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Postconditioning with Lactate-enriched Blood for Cardioprotection in ST-segment Elevation Myocardial Infarction
Published on: May 28, 2019
[Acute coronary occlusion during transluminal angioplasty: role of coronary thrombosis]
1Servizio di Cardiologia, Ospedale Civile Maggiore, Verona.
Insights
Transluminal coronary angioplasty complicated by thrombus formation can be successfully managed conservatively. Conservative treatment with thrombolytics, anticoagulants, and platelet inhibitors restored vessel patency in these cases.
Area of Science:
- Cardiology
- Interventional Cardiology
- Thrombosis
Background:
- Intracoronary thrombus formation can complicate transluminal coronary angioplasty (TCA).
- Successful mechanical dilatation may paradoxically activate thrombotic processes, leading to vessel occlusion.
Observation:
- Two patients undergoing TCA presented with baseline intracoronary thrombus.
- Mechanical dilatation led to clot proliferation and vessel occlusion in both cases.
- Intracoronary streptokinase partially slowed but did not inhibit the thrombotic process or restore patency.
Findings:
- Conservative management with anticoagulants and platelet inhibitors, alongside thrombolytic therapy, resulted in patent coronary arteries at short-term angiography.
- One patient experienced moderate myocardial enzyme release, while the other did not.
Implications:
- Acute coronary occlusion during TCA caused by identified thrombus can be managed conservatively with thrombolytic therapy.
- This approach may obviate the need for emergency coronary surgery, especially if occlusion is short-lived or collateral circulation is adequate.
- Spontaneous activation of lytic systems can restore vessel patency, potentially preventing myocardial infarction.
Abstract:
We here report on 2 patients treated by transluminal coronary angioplasty, who presented baseline angiographic aspects of an intracoronary thrombus upon vessel stenosis. In both cases mechanical dilatation was successful in increasing vessel diameter, but was complicated by activation of the thrombotic process with clot proliferation--as shown by multiple coarse filling defects irregularly stained by contrast material--and vessel occlusion. The intracoronary injection of streptokinase achieved partial slowing of the thrombotic process, but did not succeed in inhibiting it completely or in restoring vessel patency. As clinical conditions were stable, the patients were not sent to emergency surgery, but were treated conservatively with anticoagulants and platelet inhibitors: in only one patient the procedure was followed by moderate myocardial enzyme release. In both cases the coronary artery was patent at short term angiographic control. These 2 cases confirm that in the outset of transluminal angioplasty an acute coronary occlusion can be managed conservatively by thrombolytic treatment when thrombus formation can be clearly identified the cause of vessel occlusion: the activation of spontaneous lytic systems can completely restore vessel patency. If coronary occlusion was of short duration or collateral supply was adequate, myocardial infarction may not occur and emergency coronary surgery will not be necessary.
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