scholarly journals Effect of postprandial hyperglycaemia on culprit plaque rupture in diabetic patients with non-ST segment elevation acute coronary syndrome

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
G Su ◽  
S.W Zhuang ◽  
T Zhang ◽  
H.X Yang ◽  
W.L Dai ◽  
...  

Abstract Background Postprandial hyperglycemia was reported to play a key role in established risk factors of coronary artery diseases (CAD) and cardiovascular events. Serum 1,5-anhydroglucitol (1,5-AG) levels are known to be a clinical marker of postprandial hyperglycemia and short-term glycemic excursions. Low serum 1,5-AG levels have been associated with occurrence of CAD; however, the relationship between 1,5-AG levels and coronary plaque rupture has not been fully elucidated. The aim of this study was to evaluate 1,5-AG as a predictor of coronary plaque rupture in diabetic patients with non-ST segment elevation acute coronary syndrome (NSTE-ACS). Methods A total of 132 diabetic patients with NSTE-ACS were included in this study. All patients underwent intravascular ultrasound examination, which revealed 38 patients with plaque rupture and 94 patients without plaque rupture in the culprit lesion. Fasting blood glucose (FBS), hemoglobin A1c (HbA1c) and 1,5-AG levels were measured before coronary angiography. Fasting urinary 8-iso-prostaglandin F2α (8-iso-PGF2α) level was measured and corrected by creatinine clearance. Results Patients with ruptured plaque had significantly lower serum 1,5-AG levels and a tendency of higher hemoglobin A1c levels than patients without ruptured plaque in our study population. In multivariate analysis, low 1,5-AG levels were an independent predictor of plaque rupture (odds ratio 3.3; p=0.006) in diabetic patients with NSTE-ACS, but HbA1c was not. The area under the receiver-operating characteristic curve for 1,5-AG (0.678, p=0.001) to predict plaque rupture was superior to that for HbA1c (0.618, p=0.034). Levels of 1,5-AG were significantly correlated with urinary 8-iso-PGF2α (r=−0.224, p=0.010). Conclusions Postprandial hyperglycaemia appeared to be superior to long-term average blood glucose levels in predicting plaque rupture in culprit lesions, which may be useful to assess the cardiovascular outcomes in diabetic patients. Funding Acknowledgement Type of funding source: Public Institution(s). Main funding source(s): Outstanding Clinical Discipline Project of Shanghai Pudong, Beijing Health Special Foundation

2020 ◽  
Author(s):  
Gong Su ◽  
Ming-Xi Gao ◽  
Wei-Feng Yao ◽  
Xi-Xi Dai ◽  
Gen-Ling Shi ◽  
...  

Abstract Background Postprandial hyperglycemia was reported to play a key role in established risk factors of coronary artery diseases (CAD) and cardiovascular events. Serum 1,5-anhydroglucitol (1,5-AG) levels are known to be a clinical marker of short-term postprandial glucose (PPG) excursions. Low serum 1,5-AG levels have been associated with occurrence of CAD; however, the relationship between 1,5-AG levels and coronary plaque rupture has not been fully elucidated. The aim of this study was to evaluate 1,5-AG as a predictor of coronary plaque rupture in diabetic patients with non-ST segment elevation acute coronary syndrome (NSTE-ACS).Methods A total of 132 diabetic patients with NSTE-ACS were included in this study. All patients underwent intravascular ultrasound examination, which revealed 38 patients with plaque rupture and 94 patients without plaque rupture in the culprit lesion. Fasting blood glucose (FBS), hemoglobin A1c (HbA1c) and 1,5-AG levels were measured before coronary angiography. Fasting urinary 8-iso-prostaglandin F2α (8-iso-PGF2α) level was measured and corrected by creatinine clearance. Results Patients with ruptured plaque had significantly lower serum 1,5-AG levels and a tendency of higher HbA1c levels than patients without ruptured plaque in our study population. In multivariate analysis, low 1,5-AG levels were an independent predictor of plaque rupture (odds ratio 3.3; p = 0.006) in diabetic patients with NSTE-ACS, but HbA1c was not. The area under the receiver-operating characteristic curve for 1,5-AG (0.678, p = 0.001) to predict plaque rupture was superior to that for HbA1c (0.618, p = 0.034). Levels of 1,5-AG were significantly correlated with urinary 8-iso-PGF2α levels (r=-0.224, p = 0.010).Conclusions Serum 1,5-AG may identify high risk for coronary plaque rupture in diabetic patients with NSTE-ACS, which suggests PPG excursions are related to the pathogenesis of plaque rupture in diabetes.


