scholarly journals Improving the outcome of primary PCI: protection from reperfusion injury

2017 ◽  
Vol 113 (10) ◽  
pp. e33-e34 ◽  
Author(s):  
Gerd Heusch
2021 ◽  
Vol 42 (Supplement_1) ◽  
Author(s):  
M Reindl ◽  
I Lechner ◽  
C Tiller ◽  
M Holzknecht ◽  
A Rangger ◽  
...  

Abstract Background Failed myocardial tissue reperfusion due to microvascular injury despite successful culprit lesion percutaneous coronary intervention (PCI) is associated with poor clinical outcome in patients with ST-elevation myocardial infarction (STEMI). A possible influence of dysglycaemia on myocardial reperfusion injury is unclear. Objectives To investigate the association between glycaemic status and microvascular injury determined by magnetic resonance imaging in STEMI patients. Methods This prospective observational cohort study included 260 consecutive STEMI patients undergoing primary PCI between 2016 and 2019. Peripheral venous blood samples for glucose and HbA1c measurements were drawn on admission. Primary microvascular injury endpoint was defined as presence of intramyocardial haemorrhage (IMH) assessed by cardiac magnetic resonance T2* mapping at 4 (interquartile range [IQR]:2–5) days after PCI. Results HbA1c (odds ratio [OR]: 1.73 [95% CI: 1.24–2.40]; p=0.001), pre-diagnosis of diabetes (OR: 2.63 [95% CI: 1.18–5.90]; p=0.02) and glucose concentration (OR: 1.01 [95% CI: 1.00–1.01]; p=0.01) significantly predicted IMH, which was present in 90 (35%) patients. Of these three parameters, only HbA1c remained significantly associated with IMH (OR: 2.12 [95% CI: 1.12–3.99]; p=0.02) after adjusting for total ischemic time, culprit lesion location, pre- and post-interventional TIMI flow and peak biomarker concentrations (troponin, N-terminal pro-B-type natriuretic peptide and C-reactive protein). The rate of IMH was 24% in patients with HbA1c <5.7%, 43% in patients with HbA1c ≥5.7 to 6.4% and 59% in patients with HbA1c ≥6.5% (p<0.001). Conclusions In STEMI patients undergoing primary PCI, admission HbA1c was independently associated with reperfusion injury as determined by IMH. These findings suggest that IMH could represent the underlying pathophysiological link between dysglycaemia and adverse outcomes following STEMI. FUNDunding Acknowledgement Type of funding sources: Public grant(s) – EU funding. Main funding source(s): FWF - Austrian Science Fund; ÖKG - Austrian Society of Cardiology Figure 1. This figure illustrates the relation between HbA1c and IMH by two patient examples successfully treated with PCI (intervention with stent implantation schematically shown on the very left side). The first patient (upper line), representing the patient group with HbA1c <5.7% (associated IMH risk 24%), showed an anterior wall STEMI without IMH (T2* mapping on the very right, corresponding schematic picture of the infarct area without IMH next on the left). The second patient (lower line), representing the patients with HbA1c ≥5.7% (associated IMH risk 47%), showed an anterior wall STEMI with large IMH (arrows point to the hypo-intense core on the T2* mapping image and to the corresponding dark-red area in the schematic illustration). The zoomed view of one microvessel indicates the complex pathophysiology of IMH (including endothelial destruction, embolisation of thrombotic material and inflammation). (Created with BioRender)


2013 ◽  
Vol 34 (23) ◽  
pp. 1714-1722 ◽  
Author(s):  
Georg M. Fröhlich ◽  
Pascal Meier ◽  
Steven K. White ◽  
Derek M. Yellon ◽  
Derek J. Hausenloy

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Holger Thiele ◽  
Ingo Eitel ◽  
Lysann Hildebrand ◽  
Carmen Schirdewahn ◽  
Volker Adams ◽  
...  

STEMI patients undergoing PCI are at high risk for contrast-induced nephropathy (CIN) because of hemodynamic instability and lack of effective prophylaxis. High-dose N-Acetylcystein (N-ACC) reduced the incidence of CIN in patients with high contrast volumes. In addition, previous animal trials showed that the antioxidant effects of N-ACC reduce reperfusion injury. Aim of this randomized, controlled, single-blinded trial was to assess the effects of N-ACC on CIN and reperfusion injury in patients undergoing primary PCI with moderate contrast volumes. Two hundred-fifty patients undergoing primary PCI were randomized to either high-dose N-ACC (2x1200 mg/d for 48 hours) or placebo plus optimal hydratation. The two primary endpoints were: 1) occurrence of CIN defined as an increase in the serum creatinine concentration of >25% from the baseline value within 72 h; 2) Myocardial salvage measured by T2-weighted STIR-images and delayed enhancement MRI at day 2– 4 after primary PCI. Secondary endpoints were infarct size and microvascular obstruction, ST-resolution at 90 minutes and occurrence of MACE at 30 day follow-up. The median volume of an isoosmolar contrast agent during PCI was 190 ml (IQR 130, 250 ml) in the N-ACC and 180 (IQR 143; 228 ml) in the placebo group (p=n.s.). Baseline creatinine and creatinine clearance were 88 vs 86 μmol/l and 90 vs 95 ml/min, respectively. The primary endpoint CIN occurred in 14% in the N-ACC group and in 18% in the placebo group (p=n.s.). The primary endpoint reperfusion injury measured by myocardial salvage was also not different between both treatment groups (25.4%; IQR 14.1; 38.1 versus 22.5%; IQR 16.8; 36.5; p=n.s.). In addition, no differences in infarct size and microvascular obstruction as well as in ST-segment resolution were observed. The MACE rate after N-ACC was similar to placebo (19.4% versus 19.4%, p=n.s.). Lipid peroxidation as a marker for oxidative stress was reduced by 20% in the N-ACC group (p<0.05), whereas no change was evident in placebo. High-dose N-ACC reduces oxidative stress. However, it does not provide an additional clinical benefit to placebo with respect to CIN and prevention of myocardial reperfusion injury in patients undergoing PCI with moderate doses of contrast medium and optimal hydratation.


2004 ◽  
Vol 171 (4S) ◽  
pp. 487-487
Author(s):  
Motoo Araki ◽  
Masayoshi Miura ◽  
Hiromi Kumon ◽  
John Belperio ◽  
Robert Strieter ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document