The stress hyperglycaemia ratio is associated with left ventricular remodelling after first acute ST-segment elevation myocardial infarction.

BACKGROUND: Left ventricular negative remodelling after ST-segment elevation myocardial infarction (STEMI) is considered as the major cause for the poor prognosis. But the predisposing factors and potential mechanisms of left ventricular negative remodelling after STEMI remain not fully understood. The present research mainly assessed the association between the stress hyperglycaemia ratio (SHR) and left ventricular negative remodelling. METHODS: We recruited 127 first-time, anterior, and acute STEMI patients in the present study. All enrolled patients were divided into 2 subgroups equally according to the median value of SHR level (1.191). Echocardiography was conducted within 24 h after admission and 6 months post-STEMI to measure left ventricular ejection fraction (LVEF), left ventricular end-diastolic diameter (LVEDD), and left ventricular end-systolic diameter (LVESD). Changes in echocardiography parameters (δLVEF, δLVEDD, δLVESD) were calculated as LVEF, LVEDD, and LVESD at 6 months after infarction minus baseline LVEF, LVEDD and LVESD, respectively. RESULTS: In the present study, the mean SHR was 1.22 ± 0.25 and there was significant difference in SHR between the 2 subgroups (1.05 (0.95, 1.11) vs 1.39 (1.28, 1.50), p < 0.0001). The global LVEF at 6 months post-STEMI was significantly higher in the low SHR group than the high SHR group (59.37 ± 7.33 vs 54.03 ± 9.64, p = 0.001). Additionally, the global LVEDD (49.84 ± 5.10 vs 51.81 ± 5.60, p = 0.040) and LVESD (33.27 ± 5.03 vs 35.38 ± 6.05, p = 0.035) at 6 months after STEMI were lower in the low SHR group. Most importantly, after adjusting through multivariable linear regression analysis, SHR remained associated with δLVEF (beta = -9.825, 95% CI -15.168 to -4.481, p < 0.0001), δLVEDD (beta = 4.879, 95% CI 1.725 to 8.069, p = 0.003), and δLVESD (beta = 5.079, 95% CI 1.421 to 8.738, p = 0.007). CONCLUSIONS: In the present research, we demonstrated for the first time that SHR is significantly correlated with left ventricular negative remodelling after STEMI.

Augmented glycaemic gap is a marker for an increased risk of post-infarct left ventricular systolic dysfunction.

BACKGROUND: Left ventricular systolic dysfunction (LVSD) occurs frequently after acute ST-segment elevation myocardial infarction (STEMI). The predisposing factors and underlying mechanism of post-infarct LVSD are not fully understood. The present study mainly investigated the correlation between glycaemic gap, a novel index of stress-induced hyperglycaemia (SIH), and post-infarct LVSD. METHODS: A total of 274 first STEMI patients were enrolled in this cross-sectional study. Transthoracic echocardiography was performed within 48 h after admission and at 6 months after discharge to obtain left ventricular ejection fraction (LVEF). The change in LVEF was calculated as LVEF at 6 months after discharge minus baseline LVEF. Additionally, post-infarct LVSD was defined as LVEF ≤ 50%. Most importantly, glycaemic gap was calculated as admission blood glucose (ABG) minus the estimated average glucose over the previous 3 months. RESULTS: In patients without diabetes mellitus (DM), multivariate linear regression analysis revealed that both glycaemic gap (Beta = - 1.214, 95% CI - 1.886 to - 0.541, p < 0.001) and ABG (Beta = - 1.124, 95% CI - 1.795 to - 0.453, p = 0.001) were associated with change in LVEF. In DM patients, only glycaemic gap was still associated with change in LVEF, although this association was not observed in univariate linear regression analysis. Regarding the association between SIH and post-infarct LVSD, multivariate logistic regression analysis revealed that both glycaemic gap (OR = 1.490, 95% CI 1.043 to 2.129, p = 0.028) and ABG (OR = 1.600, 95% CI 1.148 to 2.229, p = 0.005) were associated with an increased risk of having post-infarct LVSD in non-DM patients. However, after multivariate adjustment in DM patients, only glycaemic gap (OR = 1.399, 95% CI 1.021 to 1.919, p = 0.037) remained associated with an increased risk of having post-infarct LVSD. Furthermore, the predictive value of glycaemic gap for post-infarct LVSD was not inferior to ABG in non-DM patients (p = 0.499), and only glycaemic gap, instead of ABG, could significantly predict post-infarct LVSD in DM patients (AUC = 0.688, 95% CI 0.591 to 0.774, p = 0.002). CONCLUSIONS: Glycaemic gap was strongly associated with a change in LVEF and an increased risk of having post-infarct LVSD in patients following STEMI. In STEMI patients with DM, glycaemic gap could provide more valuable information than ABG in identifying patients at high risk of developing post-infarct LVSD.