2019 ◽  
Vol 9 (4) ◽  
pp. 657
Author(s):  
Nevio Taglieri ◽  
Cristina Nanni ◽  
Gabriele Ghetti ◽  
Rachele Bonfiglioli ◽  
Francesco Saia ◽  
...  

Objectives: High cystatin C(CysC) levels are associated with impaired cardiovascular outcome. Whether CysC levels are independently related to the atherosclerosis burden is still controversial. Methods: We enrolled 31 non-ST-segment elevation acute coronary syndrome patients undergoing percutaneous coronary intervention. Patients were divided into 2 groups on the basis of median value of serum CysC. Using the high CysC group as a dependent variable, univariable and multivariable analyses were used to evaluate the association between CysC and three different features of atherosclerosis: 1) coronary plaque vulnerability as assessed by optical coherence tomography (OCT), 2) coronary artery calcium (CAC) by means of computed tomography scan, and 3) aortic wall metabolic activity, as assessed using 18F-Fluorodeoxyglucose-positron emission tomography (18F-FDG-PET). Results: After univariable and multivariable analyses, 18F-FDG uptake in the descending aorta (DA) was independently associated with a low level of CysC [(Odds Ratio = 0.02; 95%CI 0.0004–0.89; p = 0.044; 18F-FDG uptake measured as averaged maximum target to blood ratio); (Odds Ratio = 0.89; 95%CI 0.82–0.98, p = 0.025; 18F-FDG uptake measured as number of active slices)]. No trend was found for the association between CysC and characteristics of OCT-assessed coronary plaque vulnerability or CAC score. Conclusions: In patients with non-ST-segment elevation acute coronary syndrome (NSTE-ACS), 18F-FDG uptake in the DA was associated with a low level of serum CysC. There was no relation between CysC levels and OCT-assessed coronary plaque vulnerability or CAC score. These findings suggest that high levels of CysC may not be considered as independent markers of atherosclerosis.


2010 ◽  
Vol 23 (4) ◽  
pp. 324-334
Author(s):  
Paul P. Dobesh ◽  
Toby C. Trujillo

There are currently over 1 million patients admitted to hospitals in the United States with the diagnosis of non-ST-segment elevation acute coronary syndrome (NSTE ACS). Due to the significant morbidity and mortality associated with NSTE ACS, appropriate use of the numerous medications employed is critical in ensuring optimal outcomes. Because atherosclerotic plaque rupture and thrombus formation are the central pathophysiologic process in patients with NSTE ACS, it is important to utilize effective and safe combinations of antiplatelet and anticoagulant drug therapy. There are a number of different anticoagulant agents available for use in patients with NSTE ACS, but it is essential to have an in-depth knowledge of the setting in which these agents have been investigated, what current consensus guidelines recommend, as well as an appreciation for the treatment approach and philosophy of the institution for management of patients with NSTE ACS. In this review manuscript, the reader will find an evaluation of the current guidelines concerning the use of anticoagulant therapy in patients with NSTE ACS, as well as a detailed examination of the literature with critical analysis on issues that should be considered when deciding on the appropriate implementation of anticoagulant therapy in protocols for NSTE ACS patients.


2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
R Wereski ◽  
K.K Lee ◽  
S Smith ◽  
A.R Chapman ◽  
D Lowe ◽  
...  

