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• Plasma HO-1 levels were significantly higher in patients with CAD, especially in 1-VD, than in those without CAD. • In contrast, serum bilirubin levels were significantly lower in patients with CAD than in those without CAD. • There was no correlation between HO-1 and bilirubin levels. • In a multivariate analysis, HO-1, but not bilirubin, level was an independent factor for CAD. Heme oxygenase-1 (HO-1) degrades heme to CO, iron, and biliverdin/bilirubin. Although serum bilirubin levels were often reported in patients with coronary artery disease (CAD), HO-1 levels in patients with CAD and the association between HO-1 and bilirubin levels have not been clarified. We measured plasma HO-1 and serum total bilirubin levels in 262 patients undergoing coronary angiography. HO-1 levels were higher in patients with CAD than without CAD (median 0.46 vs. 0.35 ng/mL, P < 0.01), but bilirubin were lower in patients with CAD than without CAD (0.69 vs. 0.75 mg/dL, P < 0.02). Notably, HO-1 levels in CAD(−), 1-vessel, 2-vessel, and 3-vessel disease were 0.35, 0.51, 0.45, and 0.44 ng/mL, and were highest in 1-vessel disease (P < 0.05). Bilirubin levels in CAD(−), 1-vessel, 2-vessel, and 3-vessel disease were 0.75, 0.70, 0.68, and 0.66 mg/dL (P = NS). No correlation was found between HO-1 and bilirubin levels. In multivariate analysis, HO-1 levels were a significant factor for CAD independent of atherosclerotic risk factors and bilirulin levels. Odds ratio for CAD was 2.32 (95%CI = 1.29–4.17) for high HO-1 (>0.35 ng/mL). Patients with CAD were found to have high HO-1 and low bilirubin levels in blood, but no correlation was found between HO-1 and bilirubin levels. [ABSTRACT FROM AUTHOR]

Aims. Betatrophin is a recently identified circulating adipokine that may affect lipid and glucose metabolism. However, the association between plasma betatrophin levels and carotid atherosclerosis has not been elucidated. Methods. We investigated plasma betatrophin levels in 153 subjects undergoing carotid ultrasonography. The severity of plaque was evaluated as plaque score. Results. Of the 153 subjects, plaque was found in 63 (41%). Plasma betatrophin levels were higher in 63 subjects with plaque than in 90 without plaque (median 906 vs. 729 pg/mL, P<0.025). A stepwise increase in betatrophin levels was found depending on the plaque score: 729 pg/mL in score=0 (n=90), 802 pg/mL in score=1 (n=31), and 978 pg/mL in score≥2 (n=32) (P<0.01). In particular, betatrophin levels in subjects with score≥2 were higher than in those with score=0 (P<0.05). Moreover, betatrophin levels correlated with plaque score (r=0.23, P<0.01), but no significant correlation was found between betatrophin levels and triglyceride or HbA1c levels. The percentage of subjects with betatrophin>800 pg/mL was higher in subjects with plaque than in those without plaque (65% vs. 44%) and was highest in score≥2 (78%) (P<0.005). In the multivariate analysis, betatrophin level was not a significant factor for the presence of plaque but was a significant factor for plaque score≥2, independent of atherosclerotic risk factors. The odds ratio for score≥2 was 4.9 (95% CI=1.9-12.8) for betatrophin>800 pg/mL. Conclusions. Plasma betatrophin levels were found to be high in subjects with carotid plaque and to be associated with the severity of plaque. Betatrophin may play a role in the progression of carotid atherosclerosis. [ABSTRACT FROM AUTHOR]

