Post Conditioning in PCI for Acute ST Elevation Myocardial Infarction

• Infarct size as measured by: salvage index = total area at risk - infarct size/total area at risk [ Time Frame: 3-5 days post MI ] [ Designated as safety issue: No ]
  

• Corrected TIMI frame count (cTFC) [ Time Frame: Immediately post PCI ] [ Designated as safety issue: No ]
  
• Myocardial blush score [ Time Frame: Immediately post PCI ] [ Designated as safety issue: No ]
  
• CK release (under the curve) [ Time Frame: 1st 48 hours post MI ] [ Designated as safety issue: No ]
  
• ST segment resolution by 48 hrs compared with admission [ Time Frame: 1st 48 hours post MI ] [ Designated as safety issue: No ]
  
• MRI infarct size [ Time Frame: 3-5 days and 6 months ] [ Designated as safety issue: No ]
  
• MRI maximal transmural extent of irreversible injury [ Time Frame: 3-5 days and 6 months ] [ Designated as safety issue: No ]
  
• CMR regional end-systolic wall stress [ Time Frame: 3-5 days and 6 months ] [ Designated as safety issue: No ]
  
• CMR Myocardial perfusion [ Time Frame: 3-5 days and 6 months ] [ Designated as safety issue: No ]
  
• CMR Myocardial oxygenation [ Time Frame: 3-5 days and 6 months ] [ Designated as safety issue: No ]
  
• Peripheral endothelial function testing (brachial u/s and pulse arterial tonometry) in hospital [ Time Frame: 3-5 days post MI ] [ Designated as safety issue: No ]
  
• CMR quantification of volume of no-reflow [ Time Frame: 3-5 days and 6 months ] [ Designated as safety issue: No ]
  

Procedure: Post conditioning
4 cycles of balloon inflation /deflation (post-conditioning) within first minute of opening up artery in primary PCI for STEMI vs usual balloon inflation sequence

In patients who suffer a myocardial infarction, the blood flow usually ceases due to plaque rupture leading to thrombus formation and vessel occlusion. The resultant entity is known as ST Elevation segment myocardial infarction (STEMI) and is a significant health issue in industrialized countries. There are over 50,000 STEMI's every year in Canada and up to 10% of these patients die in hospital and another 10% die within the first year after their heart attack. The more common problem however is not death, but irreparable damage to the left ventricle leading to LV dysfunction and subsequent heart failure and arrythmias. Re-establishing blood flow promptly by administering plasminogen activators (lytics) or mechanically by performing angioplasty is possible and has lowered the mortality rate dramatically.

Although reperfusion is necessary, it gives rise to an entity known as ischemia-reperfusion where acutely re-establishing blood flow and oxygen levels of the heart has detrimental effects. Clinically this is manifested as no-reflow that causes subsequent damage to the left ventricle and decreases the beneficial affect of early reperfusion by PCI. The ischemia-reperfusion effect sets off a molecular cascade of events involving unfavorable interaction between neutrophils, platelets and endothelium, that is fairly well identified. Efforts to pharmacologically block this effect have not proven to be particularly effective.

Post conditioning follows from a concept of pre-conditioning in animals that showed a decrease in myocardial infarct size. Pre-conditioning is not useful as it requires to be performed prior to the development of ischemia/injury. Post conditioning in preliminary studies with animals and one small study in humans have shown promising results for decrease in infarct size. Post conditioning is a procedure of gradual conditioning in which the artery is opened and closed in cycles with inflation/deflation of the culprit artery followed immediately by standard PCI and placement of stent.