Relationship between the elevated mean platelet volume and coronary microvascular function in patients with idiopathic dilated cardiomyopathy

To the editor

We have read with great interest the recently published report of Erdogan et al. [1], related to the relationship of mean platelet volume (MPV) and coronary microvascular function in patients with idiopathic dilated cardiomyopathy. In this recent study, patients with idiopathic dilated cardiomyopathy have underwent echocardiographic examination including coronary flow reserve (CFR) measurement, and patients with lower CFR were found to have higher MPV values. Also, MPV was found to be the independent predictor of lower CFR.

As it is known, platelet volume is a marker of platelet activation and function, and is measured using MPV [2]. Although MPV levels reflect the changes in thrombopoiesis, inflammatory changes can also cause increases in MPV levels [3]. In patients with established cardiovascular disease, elevated MVP may be marker for adverse cardiovascular events [4]. Large platelets are metabolically and enzymatically more active than small platelets [5], [6]. Larger platelets are denser and contain more α-granules, which can release prothrombotic substances, including thromboxane A2, platelet factor 4, P-selectin, platelet derived growth factor, and chemotactic and mitogenic factors contributing to vascular neointimal proliferation [5], [7]. Several reports have demonstrated that MPV was associated with impaired myocardial perfusion after primary angioplasty [8], [9].

Moreover in a recent study of Açikgoz et al. [10], in patients with ischemic and idiopathic cardiomyopathies, elevated MPV was found to be positively correlated with the increased left ventricular (LV) diameter and inversely correlated with the low ejection fraction. Furthermore, Yilmaz et al. [11] showed that MPV increased in patients with dilated cardiomyopathy and LV thrombosis. In another study [12], it was demonstrated that platelet survival is shortened in patients with dilated cardiomyopathy, which in turn can cause the production of megakaryocytes in the bone marrow.

On the other hand, attenuated CFR has been reported in patients with idiopathic dilated cardiomyopathy because of coronary microvascular dysfunction [13]. Although the mechanism of the altered CFR in idiopathic dilated cardiomyopathy is not fully understood, impairment of CFR may lead to myocardial ischemia, progression of LV dysfunction, congestive heart failure, and increased mortality [14], [15].

In conclusion, we can say that attenuated CFR is a poor prognostic marker in patients with idiopathic dilated cardiomyopathy. On the other hand, although in some studies, increased MPV levels were found to be associated with adverse cardiovascular events, for now MPV is an important, simple, effortless, and cost effective tool which reflects the changes in thrombopoiesis. Larger platelets may play a role in the pathogenesis of microvascular dysfunction through the secretion of prothrombotic, vasoconstrictor, and inflammatory mediators. So, in the light of this study [1], in patients with dilated idiopathic cardiomyopathy, high MPV could be considered as a biomarker of impairment of coronary flow. Therefore, in this group of patients, it can be suggested that new studies should be carried out in order to assess if tailoring therapy can impact on microcirculatory function.