Response to Kurtoglu and Balta

Abstract

As response to their comments: Our subjects can well be considered as healthy controls based on the fact that they did not have any symptoms of coronary artery disease and their physical examination did not reveal any suspicion of heart disease. In addition, their exercise test and myocardial perfusion study were normal. Their medical history was free from thyroid disorders, peripheral artery diseases, chronic obstructive pulmonary diseases and anaemia but, to keep the text condensed, the complete list of excluded disorders was not expressed in the article. As suggested by Kurtoglu and Balta, cardiac diastolic function is one of the factors that can influence cardiac autonomic control. Unfortunately, diastolic function was not assessed in our study. We also agree with Kurtoglu and Balta that psychosocial factors can influence HRV. As our subjects represent normal population, there is no reason to assume that results would have been biased on the group level by psychosocial factors. On the other hand, long-lasting psychosocial stress may also predispose to atherogenesis itself. The possible effects of psychosocial factors on HRV and atherogenesis, however, remained beyond the scope of the current study. Kurtoglu and Balta raised an interesting hypothesis about the possible role of specific sinoatrial (SA) node artery and atrioventricular node artery stenosis behind HRV alterations. The SA node receives blood supply from the SA node artery, which typically originates from the proximal right coronary artery (RCA). Thus, hypoxia of the SA node could result in reduced HRV. However, in our study none of the study subjects showed a significant stenosis of their very proximal RCA. Thus, the involvement of SA node perfusion in our study is an unlikely explanation for reduced HRV. On the other hand, the blood supply of the AV node is via the AV nodal artery which is often a branch of the right posterolateral artery, i.e. more distal part of RCA. As suggested by Kurtoglu and Balta, indeed, it is possible that reduced perfusion for the AV node could be one possible link between coronary atherosclerosis and impaired HRV.