Nuovi target e opportunità terapeutiche del danno da riperfusione nello STEMI
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1 GUIDATI DA PARADIGMI SEMPRE NUOVI, GLI SCIENZIATI ADOTTANO NUOVI STRUMENTI E PROGETTANO NUOVI STUDI GUARDANDO VERSO NUOVE DIREZIONI Nuovi target e opportunità terapeutiche del danno da riperfusione nello STEMI Filippo Ottani, MD
2 Myocardial Reperfusion Injury: Definition Features of Reperfusion Injury : I. Myocardial Stunning (reversible) II. No-Reflow Phenomenon (reversible/irreversible) III. Reperfusion Arrhytmias IV. Lethal Reperfusion Injury (reversible) Lethal reperfusion injury is a paradoxical type of myocardial injury caused by the restoration of coronary blood flow after an ischemic episode that might be prevented by an intervention
3 Prasad A et al. Circualtion 2009; 120: 2105 Major Mediators of Lethal Reperfusion Injury
4 Contribution of Lethal Reperfusion Injury to Final Myocardial Infarct Size Yellon D. NEJM 2007;357:
5 Major Differences between Animal Models and Clinical Studies of Patients with Acute Myocardial Infarction
6 Hypothetical Construt of the Therapeutic Window for Cardioprotection Prasad A et al. Circualtion 2009; 120: 2105
7 Infarct Size: a Determinant of Mortality Gibbons et al. JACC 2004; 44:
8 New Strategies for Preventing Lethal Reperfusion Injury: An Overview on Ischemic Conditioning Ischemic Conditioning : an adaptative phenomenon which renders the myocardium more resistant to the detrimental effect of acute ischemiareperfusion injury 3 to 48 hrs Remote & POST- Conditioning Ischemia Reperfusion No Conditioning 1st & 2 Window of protection By Ischemic PRE- Conditioning Conditioned
9 Preconditioning in Humans: Prodromal angina and primary Angioplasty Angina positive p<0.05 vs ANGINA-ve Angina negative 0 Area at Risk Infarct Size EF Basal EF Control 0 Area at Risk Infarct Size EF Basal N of Chord % N of % Chord EF Control Ottani F, JACC 2005
10 Ischemic postconditioning in patients: Original description: Stat et al, Circulation 2005 Long term benefit: Thibault et al, Circulation 2008 Thibault H, Circulation 2008; Six randomized trials on IPC, 244 pts: Reduced CK (p=0.005) Increased LVEF (p=0.0001) Hansen PR, Int J Cardiol 2009
11 Protecting the heart against reperfusion injury: endogenous protection Prehospital remote ischaemic conditioning increases myocardial salvage in acute myocardial infarction. Lancet 2010;in press. Botker HE, Kharbanda RK, Schmidt MR, Bottcher M, Kaltoft AK, Terkelsen CJ, Munk K, Anderson NH, Hansen TM, Trautner S, Lassen JF, Christiansen EH, Krusell LR, Kristensen SD, Thuesen L, Nielsen SS, Rehling M, Sorensen HF, Redington AN, Nielsen TT. Intermitent arm ischemia before reperfusion Reduced reperfusion injury at PPCI
12 New Strategies for Preventing Lethal Reperfusion Injury Pre-, Post- Remote Conditioning Adenosine, Bradykinin, Opiods G proteincoupled Receptors RISK Activator (eg, ADO, EPO, Statins) PKG/PKCε Activators (eg, ANP) mptp inhibitor (eg, Cyclosporin A) mk ATP opener (eg, Nicorandil) RISK Akt/Erk PKG/PKCε NO and ROS mptp K ATP Mitochondria Yellon D. NEJM 2007;357: Reduction in Myocardial Infarction
13 Intracoronary adenosine during PCI in STEMI Randomized, placebo controlled studies Start Publ n Onset TIMI grade Dose (mg) F/U IS IS/AR ST resol No reflow Marzilli Grygier Circ 2000 AJC h h SALVAGE Jan 2006 EHJ h = = (> 4 h) = PROMISE Oct h mo COMPLETED NOV 2011
14 (p=0.016)
