Elevated plasma homocysteine levels in patients with isolated coronary artery ectasia

OBJECTIVE: Coronary artery ectasia is a variant of coronary atherosclerosis. Hyperhomocysteinemia has emerged as a major, independent risk factor for cardiovascular diseases. The purposes of this study were to determine plasma hyperhomocysteine levels in patients with coronary artery ectasia, and to compare patients with coronary artery ectasia, coronary artery disease, and controls with normal coronary angiogram. METHOD: The study population included 37 patients with coronary artery ectasia and 36 patients with coronary artery disease. The control group consisted of 32 patients with angiographically proven normal coronary arteries. Plasma hyperhomocysteine levels were measured in all study patients with an enzyme-linked immunosorbent assay. RESULTS: Plasma homocysteine levels were significantly higher in patients with both coronary artery ectasia and coronary artery disease than in the controls (14.8+/-1.1 and 15.9+/-0.8 vs. 2.5+/-0.6 micromol/l; P<0.001 and P<0.001, respectively). No significant differences in plasma homocysteine levels were found among CAE and CAD groups (P>0.05). CONCLUSIONS: We have demonstrated that patients with coronary artery ectasia and coronary artery disease have increased plasma hyperhomocysteine levels compared with the controls. These findings suggest that hyperhomocysteinemia may play an important role in the pathogenesis of coronary artery ectasia as in coronary artery disease.     

Increased plasminogen activator inhibitor-1 levels in patients with isolated coronary artery ectasia

Isolated coronary artery ectasia (ICAE) is defined as the ectasia of the coronary arteries without concomitant coronary artery stenosis. The etiology and the clinical course of ICAE are still not clear. Increased levels of plasminogen activator inhibitor-1 (PAI-1) inhibit vasa vasorum, leading to diminished vessel wall supply and thus contributes to aortic aneurysm expansion. Whether the same process has role in coronary artery ectasia is not known. The aim of this study is to investigate the association between PAI-1 and coronary artery ectasia in patients without concomitant obstructive coronary artery disease. Among 2830 patients who underwent coronary angiography between March 2010 and 2011, 55 patients (40 male, 15 female, mean age 60?±?8?years) with ICAE, formed our study group. 27 patients with similar patient characteristics, with angiographically proven normal coronary arteries, were enrolled as the control group. The basal characteristics were similar between two groups. PAI-1 levels were statistically higher in the ICAE group compared to the control group (104.13?±?56.65 and 63.39?±?35.01?ng/dl, respectively) (P?=?0.008). A significant positive correlation between CAE and PAI-1 (r?=?0.358, P?=?0.007) was also demonstrated. Serum high sensitive C reactive protein (hsCRP) levels did not differ between two groups (P?>?0.05). The plasma PAI-1 levels were significantly higher in ICAE patients compared to normal coronary artery group. Increased PAI-1 levels may diminish vasa vasorum by antiangiogenic activity leading to coronary ectasia.     

Neutrophil gelatinase-associated lipocalin levels in isolated coronary artery ectasia

Background

The pathophysiology of coronary artery ectasia (CAE) is still unknown. Inflammation and degradation of connective tissue may have a role in the development of coronary ectasia. In the present study, the authors examined neutrophil gelatinase-associated lipocalin (NGAL) levels in isolated CAE patients.

Methods

Thirty-five patients with isolated CAE (25 males; mean age, 59 ± 10 years) and 35 age- and sex-matched healty volunteers (22 males; mean age, 57 ± 11 years) who had been shown to have normal coronary arteries were included in the study. Basal characteristics were recorded. Serum NGAL levels were determined with an enzyme-linked immunosorbent assay kit.

Results

NGAL levels were significantly higher in the isolated CAE group than in the control group (65.1 ± 13 vs 53.7 ± 19 ng/mL; P = 0.006). There were also significant difference in NGAL levels according to the number of ectatic coronary arteries (58.1 ± 13, 70.9 ± 9, and 71.1 ± 11 ng/mL for 1, 2, and 3 arteries, respectively; P = 0.015). Level of NGAL was lowest in patients who have only 1 ectatic coronary artery.

Conclusion

Serum NGAL levels increased in patients with isolated CAE, and NGAL may play a crucial role in the development and/or progression of coronary artery ectasia.     

