BMC Cardiovascular Disorders Volume 8
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Research articleHyperhomocysteinemia and recurrent carotid stenosisRenata Hillenbrand* 1 , Andreas Hillenbrand* 2 , Florian Liewald3 and Julian Zimmermann3  1Department of Vascular and Thoracic Surgery, University of Ulm, Ulm, German 2Department of General, Visceral and Transplantation Surgery, University of Ulm, Ulm, Germany 3Department of Vascular and Thoracic Surgery, Clinic Esslingen; Esslingen a. N; Germany author email corresponding author email* Contributed equally
BMC Cardiovascular Disorders 2008,
8:1doi:10.1186/1471-2261-8-1
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| Published: |
17 January 2008 |
Abstract
Background
Hyperhomocysteinemia has been identified as a potential risk for atherosclerotic disease in epidemiologic studies. This study investigates the impact of elevated serum homocysteine on restenosis after carotid endarterectomy (CEA).
Methods
In a retrospective study, we compared fasting plasma homocysteine levels of 51 patients who developed restenosis during an eight year period after CEA with 45 patients who did not develop restenosis. Restenosis was defined as at least 50% stenosis and was assessed by applying a routine duplex scan follow up investigation. Patients with restenosis were divided into a group with early restenosis (between 3 and 18 months postoperative, a total of 39 patients) and late restenosis (19 and more months; a total of 12 patients).
Results
The groups were controlled for age, sex, and risk factors such as diabetes, nicotine abuse, weight, hypertension, and hyperlipidemia. Patients with restenosis had a significant lower mean homocysteine level (9.11 μmol/L; range: 3.23 μmol/L to 26.49 μmol/L) compared to patients without restenosis (11.01 μmol/L; range: 5.09 μmol/L to 23.29 μmol/L; p = 0.03).
Mean homocysteine level in patients with early restenosis was 8.88 μmol/L (range: 3.23–26.49 μmol/L) and 9.86 μmol/L (range 4.44–19.06 μmol/L) in late restenosis (p = 0.50).
Conclusion
The finding suggests that high plasma homocysteine concentrations do not play a significant role in the development of restenosis following CEA. |