15 A single dose of erythropoietin in ST-elevation myocardial infarction. HEBE III study Primary endpoint Secondary endpoints. All cardiovascular events Cardiovascular death EPO, n=263 Emergency re-pci for In-stent thrombosis/reinfarction Unstable angina Control, n=266 P-value Stroke Heart failure LVEF by planar radionucleide VTG-500 MBq of 99mTc-pertechnetate mean left ventricular ejection fraction (± SD), 6 weeks after a successful primary coronary intervention. Voors A A et al. Eur Heart J 2010;31:
16 Protecting the heart against reperfusion injury: pharmacological protection csa CK release NMR imagaing
17 Studio CYCLE Efficacia della ciclosporina A nell infarto miocardico acuto riperfuso Firenze, 12 maggio, 2011
18 CYCLE inclusion criteria Male and female patients with large STEMI not older than 4 hours, defined as angina pectoris or equivalent symptoms of more than 20 minutes duration within last 4 hours, and an ST elevation in at least 3 anterior leads and/or a deviation in at least 4 inferior leads, TIMI flow 0 or 1 in identified culprit artery Intended acute primary PCI Age 18 years Ability to understand the nature, scope, and possible consequences of the study participation / legal capacity Written informed consent
19 Transfer to ER Informed consent CYCLE flow chart Coronary angiography If pt eligible, Randomization ECG (baseline), blood sampling #1: core lab. Coronary angioplasty CCU-hospital Hospital discharge 4 weeks 6 months Start infusion of CsA (over ½ min) Angioplasty (check for effective reperfusion!) 60-min ECG (primary endpoint: ST resolution) Transfer pt to CCU Morning after randomization: blood sampling #2: core lab Hospital day 4: -blood sampling #3: core lab, -echocardiography. Clinical visit Clinical visit: -blood sampling #4: core lab, -echocardiography.
20 6. Protection against reperfusion injury in STEMI is now a really promising, competitive field of translational CV research Conclusion 1. Pre, post, and remote conditioning demonstrate that reperfusion injury is a clinically relevant fact fact 2. Mechanistic and pre-clinical research should address many still open questions 3. Drugs against orphan targets have to be developed 4. Well designed and powered infarct size/area at risk proof of concept studies are still necessary 5. Initially effective interventions need to be evaluated by clinical outcome studies
21 Major Mediators of Lethal Reperfusion Injury 1. Oxygen Paradox 2. Calcium Paradox 3. ph Paradox 4. Inflammation 5. Metabolic Modulation 6. Magnesium Therapy 7. Therapeutic Hypothermia 8. Mitochondrial PTP Yellon D. NEJM 2007;357:
22 New Cardioprotective Strategies for Reducing Lethal Reperfusion Injury Yellon D. NEJM 2007;357:
23 The Time Dependent Open Artery and Open Microvascular Hypothesis Non Occlusive UA / NSTEMI Plaque rupture/erosion/fissure Platelet thrombus Occlusive STEMI TIMI 2 Flow Embolization Vasoconstriction Edema Inflammation TIMI 0 Flow Impaired tissue level perfusion Time Dependent Necrosis + Troponin / CK Arrhythmias / CHF Death
24 Infarct size Myocardial Infarction: a two-component damage Ischemia Reperfusion reperfusion injury ischemic injury coronary occlusion time
25 Mechanistic Pathway of Ischemic Conditioning Pre-, Post- Remote Conditioning Common signal transduction pathway underlying PC comprise GPCR, protein kinases, NO, ROS, mkatp, and mptp Adenosine, Bradykinin, Opiods G proteincoupled Receptors Risk Akt/Erk PKG/PKCε NO and ROS mptp K ATP Mitochondria Yellon D. NEJM 2007;357: Reduction in Myocardial Infarction
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