Increased platelet activity in patients with isolated coronary artery ectasia

BACKGROUND: The common coexistence with coronary artery disease has led to the suggestion that coronary artery ectasia (CAE) is a variant of coronary artery disease. The mechanisms, however, responsible for CAE formation during the atherosclerotic process and the exact clinical significance are not well known. In this study, we aimed to investigate platelet activity in patients with isolated CAE by using specific markers of platelet activation as P-selectin, beta-thromboglobulin (beta-TG) and platelet factor 4 (PF4). METHODS: Thirty-two patients with isolated CAE without significant stenosis and 30 control participants with angiographically normal coronary arteries were included in this study. According to the angiographic definition used in the Coronary Artery Surgery Study, a vessel is considered to be ectasic when its diameter is > or = 1.5 times that of the adjacent normal segment in segmental ectasia. Plasma P-selectin, beta-TG and PF4 levels were measured in all patients and control participants using enzyme-linked immunosorbent assay method. RESULTS: Patients with isolated CAE were detected to have significantly higher levels of plasma P-selectin, beta-TG and PF4 in comparison with control participants with angiographically normal coronary arteries (P-selectin: 248+/-46 vs. 154+/-32 ng/ml, respectively, P<0.001; beta-TG: 51+/-19 vs. 21+/-9 ng/ml, respectively, P<0.001; PF4: 58+/-23 vs. 33+/-11 ng/ml, respectively, P<0.001). CONCLUSION: In conclusion, we have shown for the first time that patients with isolated CAE have raised levels of plasma P-selectin, beta-TG and PF4 compared with control participants with angiographically normal coronary arteries, suggesting increased platelet activation in patients with CAE.     

Plasma interleukin-6 levels are increased in coronary artery ectasia

OBJECTIVE: Recent studies have suggested a cytokine-induced tissue inflammation in the pathogenesis of abdominal aortic aneurysms and it has been documented that circulating interleukin-6 (IL-6) levels in these patients are increased. The aim of this study was to investigate whether a similar association also exists for patients with coronary ectasia, which may also be regarded as an abnormal dilatation of the arterial system. METHODS AND RESULTS: The study group was composed of 43 patients with coronary ectasia and 48 patients with normal coronary arteries constituted the control group. Coronary diameters were measured by quantitative angiography. A coronary diameter index was defined for each segment as the coronary diameter divided by the body surface area (BSA). A coronary segment with a diameter index of more than 1.5 fold of the control group was defined as ectatic. Baseline characteristics of the two groups were similar. Serum IL-6 levels were significantly higher in patients with coronary ectasia (5.18 +/- 2.04 pg/ml vs. 4.13 +/- 0.5 pg/ml, p = 0.002). There was no significant correlation with the maximal diameter of the most dilated coronary segment and IL-6 levels in patients with coronary ectasia (r = 0.10, p = 0.50). CONCLUSIONS: Results of this study have demonstrated increased levels of circulating IL-6 in patients with coronary ectasia which might indicate a possible role of inflammatory processes. Absence of a significant correlation between the dimensions of the ectatic segments and IL-6 levels might be due to the narrower range of the diameters of the coronary arteries compared with the abdominal aorta.     

Carotid intima-media thickness in patients with isolated coronary artery ectasia

OBJECTIVE: Carotid artery intima-media thickness (IMT) is now widely used as a surrogate marker for atherosclerotic disease. Carotid IMT measured by ultrasound has been shown to be correlated with coronary artery disease as defined by angiography. However, the relation between carotid IMT and isolated coronary artery ectasia (CAE) has not been investigated. The aim of our study was to assess this relation. METHODS: Twenty-five patients with isolated CAE without stenosis and 25 control subjects with angiographically normal coronary arteries were included in this study. These were examined by B-mode ultrasound to measure the IMT at the far wall of the common carotid artery. RESULTS: Patients with isolated CAE had significantly higher carotid IMT compared to control subjects with angiographically normal coronary arteries (0.95+/-0.12 versus 0.71+/-0.10mm respectively, p<0.0001). In addition, we detected a significant positive correlation between the presence of CAE and carotid IMT (r=0.748, p<0.001). CONCLUSION: We have shown for the first time an association between increased carotid IMT and isolated CAE, suggesting that atherosclerosis may be involved in the pathogenesis of isolated CAE in the adult population.     

