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Reduction of infarct size and heart failure in patients with ST-elevation myocardial infarction 

Danish study shows it is possible to reduce infarct size and heart failure in patients with ST-elevation myocardial infarction undergoing percutaneous coronary intervention (PCI)

Topics: Acute Coronary Syndromes (ACS)
Date: 01 Apr 2009
A Danish study has shown that it is possible to significantly reduce infarct size and heart failure in patients with ST-elevation myocardial infarction (STEMI) undergoing percutaneous coronary intervention (PCI) by repetitive interruptions of coronary blood flow applied immediately after a period of ischemia. This process is known as postconditioning.

“In general, mortality after an acute MI is high. It is very important to reduce this mortality,” said Thomas Engstrøm,DSci, Ph.D., chief consultant in the department of cardiology, Rigshospitalet, Copenhagen, Denmark, who presented this study during the American College of Cardiology’s 58th Scientific Session. “Postconditioning, which involves reopening the artery by means of a wire and a balloon for 30 seconds, and then occluding it again for four consecutive times before the artery is permanently reopened and stented, can reduce infarct size and heart failure after STEMI by slowing the reperfusion rate.”

Postconditioning has been suggested to reduce myocardial damage during PPCI in patients with ST-segment elevation myocardial infarction (STEMI). However clinical experience is limited. We examined the cardioprotective effects of postconditioning in patients treated with primary percutaneous intervention (PPCI) using cardiac magnetic resonance imaging (CMR). 118 patients with STEMI referred for PPCI were randomly assigned to have either conventional PPCI or PPCI with postconditioning. Postconditioning was performed immediately after obtained reperfusion with 4 balloon occlusions, each lasting 30 sec, followed by 30 sec of reperfusion. The primary endpoint was myocardial salvage after 3 months judged by delayed enhancement CMR.

“We found a 19% relative reduction of infarct size in the postconditioning group (51±16% of total area at risk vs. 63±17%, p=0.007), corresponding to a 31% increase in salvage ratio. No significant evidence of interaction between the impact of postconditioning and the location of the culprit lesion or size of the myocardium at risk was detected, (p=0.213 and p= 0.705).”

Clinical follow-up in 116 patients (2 patients died) showed similar levels of angina between the 2 groups, but postconditioning was associated with significantly less heart failure. After treatment, 68 patients were in NYHA class I and 27 were in class II-IV, whereas the control group had 53 patients in NYHA class I vs. 46 in class II-IV (P=0.048). Other clinical outcomes, such as repeat MI, stent thrombosis, repeat revascularization with PCI or CABG, death, and pacemaker use were comparable between groups.

In conclusion, mechanical postconditioning reduces infarct size in patients with STEMI treated with PPCI and improves functional class. The impact of mechanical postconditioning seems to be independently of the size of myocardium at risk.

Dr. Engstrøm's group is currently investigating the pharmacologic hormone analogue exenatide for use in postconditioning. For that study, both baseline and follow-up CMR are being conducted. Exenatide is an analoque of GLP 1, a hormone that is produced in the gut, which has been shown to lower blood sugar in patients with diabetes.

"We believe that it might also have a postconditioning effect. We have already shown this in animal models and now we are studying this in humans. To date we have enrolled 46 patients," states Dr.Engstrøm.

 

Authors: Thomas Engstrøm, Ph.D., chief consultant in the department of cardiology, Rigshospitalet, Copenhagen, Denmark

Co-authors
Erik Jørgensen, M.D. *; Steffen Helqvist, M.D., DMSc *; Kari Saunamäki, M.D., DMSc *; Peter Clemmensen, M.D., DMSc *; Lene Holmvang, M.D., DMSc *; Marek Treiman, M.D., Jacob T Lønborg, M.D *; Henning Kelbæk, M.D., DMSc *; Niels Vejlstrup, M.D., PhD *; DMSc **, Jan S Jensen, M.D., PhD, DMSc **; Thomas Engstrøm, M.D., PhD, DMSc *

* Department of Cardiology, The Heart Centre, Rigshospitalet, Copenhagen, Denmark
** Department of Cardiovascular Physiology, Panum Institute, University of Copenhagen, Denmark
*** Department of Cardiology, Gentofte Hospital, Copenhagen, Denmark

Notes to editor
Study presented at i2 Summit of the American College of Cardiology’s 58th Scientific Session, March 2009