Betatrophin, also called angiopoietin-llike protein 8, is a recently identified adipokine, mainly produced in liver and adipose tissue, which is recognized to play a dual role in lipid and glucose metabolism. However, any association between plasma betatrophin levels and atherosclerotic diseases, such as coronary artery disease (CAD) and peripheral artery disease (PAD), has not been elucidated yet. We investigated plasma betatrophin levels by ELISA in 457 patients (pts) undergoing elective coronary angiography who also had ankle-brachial index (ABI) test for PAD screening. Pts with ACS or a history of PCI were excluded. Results: Of the 457 study pts, CAD was present in 241 (53%), of whom 99 had 1-vessel, 71 had 2-vessel, 71 had 3-vessel disease (3-VD). Plasma betatrophin levels were higher in 241 pts with CAD than in 216 without CAD (median 1120 vs. 909 pg/mL, P<0.001). A stepwise increase in betatrophin levels was found depending on the number of >50% stenotic coronary vessels: 909 in CAD(-), 962 in 1-VD, 1097 in 2-VD and 1393 pg/mL in 3-VD (P<0.001). Betatrophin levels also correlated with the numbers of >50% and >25% stenotic coronary segments (r=0.22 and r=0.24, P<0.001). Moreover, betatrophin levels correlated with HbA1c (r=0.18, P<0.001) but not with FPG and triglyceride levels. In multivariate analysis, betatrophin levels were not a factor for CAD but were a significant factor for 3-VD independent of atherosclerotic risk factors. Odds ratio for 3-VD was 1.06 (95%CI=1.01-1.11, P<0.02) for a 100 pg/mL increase in betatrophin levels. Of the 457 pts, PAD (ABI<0.9) was found in 41 (9%). Betatrophin levels were also higher in 41 pts with PAD than in 416 without PAD (median 1354 vs. 981 pg/mL, P<0.001). Notably, pts with PAD more often had CAD (85% vs. 65%), especially 3-VD (46% vs. 13%) (P<0.001). In multivariate analysis, betatrophin levels were a significant factor for PAD independent of atherosclerotic risk factors and CAD. Odds ratio for PAD was 1.08 (95%CI=1.01-1.14, P<0.02) for a 100 pg/mL increase in betatrophin levels. Conclusions: Plasma betatrophin levels were found to be associated with the presence and severity of CAD as well as PAD independent of atherosclerotic risk factors. Betatrophin may play a role in the development of atherosclerotic diseases. [ABSTRACT FROM AUTHOR]

Nesfatin-1 is a recently identified anorexigenic peptide mainly secreted from the brain and adipose tissue. Although nesfatin-1 may have pro-inflammatory and apoptotic properties, the association between plasma nesfatin-1 levels and coronary artery disease (CAD) has not been clarified yet. We investigated plasma nesfatin-1 levels in 302 patients undergoing elective coronary angiography. Of the 302 study patients, CAD was present in 172 (57%), of whom 67 had 1-vessel, 49 had 2-vessel, and 56 had 3-vessel disease. Compared with 130 patients without CAD, 172 with CAD had higher plasma nesfatin-1 levels (median 0.21 vs. 0.17 ng/mL, P < 0.01). A stepwise increase in nesfatin-1 levels was found depending on the number of > 50% stenotic coronary vessels: 0.17 in CAD(−), 0.20 in 1-vessel, 0.21 in 2-vessel, and 0.22 ng/mL in 3-vessel disease (P < 0.05). A high nesfatin-1 level (> 0.19 ng/mL) was found in 43% of patients with CAD(−), 55% of those with 1-vessel, 55% of those with 2-vessel, and 68% of those with 3-vessel disease (P < 0.05). Nesfatin-1 levels significantly correlated with the number of > 50% stenotic coronary segments (r = 0.14, P < 0.02). In multivariate analysis, plasma nesfatin-1 levels were a significant factor for CAD independent of atherosclerotic risk factors. The odds ratio for CAD was 1.71 (95% CI 1.01–2.91) for high nesfatin-1 level of > 0.19 ng/mL (P < 0.05). Thus, plasma nesfatin-1 levels were found to be high in patients with CAD and were associated with CAD independent of atherosclerotic risk factors, suggesting that high nesfatin-1 levels in patients with CAD may play a role in the development of coronary atherosclerosis. [ABSTRACT FROM AUTHOR]