Mean platelet volume in patients with isolated coronary artery ectasia

Coronary artery ectasia (CAE) is frequently considered to be an incidental angiographic finding; however, several reports have shown an association with myocardial ischemia and infarction. In this study, we aimed to evaluate the mean platelet volume (MPV), which is a marker of platelet reactivity, in patients with isolated CAE. In this study we investigated the platelet functions by MPV measurement in patients with isolated CAE. The study population consisted of 23 patients (17 males, 6 females) with isolated CAE (Group-I). Sex-age matched 30 patients (22 males, 8 females) with angiographically proven normal coronary arteries served as the control group (Group-II). Serum total cholesterol, HDL-C, LDL-C, triglyceride level, hemoglobin, white blood cell count, CRP, platelet count and MPV were compared in both groups. There was no significant difference between two groups in terms of age, gender, body mass index, blood pressure and heart rate. Serum total cholesterol, HDL-C, LDL-C, triglyceride level, hemoglobin, white blood cell count, platelet count were also similar in both groups. However, the MPV values of patients with isolated CAE were significantly higher than those of controls (P < 0.0001). In addition to that, CRP levels were found to be significantly higher in patients with isolated CAE (P < 0.002). Increased MPV may indicate the altered platelet reactivity and aggregation and thereby may be associated with ischemic events, observed in patients with isolated CAE.     

Plasma homocysteine levels in patients with early coronary artery stenosis and high risk factors

The aim of this study was to study the relationship between plasma homocysteine (Hcy), folic acid, vitamin B12 and early coronary artery disease (early-CAD) and high coronary risk factors. The plasma Hcy levels of 58 cases with early-CAD and 31 subjects without CAD were measured using high-performance liquid chromatography (HPLC) with fluorescence detection. Plasma folic acid and Vitamin B12 levels were measured with radioassay method. The plasma Hcy level was significantly higher in the early-CAD patients than in the controls [(13.7 +/- 5.1) micromol/L vs (10.3 +/- 5.7) micromol/L]. The plasma folic acid and Vitamin B12 levels were significantly lower in the early-CAD patients than in the controls. The plasma Hcy level was higher in patients with more than 3 risk factors of CAD than in patients with 1 or 2 risk factors and in the controls [(17.3 +/- 5.1) micromol/ L vs (12.9 +/- 4.8) micromol/L, (7.8 +/- 2.5) micromol/L]. Other than gender, all classical coronary risk factors were related to the elevated Hcy level. Hcy levels were elevated in patients with early-CAD and with high risk factors. Hyperhomocysteinemia plays an important role in the pathogenesis of CAD.     

Adiponectin levels in coronary artery ectasia

Etiopathogenesis of coronary artery ectasia (CAE), which is defi ned as abnormal dilatation of a segment of the coronary artery to 1.5 times of an adjacent normal coronary artery segment, is unclear. However, it is speculated that CAE develops in the atherosclerosis process through degeneration of coronary artery media layer. Our objective in this study is to compare levels of adiponectin between cases with CAE and normal coronary anatomy, and to examine whether adiponectin plays a role in CAE etiopathogenesis. The study registered a total of 66 cases, consisting of CAE cases (group 1, n = 36) and cases with normal coronary anatomy (group 2, n = 30). Taking coronary artery diameters of the control group cases as the reference, patients with abnormal segments 1.5 times larger than the adjacent segments were accepted as CAE. Serum adiponectin levels were 4.31 ± 2.02 μg/ml in group 1 and 6.73 ± 4.0 μg/ml in group 2 (P = 0.02). High-sensitivity Creactive protein was 4.8 ± 3.8 mg/l in group 1 and 3.6 ± 3.4 mg/l in group 2 (P > 0.05). There was a negative correlation between ectatic coronary artery diameter and plasma adiponectin level (P = 0.03; r = −0.339). It was known that adiponectin levels dropped in atherosclerotic heart disease. In this study we found low plasma adiponectin levels in acquired CAE, attributed to atherosclerosis. Therefore, we think that adiponectin might be playing a role in etiopathogenesis and progression of CAE. This in turn may indicate that hypo-adiponectinemia may be useful in revealing a realized risk in CAE. However, larger, randomized, multicenter studies are required to examine the role of adiponectin in the development of CAE.     

