Authors: TELAT KELEŞ, TAHİR DURMAZ, NİHAL AKAR BAYRAM, MURAT AKÇAY, EKREM YETER, HÜSEYİN AYHAN, ENGİN BOZKURT
Abstract: Aim: Homocysteine is known to inhibit endothelial cell proliferation, which is a key event in angiogenesis. Factors responsible for the presence or absence of coronary collateral circulation are poorly understood. Therefore, in this study we investigated the effect of plasma homocysteine level on the early formation of angiographically visible collaterals after acute myocardial infarction. Materials and Methods: The study included 60 patients that had ST-segment elevation myocardial infarction (STEMI). All the patients underwent coronary angiography 1-4 days after admission (mean: 2.3 ± 1.2 days). Patients were graded according to Rentrop classification. Patients with grade 0 or 1 collateral vessels were classified as poor collaterals; patients with grade 2 or 3 collateral vessels were classified as good collaterals. Results: In all, 35 (58.3%) patients had poor collateral vessel filling and the remaining 25 (41.7%) patients had good collateral filling. Plasma homocysteine concentration in patients with poor and good collateral formation was 18.2 ± 8.6 µmol/l and 12.7 ± 2.4 µmol/l, respectively (P = 0.008). There was a negative linear correlation between Rentrop subclasses and plasma homocysteine concentration (r = –0.391, P = 0.002). We assessed the effect of demographic variables, such as age, gender, hypertension, diabetes mellitus, smoking, lipid parameters, and plasma homocysteine concentration, on the development of collaterals. The only independent variable that affected the development of collaterals was homocysteine level (OR: 0.71; 95% CI = 0.57-0.89, P = 0.003). Conclusions: This study demonstrates for the first time that there is an inverse relationship between the early development of collateral circulation after acute myocardial infarction and plasma homocysteine concentration.
Keywords: Collateral circulation, homocysteine, acute myocardial infarction
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