Neuropeptide Y-induced coronary microvascular dysfunction: A significant contributor to the adverse outcomes in stress cardiomyopathy?

Abstract

⁎ Corresponding author. E-mail address: kyalta@gmail.com (K. Yalta). In their recently published article, Szardien et al. reported a 78year-old female patient who had suffered stress cardiomyopathy (SCM) accompanied by increased serum levels of neuropeptide Y (NPY) [1]. We agree with the authors that increased serum NPY levels may contribute to myocardial contractile dysfunction and hence may also be regarded as a prognostic marker in patients with SCM [1]. However, in the setting of SCM with substantial NPY levels, NPYinduced coronary microvascular dysfunction, as described below, may also contribute significantly to the adverse clinical outcomes including ischemic malign arrhythmias, etc. Transient wall motion abnormalities including left ventricular apical ballooning have been regarded as one of the main characteristics of SCM [2]. Catecholamine-induced myocardial dysfunction, coronary microvascular dysfunction and coronary spasm etc have been suggested as potential etiologies of this entity. Recently, NPY has also been suggested to contribute to myocardial dysfunction in SCM indicating its potential prognostic value [1]. Notwithstanding the generally accepted benign nature of SCM, relatively high rates of malign ventricular arrhythmias and mortality were reported in some patient series [3]. Even though the exact mechanisms leading to adverse events (malign ventricular arrhythmia, etc.) in SCM is still largely unknown, severe coronary microvascular dysfunction may be considered as a potential trigger in some patients. Endothelial dysfunction [4] and increased serum NPY (a vasoconstrictor hormone) [5] levels are well known to play the central role in the pathogenesis of coronary microvascular syndromes. Among these syndromes, coronary syndrome Y (characterized by coronary slow flow (CSF)) is associated with enhanced coronary resistance, and may present with the clinical picture of acute coronary syndrome (ACS) along with an increased proclivity to cardiac arrhythmias [4]. Similarly, in the setting of SCM, severe and transient coronary microvascular dysfunction induced by excessive levels of NPY may be associated with adverse clinical outcomes including ischemic malign arrhythmic events and sudden cardiac death (SCD), etc. (regardless of the presence of severe left ventricular systolic dysfunction). Therefore, besides clinical presentation, SCM with excessive NPY levels may resemble ACSs in terms of prognostic features. Even though, the case reported by Szardien et al. [1] did not suffer any SCM-related adverse event, substantial levels of NPY might indicate the possibility of severe coronary microvascular dysfunction (with or without CSF) in this case. It may be suggested that NPY-induced severe coronary microvascular dysfunction may account for life-threatening ischemic adverse events including malign ventricular arrhythmias in SCM patients with substantial levels of NPY during the disease course. Therefore, these patients may be regarded as a subgroup with potentially worse prognosis due to severe coronary microvascular dysfunction indicating the need for close monitoring and aggressive management as in the event of ACSs. Besides conventional therapeutic strategies including management of heart failure, arrhythmias and anticoagulation, etc., targeting enhancement of coronary blood flow along with the use of intensive anti-ischemic regimens may be of clinical value during the disease course and may help improve prognosis in SCM patients with substantial serum levels of NPY. The authors of this manuscript have certified that they comply with the Principles of Ethical Publishing in the International Journal of Cardiology [6].