Abstract

⁎ Corresponding author. E-mail address: kyalta@gmail.com (K. Yalta). In their recently published article, Muxel S et al. reported amalewith coronary slow flow (CSF) as measured with increased thrombolysis in myocardial infarction (TIMI) frame counts (TFC), and comment on the different clinical presentations and pathophysiological mechanisms of coronary syndromeXandY [1].We agreewith the authors that coronary syndrome X is generally characterized by impaired coronary vasodilation andcoronaryflow reservewhile coronary syndromeYoccurs due to enhanced coronary resistance leading to CSF [1]. Endothelial dysfunction plays the central role in the pathogenesis of coronary syndrome X and Y [1] indicating their potential co-existence in a portion of cases. However, compared to isolated coronary syndrome X, coronary syndrome Y is more likely to accompany and/or be associated with extra-cardiac pathologies potentially associated with endothelial dysfunction and subclinical myocardial fibrosis, etc. The association between renal disease and coronary syndrome Y, as described below, may potentially harbour some diagnostic, therapeutic and prognostic implications, and has recently drawn particular attention in the clinical setting. Chronic renal failure (CRF) is well known to induce endothelial dysfunction and consequent coronary atherosclerosis possibly due to a variety of CRF-induced pathologies including increased levels of asymmetric-dimethylarginine (ADMA) [2], inflammatory response and oxidative stress, accompanying hypertension, etc. Similarly, coronary syndrome Y (characterized by CSF) may be encountered in the setting of CRF, and may be regarded as a marker of coronary microvascular dysfunction that is largely attributable to increased microvascular resistance associated with endothelial dysfunction, subclinical myocardial fibrosis and hypertrophy [2,3], etc. Endothelial dysfunction is alsowell known to contribute to the pathogenesis of CRF. Therefore, coronary syndrome Y, coronary atherosclerosis and CRFmay share the same clinicopathological background, to some extent indicating the complex relationship among these entities. A recently published study demonstrated significant reductions in coronary blood flow in patients with end-stage renal disease (ESRD) regardless of the degree of epicardial coronary artery stenosis [3]. In another previous study by our group including patients with mild to moderate renal dysfunction and angiographically normal coronary arteries, we were able to demonstrate significant reductions in coronary blood flow as measured with increased TFC values compared to the control group with normal coronary arteries and renal functions [2]. It is also of note that in the patient group of our study, the values of TFC and calculated glomerular filtration rate (GFR) were also found to be independently correlated [2] indicating the close link between coronary syndrome Y and renal failure. Therefore, in the clinical setting, renal failure may accompany (as a result of generalized endothelial dysfunction) and/or beassociatedwith coronary syndromeY. Even though the renal statusof the case reported by Muxel S et al. [1] was not reported, the patient might have suffered some kind of subclinical or incipient renal failure (even with normal blood-urea-nitrogen (BUN) and creatinine levels), and hence may need to be thoroughly evaluated via other diagnostic modalities (GFR calculation, renal imaging, etc.) along with subsequent close follow-up for the possible emergence or progression of renal failure. Itmay be suggested that among coronarymicrovascular syndromes, coronary syndrome Y is more likely to accompany and/or be associated with extra-cardiac conditions (renal disease, etc. even in the subclinical stage) indicating the need for thorough evaluation of patients with this syndrome via various diagnostic modalities. In the setting of coronary syndrome Y (isolated or in combination with coronary syndrome X), besides targeting enhancement of coronary bloodflow, earlier diagnosis andmanagementof associated conditions including renal failuremaybe of utmost clinical value in the management of coronary microvascular dysfunction, and may possibly improve clinical outcomes including renal and cardiac adverse events. The authors of this manuscript have certified that they comply with the Principles of Ethical Publishing in the International Journal of Cardiology [4].

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