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Authors: Oğuzhan Çelik, Erkan Demirci, Mustafa Aydın, Turgut Karabag and Macit Kalçık

Background

Ghrelin has recently been reported to have beneficial effects on cardiac contractile functions and coronary blood flow. The main purpose of this study was to investigate the role of ghrelin in the pathogenesis of coronary slow flow (CSF) together with endothelial functions.

Methods

Twenty-five patients having normal coronary arteries with CSF and 25 controls with normal coronary flow were included into the study. The quantitative measurement of coronary blood flow was performed for each coronary artery using the thrombolysis in myocardial infarction (TIMI) frame count (TFC) method. Ghrelin levels were measured using the enzyme-linked immunosorbent assay method from venous blood samples. Endothelial functions were evaluated from the brachial artery with the flow-mediated dilation (FMD) and nitrate-related dilation methods.

Results

There was a significant difference in terms of mean TFC values between the control and CSF groups (p < 0.001 for all coronary arteries). The mean FMD percentage among patients with CSF was lower than that of the control group (5.9 ± 0.8 vs. 10.7% ± 1.1%; p < 0.001). A moderate negative correlation was observed between the FMD percentages and the TFCs. There was no relationship between the TFC and ghrelin levels.

Conclusion

Plasma ghrelin levels seem to be uninfluential while impaired endothelial functions play an important role in the etiopathogenesis of CSF.

Open access
Authors: Erkan Demirci, Oğuzhan Çelik, Macit Kalçık, Lütfü Bekar, Mucahit Yetim and Tolga Doğan

Background

Previous studies have demonstrated that homocysteine and asymmetric dimethyl arginine (ADMA) levels were strongly associated with cardiovascular diseases including coronary artery disease. The aim of this study was to investigate the role of plasma homocysteine and ADMA levels in the pathogenesis of coronary slow flow (CSF) phenomenon.

Methods

Twenty-three patients with CSF and 25 controls with normal coronary flow were included in this study. The quantitative measurement of coronary blood flow was performed using the thrombolysis in myocardial infarction frame count method. Plasma homocysteine and ADMA levels were determined using enzymatic assays from venous blood samples.

Results

The patients with CSF had significantly higher plasma homocysteine levels than controls (16.2 ± 7.6 vs. 12.2 ± 2.2 μM/L; p = 0.023). The uric acid levels were significantly higher in CSF group than controls (5.4 ± 1.1 vs. 4.6 ± 0.9 mg/dl; p = 0.011). Plasma ADMA levels were also higher in the CSF group; however, this was not statistically significant (0.6 ± 0.1 vs. 0.5 ± 0.2 μM/L; p = 0.475).

Conclusions

Increased homocysteine and uric acid levels may play an important role in the pathogenesis of CSF. Further large scale studies are required to determine the relationship between ADMA levels and CSF.

Open access