scholarly journals Relationship of Platelet Reactivity and Inflammatory Markers to Recurrent Adverse Events in Patients with ST-Elevation Myocardial Infarction

2019 ◽  
Vol 119 (11) ◽  
pp. 1785-1794 ◽  
Author(s):  
Krishma Adatia ◽  
Mohamed F. Farag ◽  
Ying X. Gue ◽  
Manivannan Srinivasan ◽  
Diana A. Gorog
Keyword(s):  
Myocardial Infarction ◽  
Adverse Events ◽  
Platelet Reactivity ◽  
Point Of Care ◽  
High Sensitivity ◽  
St Elevation Myocardial Infarction ◽  
Major Adverse Cardiovascular Events ◽  
Neutrophil Lymphocyte Ratio ◽  
St Elevation ◽  
Hs Crp

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.

Abstract 346: Platelet Reactivity to Aspirin and Clopidogrel in Patients with Acute ST Elevation Myocardial Infarction and its Correlation with High Sensitivity C- Reactive Protein

2013 ◽  
Vol 33 (suppl_1) ◽  
Author(s):  
Archana Rajdev ◽  
Oana Penciu ◽  
Jacqueline Bradley ◽  
Cristina Mihu ◽  
Alan Siqueros ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Platelet Reactivity ◽  
High Sensitivity ◽  
St Elevation Myocardial Infarction ◽  
Diabetic Patients ◽  
C Reactive Protein ◽  
Reactive Protein ◽  
Significant Difference ◽  
St Elevation ◽  
Hs Crp

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

P327Predictive value of platelet reactivity, neutrophil to lymphocyte ratio, and hs-CRP at presentation in patients with ST-elevation myocardial infarction treated with percutaneous coronary intervention

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
K Adatia ◽  
M Farag ◽  
Y X Gue ◽  
M Srinivasan ◽  
D A Gorog
Keyword(s):  
Myocardial Infarction ◽  
Percutaneous Coronary Intervention ◽  
Platelet Reactivity ◽  
Coronary Intervention ◽  
St Elevation Myocardial Infarction ◽  
Occlusion Time ◽  
Lymphocyte Ratio ◽  
Percutaneous Coronary ◽  
St Elevation ◽  
Hs Crp

Abstract Background Patients with ST-elevation myocardial infarction (STEMI) exhibit enhanced platelet reactivity and a rise in inflammatory biomarkers such as neutrophil to lymphocyte ratio (NLR) and high-sensitivity C-reactive protein (hs-CRP). The extent of the prothrombotic and inflammatory state are predictive of adverse outcomes in patients with acute coronary syndromes. The relationship of these markers of inflammation and thrombosis in the hyperacute phase of STEMI and, whether together, they improve cardiovascular outcome prediction, is not known. Purpose The aim of this study was to assess the individual and combined predictive values of NLR, hs-CRP, and platelet reactivity for clinical outcomes in patients with STEMI. Method In a prospective study of 541 patients presenting with STEMI, acute admission bloods taken prior to emergency percutaneous coronary intervention, were analysed for NLR and hs-CRP. Platelet reactivity was measured using the point-of-care Global Thrombosis Test, which assesses platelet reactivity in native whole blood under high shear, and measures the occlusion time (OT, sec). Shorter occlusion time represents higher platelet reactivity. The study endpoint was occurrence of major adverse cardiovascular events (MACE, defined as composite of cardiovascular death [CVD], myocardial infarction [MI] or stroke [CVA]) at 30 days and 12 months. Results There was a weak, but significant, correlation between hs-CRP and NLR (r=0.25, p<0.001), and hs-CRP and platelet reactivity (r=0.14, p=0.003) on admission. There was no correlation between platelet reactivity and NLR. Amongst 541 patients, 42 patients experienced a MACE within the first 30 days, and 50 within 12 months. Cut-values associated with the highest specificity and sensitivity for 12-month MACE were NLR 5.6, hs-CRP 8 mg/L and OT 302 sec. Platelet reactivity and hs-CRP were each only weakly predictive of MACE at 30 days (platelet reactivity: hazard ratio [HR] 1.004 [95% confidence interval (CI) 1.002–1.006,] p<0.001; hs-CRP: HR 1.005 [95% CI 1.0009–1.009], p=0.016) and 12 months (platelet reactivity HR 1.004 (95% CI 1.002–1.006), p<0.001; hs-CRP HR 1.005 (95% CI 1.001–1.01), p=0.014). NLR was not predictive of MACE at either 30 days or 12 months (p=NS). When patients were divided into quartiles based on hs-CRP and platelet reactivity, patients in the highest quartile for both hs-CRP and platelet reactivity had an HR 3.46 (95% CI 1.81–6.63), p<0.001 compared to those in the lowest quartile for both (HR 0.04 (95% CI 0.005–0.27), p=0.001). The combination of enhanced platelet reactivity and raised hs-CRP was the strongest predictor of MACE at 30 days (HR 2.32 [95% CI 1.71–3.13], p<0.001) and 12 months (HR 2.31 [95% CI 1.71–3.11], p<0.001). Conclusion Both hs-CRP and platelet reactivity are very weakly predictive of MACE, but in combination provide a strong predictor of adverse outcome in STEMI.

