Biochemical parameters of endothelial dysfunction in cardiological syndrome X

Kolasińska-Kloch, W; Leśniak, Wiktoria; Kieć‐Wilk, Beata; Malczewska-Malec, Małgorzata

doi:10.1080/003655102753517145

Cited by 22 publications

(19 citation statements)

References 5 publications

(5 reference statements)

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“…22 In another study, Kolasionska-Kloch showed a statistical difference in NO/ET-1 ratio (though not in ET-1 levels per se) between CSX patients and control subjects. 23 Similarly, this study showed no elevation in ET-1 levels in CSX patients and no significant correlation between ET-1 levels and EIVD or EDVD. This suggests that ET-1 may not play a direct role in the pathogenesis of CSX.…”

Section: Discussionsupporting

confidence: 49%

Brachial Artery Flow-Mediated Vasodilation in Patients With Cardiac Syndrome X

Lee

Chen

et al. 2008

Angiology

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Cardiac syndrome X (CSX) differs from coronary artery disease (CAD) and is characterized by angina, positive stress test, and patent coronary arteries. The probable mechanism is a microvascular disorder associated with endothelial dysfunction. In this study, brachial artery flow-mediated vasodilation was used as well as the endothelin-1 assay to assess endothelial function in patients with cardiac syndrome X (CSX), coronary artery disease (CAD), and healthy controls. All subjects underwent a 2-step brachial artery flow-related vasodilatation test. Serum endothelin-1, one of the most potent constricting factors, was measured for all participants. Patients with CSX had a lower brachial artery dilation ratio than controls but higher than that of CAD patients. Control subjects and CSX patients had higher endothelin-1 levels than CAD patients. CSX patients were found to have worse endothelial function than healthy volunteers, but patients with CAD had even worse endothelium function than CSX patients.

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Section: Discussionsupporting

confidence: 49%

Brachial Artery Flow-Mediated Vasodilation in Patients With Cardiac Syndrome X

Lee

Chen

et al. 2008

Angiology

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“…8 The presence of microvascular dysfunction has been confirmed by several studies, demonstrating an impairment of both endothelium-dependent and endothelium-independent coronary vasodilatation. 19 The endothelium produces diverse vasoactive substances such as vasodilator NO and vasoconstrictor endothelin and the balanced opposition of these substances determine vascular tone.…”

Section: Discussionmentioning

confidence: 84%

Intron 4 VNTR Polymorphism of eNOS Gene is Protective for Cardiac Syndrome X

Sinici¹,

Atalar²,

Kepez³

et al. 2010

Journal of Investigative Medicine

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Microvascular abnormalities caused by endothelial dysfunction seem to be responsible for the myocardial ischemia in patients with cardiac syndrome X (CSX). Nitric oxide is a key mediator of endothelial function and is synthesized by endothelial nitric oxide synthase (eNOS). We investigated if the 3 potential polymorphisms of the eNOS gene (VNTR in intron 4, T786C polymorphism in the promoter region, and G894T polymorphism in exon 7) are independent risk factors for CSX. Sixty-nine patients with CSX and 73 healthy controls were studied. Genotypes were determined through polymerase chain reaction with or without restriction endonuclease digestions. Genotype distribution was significantly different between patients with CSX and controls for intron 4aa (allele for 4 repeats of 27 bp), intron 4aa genotype frequency being 3.2% and 6.8%, respectively. The presence of intron 4a is 3.2 (odds ratio) times protective (95% confidence interval, 1.5-6.8) for the risk of CSX disease. The protective effect of intron 4a polymorphism also holds after adjustment for age and sex and when the study group is limited to those without hypertension and hyperlipidemia. No significant difference was observed in genotype distribution of G894T and T786C polymorphism between patients with CSX and controls. In conclusion, intron 4aa genotype of eNOS gene is protective for CSX. No association was found between promoter and exon 7 polymorphisms of eNOS gene and CSX.

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“…Lerman et al [35,36] demonstrated that coronary endothelial dysfunction in humans is characterized by increased coronary and circulating endothelin-1 with a higher increase after pacing [34]. Moreover, the nitric oxide/endothelin-1 ratio was found decreased in patients with cardiac syndrome X [32], while endothelin-1 levels positively correlated with fasting asymmetric dimethylarginine levels [48].…”

Section: Endothelin-1 and Cardiac Syndrome Xmentioning

confidence: 99%

Role of Endothelial Dysfunction and Insulin Resistance in Angina Pectoris and Normal Coronary Angiogram

Monti

Piatti²

2005

Herz

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Angina pectoris and a normal coronary angiogram or cardiac syndrome X is a heterogeneous syndrome that probably encompasses different pathophysiological entities. Patients affected by cardiac syndrome X are often women presenting with severe, invalidating chest pain. However, there is a significant discrepancy among the severity of symptoms, the lack of hemodynamic evidence of myocardial ischemia and the relatively benign long-term prognosis. The vascular endothelium has numerous important functions, including the regulation of vascular tone, blood flow and permeability, secreting both vasorelaxing and vasoconstricting factors. It has been found that both endothelium and non-endothelium-mediated coronary blood flow are impaired in patients with cardiac syndrome X. Interestingly, it has been shown that impaired nitric oxide-dependent vasodilation could increase coronary microvessel tone and produce spasm. It has also been reported that circulating endothelin-1 levels are elevated with a direct relationship between endothelin-1 levels and impaired coronary flow reserve in these patients. In addition, patients with high endothelin-1 levels showed a time onset of chest pain during exercise significantly lower compared to patients with low endothelin-1 concentrations. Moreover, the nitric oxide/endothelin-1 ratio was found decreased in patients with cardiac syndrome X and endothelin-1 levels were also positively correlated with fasting asymmetric dimethylarginine levels. All in all, these data suggest a role of endothelial dysfunction as a cause of regional myocardial and peripheral blood flow abnormalities. Further studies are necessary to characterize the prevailing mechanisms determining alterations in nitric oxide/endothelin-1 pathway in these patients, in order to find new therapies able to improve both quality of life and prognosis.

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Biochemical parameters of endothelial dysfunction in cardiological syndrome X

Cited by 22 publications

References 5 publications

Brachial Artery Flow-Mediated Vasodilation in Patients With Cardiac Syndrome X

Brachial Artery Flow-Mediated Vasodilation in Patients With Cardiac Syndrome X

Intron 4 VNTR Polymorphism of eNOS Gene is Protective for Cardiac Syndrome X

Role of Endothelial Dysfunction and Insulin Resistance in Angina Pectoris and Normal Coronary Angiogram

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