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Increased carotid wall stress in vascular Ehlers-Danlos syndrome.
Circulation. 2004 Mar 30; 109(12):1530-5.Circ

Abstract

BACKGROUND

Vascular Ehlers-Danlos syndrome (vEDS), also known as EDS type IV, an inherited disorder of connective tissue, results from mutations in the gene encoding type III procollagen (COL3A1). Affected patients are at risk for arterial dissection or rupture, the main cause of death. To understand the pathogenesis of the vascular lesions, we used a biomechanical approach and determined steady and pulsatile wall stress.

METHODS AND RESULTS

Sixteen patients with vEDS and 16 age-, gender-, and blood pressure-matched control subjects were included in this cross-sectional noninvasive study. Circumferential wall stress was determined under steady and pulsatile conditions at the site of an elastic (common carotid) and a muscular (radial) artery from the measurements of intima-media thickness and internal diameter with high-resolution echo-tracking systems and either mean blood pressure or pulse pressure, respectively. At the site of the carotid artery, steady circumferential wall stress was 43% higher in vEDS patients than in control subjects (68.9+/-14.3 versus 48.2+/-12.1 kPa, P<0.001), and pulsatile circumferential wall stress was 22% higher (28.2+/-7.7 versus 23.1+/-5.7 kPa, P<0.001). Carotid intima-media thickness was 32% lower (408+/-56 versus 598+/-171 microm, P<0.001) in vEDS patients, and internal diameter was not different between groups. Radial artery parameters were not significantly different between groups.

CONCLUSIONS

In vEDS patients, an abnormally low intima-media thickness generates a higher wall stress than in control subjects at the site of an elastic artery, which may increase the risk of arterial dissection and rupture.

Authors+Show Affiliations

Department of Pharmacology and INSERM EMI 0107, Hôpital Européen Georges Pompidou, Paris, France.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Comparative Study
Journal Article

Language

eng

PubMed ID

15007000

Citation

Boutouyrie, Pierre, et al. "Increased Carotid Wall Stress in Vascular Ehlers-Danlos Syndrome." Circulation, vol. 109, no. 12, 2004, pp. 1530-5.
Boutouyrie P, Germain DP, Fiessinger JN, et al. Increased carotid wall stress in vascular Ehlers-Danlos syndrome. Circulation. 2004;109(12):1530-5.
Boutouyrie, P., Germain, D. P., Fiessinger, J. N., Laloux, B., Perdu, J., & Laurent, S. (2004). Increased carotid wall stress in vascular Ehlers-Danlos syndrome. Circulation, 109(12), 1530-5.
Boutouyrie P, et al. Increased Carotid Wall Stress in Vascular Ehlers-Danlos Syndrome. Circulation. 2004 Mar 30;109(12):1530-5. PubMed PMID: 15007000.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Increased carotid wall stress in vascular Ehlers-Danlos syndrome. AU - Boutouyrie,Pierre, AU - Germain,Dominique P, AU - Fiessinger,Jean-Noël, AU - Laloux,Brigitte, AU - Perdu,Jérôme, AU - Laurent,Stéphane, Y1 - 2004/03/08/ PY - 2004/3/10/pubmed PY - 2004/7/16/medline PY - 2004/3/10/entrez SP - 1530 EP - 5 JF - Circulation JO - Circulation VL - 109 IS - 12 N2 - BACKGROUND: Vascular Ehlers-Danlos syndrome (vEDS), also known as EDS type IV, an inherited disorder of connective tissue, results from mutations in the gene encoding type III procollagen (COL3A1). Affected patients are at risk for arterial dissection or rupture, the main cause of death. To understand the pathogenesis of the vascular lesions, we used a biomechanical approach and determined steady and pulsatile wall stress. METHODS AND RESULTS: Sixteen patients with vEDS and 16 age-, gender-, and blood pressure-matched control subjects were included in this cross-sectional noninvasive study. Circumferential wall stress was determined under steady and pulsatile conditions at the site of an elastic (common carotid) and a muscular (radial) artery from the measurements of intima-media thickness and internal diameter with high-resolution echo-tracking systems and either mean blood pressure or pulse pressure, respectively. At the site of the carotid artery, steady circumferential wall stress was 43% higher in vEDS patients than in control subjects (68.9+/-14.3 versus 48.2+/-12.1 kPa, P<0.001), and pulsatile circumferential wall stress was 22% higher (28.2+/-7.7 versus 23.1+/-5.7 kPa, P<0.001). Carotid intima-media thickness was 32% lower (408+/-56 versus 598+/-171 microm, P<0.001) in vEDS patients, and internal diameter was not different between groups. Radial artery parameters were not significantly different between groups. CONCLUSIONS: In vEDS patients, an abnormally low intima-media thickness generates a higher wall stress than in control subjects at the site of an elastic artery, which may increase the risk of arterial dissection and rupture. SN - 1524-4539 UR - https://www.unboundmedicine.com/medline/citation/15007000/Increased_carotid_wall_stress_in_vascular_Ehlers_Danlos_syndrome_ L2 - https://www.ahajournals.org/doi/10.1161/01.CIR.0000121741.50315.C2?url_ver=Z39.88-2003&amp;rfr_id=ori:rid:crossref.org&amp;rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -