Byung Gyu Kim et al.: Reduced systemic vascular resistance is the underlying hemodynamic mechanism in nitrate-stimulated vasovagal syncope during head-up tilt-table test.

Dear Editor

We read with great interest the well-crafted article by Kim et al. [1], which reported that presyncopal symptoms during nitrate-stimulated tilt-testing could be explained by decreased systemic vascular resistance (SVR) rather than reduced cardiac output (CO). The study setup is sound, but being accustomed to this methodology [2], [3], we noticed inaccuracies in Tables 2 and 3. The SVR values appear correct, whereas the systemic vascular resistance index (SVRI) values presented seem incorrect. SVR is calculated as 80*(MAP-CVP)/CO, where MAP is mean arterial pressure and CVP is central venous pressure. The normal values of SVR range from 800 to 1200 dynes s/cm5 [4], consistent with the original article [1]. SVRI is calculated as 80*(MAP-CVP)/CI, where CI is cardiac index [5]; and the formula equals 80*(MAP-CVP)/(CO/BSA), where BSA is body surface area. This formula may also be presented as SVRI=SVR*BSA, and the normal values of SVRI range from 1900 to 2400 dynes s m2/cm5 [2], [3], [5]. Notably, the reported SVRI values in the article by Kim et al. [1] range from 612 to 683 and the units are given as dynes s/cm5/m2, indicating that the SVR values were divided and not multiplied by BSA. The correct SVRI units should be presented as either dynes s/(cm5/m2) or dynes s*m2/cm5. We estimated that the proper SVRI values in the study conducted by Kim et al. [1] would range from 1900 to 2300 dynes s m2/cm5. We agree with the general results and conclusions of the article; however, the SVRI results should be recalculated.

Conflict of interest

All authors declare no conflict of interest related to this study.