Value of oral glucose tolerance test in the acute phase of myocardial infarction

<p>Abstract</p> <p>Background</p> <p>Although European guidelines advise oral glucose tolerance test (OGTT) in patients with acute myocardial infarction (AMI) before or shortly after hospital discharge, data supporting this recommendation are inconclusive. We aimed to analyze whether disturbances in glucose metabolism diagnosed before hospital discharge in AMI patients represents a latent pre-existing condition or rather temporary finding. Additionally, we planned to investigate the value of pre-selected glycemic control parameters as predictors of long-term glucometabolic state.</p> <p>Methods</p> <p>We assessed admission glycemia, glycated hemoglobin, mean blood glucose concentration on days 1 and 2 in 200 patients with a first AMI but without overt disturbances of glucose metabolism. We also performed OGTT at discharge and 3 months after discharge.</p> <p>Results</p> <p>The prevalence of disturbances in glucose metabolism (as assessed by OGTT) at 3 months was significantly lower than at discharge (29% <it>vs</it>. 48%, p = 0.0001). Disturbances in glucose metabolism were not confirmed in 63% of patients with impaired glucose tolerance and in 36% of patients with diabetes mellitus diagnosed during the acute phase of AMI. Age >77 years, glucose ≥12.06 mmol/l at 120 minutes during OGTT before discharge and mean blood glucose level on day 2 >7.5 mmol/l were identified as independent predictors of disturbances in glucose metabolism at the 3-month follow-up.</p> <p>Conclusions</p> <p>Disturbances in glucose metabolism observed in patients with a first AMI are predominantly transient. Elderly age, high plasma glucose concentration at 120 minutes during OGTT at discharge and elevated mean blood glucose level on day 2 were associated with sustained disturbances in glucose metabolism.</p

Personalized antiplatelet therapy with P2Y12 receptor inhibitors: benefits and pitfalls.

Antiplatelet therapy with P2Y12 receptor inhibitors has become the cornerstone of medical treatment in patients with acute coronary syndrome, after percutaneous coronary intervention and in secondary prevention of atherothrombotic events. Clopidogrel used to be the most broadly prescribed P2Y12 receptor inhibitor with undisputable benefits especially in combination with aspirin, but a considerable number of clopidogrel-treated patients experience adverse thrombotic events in whom insufficient P2Y12-inhibition and a consequential high on-treatment platelet reactivity is a common finding. This clinically relevant limitation of clopidogrel has driven the increased use of new antiplatelet agents. Prasugrel (a third generation thienopyridine) and ticagrelor (a cyclopentyl-triazolo-pyrimidine) feature more potent and predictable P2Y12-inhibition compared to clopidogrel, which translates into improved ischemic outcomes. However, excessive platelet inhibition and consequential low on-treatment platelet reactivity comes at the price of increased risk of major bleeding. The majority of randomized clinical trials failed to demonstrate improved clinical outcomes with platelet function testing and tailored antiplatelet therapy, but results of all recent trials of potent antiplatelets and prolonged antiplatelet durations point towards a need for individualized antiplatelet approach in order to decrease thrombotic events without increasing bleeding. This review focuses on potential strategies for personalizing antiplatelet treatment

Usefulness of C-reactive protein as a marker of early post-infarct left ventricular systolic dysfunction

Objective To assess the usefulness of in-hospital measurement of C-reactive protein (CRP) concentration in comparison to well-established risk factors as a marker of post-infarct left ventricular systolic dysfunction (LVSD) at discharge. Materials and methods Two hundred and four consecutive patients with ST-segment-elevation myocardial infarction (STEMI) were prospectively enrolled into the study. CRP plasma concentrations were measured before reperfusion, 24 h after admission and at discharge with an ultra-sensitive latex immunoassay. Results CRP concentration increased significantly during the first 24 h of hospitalization (2.4 ± 1.9 vs. 15.7 ± 17.0 mg/L; p\0.001) and persisted elevated at discharge (14.7 ± 14.7 mg/L), mainly in 57 patients with LVSD (2.4 ± 1.8 vs. 25.0 ± 23.4 mg/L; p\0.001; CRP at discharge 21.9 ± 18.6 mg/L). The prevalence of LVSD was significantly increased across increasing tertiles of CRP concentration both at 24 h after admission (13.2 vs. 19.1 vs. 51.5 %; p\0.0001) and at discharge (14.7 vs. 23.5 vs. 45.6 %; p\0.0001). Multivariate analysis demonstrated CRP concentration at discharge to be an independent marker of early LVSD (odds ratio of 1.38 for a 10 mg/L increase, 95 % confidence interval 1.01–1.87; p\0.04). Conclusion Measurement of CRP plasma concentration at discharge may be useful as a marker of early LVSD in patients after a first STEMI

