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Published on: May 3, 2018
Increased carotid artery stiffness without atherosclerotic change in patients with aortic dissection
Shinji Makita1, Atsushi Ohira, Yujiro Naganuma
1Department of Medicine II, Iwate Medical University, Morioka, Japan. makitas@seagreen.ocn.ne.jp
Insights
Aortic dissection (AD) patients show reduced arterial distensibility without severe intimal disease, unlike arteriosclerosis obliterans (ASO) or coronary artery disease (CAD). Arterial alterations in AD may include structural abnormalities, differing in subtypes like intramural hematoma (IMH) or thrombosed false lumen (TLF).
Area of Science:
- Vascular Biology
- Cardiovascular Medicine
- Medical Imaging
Background:
- Aortic dissection (AD) pathogenesis and arterial properties are not fully understood.
- Existing research often focuses on atherosclerosis, necessitating a deeper look into AD-specific arterial changes.
Purpose of the Study:
- To investigate and characterize the arterial properties in patients with aortic dissection (AD).
- To compare carotid artery ultrasonographic findings in AD patients with those in arteriosclerosis obliterans (ASO), coronary artery disease (CAD), and healthy controls (HC).
Main Methods:
- Ultrasonographic assessment of carotid artery intima-media thickness (IMT), plaque formation, luminal diameter, and distensibility.
- Comparative analysis between AD patients (n=86) and cohorts with ASO (n=151), CAD (n=163), and HC (n=77).
- Subgroup analysis within AD based on intramural hematoma (IMH), thrombosed false lumen (TLF), and coexisting abdominal aortic aneurysm (AAA).
Main Results:
- AD patients exhibited milder atherosclerotic intimal changes (IMT, plaque) compared to ASO and CAD groups.
- Luminal distensibility was reduced in AD compared to HC, but similar to ASO and CAD.
- Patients with IMH or TLF showed higher IMT; those with coexisting AAA had more severe plaque formation.
- Reduced distensibility was observed in AD without significant intimal disease.
Conclusions:
- Aortic dissection is associated with arterial alterations, including reduced distensibility and structural abnormalities, independent of severe intimal atherosclerosis.
- Specific AD subtypes (IMH, TLF, AAA) present distinct arterial characteristics, suggesting varied underlying pathogenetic mechanisms.
- Further research into these arterial properties may elucidate the initiating causes of aortic dissection.
Abstract:
The arterial properties and pathogenesis of aortic dissection remain obscure. To examine the arterial properties of patients with aortic dissection, the authors studied the ultrasonographic characteristics of the carotid artery in patients with an aortic dissection (AD, n = 86), and compared these findings with data of patients suffering from arteriosclerosis obliterans (ASO, n = 151), coronary artery disease (CAD, n = 163), and with healthy controls (HC, n = 77). Atherosclerotic intimal changes, such as intima-media thickness (IMT) and plaque formation, were milder in AD than in ASO or CAD (IMT: 0.83 +/- 0.16 vs 0.93 +/- 0.20/0.86 +/- 0.17 mm, p < 0.05; plaque number: 0.6 +/- 1.1 vs 2.7 +/- 2.4/2.5 +/- 2.1, p <0.05). Luminal diameter in AD, ASO, and CAD was significantly higher than in HC. The luminal distensibility in AD was decreased compared with HC but was the same as in ASO and CAD. Intra-AD group analysis showed that in patients with an intramural hematoma (IMH) or a dissection with a thrombosed false lumen (TLF) the IMT was higher than in patients with a classic dissection. In addition, plaque formation was more severe in AD patients with a coexisting abdominal aortic aneurysm (AAA). Reduced distensibility without severe intimal disease was found in AD. These findings suggest that patients with AD may have several arterial alterations, including structural abnormalities. Patients with IMH, TFL, or coexisting AAA may differ from patients who have a classic type of dissection or who do not have AAA, in terms of arterial characteristics including intimal disease and wall elastic property, and the initiating cause of the dissection.
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