P826Peri-procedural treatment with high dose Rosuvastatin reduces soluble TNF receptor 1 in patients treated with primary percutaneous coronary intervention for ST elevation myocardial infarction

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
A I Larsen ◽  
N Butt ◽  
P Aukrust ◽  
P S Munk ◽  
J M Nilsen ◽  
...  

Abstract Background The extent of cardiac injury in ST elevation myocardial infarction (STEMI) depends on the level of inflammation and subsequent immune cell recruitment. An inflammatory phase that is disproportionately prolonged, of excessive magnitude, or insufficiently suppressed, can lead to sustained tissue damage and improper healing, promoting infarct expansion, adverse remodelling and chamber dilatation. Soluble TNF receptor 1 (sTNFR-1) is believed to mirror systemic pan-inflammatory status more closely than a single cytokine antigenic level. sTNFR-1 levels might give prognostic information, independent from and, at the same time, additive with some well-recognized outcome predictors such as left ventricular ejection fraction. Purpose We hypothesised that sTNFR-1 and other inflammatory markers could be modulated by statins. Methods Plasma levels of inflammatory markers were measured at baseline, 2 days, 7 days and 2 months in consecutive patients with first time STEMI with single vessel disease. Twenty-five patients (treatment group (TG)) were treated with 80 mg Rosuvastatin daily with first dose before primary percutaneous coronary intervention (PCI) whereas the control group (CG) consisted of 34 patients in whom treatment with 20 mg simvastatin daily were initiated the day after PPCI. Results sTNFR1 increased during the first 48 hours following PCI and this increase was larger in the CG compared with the TG (0.22±0.30 ng/mL vs 0.08±0.19 ng/nmL, p=0.025). The difference in increase during one week was only borderline statistically significant (0.21±0.30 ng/mL vs 0.08±0.26 ng/mL, p=0.081). These differences in the kinetics of sTNRF-1 were mirrored by changes in Pentraxin 3 (PTX3) between groups from baseline to 1 week, CG vs TG. (0.28±0.70 μmol/l vs 0.10±0.05 ng/mL, p=0.014) and at 2 months (−0.42±0.56 ng/mL vs 0.08±0.60 μmol/l, p=0.032) Conclusion High dose Rosuvastatin therapy initiated peri-procedural during PPCI for STEMI reduces pan inflammation as reflected by sTNFR1 and is associated with a less abrupt fall in PTX3 at 1 week and 2 months supporting recent research suggesting that PTX3 plays a cardiovascular protective effect in cardiovascular disease and healing. Acknowledgement/Funding Western Norway Regional Health Authority

2012 ◽  
Vol 7 (2) ◽  
pp. 81
Author(s):  
Bruce R Brodie ◽  

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.


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