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Clinically stable angina pectoris is not necessarily associated with histologically stable atherosclerotic plaques
A C van der Wal1, A E Becker, K T Koch
1Department of Cardiovascular Pathology, University of Amsterdam, Netherlands.
Insights
Inflammation in coronary artery plaques is lower in patients with stable angina compared to unstable angina. However, some stable angina patients have unstable plaque characteristics, indicating a need for further plaque assessment.
Area of Science:
- Cardiovascular Medicine
- Pathology
- Immunology
Background:
- Coronary artery disease (CAD) is a leading cause of mortality worldwide.
- Plaque inflammation plays a critical role in the pathogenesis of CAD.
- Understanding the relationship between plaque characteristics and clinical presentation is crucial for risk stratification and treatment.
Purpose of the Study:
- To investigate the extent of plaque inflammation in culprit lesions of patients with chronic stable angina.
- To compare inflammatory markers in plaques of patients with stable angina versus those with unstable angina.
Main Methods:
- Retrospective study of 58 patients undergoing directional coronary atherectomy.
- Patients were categorized into chronic stable angina (Group 1), unstable angina Braunwald class II (Group 2), and unstable angina Braunwald class III (Group 3).
- Histological analysis quantified areas of smooth muscle cells, macrophages, T cells, and HLA-DR positive cells within culprit lesions.
Main Results:
- Areas rich in smooth muscle cells were larger in stable angina patients compared to unstable angina patients (p < 0.004 for Group 1 vs. Group 3).
- Macrophage, T cell, and HLA-DR positive cell areas were significantly smaller in stable angina patients than in unstable angina patients (p < 0.02 for Group 1 vs. Group 2, p < 0.001 for Group 1 vs. Group 3).
- Despite these differences, considerable overlap in inflammatory markers was observed between groups.
Conclusions:
- The findings support the concept that reduced plaque inflammation is associated with clinical plaque stabilization.
- However, the overlap in histological findings suggests that some patients with clinically stable angina may have histologically unstable plaques.
- Further research into plaque characteristics is warranted for improved risk assessment in angina patients.
Objective:
To investigate the extent of plaque inflammation in culprit lesions of patients with chronic stable angina.
Design:
Retrospective study.
Setting:
Amsterdam reference centre.
Subjects:
89 consecutive patients who underwent directional coronary atherectomy, 58 of whom met the following inclusion criteria: chronic stable angina (Canadian Cardiovascular Society classification 1-3 (group 1, n = 28)); unstable angina (Braunwald class II (group 2, n = 18)); unstable angina (Braunwald class III (group 3, n = 12)).
Interventions:
Directional atherectomy in patients with angina pectoris.
Main Outcome Measures:
Tissue areas of culprit lesions occupied by inflammatory cells and smooth muscle cells related to clinically defined ischaemic syndrome.
Results:
Areas (% of total surface area (mean (SEM)) rich in smooth muscle cells were larger in patients with chronic stable angina (group 1, 51.2 (20.9)) than in those with unstable angina (group 2, 42.1 (20.5); group 3, 29.5 (19.4)) (1 v 2 and 2 v 3, NS; 1 v 3, P < 0.004). Macrophage rich areas were significantly smaller in patients with stable angina (group 1, 21.8 (11.9)) than in those with unstable angina (group 2, 31.5 (14.6); group 3, 46.4 (16.7)) (1 v 2, P < 0.02; 2 v 3, P < 0.02; 1 v 3, P < 0.001). Mean numbers of T cells per mm2 were as follows: group 1, 17 (9.4); group 2, 25 (15.9); group 3, 41 (30.6) (1 v 2, P 0.04; 2 v 3, P 0.07; 1 v 3, P < 0.001). Areas with HLA-DR positive cells showed the same pattern as macrophages and T cells and were smaller in stable (29.9 (12.4)) than in unstable angina (group 2, 40.4 (17.6); group 3, 52.4 (12.0)) (1 v 2, P < 0.02; 2 v 3, P < 0.05; 1 v 3, P < 0.001).
Conclusion:
The inverse relation between the extent of inflammatory activity in plaque tissues of culprit lesions and the clinical stability of the ischaemic syndrome supports the concept that reduction of inflammation favours plaque stabilisation. At the same time, the considerable overlap between groups indicates that patients with clinically stable angina do not all have histologically stable plaques.