Abstract Background The widespread adoption of high-sensitivity cardiac troponin testing has encouraged the use of pathways to accelerate the rule-out and rule-in myocardial infarction in the Emergency Department. These pathways are not recommended for patients with ST-segment elevation, but there is a risk they may be applied incorrectly given that interpretation of the electrocardiogram is subjective, dependent on experience, and signs may be masked in those with posterior myocardial infarction. Methods Consecutive patients with suspected acute coronary syndrome were enrolled in a stepped-wedge cluster randomized controlled trial across ten hospitals in Scotland. The index diagnosis was adjudicated two clinicians independently in all patients with high-sensitivity cardiac troponin I concentrations above the sex-specific 99th centile on serial testing and abnormalities on the electrocardiogram recorded. The proportion of patients with ST-segment elevation myocardial infarction and concentrations below the rule-out threshold (<5 ng/L), 99th centile (<16 ng/L and <34 ng/L for women and men) and rule-in threshold (<52 ng/L) at presentation were determined. Results In total 48,282 patients were recruited between June 2013, and March 2016 of which 22% (10,360/48,282) had peak cardiac troponin concentrations above the 99th centile. The adjudicated diagnosis was type 1 myocardial infarction in 55% (4,981/9,115) of patients and 10% (925/9,115) had ST-segment elevation myocardial infarction (age 65 [14] years, 68% men). The majority presented within 6 hours of symptom onset (67%, 619/925), and 84% (772/925) had cardiac troponin concentrations above the 99th centile at presentation. However, troponin concentrations were below the rule-out threshold in 2% (20/925) and the rule-in threshold in 26% (240/925) of patients with ST-segment elevation myocardial infarction. Discussion In patients with suspected acute coronary syndrome who have a final diagnosis of ST-segment elevation myocardial infarction, high-sensitivity cardiac troponin concentrations are below the rule-out and rule-in threshold at presentation in 1 in 50 and 1 in 4 patients, respectively. Clinicians should not rely on cardiac troponin concentrations to guide initial treatment decisions in patients with possible ST-segment elevation myocardial infarction. Funding Acknowledgement Type of funding source: Foundation. Main funding source(s): British Heart Foundation


Folia Medica ◽  
2013 ◽  
Vol 55 (2) ◽  
pp. 16-25
Author(s):  
Nikolay G. Dimitrov ◽  
Iana I. Simova ◽  
Hristo F. Mateev ◽  
Maria R. Kalpachka ◽  
Pavlin S. Pavlov ◽  
...  

ABSTRACT INTRODUCTION: Patients with acute coronary syndrome without ST segment elevation are a heterogeneous group with respect to the risk of having a major adverse cardiac event (MACE). A history of diabetes mellitus (DM) is no doubt one of the factors that define a patient as being at a higher risk of having the syndrome. AIM: To compare early invasive strategy with selective invasive strategy indicated for patients with and without DM. PATIENTS AND METHODS: The study enrolled 178 patients with unstable angina or non-ST elevation myocardial infarction (UA/NSTEMI), and of these 52 (29.2%) had DM. Patients were randomly assigned to an early invasive strategy (these were scheduled to undergo coronary arteriography and percutaneous coronary intervention within 24 hours after admission) or to a selective invasive strategy (at first these were medically stabilized, with coronary arteriography required only in case of angina recurrence and/or evidence of inducible myocardial ischemia). The patients were followed up for a mean period of 22.8 ± 14 months. RESULTS: In the follow up the diabetics allocated to an early invasive strategy were found to have a significantly lower angina recurrence incidence (p = 0.005), rehospitalization rate (p = 0.001), fewer arteriographies (p = 0.001) and coronary interventions (p = 0.001) and low cumulative incidence of MACE (p = 0.008) in comparison with the diabetics assigned to selective invasive strategy. We also found, using the Kaplan-Meier curves survival analysis, that the time to MACE in patients assigned to an early invasive strategy was significantly longer than that in the group of selective invasive strategy. In the follow-up of non-diabetics we found no significant difference in MACE rate between the patients allocated to early invasive strategy and those assigned to selective invasive strategy. In the selective invasive strategy group, however, the cardiovascular adverse events tended to occur earlier than in the early invasive strategy group. CONCLUSIONS: Early invasive strategy in diabetic patients with non-ST-segment elevation acute coronary syndrome is associated with a reduced MACE rate compared with the selective invasive strategy used in these patients. Early invasive strategy applied in diabetic patients is also associated with a significantly longer time to MACE. In non-diabetics the advantages of early over selective invasive strategy are not so clearly differentiated.