Nesfatin-1 is a recently identified anorexigenic peptide derived from nucleobindin 2, which is mainly secreted from brain and adipose tissue. Although nesfatin-1 was suggested to have anti-inflammatory and anti-apoptotic properties, the association between plasma nesfatin-1 levels and atherosclerotic disease, such as coronary artery disease (CAD), has not been elucidated. We investigated plasma nesfatin-1 levels by ELISA in 302 patients (pts) undergoing elective coronary angiography for suspected CAD. Pts with ACS, heart failure, malignancy or a history of PCI were excluded. The severity of CAD was represented as the numbers of >50% stenotic vessels and segments, and the severity score of stenosis. The degree of coronary stenosis in each segment was scored 0 to 4 points (0, ≤25%; 1, 26-50%; 2, 51-75%; 3, 76-90%; 4, >90% stenosis), and the severity score was defined as the sum of scores of all segments. Results: Of the 302 study pts, CAD was present in 172 (57%), of whom 67 had 1-vessel, 49 had 2-vessel, 56 had 3-vessel disease (3-VD). Compared with 130 pts without CAD, 172 with CAD more often had hypertension, hyperlipidemia and DM (P<0.05). Plasma nesfatin-1 levels were higher in pts with CAD than without CAD (median 0.21 vs. 0.17 ng/mL, P<0.01). A stepwise increase in nesfatin-1 levels was found depending on the number of >50% stenotic coronary vessels: 0.17 in CAD(-), 0.20 in 1-VD, 0.21 in 2-VD and 0.22 ng/mL in 3-VD (P<0.05). High nesfatin-1 level (>0.19 ng/mL) was found in 43% of pts with CAD(-), 55% of 1-VD, 55% of 2-VD and 68% of 3-VD (P<0.05). Nesfatin-1 levels also correlated with the number of stenotic segments and the severity score (r=0.14 and r=0.13, P<0.02), but they did not correlate with body mass index or HbA1c level. In multivariate analysis, nesfatin-1 levels were a significant factor associated with CAD, especially 3-VD, independent of atherosclerotic risk factors. The odds ratios for CAD and 3-VD were 1.71 (95%CI=1.01-2.91) and 1.96 (95%CI=1.02-3.76) for high nesfatin-1 level of >0.19 ng/mL (P<0.05). Conclusions: Plasma nesfatin-1 levels were found to be associated with the presence and severity of CAD independent of atherosclerotic risk factors. High nesfatin-1 levels in CAD pts may be aimed at preventing the progression of coronary atherosclerosis. [ABSTRACT FROM AUTHOR]

Aims. Heme oxygenase-1 (HO-1) is an intracellular enzyme that catalyzes the oxidation of heme to generate CO, biliverdin, and iron. Since these products have antiatherogenic properties, HO-1 may play a protective role against the progression of atherosclerosis. However, plasma HO-1 levels in patients with atherosclerotic diseases, such as coronary artery disease (CAD) and peripheral artery disease (PAD), have not been clarified yet. Methods. We investigated plasma HO-1 levels by ELISA in 410 consecutive patients undergoing elective coronary angiography who also had an ankle-brachial index (ABI) test for PAD screening. Results. Of the 410 study patients, CAD was present in 225 patients (55%) (1-vessel (1-VD), n=91; 2-vessel (2-VD), n=66; 3-vessel disease (3-VD), n=68). PAD (ABI < 0.9) was found in 36 (9%) patients. Plasma HO-1 levels did not differ between 225 patients with CAD and 185 without CAD (median 0.44 versus 0.35 ng/mL), but they were significantly lower in 36 patients with PAD than in 374 without PAD (0.27 versus 0.41 ng/mL, P<0.02). After excluding the 36 patients with PAD, HO-1 levels were significantly higher in 192 patients with CAD than in 182 without CAD (0.45 versus 0.35 ng/mL, P<0.05). HO-1 levels in 4 groups of CAD(−), 1-VD, 2-VD, and 3-VD were 0.35, 0.49, 0.44, and 0.44 ng/mL, respectively, and were highest in 1-VD (P<0.05). In the multivariate analysis, HO-1 levels were inversely associated with PAD, whereas they were also associated with CAD. The odds ratios for PAD and CAD were 2.12 (95% CI = 1.03–4.37) and 0.65 (95% CI = 0.42–0.99) for the HO-1 level of <0.35 ng/mL, respectively. Conclusions. Plasma HO-1 levels were found to be low in patients with PAD, in contrast to high levels in patients with CAD. [ABSTRACT FROM AUTHOR]