scholarly journals Endothelial function after ST-elevation myocardial infarction in patients with high levels of high-sensitivity CRP and Lp-PLA 2 : A substudy of the RESPONSE randomized trial

2017 ◽  
Vol 18 (3) ◽  
pp. 202-206 ◽  
Author(s):  
Jasveen J. Kandhai-Ragunath ◽  
Bjorn de Wagenaar ◽  
Cees Doelman ◽  
Jan van Es ◽  
Harald T. Jørstad ◽  
...  
2013 ◽  
Vol 33 (suppl_1) ◽  
Author(s):  
Archana Rajdev ◽  
Oana Penciu ◽  
Jacqueline Bradley ◽  
Cristina Mihu ◽  
Alan Siqueros ◽  
...  

INTRODUCTION Implantation of bare metal or drug eluting stents supported by dual antiplatelet therapy (DAPT) is standard treatment for the management of patients with ST elevation myocardial infarction (STEMI). Individual response to aspirin and clopidogrel is heterogeneous, and decreased response is associated with thrombotic events following stenting. We postulated that systemic inflammation at the time of STEMI would diminish responsiveness to DAPT. The aim of this study is to evaluate the correlation between elevated high-sensitivity C-reactive protein (hs-CRP) as a marker of inflammation and decreased platelet sensitivity to DAPT in STEMI. METHODS We recruited patients with STEMI undergoing percutaneous coronary intervention (PCI) who received oral clopidogrel 600 mg loading dose followed by 75 mg daily maintenance dose and aspirin 325 mg daily. Platelet reactivity and hs-CRP were measured within 72 hours of PCI and at 6 weeks. For patients receiving eptifibatide, blood samples were taken 48 hours after discontinuation. Platelet reactivity was assessed using the VerifyNow platelet function analyzer. A cut-off value of 208 platelet reaction units (PRU) was used to define high on-clopidogrel platelet reactivity (HCPR) and a value of 454 aspirin reaction units (ARU) was used to define high on-aspirin platelet reactivity (HAPR). RESULTS In 20 patients aged 31 to 85, in hospital and 6 weeks after STEMI, hs-CRP was 6.7 (SD 4.0) and 2.6 (SD 3.2) respectively, p< 0.01. Changes in ARU from 408.3 (SD 54.3) to 425.2 (SD 68.2) and PRU from 157.8 (SD 74.7) to 164.2 (SD 75) were not statistically significant. 2 patients had HAPR in hospital; 1 became sensitive at follow up. 2 patients developed HAPR and HCPR. We saw a trend towards higher PRU in diabetic patients and those prescribed statins. CONCLUSIONS Although we found a significant difference in hs-CRP levels between the first and second time point, no significant difference was found in on-aspirin and on-clopidogrel platelet reactivity between the time points.Thus, in this small series, the acute inflammatory state associated with STEMI did not appear to influence the on-DAPT reactivity at the dosages used. Trends among those with diabetics and prescribed statins will be discussed


2019 ◽  
Vol 119 (11) ◽  
pp. 1785-1794 ◽  
Author(s):  
Krishma Adatia ◽  
Mohamed F. Farag ◽  
Ying X. Gue ◽  
Manivannan Srinivasan ◽  
Diana A. Gorog

Background Patients with ST-elevation myocardial infarction (STEMI) exhibit pro-thrombotic and pro-inflammatory states. Markers of enhanced platelet reactivity and inflammation are predictive of adverse outcome. However, the relationship between these biomarkers, and their combined usefulness for risk stratification, is not clear. Methods In a prospective study of 541 patients presenting with STEMI, blood samples were taken on arrival to measure high-sensitivity C-reactive protein (hs-CRP), neutrophil/lymphocyte ratio (NLR) and platelet reactivity using the point-of-care Global Thrombosis Test. These biomarkers, alone and in combination, were related to the occurrence of major adverse cardiovascular events (MACE, defined as composite of cardiovascular death, myocardial infarction and cerebrovascular accident) at 30 days and 12 months. Results Platelet reactivity and hs-CRP, but not NLR, were weakly predictive of MACE at 30 days and 12 months. The combination of enhanced platelet reactivity and raised hs-CRP was strongly predictive of MACE at 30 days (hazard ratio [HR] 3.46 [95% confidence interval [CI] 1.81–6.62], p < 0.001) and 12 months (HR 3.46 [95% CI 1.81–6.63], p < 0.001). Combination of all three biomarkers (NLR, hs-CRP and platelet reactivity) provided the best prediction of MACE at 30 days (HR 3.73 [95% CI 1.69–8.27], p < 0.001) and 12 months (HR 3.85 [95% CI 1.72–8.60], p < 0.001), and improved the prediction of MACE when added to Thrombolysis In Myocardial Infarction score (net reclassification index 0.296, p < 0.001). Conclusion A combination of three easy to measure biomarkers on arrival, namely hs-CRP, NLR and platelet reactivity, can help identify STEMI patients at high risk of recurrent adverse events over the subsequent year.


2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
C Puelacher ◽  
M Gugala ◽  
P D Adamson ◽  
A S V Shah ◽  
A R Chapmann ◽  
...  

Abstract Objective Assess the incidence and compare characteristics and outcome of unstable angina (UA) and Non-ST-Elevation myocardial infarction (NSTEMI) Design Two independent prospective multicenter diagnostic studies (Advantageous Predictors of Acute Coronary Syndromes Evaluation (APACE) and High-Sensitivity Troponin in the Evaluation of Patients With Acute Coronary Syndrome (High-STEACS)) enrolling patients with acute chest discomfort presenting to the emergency department. Central adjudication of the final diagnosis was done by two independent cardiologists using all clinical information including serial measurements of high-sensitivity cardiac troponin (hs-cTn). All-cause death and future non-fatal MI were assessed at 30-days and 1-year. Results 8992 patients were enrolled at 11 centres. UA was adjudicated in 366/4122 (8.9%) and 137/4870 (2.8%) patients in APACE and High-STEACS, respectively, and NSTEMI in 622 (15.1%) and 651 (13.4%). Coronary artery disease was pre-existing in 73% and 76% of patients with unstable angina. At 30-days, all-cause mortality in UA was substantially lower as compared to NSTEMI (0.5% versus 3.7%, p=0.002 in APACE, 0.7% versus 7.4%, p=0.004 in High-STEACS). Similarly, at 1-year in UA all-cause mortality was 3.3% [95% CI 1.2–5.3] vs 10.4% [7.9–12.9] in APACE, and 5.1% [0.7–9.5] vs 22.9% [19.3–26.4] in High-STEACS, and similar to non-cardiac chest pain (NCCP). In contrast, future non-fatal MI in APACE was comparable in UA and NSTEMI (11.2%, [7.8–14.6] and 7.9%, [5.7–10.2]), and higher than in NCCP (0.6%, [0.2–1.0]). 1-year survival free from future AMI Conclusions The incidence and the mortality of UA is substantially lower than that of NSTEMI, while the rate of future non-fatal MI is similar. Acknowledgement/Funding Swiss National Science Foundation, Swiss Heart Foundation, Cardiovascular Research Foundation Basel, British Heart Foundation Project Grants, Butler S


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