May 28, 2002Open Access
View Full PaperIntimomedial Interface Damage and Adventitial Inflammation Is Increased Beneath Disrupted Atherosclerosis in the Aorta
Key Result
Rupture of the internal elastic lamina was identified as an independent predictor for fibrous cap disruption in human aortic plaques (P=0.0001).
Study Design
Type
Observational (n=598)
Structured PICO
Are disrupted atherosclerotic plaques associated with increased intimomedial interface damage and adventitial inflammation compared to nondisrupted plaques?
P
Population
598 human aortic plaques classified according to the AHA classification
I
Intervention
Disrupted atherosclerotic plaques
C
Comparator
Nondisrupted atherosclerotic plaques
O
Outcome
Histopathological features including internal elastic lamina (IEL) rupture, medial and adventitial inflammation, medial fibrosis, and medial atrophysurrogate
Disrupted atherosclerotic plaques are associated with increased internal elastic lamina rupture, medial/adventitial inflammation, and medial atrophy, suggesting these changes play a role in plaque instability.
Main Result
p-value: p=0.0001
Abstract
BACKGROUND: Atherosclerotic plaque progression is frequently accompanied by compensatory enlargement to preserve the lumen. These enlarging plaques develop features of vulnerability, however, leading to disruption and lumen obstruction. This complex transition from compensatory expansion to plaque disruption may not derive solely from progressive intimal disease. Concurrent changes at the intimomedial interface and within the tunica media and adventitia may play a role in plaque instability. We tested this hypothesis by investigating whether interface changes, including internal elastic lamina (IEL) rupture, and medial and adventitial changes, including inflammation, fibrosis, and atrophy, more frequently accompany disrupted than nondisrupted atherosclerotic plaques. METHODS AND RESULTS: Computerized planimetry and ocular micrometry were used for systematic quantification of intimal, medial, and adventitial histopathological features in 598 human aortic plaques according to the AHA classification. Disrupted plaques exhibited larger plaque and lipid pool areas (P=0.0001) and a higher incidence of rupture of the IEL (P=0.0001). Medial and adventitial inflammation (P=0.01), medial fibrosis (P=0.0001), and medial atrophy (P=0.0001) were also higher in disrupted plaques. Furthermore, medial thickness was reduced in disrupted plaques (P=0.0001). Logistic regression analysis identified rupture of the IEL as an independent predictor for fibrous cap disruption (P=0.0001). CONCLUSIONS: Compared with nondisrupted plaques, disrupted plaques have an increased incidence of IEL rupture, medial and adventitial inflammation, medial fibrosis, and medial atrophy. These intimomedial interface and adventitial changes may play a role in the natural history of complex atherosclerotic lesions. The interaction between medial and adventitial pathology and the intimal atherosclerotic process deserves further investigation.