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Intracoronary thrombus in syndromes of unstable myocardial ischemia
Insights
Intracoronary thrombi were observed in patients experiencing unstable myocardial ischemia without infarction. These thrombi appeared as filling defects in coronary arteries, suggesting a role in acute coronary syndromes.
Area of Science:
- Cardiology
- Interventional Cardiology
- Vascular Medicine
Background:
- Coronary thrombosis is typically associated with transmural myocardial infarction.
- Recent observations suggest intracoronary thrombi may also occur in unstable myocardial ischemia without infarction.
Observation:
- The study reviewed angiograms of 129 patients with unstable angina or intermediate coronary syndrome.
- Eight patients (6.2%) exhibited intracoronary filling defects consistent with thrombus.
- These defects were located distal to severe coronary stenosis (80-99%) in well-opacified vessels.
Findings:
- The observed defects were hazy, nonoccluding, or nonopacified, consistent with thrombus.
- Repeat angiography in three patients showed defect enlargement, and two experienced fragment embolization.
- Angiographic characteristics were similar to defects seen after streptokinase recanalization.
Implications:
- Intracoronary thrombus may be a significant finding in unstable myocardial ischemia.
- These findings challenge the traditional view linking thrombus solely to transmural infarction.
- Further research is warranted to understand the role and management of thrombus in non-ST elevation acute coronary syndromes.
Abstract:
The association of coronary thrombosis and transmural myocardial infarction is well documented. We have recently observed apparent intracoronary thrombi in patients with unstable myocardial ischemia without transmural infarction. To assess the frequency and angiographic characteristics of intracoronary defects consistent with thrombi, we reviewed the angiograms of all patients undergoing catheterization within 1 month of the onset of unstable angina or the intermediate coronary syndrome. Of 129 such patients, eight (6.2%) had nonoccluding, hazy, or nonopacified intracoronary filling defects consistent with thrombus in angiographically well-opacified vessels. All defects were just distal to a significant (80% to 99%) coronary stenosis. In each instance the thrombus-involved vessel supplied a myocardial segment referable to the electrocardiographically defined area of ischemia. Support for the theory that the intracoronary defects were thrombi includes three patients with enlargement of the filling defects, who underwent repeat angiography within 7 days, and two patients with embolization of defect fragments. Furthermore these defects were angiographically similar to poststenotic intraluminal defects seen transiently in some patients after partial intracoronary streptokinase recanalization. In conclusion, we have observed, angiographically, intracoronary filling defects consistent with thrombus in some patients with unstable myocardial ischemia.