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The effects of early coronary patency on the evolution of myocardial infarction: a prospective arteriographic study
A D Timmis1, B Griffin, J C Crick
1Department of Cardiology, Guy's Hospital, London.
Insights
Early spontaneous coronary artery patency in myocardial infarction patients reduces infarct size and improves left ventricular function. This early opening, similar to successful thrombolysis, suggests natural artery recanalization improves outcomes.
Area of Science:
- Cardiology
- Cardiovascular Research
- Interventional Cardiology
Background:
- Myocardial infarction (MI) evolution is influenced by early coronary artery patency.
- Spontaneous recanalization of the infarct-related artery may impact infarct size and left ventricular (LV) function.
- Understanding the effects of early patency is crucial for optimizing MI management.
Purpose of the Study:
- To evaluate the effects of early spontaneous coronary artery patency on the evolution of myocardial infarction.
- To compare infarct size, ST-segment changes, and creatine kinase (CK) release in patients with and without early coronary patency.
- To assess the impact of early patency on left ventricular ejection fraction (LVEF) and infarction patterns.
Main Methods:
- Coronary arteriography was performed in 41 MI patients at a mean of 3.1 hours after chest pain onset, with repeat studies at 90 minutes and 3 days.
- Patients were categorized into three groups: early patent infarct artery (Group 1), early recanalization with thrombolysis (Group 2), and persistently occluded artery (Group 3).
- Infarct location, ST-segment elevation, QRS scores, serum CK activity, LVEF, and infarction patterns (Q-wave vs. non-Q wave) were analyzed.
Main Results:
- Early spontaneous patency (Group 1) and successful thrombolysis (Group 2) showed similar patterns of ST-segment changes and CK release compared to persistent occlusion (Group 3).
- Groups 1 and 2 exhibited earlier ST-segment reduction and earlier peaking of CK activity than Group 3.
- Creatine kinase release was significantly attenuated in Group 1 (peak 1242 IU/L), with better LVEF preservation (62%) and a higher frequency of non-Q wave infarction.
Conclusions:
- Early spontaneous coronary artery patency in MI patients is associated with reduced infarct size, evidenced by attenuated CK release and preserved LVEF.
- The clinical and biochemical patterns in early spontaneous patency resemble those seen after successful thrombolytic therapy.
- These findings suggest that early coronary patency, likely due to spontaneous recanalization, significantly improves MI outcomes.
Abstract:
The effects of early spontaneous coronary patency on the evolution of myocardial infarction were evaluated in 41 patients. They had coronary arteriography (mean (SEM)) 3.1 (0.2) hours after the onset of chest pain with repeat studies 90 minutes and three days later. In 12 (29%) patients the infarct related coronary artery was patent at the first arteriogram (group 1). A further 10 patients, nine of whom received thrombolytic treatment, showed early recanalisation of the infarct related coronary artery within 90 minutes of treatment (group 2). In the remainder the infarct related coronary artery was persistently occluded (group 3). Baseline values for infarct location, the sum of ST elevation in all leads, QRS scores, and serum creatine kinase activity did not permit discrimination between the groups. Nevertheless, patterns of ST segment change and enzyme release in group 1 were closely similar to those that occurred in response to thrombolysis in group 2. Thus compared with group 3, groups 1 and 2 showed earlier 50% reduction in the sum of peak ST elevation in all leads and earlier peaking of serum creatine kinase activity. Importantly, creatine kinase release was significantly attenuated in group 1, rising to a peak serum activity (mean (SEM)) of only 1242 (415) IU/1. Analysis of angiographic left ventricular ejection fractions at three days indicated limitation of infarct size in groups 1 and 2 compared with group 3. Mean (SEM) ejection fraction, however, was best preserved in group 1 (62(6)%) and in this group the frequency of non-Q wave infarction was higher than in groups 2 and 3. Thus in patients who present with a patent infarct related coronary artery early during infarction: (a) there is a reduction in the pattern of infarct size as reflected by attenuation of release of creatine kinase, preservation of left ventricular ejection fraction, and a relatively high frequency of non-Q wave infarction; (b) patterns of ST segment change and creatine kinase release resemble those that occur after successful thrombolytic treatment, suggesting that early coronary patency is the result of spontaneous recanalisation of a previously occluded artery.