Plasma total homocysteine levels in postmenopausal women with unstable coronary artery disease

An elevated plasma total homocysteine (tHcy) level is considered a risk factor for coronary artery disease (CAD), but the relationship between plasma tHcy and well-defined CAD in women is still unclear. Plasma tHcy concentrations and the covariates serum folate, vitamin B12, and creatinine were analysed in 157 angiographically examined postmenopausal women with unstable CAD and in 101 healthy controls. At coronary angiography, 16% had normal vessels and 84% had coronary atherosclerosis. Mean plasma tHcy concentration (micromol/l, 95% confidence interval) did not differ in patients compared to controls (13.1 (12.3-13.8) vs. 12.5 (11.6-13.5)) or in patients with or without coronary atherosclerosis (13.3 (12.4-14.1) vs. 12.0 (10.8-13.2)). A trend to an increasing plasma tHcy with increasing degree of coronary atherosclerosis was attenuated after adjustment for age and the previous mentioned covariates. Odds ratio for the risk of coronary artery disease and coronary atherosclerosis in hyperhomocysteinemic patients (> or =90th percentile in controls) was approximately 3. However, the confidence interval included unity in half of the groups and the significance was therefore difficult to judge. Receiver operating characteristics showed age to be the only variable with a significant discriminatory ability regarding the presence of coronary atherosclerosis (area 0.77). Mild hyperhomocysteinemia seems not to be related to the risk of unstable CAD in postmenopausal women. The trend towards higher plasma tHcy with increasing degree of coronary atherosclerosis may be a marker of the disease. In future studies adjustment for age and the other three covariates should be considered.     

Comparison of C-reactive protein levels in patients with coronary artery ectasia versus patients with obstructive coronary artery disease

This study evaluated plasma C-reactive protein (CRP) levels, a specific marker of inflammation, in 32 patients with isolated coronary artery ectasia (CAE) and compared the results with those of 32 patients with obstructive coronary artery disease without coronary artery ectasia and 30 subjects with angiographically normal coronary arteries. CRP levels were found to be significantly higher in patients with isolated CAE (p <0.001), suggesting that more severe inflammation may be involved in the pathogenesis of CAE.     

Plasma homocysteine levels and the left ventricular systolic function in coronary artery disease patients

BACKGROUND: Numerous studies have shown a relationship between hyperhomocysteinemia, atherothrombosis and cardiovascular mortality. However, an association between hyperhomocysteinemia and the extent of coronary artery disease (CAD) remains controversial whereas its relationship with left ventricular systolic function has not been established. METHODS: One hundred and fifty-seven patients with angiographically defined CAD were included. The relationships between hyperhomocysteinemia, severity of CAD and left ventricular systolic function were studied. Left ventricular systolic function was determined primarily by ventriculography. The severity of CAD was determined through coronary angiography using the Gensini score and the number of vessels with > or = 50% stenosis. RESULTS: The mean fasting plasma homocysteine level was 13.4 mumol/l+/-0.5 SE. Elevated levels of homocysteine correlated significantly with increased severity of CAD both by the Gensini scores (r-value = 0.344, P < 0.0005) and the total number of diseased vessels (r-value = 0.387, P < 0.0005). The patients with hyperhomocysteinemia were found to have significantly reduced left ventricular ejection fraction (r-value = -0.382, P < 0.0005). A multivariate regression analysis revealed homocysteine level to be an independent predictor of left ventricular systolic function. In addition, adjusted analysis revealed hyperhomocysteinemia to be associated with global left ventricular dysfunction. CONCLUSION: In patients with CAD, homocysteine levels correlate independently with left ventricular systolic function. The mechanism of this association between homocysteine and left ventricular systolic function is unknown but may be due to a direct effect of homocysteine on myocardial function separate from its effects on coronary atherosclerosis.     

Increased thrombolysis in myocardial infarction frame counts in patients with isolated coronary artery ectasia

