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Coronary endothelial dysfunction associated with a depressive mood in patients with atypical angina but angiographically normal coronary artery.
Kim, JH, Kim, JW, Ko, YH, Choi, CU, Na, JO, Kim, EJ, Rha, SW, Park, CG, Seo, HS, Oh, DJ
International journal of cardiology. 2010;(2):154-7
Abstract
BACKGROUND Depression is a risk factor for the development of coronary heart disease but the relationship between coronary endothelial dysfunction and depression is not yet known. This study investigated whether depressive symptomatology is associated with coronary endothelial dysfunction in patients without coronary artery disease (CAD). METHODS AND RESULTS Incremental acetylcholine (Ach; 20, 50 and 100 microg/min) and nitrate (200 microg/min) were infused into the left coronary ostium of 52 patients (male 30, 51.8 years) with depressive symptoms as indicated by a Beck Depression Inventory (BDI) score of >or=10 and a Hamilton Depression Rating Scale (HAM-D17) of >or=7 but without overt CAD or any vasoactive medications. Vascular responses to each drug were measured quantitatively at the mid-segments of the left anterior descending artery (LAD) and compared to those of 103 matched control subjects (male 64, 51.3 years) with angiographically normal looking LAD and as estimated by BDI <10 and HAM-D17 <7. Patients in the depressive group showed significant vasoconstriction compared with patients in the non-depressive group (p=0.017, 0.090, 0.004 respectively). However, endothelium-independent vasodilatation to nitrates did not differ significantly between the two groups (p=0.461). No differences in risk factors were found between the two groups. CONCLUSIONS Depressive mood is associated with coronary endothelial dysfunction in patients without CAD, suggesting a possible mechanism by which depressive mood may act as a cardiovascular risk factor.
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Smoking cessation normalizes coronary endothelial vasomotor response assessed with 15O-water and PET in healthy young smokers.
Morita, K, Tsukamoto, T, Naya, M, Noriyasu, K, Inubushi, M, Shiga, T, Katoh, C, Kuge, Y, Tsutsui, H, Tamaki, N
Journal of nuclear medicine : official publication, Society of Nuclear Medicine. 2006;(12):1914-20
Abstract
UNLABELLED Cigarette smoking is one of the risk factors of cardiovascular diseases and is related to abnormal peripheral and coronary vascular vasomotion. Coronary vascular endothelial dysfunction is caused by chronic smoking in smokers without epicardial coronary artery stenosis. The coronary endothelial vasomotion abnormality is restored by interventions such as l-arginine or vitamin C infusion. However, to our knowledge, the effect of smoking cessation on coronary vasomotor response has not been elucidated. Therefore, the aim of this study was to assess the effect of smoking cessation on coronary vasomotor response by quantitative myocardial blood flow (MBF) measurement using (15)O-water and PET. METHODS Fifteen young smokers (Brinkman index > 100; mean age +/- SD, 26 +/- 4 y) with no evidence of heart disease or cardiovascular risk factors, except for smoking, and age-matched nonsmokers (n = 12) were enrolled in this study. MBF was measured at rest, during the cold pressor test (CPT), before and at 1 and 6 mo after smoking cessation. In addition, MBF measurement during adenosine triphosphate (ATP) infusion was performed before and at 6 mo after smoking cessation. In nonsmokers, MBF was measured at rest, during ATP infusion, and during the CPT. RESULTS MBF at rest and during ATP infusion did not differ between smokers and nonsmokers (0.73 +/- 0.12 vs. 0.80 +/- 0.15 mL/g/min and 3.15 +/- 1.43 vs. 3.69 +/- 0.76 mL/g/min, respectively; P = not significant). In contrast, MBF during the CPT in smokers was lower than that in nonsmokers (0.90 +/- 0.19 vs. 1.12 +/- 0.28 mL/g/min; P < 0.05). There was no significant difference in MBF either at rest or during ATP infusion between before and after smoking cessation, but MBF during the CPT increased at 1 mo in comparison with before cessation of smoking (0.90 +/- 0.19 vs. 1.02 +/- 0.22 mL/g/min; P < 0.01). An improvement of MBF response to the CPT was preserved at 6 mo after smoking cessation. CONCLUSION Coronary vasomotor abnormality assessed by MBF response to the CPT was improved at 1 mo after smoking cessation. These findings indicate that coronary endothelial dysfunction may be reversible within 1 mo after smoking cessation in healthy young smokers.