scholarly journals Influence of myocardial damage on serum procalcitonin in ST-elevation myocardial infarction

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
M Reindl ◽  
C Tiller ◽  
M Holzknecht ◽  
I Lechner ◽  
B Henninger ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Myocardial Injury ◽  
Release Kinetics ◽  
Myocardial Damage ◽  
High Sensitivity ◽  
St Elevation Myocardial Infarction ◽  
Funding Source ◽  
St Elevation ◽  
Hs Crp ◽  
Cmr Imaging

Abstract Background Myocardial tissue injury due to acute ST-elevation myocardial infarction (STEMI) initiates an inflammatory response with a release of systemic inflammatory biomarkers including C-reactive protein (CRP) and white blood cell count (WBCc), which, however, hampers the usefulness of these routine biomarkers to identify concomitant infections. The clinical role of Procalcitonin (PCT), a promising marker of bacterial infections, to detect concomitant infections in acute STEMI is unknown, mainly because it is unclear whether myocardial injury per se induces a systemic PCT release. Purpose To investigate release kinetics of serum PCT in the acute setting of STEMI and possible associations with myocardial injury markers as comprehensively assessed by cardiac magnetic resonance (CMR) imaging. Methods In this prospective observational study, we included 141 STEMI patients treated with primary percutaneous coronary intervention (PCI). Concentrations of PCT, high-sensitivity CRP (hs-CRP), WBCc and high-sensitivity cardiac troponin T (hs-cTnT) were measured serially at day 1 and day 2 after infarction. CMR imaging to assess infarct size (IS), extent of microvascular injury (MVI) and occurrence of intramyocardial haemorrhage (IMH) was performed within the first week following STEMI. Results Median concentrations of PCT were 0.07μg/l at both time points. In 140 patients (99%), both PCT values were within the normal range (≤0.5μg/l). Whereas hs-CRP, WBCc, and hs-TnT were significantly correlated with CMR markers of myocardial damage, PCT did not show significant correlations (all p&gt;0.10) with IS (PCT24h: r=0.07; PCT48h: r=0.13) or MVI (PCT24h: r=−0.03; PCT48h: r=0.09). Furthermore, PCT failed to discriminate between large and small IS or MVI or between presence and absence of IMH (AUC values:0.46–0.55). Conclusions In the acute phase after PCI for STEMI, circulating PCT remained unaffected by the extent of myocardial and microvascular tissue damage as visualized by CMR imaging. These data highlight the clinical potential of PCT to identify concomitant infections and to guide antibiotic treatments in STEMI patients. Funding Acknowledgement Type of funding source: Public grant(s) – National budget only. Main funding source(s): Austrian Science Fund, Tiroler Wissenschaftsförderung

Abstract 14004: Pharmacodynamic Profiles of Ticagrelor in Patients With ST-Elevation Myocardial Infarction: A Prospective Randomized Comparison of Escalating Loading Dose Regimens

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Francesco Franchi ◽  
Fabiana Rollini ◽  
Jung Rae Cho ◽  
Mona Bhatti ◽  
Christopher DeGroat ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Time Course ◽  
Peak Plasma ◽  
Platelet Reactivity ◽  
Randomized Study ◽  
Plasma Concentrations ◽  
St Elevation Myocardial Infarction ◽  
Reactivity Index ◽  
Loading Dose ◽  
St Elevation

Background: Pharmacodynamic (PD) studies have shown that in ST-elevation myocardial infarction (STEMI) patients undergoing primary percutaneous coronary intervention (PPCI), ticagrelor is associated with suboptimal platelet inhibition and elevated rates of high on-treatment platelet reactivity (HPR) in the early hours after loading dose (LD) administration. Impaired absorption affecting drug pharmacokinetics (PK) has been hypothesized as a contributing factor suggesting increasing LD regimens to improve PK/PD profiles. To date there are no randomized studies which have investigated the PK/PD effects of escalating ticagrelor LD regimens in patients undergoing PPCI. Methods: In this prospective, randomized study, STEMI patients undergoing PPCI (n=52) were randomized 1:1:1 to receive 180mg, 270mg or 360mg LD of ticagrelor. PK and PD analysis were performed before and at 6 time points after LD. PD assessments included P2Y 12 reaction units (PRU) measured by VerifyNow P2Y12 and platelet reactivity index (PRI) measured by VASP. PK assessments included plasma concentrations of ticagrelor and its metabolite AR-C124910XX. Results: At baseline there were no differences in platelet reactivity between groups. At 2 hrs (primary endpoint), there were no differences in PRU between groups (p=0.54). There were no differences in PRU between groups during the overall study time course (p=0.17; Figure). Accordingly, HPR (PRU>208) at 2 hrs was observed in 30% of patients and was not reduced by escalating ticagrelor LD regimens. Consistent PD findings were observed with VASP-PRI. PK data tracked PD results, with a non-dose related delay in peak plasma concentrations of both ticagrelor and AR-C124910XX, particularly in HPR patients. Conclusions: In STEMI patients undergoing PPCI, increasing the LD regimen of ticagrelor did not translate into more prompt or potent P2Y 12 inhibition, which is attributed to impaired absorption in the early hours after drug administration.

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