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Post-conditioning the human heart to reduce infarct size Michel OVIZE Inserm E 0226 and Cardiology Hospital Lyon France.

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Presentation on theme: "Post-conditioning the human heart to reduce infarct size Michel OVIZE Inserm E 0226 and Cardiology Hospital Lyon France."— Presentation transcript:

1 Post-conditioning the human heart to reduce infarct size Michel OVIZE Inserm E 0226 and Cardiology Hospital Lyon France

2  common (  / year in USA)  affects outcome : mortality  disabling: heart failure Acute Myocardial Infarction

3 Gibbons et al. JACC 2004;44: Infarct size is a determinant of mortality

4 Reperfusion improves outcome van Domburg et al. JACC 2005:15–20

5 Reperfusion Injury « a double edged sword »  stunning : accepted  arrhythmias :accepted  no-reflow :accepted  necrosis :debated

6 AR/LV AN/AR (% of tissue area) control PostC PreC * * Zhao ZQ et al. Am J Physiol 2003 Postconditioning

7 coronary occlusion Ischemia Reperfusion reperfusion injury ischemic injury Infarct size time PostconditioningPreC Infarction: a two-component damage

8  -blockers ACE inhibitors statins …. Current treatment of AMI Ischemic damage : YES – thrombolysis / PCIischemia time – antiplatelet agentsischemia time Reperfusion damage : NO improve post-MI outcome, but not via a reduction in infarct size Action on infarct size

9 A narrow time window Loosing protection

10 Does Postconditioning protect the human heart ? A « proof of concept » study

11 Inclusion criteria 1. Age ≥ First acute (STE)MI / chest pain onset < 6 hrs 3. Need for emergency PTCA Exclusion criteria 1. Cardiac arrest 2. Cardiogenic shock 3. Circumflex coronary artery as culprit for AMI Study population A « Human Model » of Postconditioning

12 Eligible Patient Experimental Design Coronary + LV Angio Informed consent Randomization Angioplasty TIMI 0 Collat = 0 reperf. TIMI > 2

13 1’ ReperfusionOccluded coronary artery Direct stenting Balloon inflations - deflations Postcond Control Post-Conditioning algorythm Staat et al. Circulation. 2005;112:

14 Study Endpoints Total CK release over first 72 hrs of reperfusion –every 4 hr on Day 1 –every 6 hr on Day 2 –every 8 hr on Day 3

15 Results

16 Study population - baseline characteristics Control (n = 14) Postconditioned (n = 16) p value Age (y)56±358±4ns Sex (M/F)13/112/4ns BMI27±128±1ns HBP (%)3638ns Smokers (%)5657ns Dyslipidemia (%)5080ns Diabetes (%)1320ns LV and coronary angiography Culprit artery (LAD/RCA)6/86/10ns Ejection fraction (%)49 ± 452 ± 2ns

17 Area at Risk estimation on LV angiogram LV End Diastole LV End Systole A B C D B - C A - D ACS = X 100 % Length of the Abnormally Contracting Segments of the LVED endocardial perimeter Length of the LVED endocardial perimeter Anterior infarct

18 Area at Risk size (ACS) control PostC ns (%) Duration of Ischemia ns control PostC min. Determinants of infarct size

19 Adm. 4h8h24h48h72h Control Post-Cond CK release (AUC: arbitrary units) PTCA Reperfusion - 36 % (p < 0.05) CK release during reperfusion Staat et al. Circulation. 2005;112:

20 ACS (%) CK release (AUC) Control PostC CK release versus ACS (infarct size versus area at risk)

21 0 0,5 1 1,5 2 2,5 3 C Blush grade ST segment shift (mm) PostC C * Staat et al. Circulation. 2005;112: Estimation of « no reflow »

22 Toward New Clinical Strategies Ischemic PostC Pharmaco PostC drug adenosine, NO, K + ATP openers survival kinases mPTP inhibitors, ….. PCI - thrombolysis


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