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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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An improved model for the measurement of myocardial perfusion in human beings using N-13 ammonia.
Hickey, KT, Sciacca, RR, Chou, RL, Rodriguez, O, Bokhari, S, Bergmann, SR
Journal of nuclear cardiology : official publication of the American Society of Nuclear Cardiology. 2005;(3):311-7
Abstract
BACKGROUND Oxygen 15 water and nitrogen 13 ammonia are widely used for the quantitative measurement of myocardial perfusion with positron emission tomography. However, blood flow obtained with N-13 ammonia by use of the conventional 2-compartment model frequently underestimates flow by 30% to 50% compared with O-15 water. We hypothesized that this discrepancy is a result of the model configuration of N-13 ammonia and investigated changes to the mathematical model to determine whether more accurate measurements of perfusion could be obtained. METHODS AND RESULTS Twelve healthy volunteers were sequentially studied with O-15 water and N-13 ammonia at rest and during maximal coronary vasodilation with adenosine. Perfusion measurements obtained with the conventional and modified models were compared with values obtained with O-15 water. The conventional N-13 ammonia model underestimated flow by 37% +/- 16% at rest and by 20% +/- 24% with stress when compared with flows obtained with O-15 water. The modified model yielded flow values closer to the line of identity than the conventional model (y = 1.07x + 0.04 vs y = 0.69x + 0.08; respectively; P < .01). CONCLUSIONS Model changes made N-13 ammonia myocardial blood flow estimates more comparable to those obtained with O-15 and may allow for better comparison of flows obtained with these two tracers in the future. Further efforts are warranted to evaluate the accuracy of flow models in human subjects.
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Lack of association between Chlamydia Pneumoniae serology and endothelial dysfunction of coronary arteries.
Ferrari, M, Werner, GS, Richartz, BM, Oehme, A, Straube, E, Figulla, HR
Cardiovascular ultrasound. 2005;:12
Abstract
BACKGROUND Recent publications brought up the hypothesis that an infection with Chlamydia Pneumoniae (CP) might be a major cause of coronary artery disease (CAD). Therefore, we investigated whether endothelial dysfunction (ED) as a precursor of atherosclerosis might be detectable in patients with previous infection with CP but without angiographic evidence of CAD. METHODS We included 16 patients (6 male / 10 female) of 52 consecutive patients with normal coronary angiography who had typical angina pectoris and pathologic findings in the stress test. Exclusion criteria were: active smoker, elevated cholesterol, hypertension, age > 65 years, diabetes mellitus, treatment with ACE-inhibitors, or known CAD. Blood sample analysis for serum titer against CP (aCP-IgG) was performed after coronary angiography. We looked for endothelial dysfunction analyzing the diameter of the left anterior descending coronary artery (LAD) before and after acetylcholine (ACh) i. c. Quantitative analysis of luminal diameter (LD) was performed in at least two planes during baseline conditions and after ACh for 2 minutes in dosages of 7.2 microg/min and 36 microg/min with an infusion speed of 2 ml/min. Using Doppler guide wire, the coronary flow velocity was measured continuously in the LAD. The coronary flow velocity reserve (CFVR) was measured after 20 microg adenosine i. c. RESULTS 10 patients had an elevated aCP-IgG (> 1:8). 6 patients with negative titers (aCP-IgG CONCLUSION In patients with typical symptoms of coronary ischemia but without angiographically visible CAD and absence of other factors affecting the endothelial function, a previous infection with CP is not associated with endothelial dysfunction.
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Changes in coronary plaque color and morphology by lipid-lowering therapy with atorvastatin: serial evaluation by coronary angioscopy.
