Hyperhomocysteinemia and recurrent carotid stenosis

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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).

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).

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 class=entity>μmol/L; range: 3.23 μmol/L to 26.49 μmol/L) compared to patients without restenosis (11.01 μmol/L; range: 5.09 class=entity>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).

The finding suggests that high plasma homocysteine concentrations do not play a significant role in the development of restenosis following CEA.


Compared to the best medical therapy, carotid endarterectomy (CEA) or eversions-endarteriectomy has been identified as preferred treatment for symptomatic and asymptomatic patients with high-grade extra cranial carotid stenosis [1].

The long term follow-up of such patients indicates however, that a recurrent stenosis may occur in up to 36% of patients [2], but the incidence of carotid restenosis (CR) is variable and in part dependent on the definition of restenosis and the technique used to calculate its incidence.

Symptomatic or asymptomatic CR is generally attributed to neointimal hyperplasia during the early postoperative period (within 36 months) or recurrent atherosclerosis thereafter [2]. Late CR lesions are indistinguishable from primary atherosclerosis. Neointimal hyperplasia is an intensely studied hyperpalstic reaction in the arterial wall. On gross as well as angiographic or duplex ultrasound interrogation, neointimal hyperplasia is generally smooth in appearance. The exact mechanisms for neointimal hyperplasia are still being investigated, but homocysteine seems to contribute to increased neointimal hyperplasia [3].

Homocysteine is a sulfhydryl amino acid. Its precursor, the essential amino acid methionine, is derived from dietary proteins./>/>/>/>/>/>/>



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