Monocyte-to-high-density lipoprotein ratio as a predictor for patients with Takayasu arteritis and coronary involvement: a double-center, observational study.

Background: The implication of the monocyte-to-high-density lipoprotein ratio (MHR) in Takayasu arteritis (TAK) remains unclear. Objective: We aimed to assess the predictive value of the MHR to identify coronary involvement with TAK and determine the patient prognosis. Methods: In this retrospective study, 1,184 consecutive patients with TAK were collected and assessed, and those who were initially treated and with coronary angiography were enrolled and classified according to coronary involvement or no involvement. Binary logistic analysis was performed to assess coronary involvement risk factors. Receiver-operating characteristic analysis was used to determine the MHR value to predict coronary involvement in TAK. Major adverse cardiovascular events (MACEs) were recorded in patients with TAK and coronary involvement within a 1-year follow-up, and Kaplan-Meier survival curve analysis was conducted to compare MACEs between them stratified by the MHR. Results: A total of 115 patients with TAK were included in this study, and 41 of them had coronary involvement. A higher MHR was found for TAK with coronary involvement than for TAK without coronary involvement (P = 0.014). Multivariate analysis showed that the MHR is an independent risk factor for coronary involvement in TAK (odds ratio: 92.718, 95% confidence interval (CI): 2.813-3056.291, P = 0.011). With the best cut-off value of 0.35, the MHR identified coronary involvement with 53.7% sensitivity and 68.9% specificity [area under the curve (AUC): 0.639, 95% CI: 0.544-0.726, P=0.010] and identified left main disease and/or three-vessel disease (LMD/3VD) with 70.6% sensitivity and 66.3% specificity (AUC: 0.704, 95% CI: 0.612-0.786, P = 0.003) in TAK. Combined with other variables, the MHR identified coronary involvement with 63.4% sensitivity and 90.5% specificity (AUC: 0.852, 95% CI: 0.773-0.911, P < 0.001), and identified LMD/3VD with 82.4% sensitivity and 78.6% specificity (AUC: 0.827, 95% CI: 0.720-0.934, P < 0.001) in TAK. A total of 39 patients with TAK and coronary involvement were followed up for 1 year, and 5 patients suffered a MACE. Those with an MHR >0.35 had a higher MACE incidence than their counterparts with an MHR ≤0.35 (χ2 = 4.757, P = 0.029). Conclusions: The MHR could be a simple, practical biomarker for identifying coronary involvement and LMD/3VD in TAK and predicting a long-term prognosis.

Short- and long-term functional results following drug-coated balloons versus drug- eluting stents in small coronary vessels: The RESTORE quantitative flow ratio study.

Background Immediate and long-term functional outcomes after percutaneous treatment of small vessel disease (SVD) with drug-coated balloon (DCB) versus drug-eluting stent (DES) remain unknown. The study sought to investigate whether treatment of de novo SVD with DCB yields similar functional results compared with DES, as judged with angiography-based quantitative flow ratio (QFR). Methods and results QFR was measured at pre-procedural, post-procedural and 9-month angiography in all available subjects from the non-inferiority RESTORE SVD China trial, in which patients were randomized to Restore DCB (n = 116) or Resolute DES (n = 114) study arms. Primary outcome of this analysis was 9-month QFR. Pre-procedural, post-procedural and 9-month QFR was performed in 84.8% (195/230), 83.0% (191/230) and 93.8% (181/193) cases, respectively. At 9 months, the QFR of DCB showed no significant difference to DES (0.88 ± 0.23 vs. 0.92 ± 0.12, p = 0.12). Both 9-month QFR and the QFR difference between post-procedure and 9-month follow-up were correlated with angiographic percentage of diameter stenosis and late loss, and predictive of 2-year clinical outcome. Conclusions Treatment of coronary SVD with DCB resulted in similar 9-month functional results compared with DES. This study provides evidences to the value of QFR as a mean of evaluating device performance after coronary revascularization. Clinical trial registration URL: https://www.clinicaltrials.gov; ClinicalTrial.gov: Identifier: NCT02946307.