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'Warm-up' phenomenon in diabetic patients with stable angina treated with diet or sulfonylureas.
Bilinska, M, Potocka, J, Korzeniowska-Kubacka, I, Piotrowicz, R
Coronary artery disease. 2007;(6):455-62
Abstract
BACKGROUND Classic sulfonyloureas (SUs) are known to attenuate ischaemic preconditioning. Gliclazide is an SU agent believed to be more protective. We assessed the effects of diet, glibenclamide, or gliclazide on the warm-up effect in type 2 diabetic patients with stable angina. METHODS The study group consisted of 64 men, aged 54+/-5 years: 17 patients without diabetes (G I) and 47 diabetic patients: 16 patients treated with glibenclamide (G II), 16 with gliclazide (G III) and 15 patients treated with diet (G IV). After the baseline positive exercise test (ET1), all patients reexercised after 30-min rest (ET2). We analysed exercise duration (ED, s), time to 1 mm ST depression (T-STD, s), max STD (mm), heart rate-systolic blood pressure product at 1 mm STD, or ischaemic threshold (mmHg/min x 100) and the total ischaemic time (s). RESULTS In G I, all analysed variables improved significantly during ET2 relative to ET1. Glibenclamide (G II) completely abolished the protective effect of exercise-induced ischaemia because only ED increased during ET2 (431 vs. 451, P<0.05). In G III, however, ED (486 vs. 537, P<0.001), T-STD (364 vs. 388, P<0.05) and max STD (2.5 vs. 2.0, P<0.05) improved significantly during ET2, whereas ischaemic threshold and total ischaemic time did not (PNS). In G IV, similar to G I, all variables improved significantly during ET2 relative to ET1. CONCLUSION Warm-up effect is preserved in diabetic patients with stable angina treated with diet, partially preserved in gliclazide-treated and abolished in glibenclamide-treated patients.
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Effects of vitamin C on intracoronary L-arginine dependent coronary vasodilatation in patients with stable angina.
Tousoulis, D, Xenakis, C, Tentolouris, C, Davies, G, Antoniades, C, Crake, T, Stefanadis, C
Heart (British Cardiac Society). 2005;(10):1319-23
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Abstract
OBJECTIVE To assess the effects of intravenous vitamin C administration on the vasomotor responses to intracoronary L-arginine infusion in epicardial coronary arteries. METHODS 28 patients with coronary artery disease and stable angina were enrolled in the study. Eight patients received intracoronary infusions of 150 micromol/min L-arginine before and after intravenous infusion of vitamin C, 10 patients received intracoronary infusions of 150 micromol/min L-arginine before and after intravenous infusion of normal saline, and 10 patients received intracoronary normal saline before and after intravenous infusion of vitamin C. The diameter of proximal and distal coronary artery segments was measured by quantitative angiography. RESULTS Infusion of L-arginine caused significant dilatation of both proximal (4.87 (0.96)%, p < 0.01 v normal saline) and distal (6.33 (1.38)%, p < 0.01 v normal saline) coronary segments. Co-infusion of vitamin C and L-arginine dilated proximal coronary segments by 8.68 (1.40)% (p < 0.01 v normal saline, p < 0.01 v L-arginine) and distal segments by 13.07 (2.15)% (p < 0.01 v normal saline, p < 0.01 v L-arginine). Intravenous infusion of vitamin C caused a borderline increase in proximal and distal coronary segment diameters (1.93 (0.76)% and 2.09 (1.28)%, respectively, not significant). CONCLUSIONS L-arginine dependent coronary segment vasodilatation was augmented by the antioxidant vitamin C in patients with coronary artery disease. Thus, vitamin C may have beneficial effects on nitric oxide bioavailability induced by L-arginine.
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Comparison of urinary biopyrrin levels in acute myocardial infarction (after reperfusion therapy) versus stable angina pectoris and their usefulness in predicting subsequent cardiac events.
Shimomura, H, Ogawa, H, Takazoe, K, Soejima, H, Miyamoto, S, Sakamoto, T, Kawano, H, Suefuji, H, Nishikawa, H, Arai, H, et al
The American journal of cardiology. 2002;(2):108-11
Abstract
We examined the relation between oxidative stress and cardiac events in patients with acute myocardial infarction (AMI). There is now increasing evidence that reactive oxygen species cause reperfusion injury to the previously ischemic myocardium after reperfusion. We measured urinary biopyrrin/creatinine levels, an oxidative stress marker, in 41 patients with AMI, 34 patients with stable angina pectoris (SAP), and 29 control subjects. In the patients with AMI, urine samples were taken before, at 4 and 24 hours, and at 1 and 2 weeks after reperfusion therapy. Of these 41 patients with AMI, 38 received reperfusion therapy, and the urinary biopyrrin/creatinine levels (micromol/g.creatinine) before reperfusion were significantly higher than those of the other 2 groups (AMI 4.24 +/- 0.49, SAP 2.45 +/- 0.15, control subjects 2.31 +/- 0.16; p = 0.0003 vs AMI). The onset of reperfusion significantly increased the levels of urinary biopyrrins/creatinine, and this time course was mapped out, peaking at 4 hours (8.21 +/- 0.96 vs 4.24 +/- 0.49 before, p = 0.0001), and decreasing to control levels between 24 hours and 7 days. The peak levels of urinary biopyrrins/creatinine were higher in the positive cardiac event group than in the negative cardiac event group (11.89 +/- 1.77 vs 7.57 +/- 1.00 micromol/g.creatinine, p = 0.029). These findings add further evidence that oxidative stress contributes to the complications of reperfusion injury, and suggest that urinary assessment of biopyrrins may be useful in predicting subsequent cardiac events after reperfusion in AMI.