2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
K Sopova ◽  
G Georgiopoulos ◽  
M Mueller-Hennessen ◽  
M Sachse ◽  
N Vlachogiannis ◽  
...  

Abstract Background Cathepsin S is an extracellular matrix degradation enzyme that plays an important role in atherosclerotic cardiovascular disease by inducing vasa vasorum development and atherosclerotic plaque rupture. Purpose To determine the prognostic and reclassification value of baseline serum cathepsin S after adjustment for the Global Registry of Acute Coronary Events (GRACE) score, which is a clinical guideline recommended risk score in non-ST-segment elevation acute coronary syndrome (NSTE-ACS). Methods Serum cathepsin S was measured by ELISA in 1,129 consecutive patients presenting with acute symptoms to the emergency department for whom a final adjudicated diagnosis of NSTE-ACS was made. All-cause mortality or all-cause death/non-fatal myocardial infarction (MI) after a median follow-up of 21 months were evaluated as the primary or secondary study endpoint, respectively. The Net Reclassification Index (NRI) estimated the reclassification predictive value for risk of each end-point of cathepsin S over the GRACE score. Results After a median follow-up of 21 months 101 (8.95%) deaths were reported. The combined endpoint of death or non-fatal MI occurred in 176 (15.6%) patients. Dose-response curve analysis adjusted for the effect of age, gender, diabetes mellitus, high-sensitivity-cardiac troponin T, high-sensitivity C-reactive protein, revascularization and index diagnosis revealed a non-linear association of continuous cathepsin S with all-cause death (P=0.036 for non-linearity; adjusted HR=1.60 for 80th vs. 20th percentiles, P=0.038) or with the combined endpoint (P=0.008 for non-linearity, adjusted HR=1.53 for 80th vs. 20th percentiles, P=0.011). Serum cathepsin S maintained its predictive value for all-cause death (adjusted HR=1.70 highest vs. lowest tertile, 95% CI 1.03–2.82, P=0.039) after adjusting for the GRACE Score. Similarly, cathepsin S predicted the combined endpoint of all-cause death or non-fatal MI (adjusted HR=1.67 highest vs. lowest tertile, 95% CI 1.15–2.42, P=0.007) independently of the GRACE Score. When cathepsin S was added over the GRACE Score it correctly reclassified risk for all-cause death in 20% of the population (P=0.004). Similarly, serum Cathepsin S conferred a significant reclassification value over the GRACE score for all-cause death or non-fatal MI in 15.9% of the population. Conclusions Serum cathepsin S is a predictor of mortality and improves risk stratification over the GRACE score in patients with NSTE-ACS. The clinical application of cathepsin S as a novel biomarker in NSTE-ACS should be further explored and validated. Funding Acknowledgement Type of funding source: Foundation. Main funding source(s): German Heart Foundation


Author(s):  
Siva S. Ketha ◽  
Juan Carlos Leoni Moreno

Acute coronary syndrome (ACS) encompasses all clinical manifestations caused by active myocardial ischemia and includes 3 entities: unstable angina (UA), acute non–ST-segment elevation myocardial infarction (NSTEMI), and acute ST-segment elevation myocardial infarction (STEMI). Atherosclerotic plaque rupture is the most consistent pathophysiologic event in ACS. After plaque rupture, cardiac myocytes die as a consequence of continued occlusion, thereby causing acute myocardial infarction (MI). Prompt recognition of ACS is crucial because the greatest therapeutic effect is achieved if treatment is performed soon after presentation.


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