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The systemic immune inflammation index (SII; platelet count x neutrophil-lymphocyte ratio), a new marker, predicts adverse clinical outcomes in many conditions, including acute and chronic coronary syndromes, pulmonary embolism, cancers, and contrast nephropathy. The aim of this study was to determine the relationship between SII and microvascular dysfunction in patients with Cardiac Syndrome X (CSX); 105 patients with CSX and 105 patients with normal coronary arteries were included. Microvascular dysfunction was determined angiographically using myocardial blush grade (MBG) and total myocardial blush score (TMBS). We observed that the SII levels were higher in the CSX (+) group (687 [355–2211] vs 418 [198–1614], P <.001). The SII levels were also found to be significant independent predictors for CSX in multiple regression analysis (P =.001). SII levels >440 had 83.8% sensitivity and 55.2% specificity (area under the curve [AUC]:.923, 95% CI:.895–.999, P <.001) for predicting CSX. There is a significant correlation between SII levels and CSX. [ABSTRACT FROM AUTHOR]

We compared Turkish patients with cardiac syndrome X (CSX) and controls with respect to serum pro- and anti-inflammatory cytokine levels, as well as the single-nucleotide polymorphisms located in the promoter regions of their related genes. This study included 111 consecutive patients angiographically diagnosed with CSX and 111 healthy controls with similar demographic characteristics. Serum interleukin (IL) 6, tumor necrosis factor α (TNF-α), and IL-10 levels were measured, and the genotypes of the patients and controls were determined using standard methods. Serum IL-6 and IL-10 levels were significantly higher in the CSX group than in the control group (P < .01, respectively). Serum TNF-α level was lower in the CSX group than in the control group (P < .001). On the other hand, participants with CSX and healthy controls were not significantly different with respect to the genotype distributions of IL-6, TNF-α, and IL-10 genes. As a result of our study, both pro-inflammatory and anti-inflammatory cytokines may play a role in the pathogenesis of CSX. In contrast, the studied gene polymorphisms did not influence CSX pathogenesis. [ABSTRACT FROM AUTHOR]

Up to half of patients with signs and symptoms of stable ischemic heart disease have non-obstructive coronary artery disease (NoCAD). Recent evidence demonstrates that two-thirds of patients with NoCAD have demonstrable coronary endothelial dysfunction represented by microvascular or diffuse epicardial spasm following acetylcholine challenge. Patients with coronary endothelial dysfunction are recognized to have significant health services use and morbidity as well as increased risk of developing flow-limiting coronary artery disease and myocardial events, including death. Currently, there are few centers that test for this etiology owing to lack of knowledge, limited evidence for treatment options and invasive diagnostic strategies. This article reviews the pathophysiology, epidemiology, diagnosis and treatment of coronary endothelial dysfunction as a subgroup of NoCAD. [ABSTRACT FROM AUTHOR]

Neutrophils and lymphocytes (N/L) ratio and carotid intima–media thickness (C-IMT) value have been studied as new predictors of cardiovascular risk. We aimed to investigate N/L ratio and C-IMT value in patients with cardiac syndrome X (CSX) and compare patients with coronary artery disease (CAD) and normal participants. A total of 288 participants were enrolled in the study. The N/L ratio and C-IMT value were compared among the 3 groups. There were no statistically significant differences in N/L levels between CSX and CAD groups. The N/L ratio was found significantly increased in patients with CSX and CAD, compared to the control group. Patients with CAD and CSX had significantly higher C-IMT value compared to control participants. Significant positive correlation was found between C-IMT value and plasma level of N/L ratio. The relationship among CSX and higher N/L ratio level and C-IMT suggests that endothelial dysfunction may contribute to the etiopathogenesis of the CSX. [ABSTRACT FROM PUBLISHER]

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. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]