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Nicorandil enhances myocardial tolerance to ischemia without progressive collateral recruitment during coronary angioplasty.
Sakai, K, Yamagata, T, Teragawa, H, Matsuura, H, Chayama, K
Circulation journal : official journal of the Japanese Circulation Society. 2002;(4):317-22
Abstract
Nicorandil, a hybrid nitrate and ATP-sensitive potassium channel opener, has had a preconditioning effect in some coronary angioplasty studies. The present study investigated whether the cardioprotective effects of nicorandil involve coronary collateral function. Thirty-two patients with stable angina pectoris were randomized to receive a 1-min intravenous infusion of nicorandil (100 microg/kg) or normal saline. Five minutes later they underwent three 2-min balloon inflations 5-min apart. The maximum ST-segment elevation (deltaSTmax), the sum of ST-segment elevations in all leads (sigmaST), and the chest pain score were determined at the end of each balloon inflation. The collateral flow index (CFI) was derived from simultaneous measurement of the mean aortic pressure and the coronary wedge pressure obtained from a pressure guidewire during balloon inflation. The deltaSTmax, sigmaST, and chest pain score decreased progressively during the 3 sequential balloon inflations in both groups, and the deltaSTmax and sigmaST were less in the nicorandil group than in the control group during each inflation. The CFI did not change during the 3 inflations in either group and was similar in the 2 groups during each inflation. In conclusion, pretreatment with intravenous nicorandil enhances myocardial tolerance to ischemia without progressive collateral recruitment during coronary angioplasty.
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Differential coronary calcification on electron-beam CT between syndrome X and coronary artery disease in patients with chronic stable angina pectoris.
Chen, LC, Chen, JW, Wu, MH, Liu, JC, Lan, GY, Ding, PY, Chang, MS
Chest. 2001;(5):1525-33
Abstract
STUDY OBJECTIVES The differential diagnosis of syndrome X and coronary artery disease (CAD) in patients with evidence of myocardial ischemia may be difficult. The possible difference in coronary calcium detected by electron-beam CT (EBCT) between syndrome X and CAD is rarely evaluated, especially in aged patients with chronic, stable angina. DESIGN AND SETTINGS Prospective, controlled study at a tertiary referral medical center. PATIENTS AND MEASUREMENTS Forty patients with syndrome X (85% male) and 53 patients with CAD (89% male) were enrolled. Ten control subjects (90% male) with negative exercise treadmill test results and normal coronary angiographic findings served as control subjects. EBCT determined the coronary calcium scores (CCSs), and standard cardiovascular risk factors of all study subjects were analyzed. RESULTS The 93 study patients had CCSs that ranged from 0 to 1,857. Coronary calcification was seen in 2 of the 10 control subjects (20%), 21 of the 40 syndrome X patients (52.5%), and 51 of the 53 CAD patients (96.2%) [p < 0.01]. The CCS (median [range]) was significantly lower in syndrome X patients than in CAD patients: 1 (0 to 117) vs 202 (0 to 1,857) [p < 0.001]. Receiver operating characteristic curve analyses also demonstrated that coronary calcification differentiated syndrome X from CAD (area under curve, 0.891; 95% confidence interval, 0.806 to 0.947). Of the CAD patients whose CCSs were < 117 and overlapped with CCSs of syndrome X, multivariate analyses determined CCS > 5 (odds ratio, 13.1; 95% confidence interval, 2.86 to 59.7), hypertension (odds ratio, 6.4; 95% confidence interval, 1.5 to 27.4), and hypercholesterolemia (odds ratio, 6.7; 95% confidence interval, 1.5 to 30.5) to be independent discriminators to differentiate CAD from syndrome X. Patients with CAD had more frequent hypertension than patients with syndrome X. CONCLUSIONS The coronary calcium detected noninvasively by EBCT was different, though with some overlapping, between patients with syndrome X and CAD. In addition to standard cardiovascular risk factors, CCS determined by EBCT (especially > 117 or = 0) could differentiate between syndrome X and CAD in patients with chronic, stable angina with evidence of myocardial ischemia. Larger trials would be useful to validate CCS on EBCT as a predictor of clinical outcome in these patients.