The Thrombolysis in myocardial infarction (TIMI) frame count is a simple clinical tool for assessing quantitative indexes of coronary blood flow. This measurement has been significantly correlated with flow velocity measured with a flow-wire by several investigators during baseline conditions or hyperemia. In this study we aimed to evaluate the coronary flow in patients with isolated coronary artery ectasia by means of the TIMI frame count and to compare the results with those of patients with angiographically normal coronary arteries. The study population consisted of 37 patients with coronary artery ectasia only in the right coronary artery (RCA). The control group consisted of 31 patients with angiographically proven normal coronary arteries. Coronary artery ectasia was defined as nonobstructive lesions of the coronary arteries with a luminal dilatation 1.5-fold or more of the adjacent normal coronary segments. The TIMI frame count was determined for each major coronary artery in each patient according to the methods first described by Gibson et al. The TIMI frame count of RCA in the study group was significantly higher than in that of the control group (51 ± 17 vs 25 ± 8, P 0.0001). The TIMI frame counts of the study group for the left anterior descending and left circumflex coronary artery were also significantly higher than those of the control group (corrected TIMI frame count for LAD = 42 ± 11 vs 24 ± 7, P 0.001; TIMI frame count for LCx = 44 ± 15 vs 25 ± 9, P 0.001). In patients with coronary artery ectasia, the TIMI frame count of the RCA was higher than that of the left anterior descending and left circumflex coronary artery (51 ± 17 vs 42 ± 11 and 44 ± 15, respectively, P 0.05). We have shown increased TIMI frame counts in patients with isolated coronary artery ectasia and suggest that the pathophysiological mechanism of coronary artery ectasia is not a focal disease. TIMI frame counts can be regarded as an index of the severity of impaired coronary flow in patients with coronary artery ectasia.     

The association between soluble lectin-like oxidized low-density lipoprotein receptor-1 levels and patients with isolated coronary artery ectasia

Some evidence suggests that chronic inflammation plays a critical role in the development and progression of coronary artery ectasia. Lectin-like oxidized low-density lipoprotein receptor-1 is involved in multiple phases of vascular dysfunction, including endothelial dysfunction, atherogenesis, initiation of plaque rupture, and restenosis. The objectives was to study the purpose of the current study was to determine whether soluble lectin-like oxidized low-density lipoprotein receptor-1 is associated with isolated coronary artery ectasia patients. Forty-six patients with isolated coronary artery ectasia without stenosis and 46 control subjects with angiographically normal coronary arteries were included in this study. Lectin-like oxidized low-density lipoprotein receptor-1 levels were measured in serum by sandwich enzyme-linked immunosorbent assay. Baseline characteristics of the two groups were similar. Plasma levels of lectin-like oxidized low-density lipoprotein receptor-1 were significantly higher in the coronary artery ectasia group than normal coronary artery group (1.7 ± 0.8 ng/ml vs. 1.1 ± 0.3 ng/ml, P < 0.001, respectively). No correlation was found between plasma soluble lectin-like oxidized low-density lipoprotein receptor-1 levels and different types of ectasia in patients with coronary artery ectasia. In this study, we found significantly higher levels of soluble lectin-like oxidized low-density lipoprotein receptor-1 in coronary artery ectasia patients when compared to control subjects with normal coronary arteries, suggesting that soluble lectin-like oxidized low-density lipoprotein receptor-1 may be involved in the pathogenesis of coronary artery ectasia.     

Plasma soluble adhesion molecules; intercellular adhesion molecule-1, vascular cell adhesion molecule-1 and E-selectin levels in patients with isolated coronary artery ectasia

