CONTENT

To the Editor,

I sincerely thank you for the interest and constructive comments¹ regarding my recent article.² In this study, I investigated the association between whole blood viscosity (WBV) and in-stent restenosis (ISR) in patients with chronic coronary syndrome who had undergone coronary stent implantation. I demonstrated that both high-shear rate and low-shear rate WBV were independent predictors of ISR, thereby contributing to the growing body of evidence in this field.²

As noted, the retrospective and single-center design inherently carries limitations in terms of internal validity. However, I believe that the relatively large sample size in my study helped reduce the potential impact of selection bias. Furthermore, while certain procedural details such as stent type, diameter, length, and adjunctive techniques were not fully available, I explicitly acknowledged this as a limitation. These factors are indeed recognized to influence ISR outcomes, as reported in previous literature.^3,4

In my study, WBV was not directly measured using a viscometer but instead estimated from hematocrit and plasma protein levels using the validated De Simone formula. Although this approach may be influenced by biological variability, it has been widely utilized in cardiovascular research.⁵ Importantly, the recent work of Nwose and Bwititi reaffirmed its clinical applicability, showing that the method provides acceptable sensitivity and specificity.⁶ For this reason, I consider my approach both practical and valid for large patient populations. Nevertheless, I agree that additional hemorheological parameters, such as plasma viscosity and erythrocyte deformability, could provide deeper insights into the mechanisms of ISR.

My cohort was restricted to patients undergoing angiography for chronic coronary syndrome, which inevitably limits generalizability to acute coronary syndromes, where inflammatory and rheological conditions are different. However, I believe that my findings provide preliminary evidence supporting WBV as a potential predictor of ISR and can form the basis for larger, multicenter, prospective studies.

In conclusion, I acknowledge the limitations emphasized and appreciate the perspective that further studies are warranted. I would like to highlight once more that while my results suggest a promising role for WBV, its integration into clinical decision-making will only be clarified through prospective investigations with standardized protocols and diverse populations.

Footnotes

Declaration of Interests: The author has no conflicts of interest to declare.

References

1. Süygün H. Comments on “evaluation of whole blood viscosity to predict stent restenosis”. Anatol J Cardiol. 2026;30(1):66-67.
2. Çalapkulu Y, Erdoğan M, Aslan AN. Evaluation of whole blood viscosity to predict stent restenosis in patients with coronary artery disease. Anatol J Cardiol. 2025;29(9):503-511.
3. Buccheri D, Piraino D, Andolina G, Cortese B. Understanding and managing in-stent restenosis: a review of clinical data, from pathogenesis to treatment. J Thorac Dis. 2016;8(10):E1150-E1162.
4. Alfonso F, Byrne RA, Rivero F, Kastrati A. Current treatment of in-stent restenosis. J Am Coll Cardiol. 2014;63(24):2659-2673.
5. De Simone G, Devereux RB, Chien S, Alderman MH, Atlas SA, Laragh JH. Relation of blood viscosity to demographic and physiologic variables and to cardiovascular risk factors in apparently normal adults. Circulation. 1990;81(1):107-117.
6. Nwose E, Bwititi P. Whole blood viscosity: affordances and re-evaluation of sensitivity and specificity for clinical use. Int J Biomed Lab Sci (IJBLS). 2022;11(2):96-103.