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Intracoronary thrombus in nontransmural myocardial infarction and in unstable angina pectoris
Insights
Intracoronary thrombus formation is implicated in myocardial infarction (MI). This study investigated its role in unstable angina (UA) and non-transmural MI, finding evidence of thrombolysis in these conditions.
Area of Science:
- Cardiology
- Interventional Cardiology
- Vascular Medicine
Background:
- Intracoronary thrombus is a known factor in acute transmural myocardial infarction (MI).
- The role of intracoronary thrombus in unstable angina (UA) and non-transmural MI remains unclear.
- Understanding thrombus formation in these syndromes is crucial for effective treatment strategies.
Purpose of the Study:
- To investigate the presence and significance of intracoronary thrombus in patients with unstable angina and non-transmural MI.
- To assess the response to intracoronary interventions aimed at thrombus dissolution.
Main Methods:
- Coronary arteriography was performed in 17 patients presenting with unstable angina or non-transmural MI.
- Interventions included intracoronary nitroglycerin and streptokinase infusion.
- Vessel patency, stenotic diameter, and intracoronary filling defects were assessed before, during, and after infusions.
Main Results:
- Intracoronary nitroglycerin showed limited response in patients with non-transmural MI and UA.
- Streptokinase infusion resulted in vessel opening, increased diameter, or defect dissolution in several patients with non-transmural MI and UA.
- Evidence of thrombolysis was observed within one week of symptom onset; no thrombolysis was seen in later studies.
Conclusions:
- Intracoronary thrombus formation appears to play a significant pathogenetic role in a subset of patients with unstable angina and non-transmural MI.
- Thrombolysis with streptokinase demonstrates the presence of intracoronary thrombi in these syndromes.
- The timing of intervention is critical, as thrombolytic evidence diminishes after one week.
Abstract:
Although intracoronary thrombus formation plays a major role in acute transmural myocardial infarction (MI), its occurrence in unstable angina (UA) and nontransmural MI has not clearly been established. To determine whether intracoronary thrombus does occur in these syndromes, coronary arteriography was performed before, during, and after intracoronary nitroglycerin and streptokinase infusion in 17 patients. None of the 8 patients with nontransmural MI and 1 of the 9 patients with UA responded to intracoronary nitroglycerin. Seven of 8 patients with nontransmural MI and 4 of 9 patients with UA responded to streptokinase infusion with opening of an occluded vessel, an increase in stenotic diameter, dissolution of an intracoronary filling defect, or a combination of these. Serial opening and closing of ischemia-related vessels occurred spontaneously and in response to streptokinase in some patients in whom thrombolysis was demonstrated. Evidence of thrombolysis was not seen in any patient studied longer than 1 week from the onset of the rest pain syndrome. The finding of thrombolysis in several patients with nontransmural MI and UA suggests that intracoronary thrombus formation plays a pathogenetic role in some patients with these ischemic syndromes.