Endothelial Function and Coronary Spastic Angina

Kawano, Hiroaki; Ogawa, Hisao

doi:10.2169/internalmedicine.44.91

Cited by 61 publications

(37 citation statements)

References 85 publications

(54 reference statements)

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“…20 It is well known that variant angina could be caused by coronary endothelial dysfunction, at least in part. 21 In the present study, we showed that CPT%PDV was positively associated with plasma free IGF-I in the entire study population, and subjects with vasospasm to intracoronary acetylcholine had lower plasma free IGF-I and CPT%PDV than the others. IGF-I has been known to protect directly against endothelial dysfunction, atherosclerotic plaque development, clinical instability, and ischemic myocardial damage by induction of NO production, 8 although it had been considered a mediator of cardiovascular disease previously.…”

Section: Discussionsupporting

confidence: 57%

Change of Coronary Flow Velocity During the Cold Pressor Test Is Related to Endothelial Markers in Subjects With Chest Pain and a Normal Coronary Angiogram

Hwang

Youn

Lee

et al. 2011

Clinical Cardiology

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Background: Several studies demonstrated that endothelial or atherosclerotic biomarkers, including plasma free insulin-like growth factor-I(IGF-I), soluble CD40 ligand (sCD40L), adiponectin, and leptin have an influence on coronary endothelial function. Hypothesis: The aim of the present study was to investigate whether change of coronary flow velocity of the distal left anterior descending artery (LAD) during the cold pressor test (CPT) with transthoracic Doppler echocardiography (TTE) was associated with these biomarkers in subjects with chest pain and a normal coronary angiogram. Methods: In 190 subjects (mean age, 54 ± 11 years; male:female, 113:77) with chest pain and a normal coronary angiogram, peak diastolic velocity (PDV) of the distal LAD during the CPT with TTE was assessed. Acetylcholine provocation test was performed in 58 subjects (mean age, 51 ± 10 years) who were clinically suspected of vasospasm. CPT%PDV was defined as the percent change in PDV during the CPT. Associations between CPT%PDV and clinical parameters were analyzed. Results: According to multiple regression analysis, CPT%PDV was associated with plasma free IGF-I in the entire study population (β = 0.295, P < 0.001 in all subjects; β = 0.341, P = 0.001 in males; β = 0.243, P = 0.037 in females; β = 0.303, P = 0.002 in nonsmokers; and β = 0.256, P = 0.047 in smokers), and sCD40L in males (β = −0.269, P = 0.008)and smokers (β = −0.261, P = 0.046). Subjects with vasospasm to intracoronary acetylcholine had lower plasma free IGF-I(6.9 ± 3.3 vs 8.9 ± 3.4, P = 0.026) and CPT%PDV (8.8 ± 24.9 vs 52.7 ± 26.0, P < 0.001) than the others. Plasma adiponectin and leptin were not associated with CPT%PDV. Conclusions: Change of coronary flow velocity assessed using the CPT with TTE may be related to endothelial markers, especially plasma free IGF-I.

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Section: Discussionsupporting

confidence: 57%

Change of Coronary Flow Velocity During the Cold Pressor Test Is Related to Endothelial Markers in Subjects With Chest Pain and a Normal Coronary Angiogram

Hwang

Youn

Lee

et al. 2011

Clinical Cardiology

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“…3,5 Endothelial dysfunction is caused by risk factors related to atherosclerosis, such as hyperlipidemia, smoking and diabetes. 29 Although the causal mechanism of endothelial dysfunction remains elusive, available evidence suggests that chronic low-grade inflammation in arteries including the endothelium has an important function in the induction of endothelial dysfunction with coronary artery spasm and atherosclerotic changes.…”

Section: Discussionmentioning

confidence: 99%

“…Some reports indicated that coronary artery spasm is related to the extent of atherosclerotic changes 4 and endothelial dysfunction. 5 Endothelial dysfunction was initially characterized by impaired vasodilation to specific stimuli, such as acetylcholine that can induce vasodilation by release of nitric oxide from the endothelium. 6,7 The broader understanding of endothelial dysfunction includes proinflammatory and prothrombotic states of the endothelium.…”

