclerosis. METHODS AND RESULTS: In this retrospective study, we enrolled 1437 patients with multiple risk factors for atherosclerosis. Patients were categorized into two groups according to their baseline UA level. Multivariate logistic regression analysis and restricted cubic spline curves were used to assess the relationship between HDL-C and carotid atherosclerosis (abnormal carotid intima-media thickness [cIMT] and carotid artery plaque) at different UA levels. Compared to patients with normouricemia, patients with hyperuricemia were older and had a more extensive history of disease and unhealthy behavior. In the normouricemia group, multivariate-adjusted odds ratios (95% CIs) for HDL-C were 0.55 (0.33-0.92) for abnormal mean cIMT, 0.59 (0.35-1.00) for abnormal maximum cIMT, and 0.53 (0.29-0.94) for the occurrence of carotid artery plaque, while the correlation between each of these three indicators with HDL-C were not significant in those with hyperuricemia. Spline regression models yielded similar results. The effect of UA on the association between HDL-C and carotid atherosclerosis remained in the subset of patients with optimal low-density lipoprotein cholesterol. CONCLUSION: Elevated UA marks a pre-inflammatory state and impacts the role of HDL-C on carotid atherosclerosis.