scholarly journals EFFECTS OF BASELINE PLATELET REACTIVITY IN FIBRINOLYSIS-TREATED ST ELEVATION MYOCARDIAL INFARCTION PATIENTS UNDERGOING EARLY PERCUTANEOUS CORONARY INTERVENTION

2018 ◽  
Vol 34 (10) ◽  
pp. S13-S14
Author(s):  
P. Sin ◽  
A. Yang ◽  
Q. Pon ◽  
A. Lavoie ◽  
J. Crawford ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Percutaneous Coronary Intervention ◽  
Platelet Reactivity ◽  
Coronary Intervention ◽  
St Elevation Myocardial Infarction ◽  
Percutaneous Coronary ◽  
St Elevation

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.

Efficacy of prasugrel administration immediately after percutaneous coronary intervention in ST-elevation myocardial infarction

2017 ◽  
Vol 117 (01) ◽  
pp. 99-104 ◽  
Author(s):  
Ulrike Flierl ◽  
Florian Zauner ◽  
Jan-Thorben Sieweke ◽  
Christine Berliner ◽  
L. Christian Napp ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Percutaneous Coronary Intervention ◽  
Platelet Reactivity ◽  
Coronary Intervention ◽  
Rapid Onset ◽  
St Elevation Myocardial Infarction ◽  
Primary Pci ◽  
Acute Stemi ◽  
Percutaneous Coronary ◽  
St Elevation

SummaryPrasugrel, a potent thienopyridine, achieves stronger inhibition of platelet activation than clopidogrel. However, onset of inhibition is significantly delayed in patients with acute ST-elevation myocardial infarction (STEMI), as haemodynamic instability and morphine application seem to exhibit significant influence. Since rapid onset of effect was demonstrated in non-STEMI patients when prasugrel was administered only after percutaneous coronary intervention (PCI) without increasing cardiovascular event rates we assessed the efficacy of prasugrel loading immediately after PCI for STEMI instead of pre-loading before revascu-larisation. We investigated 50 consecutive patients with acute STEMI (mean age 56 ± 10 years) admitted for primary PCI. Prasugrel efficacy was assessed by platelet reactivity index (PRI; VASP assay) before, 1, 2, 4, 6, 12, and 24 hours following an oral loading dose of 60 mg immediately after PCI. High on-treatment platelet reactivity (HTPR) was de-fined as PRI>50 %. Prasugrel significantly and rapidly reduced platelet reactivity in acute STEMI patients (p<0.0001 at each time point vs control). Morphine application resulted in a significantly higher HTPR rate among patients having received morphine less than 1 hour before pra-sugrel loading (p<0.001) while concomitant metoclopramide (MCP) treatment did not significantly affect prasugrel efficacy. In conclusion, in contrast to previous reports describing a significant delay in onset of prasugrel-mediated P2Y12 inhibition in acute STEMI, we observed a rapid onset with low HTPR rates comparable to those observed in stable non-STEMI patients. Prasugrel administered directly after primary PCI might therefore be a useful therapeutic strategy in patients with STEMI to provide strong and effective P2Y12 inhibition.

Optimum Therapies for ST-Elevation Myocardial Infarction Managed with Primary Percutaneous Coronary Intervention

2012 ◽  
Vol 7 (2) ◽  
pp. 81
Author(s):  
Bruce R Brodie ◽  
Keyword(s):  
Myocardial Infarction ◽  
Percutaneous Coronary Intervention ◽  
Primary Percutaneous Coronary Intervention ◽  
Great Majority ◽  
Coronary Intervention ◽  
St Elevation Myocardial Infarction ◽  
Stent Deployment ◽  
Aspiration Thrombectomy ◽  
Percutaneous Coronary ◽  
St Elevation

This article reviews optimum therapies for the management of ST-elevation myocardial infarction (STEMI) with primary percutaneous coronary intervention (PCI). Optimum anti-thrombotic therapy includes aspirin, bivalirudin and the new anti-platelet agents prasugrel or ticagrelor. Stent thrombosis (ST) has been a major concern but can be reduced by achieving optimal stent deployment, use of prasugrel or ticagrelor, selective use of drug-eluting stents (DES) and use of new generation DES. Large thrombus burden is often associated poor outcomes. Patients with moderate to large thrombus should be managed with aspiration thrombectomy and patients with giant thrombus should be treated with glycoprotein IIb/IIIa inhibitors and may require rheolytic thrombectomy. The great majority of STEMI patients presenting at non-PCI hospitals can best be managed with transfer for primary PCI even with substantial delays. A small group of patients who present very early, who are at high clinical risk and have long delays to PCI, may best be treated with a pharmaco-invasive strategy.

Risk factors of coronary microvascular obstruction (Preprint)

2020 ◽  
Author(s):  
Yong Li ◽  
Shuzheng Lyu
Keyword(s):  
Risk Factors ◽  
Myocardial Infarction ◽  
Percutaneous Coronary Intervention ◽  
Logistic Regression ◽  
Microvascular Obstruction ◽  
Coronary Intervention ◽  
St Elevation Myocardial Infarction ◽  
Neutrophil Percentage ◽  
Percutaneous Coronary ◽  
St Elevation

BACKGROUND Coronary microvascular obstruction /no-reflow(CMVO/NR) is a predictor of long-term mortality in survivors of ST elevation myocardial infarction (STEMI) underwent primary percutaneous coronary intervention (PPCI). OBJECTIVE To identify risk factors of CMVO/NR. METHODS Totally 2384 STEMI patients treated with PPCI were divided into two groups according to thrombolysis in myocardial infarction(TIMI) flow grade:CMVO/NR group(246cases,TIMI 0-2 grade) and control group(2138 cases,TIMI 3 grade). We used univariable and multivariable logistic regression to identify risk factors of CMVO/NR. RESULTS A frequency of CMVO/NR was 10.3%(246/2384). Logistic regression analysis showed that the differences between the two groups in age(unadjusted odds ratios [OR] 1.032; 95% CI, 1.02 to 1.045; adjusted OR 1.032; 95% CI, 1.02 to 1.046 ; P <0.001), periprocedural bradycardia (unadjusted OR 2.357 ; 95% CI, 1.752 to 3.171; adjusted OR1.818; 95% CI, 1.338 to 2.471 ; P <0.001),using thrombus aspirationdevices during operation (unadjusted OR 2.489 ; 95% CI, 1.815 to 3.414; adjusted OR1.835; 95% CI, 1.291 to 2.606 ; P =0.001),neutrophil percentage (unadjusted OR 1.028 ; 95% CI, 1.014 to 1.042; adjusted OR1.022; 95% CI, 1.008 to 1.036 ; P =0.002) , and completely block of culprit vessel (unadjusted OR 2.626; 95% CI, 1.85 to 3.728; adjusted-OR 1.656;95% CI, 1.119 to 2.45; P =0.012) were statistically significant ( P <0. 05). The area under the receiver operating characteristic curve was 0.6896 . CONCLUSIONS Age , periprocedural bradycardia, using thrombus aspirationdevices during operation, neutrophil percentage ,and completely block of culprit vessel may be independent risk factors for predicting CMVO/NR. We registered this study with WHO International Clinical Trials Registry Platform (ICTRP) (registration number: ChiCTR1900023213; registered date: 16 May 2019).http://www.chictr.org.cn/edit.aspx?pid=39057&htm=4. Key Words: Coronary disease ST elevation myocardial infarction No-reflow phenomenon Percutaneous coronary intervention

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