Section: Introductionmentioning

confidence: 99%

Mutation of ARHGAP9 in patients with coronary spastic angina

et al. 2009

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Coronary artery spasm has an important function in the etiology of variant angina and other acute coronary syndromes. Abnormal activation of Rho-family GTPases has been observed in cardiovascular disorders, but the function of genetic variability in Rho-family GTPases remains to be evaluated in cardiovascular disorders. We examined the genetic variability of Rho-family GTPases and their regulators in coronary artery spasm. We performed a comprehensive candidate gene analysis of 67 single nucleotide polymorphisms with amino-acid substitution in Rho-family GTPases and their regulators in 103 unrelated Japanese patients with acetylcholine-induced coronary artery spasm and 102 control Japanese subjects without acetylcholine-induced coronary artery spasm. We noted an association of the single nucleotide polymorphism of ARHGAP9 (rs11544238, Ala370Ser) with coronary artery spasm (odds ratio¼2.67). We found that ARHGAP9 inactivated Rac as RacGAP and that the mRNA level of ARHGAP9 was strongly detected in hematopoietic cells. ARHGAP9 negatively regulated cell migration. The Ala370Ser polymorphism counteracted ARHGAP9-reduced cell migration, spreading and adhesion. The Ala370Ser polymorphism in the ARHGAP9 gene is associated with coronary artery spasm. These data suggest that the polymorphism of ARHGAP9 has a critical function in the infiltration of hematopoietic cells into the endothelium and inflammation leading to endothelial dysfunction.

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“…The precise mechanism of coronary spasm remains obscure, but endothelial dysfunction and smooth muscle hypercontraction have been reported as important factors. 12 Kaneda et al recently reported that polymorphisms of the endothelial nitric oxide synthase gene are associated with coronary artery spasm 13 and Mashiba et al reported that VA is influenced by polymorphism of the paraoxonase 1 gene A632G. 14 Racial differences in the angiographic patterns and prevalence of coronary spasm appear to exist between Asian and Caucasians, and the prevalence of VA appears to be higher in Asians than in Caucasians.…”

Section: Discussionmentioning

confidence: 99%

Clinical and Angiographic Characteristics of Acute Myocardial Infarction Caused by Vasospastic Angina Without Organic Coronary Heart Disease

Kim

Seung

Kim

et al. 2007

Circ J

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lthough acute myocardial infarction (AMI) is mostly associated with obstructive coronary artery disease, myocardial infarction with normal epicardial coronary arteries has been documented. [1][2][3][4][5] The overall prevalence of myocardial infarction (MI) with a normal coronary angiogram is low, approximately 3%, but the incidence of this condition appears to vary with age, with higher rates in younger patients. 4,5 In some patients with a diagnosis of vasospastic angina (VA), dangerous complications such as AMI, or a high-degree of atrioventricular block, ventricular tachycardia, fibrillation or electromechanical dissociation, are observed during an ischemic attack, and all of these maladies can lead to sudden death. Coronary artery spasm has been proposed as a classic etiologic factors for AMI with normal coronary arteries, 6 but the actual prevalence of this event has remained ill-defined because of a lack of data from spasm provocation tests in a large series of patients.In the present study we evaluated the clinical and angiographic characteristics of VA with AMI in patients without organic coronary heart disease. Circulation Journal Vol.71, September 2007 Methods PatientsBetween January 2003 and June 2005, 672 coronary spasm provocation tests were performed at Kangnam St Mary's hospital and 292 patients were diagnosed with VA. Among these 292 patients, 21 had an AMI. In this study, the diagnosis of VA was made when patients met all of the following criteria: (1) burning or squeezing retrosternal chest pain, (2) positive spasm provocation test, and (3) no significant organic lesion (<50% narrowing of the coronary luminal diameter according to quantitative coronary angiography (QCA)). AMI with VA was defined by elevation of the cardiac markers (troponin-I >upper normal limit and creatine kinase-MB >3-fold the upper normal limit) with no organic coronary heart disease being identified on angiography. We excluded patients with takotsubo cardiomyopathy.After the procedure was explained, written informed consent for the spasm provocation test was given by all the patients. Spasm Provocation TestAll the patients' medications, except for nitroglycerin, were discontinued for >48 h before the start of the study, and nitroglycerin was discontinued at least >4 h before the start of the study. Cardiac catheterization was performed through the right femoral artery while the patient was in a fasting state. Control angiograms of the left coronary artery (LCA) were obtained in the right anterior oblique view with caudal projection, before imaging of the right coronary artery (RCA) in the left anterior oblique view with straight projection after the injection of 4-6 ml of contrast medium.Circ J 2007; 71: 1383 -1386 (Received June 7, 2006 revised manuscript received April 6, 2007; accepted May 24, 2007 There were 20 patients who initially visited the emergency room for AMI without suffering prior VA. One patient with a history of VA had an AMI when he discontinued his medication. Among the 21 VA patients with AMI, 14 ha...

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Endothelial Function and Coronary Spastic Angina

Cited by 61 publications

References 85 publications

Change of Coronary Flow Velocity During the Cold Pressor Test Is Related to Endothelial Markers in Subjects With Chest Pain and a Normal Coronary Angiogram

Change of Coronary Flow Velocity During the Cold Pressor Test Is Related to Endothelial Markers in Subjects With Chest Pain and a Normal Coronary Angiogram

Mutation of ARHGAP9 in patients with coronary spastic angina

Clinical and Angiographic Characteristics of Acute Myocardial Infarction Caused by Vasospastic Angina Without Organic Coronary Heart Disease

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