Present-day investigations cannot adequately determine the risk of acute coronary syndromes
1Clinical Pharmacology Unit, University of Cambridge, UK. rf226@medschl.cam.ac.uk
Insights
Current stress tests cannot identify vulnerable plaques. Pathological studies reveal plaque content, not size, determines rupture risk, offering targets for new detection methods.
Area of Science:
- Cardiology
- Pathology
- Biomedical Engineering
Background:
- Clinical stress testing (e.g., exercise electrocardiogram, stress echocardiography, coronary angiography) fails to detect vulnerable coronary plaques.
- Vulnerable plaques, a key factor in acute coronary syndromes, are often invisible to current imaging techniques.
- Pathological studies highlight thrombosis and plaque composition as critical in acute coronary syndromes.
Purpose of the Study:
- To emphasize the limitations of current stress testing in identifying vulnerable plaques.
- To highlight the importance of plaque content (lipid core, thin cap) over plaque size in determining rupture risk.
- To identify cellular and molecular features of vulnerable plaques as potential targets for new diagnostic and therapeutic strategies.
Main Methods:
- Review of landmark pathological studies on acute coronary syndromes.
- Analysis of angioscopic and necropsy findings regarding plaque rupture and thrombosis.
- Comparison of information obtained from clinical stress tests versus pathological plaque characteristics.
Main Results:
- Vulnerable plaques, characterized by a thin fibrous cap and large lipid core, are not visualized by standard stress tests.
- Plaque rupture is associated with specific cellular components (macrophages, T-lymphocytes) and enzymatic activity (matrix metalloproteinases).
- Downregulation of smooth muscle cell proliferation and collagen synthesis is observed in vulnerable plaques.
Conclusions:
- Clinical stress testing primarily assesses plaque size, not the composition that dictates rupture risk.
- Features of vulnerable plaques, such as thin caps, lipid cores, and inflammatory cell infiltration, are key targets for future diagnostic tools.
- Understanding these pathological features may lead to novel methods for detecting and potentially reversing the risk associated with vulnerable plaques.
Abstract:
It is an important irony that present-day clinical stress testing methods including exercise electrocardiogram, stress echocardiography and even coronary angiography are not able to demonstrate vulnerable coronary plaques at risk of rupture. A vulnerable plaque may in fact be invisible on clinical stress test and perhaps only visualized directly through less available techniques such as coronary angioscopy. Landmark pathological studies have deepened our understanding of the mechanisms behind acute coronary syndromes over the last decade. Thrombosis plays a key role and is a unifying feature in the pathogenesis. Platelet-rich thrombus superimposed over the disrupted atherosclerotic plaque or eroded plaque endothelium, with or without fibrin-thrombus extension, is evident in post-mortem necropsy and angioscopic studies. However features which contribute to the risk of acute events lie in the atherosclerotic plaque itself. Plaque content and not plaque size is the important factor. Clinical stress testing demonstrates plaque size but not plaque content. A plaque will be prone to rupture if it has only a thin cap and a proportionally larger lipid core. In such a plaque there is preponderance of activated macrophages and T-lymphocytes, and high activity of matrix metalloproteinases. Smooth muscle cell proliferation and collagen synthesis are downregulated. These features may serve as possible targets for devising clinical methods to detect plaques at risk or for reversing the risk in vulnerable plaques.
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