Predicting Mortality in Patients with Atrial Fibrillation and Obstructive Chronic Coronary Syndrome: The Bialystok Coronary Project

Over the next decades, the prevalence of atrial fibrillation (AF) is estimated to double. Our aim was to investigate the causes of the long-term mortality in relation to the diagnosis of atrial fibrillation (AF) and chronic coronary syndrome (CCS). The analysed population consisted of 7367 consecutive patients referred for elective coronary angiography enrolled in a large single-centre retrospective registry, out of whom 1484 had AF and 2881 were diagnosed with obstructive CCS. During follow-up (median = 2029 days), 1201 patients died. The highest all-cause death was seen in AF(+)/CCS(+) [194/527; 36.8%], followed by AF(+)/CCS(−) [210/957; 21.9%], AF(−)/CCS(+) [(459/2354; 19.5%)] subgroups. AF ([HR](AC) = 1.48, 95%CI, 1.09–2.01; HR(CV) = 1.34, 95%CI, 1.07–1.68) and obstructive CCS (HR(AC) = 1.90, 95%CI, 1.56–2.31; HR(CV) = 2.27, 95%CI, 1.94–2.65) together with age, male gender, heart failure, obstructive pulmonary disease, diabetes were predictors of both all-cause and CV mortality. The main findings are as follow among patients referred for elective coronary angiography, both AF and obstructive CCS are strong and independent predictors of the long-term mortality. Mortality of AF without CCS was at least as high as non-AF patients with CCS. CV deaths were more frequent than non-CV deaths in AF patients with CCS compared to those with either AF or CCS alone

Clinical Study Value of C-Reactive Protein in Predicting Left Ventricular Remodelling in Patients with a First ST-Segment Elevation Myocardial Infarction

Objective. To assess the value of C-reactive protein (CRP) in predicting postinfarct left ventricular remodelling (LVR). Methods. We measured in-hospital plasma CRP concentrations in patients with a first ST-segment elevation myocardial infarction (STEMI). Results. LVR was present at 6 months in 27.8% of 198 patients. CRP concentration rose during the first 24 h, mainly in LVR group. The prevalence of LVR was higher in patients from the highest quartile of CRP concentrations at 24 h as compared to those from any other quartile (odds ratio (OR) 3.48, 95% confidence interval (95% CI) 1.76-6.88). Multivariate analysis identified CRP concentration at 24 h (OR for a 10 mg/L increase 1.29, 95% CI 1.04-1.60), B-type natriuretic peptide at discharge (OR for a 100 pg/mL increase 1.21, 95% CI 1.05-1.39), body mass index (OR for a 1 kg/m 2 increase 1.10, 95% CI 1.01-1.21), and left ventricular end-diastolic volume (OR for a 1 mL increase 0.98, 95% CI 0.96-0.99) as independent predictors of LVR. The ROC analysis revealed a limited discriminative value of CRP (area under the curve 0.61; 95% CI 0.54-0.68) in terms of LVR prediction. Conclusions. Measurement of CRP concentration at 24 h after admission possesses a significant but modest value in predicting LVR after a first STEMI

Interplay between genetic and clinical variables affecting platelet reactivity and cardiac adverse events in patients undergoing percutaneous coronary intervention.

Several clinical and genetic variables are associated with influencing high on treatment platelet reactivity (HTPR). The aim of the study was to propose a path model explaining a concurrent impact among variables influencing HTPR and ischemic events. In this prospective cohort study polymorphisms of CYP2C19*2, CYP2C19*17, ABCB1, PON1 alleles and platelet function assessed by Multiple Electrode Aggregometry were assessed in 416 patients undergoing percutaneous coronary intervention treated with clopidogrel and aspirin. The rates of major adverse cardiac events (MACE) were recorded during a 12-month follow up. The path model was calculated by a structural equation modelling. Paths from two clinical characteristics (diabetes mellitus and acute coronary syndrome (ACS)) and two genetic variants (CYP2C19*2 and CYP2C19*17) independently predicted HTPR (path coefficients: 0.11 0.10, 0.17, and -0.10, respectively; p<0.05 for all). By use of those four variables a novel score for prediction of HTPR was built: in a factor-weighted model the risk for HTPR was calculated with an OR of 3.8 (95%CI: 3.1-6.8, p<0.001) for a score level of ≥1 compared with a score of <1. While MACE was independently predicted by HTPR and age in the multivariate model (path coefficient: 0.14 and 0.13, respectively; p<0.05), the coexistence of HTPR and age ≥75 years emerged as the strongest predictor of MACE. Our study suggests a pathway, which might explain indirect and direct impact of variables on clinical outcome: ACS, diabetes mellitus, CYP2C19*2 and CYP2C19*17 genetic variants independently predicted HTPR. In turn, age ≥75 years and HTPR were the strongest predictors of MACE