Plasma soluble adhesion molecules, intercellular adhesion molecule-1 (ICAM)-1, vascular cell adhesion molecule-1 (VCAM-1) and E-selectin leves of patients with isolated coronary artery ectasia (CAE), patients with obstructive coronary artery disease without CAE and subjects with angiographically normal coronary arteries were evaluated. Patients with isolated CAE were detected to have significantly higher levels of plasma soluble ICAM-1, VCAM-1 and E-selectin in comparison with patients with obstructive coronary artery disease without CAE (ICAM, 673 +/- 153 versus 381 +/- 106, respectively, P < 0.001; VCAM-1, 2366 +/- 925 versus 1136 +/- 208, respectively, P < 0.001; E-selectin, 74 +/- 21 versus 61 +/- 18, respectively, P = 0.01) and subjects with normal coronary arteries (ICAM-1, 673 +/- 153 versus 303 +/- 131, respectively, P < 0.001; VCAM-1, 2366 +/- 925 versus 729 +/- 231, respectively, P < 0.001; E-selectin, 74 +/- 21 versus 49 +/- 9, respectively, P < 0.001), suggesting the presence of a more severe and extensive chronic inflammation in the coronary circulation in patients with isolated CAE. BACKGROUND: The common coexistence of coronary artery ectasia (CAE) with coronary artery disease (CAD) suggests that it may be a variant of CAD. However, it is not clear why some patients with obstructive CAD develop CAE whereas most do not. Inflammation has been reported to be a major contributing factor to both obstructive and aneurysmatic vascular disorders and therefore, in the present study, the plasma soluble adhesion molecules, intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1) and E-selectin levels in isolated CAE were investigated. METHODS: The study population consisted of three groups: the first consisted of 32 patients with isolated CAE without stenotic lesion; the second of 32 patients with obstructive CAD without CAE; and the third group of 30 control subjects with normal coronary arteries. Coronary diameters were measured as the maximum diameter of the ectasic segment by use of a computerized quantitative coronary angiography analysis system. According to the angiographic definition used in the Coronary Artery Surgery Study, a vessel is considered to be ectasic when its diameter is > or =1.5 times that of the adjacent normal segment in segmental ectasia. Plasma soluble ICAM-1, VCAM-1 and E-selectin levels were measured in all patients and control subjects using commercially available enzyme-linked immunosorbent assay kits. RESULTS: Patients with isolated CAE were found to have significantly higher levels of plasma soluble ICAM-1, VCAM-1, and E-selectin in comparison with patients with obstructive CAD without CAE (ICAM, 673 +/- 153 versus 381 +/- 106, respectively; P < 0.001; VCAM-1, 2366 +/- 925 versus 1136 +/- 208, respectively; P < 0.001; E-selectin, 74 +/- 21 versus 61+/-18, respectively; P = 0.01) and control subjects with normal coronary arteries (ICAM-1, 673 +/- 153 versus 303 +/- 131, respectively;, P < 0.001; VCAM-1, 2366 +/- 925 versus 729 +/- 231, respectively; P < 0.001; E-selectin, 74 +/- 21 versus 49 +/- 9, respectively; P < 0.001). In addition, we detected statistically significant positive correlation between the total length of ectasic segments and the levels of plasma soluble ICAM-1 (r = 0.625; P < 0.001), VCAM-1 (r = 0.548; P = 0.001) and E-selectin (r = 0.390; P = 0.027). Multivariate logistic regression analysis revealed a significant independent relation between isolated CAE and ICAM-1 [odds ratio (OR) = 1.023; 95% confidence interval (CI) = 1.0048-1.0414; P = 0.0129] and VCAM-1 (OR = 1.0057; 95% CI = 1.0007-1.0106; P = 0.0240). CONCLUSIONS: We have shown that patients with isolated CAE have raised levels of plasma soluble ICAM-1, VCAM-1 and E-selectin in comparison with patients with obstructive CAD without CAE and control subjects with normal coronary arteries, suggesting the presence of a more severe and extensive chronic inflammation in the coronary circulation in these patients.     

Plasma homocysteine levels in acute coronary syndromes

Hyperhomocysteinemia is currently regarded as an independent and modifiable risk factor for ischemic vascular diseases and thrombosis. We measured fasting plasma total homocysteine levels by HPLC with fluorescence detection in 30 patients presenting with acute coronary syndromes and 30 age and sex-matched control subjects. Demographic data, classical risk factors (systolic blood pressure, diabetes mellitus, smoking, ethanol intake, family history of ischaemic heart disease) and life-style habits were recorded. Lipid fractions including total cholesterol, triglycerides, HDL-cholesterol, total cholesterol/HDL-cholesterol ratio, serum creatinine, LDL-cholesterol and vitamins involved in the metabolism of homocysteine, folic acid and vitamin B12 were also assessed. Total fasting homocysteine concentrations were significantly higher in the patient group (12.2 +/- 1.01 micromol/l) than in the control subjects (7.05 +/- 0.36 micromol/l; p < 0.0001). Homocysteine correlated positively with age (r = 0.617; p < 0.01) and serum creatinine (r = 0.457; p < 0.01) in the patient group. Hyperhomocysteinemia was not associated with vitamin B12 or folate deficiency states. Vitamin B12 concentration was 273 +/- 16.4 ng/l in the control group and 284.3 +/- 32.2 ng/l in the patient group (p = NS). Serum folate concentration also was not significantly different between controls and patients; 7.57 +/- 0.58 microg/l and 8.05 +/- 0.72 microg/l, respectively. Since no significant difference was observed in the lipid parameters between patients and controls, the hyperhomocysteinemia in the patient group supports the view that homocysteine is an independent risk factor for cardiovascular diseases. Our results strongly suggest that elevated homocysteine levels are among the interacting factors in the complex, multifactorial pathophysiology of ischemic heart disease.