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Updated: Aug 4, 2026
Myocardial Infarction and Functional Outcome Assessment in Pigs
Published on: April 25, 2014
[Peri-infarct angiographic behavior of "non-culprit" coronary infarct lesions]
A Loaldi1, M Bussotti, L Grancini
1Istituto di Cardiologia, Università degli Studi, Milano.
Insights
Myocardial infarction may stem from systemic coronary disease activity, not just local plaque events. This research suggests widespread coronary artery changes contribute to heart attacks, impacting non-culprit lesions significantly.
Area of Science:
- Cardiology
- Vascular Biology
- Pathophysiology
Background:
- Systemic factors like lipoproteins and infections may influence plaque rupture and coronary occlusion.
- The origin of thrombosis in coronary artery disease is debated: a local plaque event versus systemic coronary tree activity.
Purpose of the Study:
- To investigate whether coronary thrombosis is solely a local plaque event or a manifestation of systemic coronary artery disease activity.
- To compare coronary angiography findings in patients with first myocardial infarction versus those with stable angina.
Main Methods:
- Coronary angiography was performed early (days) and late (1 month) in 23 patients with first infarction.
- Changes in non-culprit lesions (>0.27 mm) were assessed for progression or regression.
- Findings were compared to a control group of stable angina patients undergoing repeat angiography after 1 month.
Main Results:
- Infarction patients showed significantly more progression (16/23) and regression (4/23) in non-culprit lesions compared to stable angina patients (2/23 progression, 1/23 regression).
- Progression was observed in 17/45 non-culprit lesions in the infarction group versus 2/45 in the stable angina group.
- Three infarction patients with interim angina at rest showed progression of a culprit lesion.
Conclusions:
- Results support the hypothesis that myocardial infarction can result from systemic coronary disease activity, not just isolated plaque events.
- The findings suggest that the 'offending plaque' may represent the maximal expression of a broader systemic process affecting the entire coronary tree.
Abstract:
Because systemic factors, such as lipoproteins, autoantigens, infectious agents, may facilitate plaque rupture, thrombus formation and coronary occlusion, the question may arise of whether thrombosis be only a local plaque event or the consequence of an acute activity of the entire coronary tree. Taking changes at the narrowest point of non culprit lesions as reflecting progression or regression of the disease when > 0.27 mm, early (within a few days) and late (within 1 month) coronarographic findings in 23 patients with first infarction were compared with those of patients with stable angina, in whom coronary angiography was performed for diagnostic purposes and was repeated 1 month later, before angioplasty. Sixteen infarction patients had progression, 4 had regression, 1 had both, and 2 had steadiness; corresponding values in stable angina group were 2 (p < 0.001), 1 (NS), 0 (NS) and 20 (p < 0.001). In the infarction group, 17 out of the 45 non culprit lesions progressed and 5 regressed; corresponding figures in stable angina group were 2 (p < 0.001) and 1 (p < 0.05). Three of the infarction patients developed interim angina at rest that was associated with progression of a culprit lesion in each of them. These results support the hypothesis that in a number of cases infarction may not reflect an arbitrary plaque event but rather a systemic coronary disease activity with maximal expression at the level of the offending plaque.
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