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Review
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Korean J Med. 2006;71(1):296-296.
- Left Ventricular Wall Rupture After Pecutaneous Coronary Stenting Following Acute Myocardial Infarction: a case report
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- Left Ventricular Wall Rupture After Pecutaneous Coronary Stenting Following Acute Myocardial Infarction: a case report
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1Department of Internal Medicine, Hanyang University College of Medicine, Seoul; 2Department of Life Science, Postech Biotech Center, Pohang University of Science and Technology, Pohang, Korea
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- Abstract
- We report the case of a 62-year-old hypertensive women, who had left ventricular free wall rupture immediately after delayed
percutaneous revascularization following acute myocardial infarction. She was admitted for 3 hour chest pain. Her
electrocardiogram showed ST elevation in lead 2, 3 and aVF, and reciprocal ST depression in lead1, aVL and V1-3. Thrombolytic
agent was infused immediately. Chest pain was relieved and ST elevation in inferior lead was decreased to baseline after
thrombolytic therapy. We did coronary angiography on 5 day after admission and observed near total obstruction in distal right
coronary artery with collateral flow from left descending artery. We decided to do percutaneous revascularization because
collateral circulation was well developed and may have viable myocardium. PTCA guidewire was easily passed via obstructed
lesion and ballooning with 2.5 × 20 mm size was done. The patient still complaint chest discomfort after deflation of balloon.
We suspected distal embolization and started to infuse glycoprotein IIbIIIa blocking agent(Agarastat ). We also put stent the
lesion. A few second later, the patients developed syncope and severe hypotension, and electrocardiogram was not changed. We
comfirmed passage of contrast to the distal arterial bed, but there was no extravasation of contrast to the pericardium.
Echocardiography showed pericardial effusion. We did pericardiocentesis and resucitation measures and transfer the patient to
the operation room. Cardiac surgean observed 2 cm sized free wall rupture and necrotic, infarcted muscle in inferior portion and
repaired with Dacron. After cardiac surgery, the patients was hemodynamically supported by artificial assist device (T-PLS) and
occured death at 3 days after emergency operation. Considering etiology of rupture immediately after revascualrization, we can
not exclude the effect of acute reperfusion injury or possibility of unrecognized, aborted rupture before procedure or effect of
thrombolytic and glycoprotein IIbIIIa blocing agent on hemorrhagic transformation in infarcted myocardium. This case highlights
the importance of reperfusion injury and careful examination of aborted cardiac rupture
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