Takano, M, Mizuno, K, Yokoyama, S, Seimiya, K, Ishibashi, F, Okamatsu, K, Uemura, R
Journal of the American College of Cardiology. 2003;(4):680-6
Abstract
OBJECTIVES Changes in coronary plaque color and morphology by statin therapy were evaluated using coronary angioscopy. BACKGROUND Coronary plaque stabilization by statin therapy has not been clarified in humans. METHODS Thirty-one patients with coronary artery disease were divided into either the comparison group (n = 16) or the atorvastatin group (n = 15). Before treatment and 12 months after, the color and complexity of 145 coronary plaques were determined according to angioscopic findings. The yellow score of the plaque was defined as 0 (white), 1 (light yellow), 2 (yellow), or 3 (dark yellow), and its disrupted score was defined as 0 (smooth surface) or 1 (irregular surface) and as 0 (without thrombus) or 1 (with thrombus). In each patient, the mean yellow score and mean disrupted score were calculated. RESULTS Mean low-density lipoprotein cholesterol (LDL-C) decreased by 45% in the atorvastatin group, whereas an increase of 9% was seen in the comparison group. The mean yellow score decreased from 2.03 to 1.13 in the atorvastatin group, whereas it increased from 1.67 to 1.99 in the comparison group. There was a good correlation between the change in the mean yellow score and the change in LDL-C levels (r = 0.81, p < 0.0001). The change in the mean yellow score and mean disrupted score differed significantly between the two groups (p = 0.002 and p = 0.03, respectively). CONCLUSIONS This is the first report clarifying detailed changes in coronary plaque by statin in humans. This study indicated that lipid-lowering therapy changes plaque color and morphology and should then lead to coronary plaque stabilization.
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Relation of peripheral flow-mediated vasodilatation and coronary arterial calcium in young patients with heterozygous familial hypercholesterolemia.
Hoffmann, U, Dirisamer, A, Heher, S, Kostner, K, Widhalm, K, Neunteufl, T
The American journal of cardiology. 2002;(1):70-3
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Early dysfunction and long-term improvement in endothelium-dependent vasodilation in the infarct-related artery after thrombolysis.
Iràculis, E, Cequier, A, Gómez-Hospital, JA, Sabaté, M, Mauri, J, Fernández-Nofrerias, E, García del Blanco, B, Jara, F, Esplugas, E
Journal of the American College of Cardiology. 2002;(2):257-65
Abstract
OBJECTIVES This study assessed the degree of endothelial dysfunction in post-acute myocardial infarction (AMI) and its subsequent status in the infarct-related artery (IRA) in patients treated with thrombolysis. BACKGROUND Coronary flow reserve alterations in the IRA after thrombolysis have been described, but the endothelium-dependent vasomotion has not been investigated, to date. METHODS Endothelial function in patients after thrombolysis was assessed by infusion of acetylcholine (ACh) at increasing doses in the IRA. Diameter changes in the distal segments were evaluated using quantitative coronary angiography. Patients with coronary atherosclerosis constituted the control group. Clinical variables, electrocardiography and biochemical markers were used to determine the timing of reperfusion and the extent of the infarct. Patients in the AMI group were re-evaluated one year later. RESULTS In the initial assessment, 16 patients showed a vasoconstriction response to ACh in the IRA compared to the control group (-20 +/- 21% vs. 4 +/- 4%; p < 0.01). Significant correlations between the degree of vasoconstriction and maximum value of the creatine kinase-MB fraction and number of new Q waves were observed. Of the 12 patients re-evaluated, 4 had complete occlusion of the IRA. In the remaining eight patients with patent artery, an improvement in response to ACh was observed relative to the initial study (+3 +/- 11%, vs. -19 +/- 15%, p < 0.05). CONCLUSIONS In patients with AMI treated with thrombolysis, severe endothelial dysfunction in the IRA is observed early. In patients who retain patency of the IRA, the endothelial dysfunction improves during the follow-up and suggests a component of stunned endothelium in the first few days post-AMI.