Renal dysfunction in syndrome Y

Abstract

We thank Dr Yalta et al. for their interest in our case report [1] and for their contribution in the definition of what we believe is a poorly understood condition [2]. Beyond endothelial dysfunction (or rather in the context of endothelial dysfunction), renal insufficiency is often associated with coronary calcifications and hemorheological abnormalities which provide a likely background for their observations [3]. On the other side, renal dysfunction is generally associated with anemia and reduced blood viscosity, which might compensate for the increased vascular tone (and TIMI frame count) brought about by the worsening of endothelial function. Both creatinine and blood urea nitrogen were normal in our patient. Admittedly, glomerular filtration rate was not assessed and therefore we cannot exclude that some subclinical degree of impairment might be present. We felt however that the possibility of a relationship between these conditions was interesting, and we tried to address it in a larger database (n=135 patients, in which the corrected thrombolysis in myocardial infarction frame count was assessed). Even in this larger cohort of patients, we found no relationship between TIMI frame count and blood parameters of renal function (R=0.004 for creatinine, R=0.03 for urea nitrogen, PN0.5). Thus, in our hands, TIMI frame count was not associated with renal function (or lack thereof). It remains open for discussion whether the assessment of renal function using more sophisticated techniques—which allow identifying subclinical renal dysfunction— may yield different results, and the hypothesis of Dr. Yalta is nonetheless well taken. We disagree with Dr. Yalta et al. when they state that, as compared with other coronary microvascular syndromes (i.e. the “traditional” syndrome X), coronary slow flow is more commonly associated with other cardiac and extracardiac conditions. We rather believe that there is a need for a classification of the slow flow phenomenon, and for the identification of “primary” syndromes (i.e. those in which the slow flow phenomenon cannot be explained by the presence of concomitant diseases), from “secondary” syndromes (for instance the slow flow that can be observed in patients with myocardial infarction, percutaneous interventions, coronary ectasia, severe bradycardia, or elevated left ventricular end diastolic pressure) [4]. We feel that the term “syndrome Y” should be used only for the former (or at least that the distinction between primary and secondary form should be acknowledged); in this sense renal dysfunction might also be considered an exclusion criteria. The slow flow phenomenon remains a poorly understood condition, andmost of the contributions are still—unfortunately—anecdotal. Further, in the absence of adequate experimental models, an evidence of association (including our own association with flow-mediated constriction) cannot be taken as a direct proof of causality. There is a need for a classification of the disease, for experimental models, and for large patient series. What we are sure of, as Dr Yalta will concur, is that the slowflowphenomenon is not “just an angiographic curiosity”: a TIMI frame count as high as 50—or even 100—reflects a severe impairment in myocardial perfusion, and should be taken as such. The authors have read and comply with the rules for ethical authorship and publishing of the International Journal of Cardiology [5].