Pulse Wave Velocity and Augmentation Index in Renal Transplant Recipients - 4.6 Years Follow Up

Abstract Background and Aims Fluid overload and vascular stiffness are two independent predictors of cardiovascular events in hemodialysis (HD) patients. To date, observational and interventional studies that investigated the effect of inter- and intradialytic fluid overload changes on vascular stiffness in HD patients are very limited. We performed a scoping review to explore existing reports about effects of fluid overload on vascular stiffness in adults receiving HD treatment and to identify knowledge gaps for future research. Method We followed the framework originally developed by Arksey and O’Malley. We searched Medline, Embase, CINAHL, and Cochrane Database of systematic reviews from inception to October 29, 2019. References of review papers were screened for relevant studies not identified from the initial search until saturation is achieved. Results Of 666 eligible studies, nineteen studies met the inclusion criteria. These included clinical observational studies (n=16) and randomized controlled trials (n=3). In general, most of the identified studies had small sample size and short term of follow up. Studies use different definitions of fluid overload and vascular stiffness. Measures of relative fluid overload like the ratio of extracellular fluid/intracellular fluid, fluid overload/extracellular fluid, and/or extracellular fluid/total body fluid were used as a representative of fluid status. Pulse wave velocity and augmentation index were used interchangeably as vascular stiffness measures. The accumulated findings were inconsistent and inconclusive. There was no consensus whether intradialytic fluid volume changes affected vascular stiffness. In the majority of the observational studies, a decrease in pulse wave velocity or augmentation index correlated with a decrease in blood pressure after fluid correction by HD treatment. The randomized clinical trials used different methods and technologies for the correction of fluid overload, thereby, results were conflicting. Conclusion Current literature is insufficient to justify whether fluid overload changes have a direct effect on vascular stiffness in HD patients. The findings were conflicting which limits the comparisons of studies and generalization of findings. These knowledge gaps urge the need for further clinical studies to enhance the understanding and to improve the quality of research in this topic. This includes standardized definitions and methodologies as well as longer term of follow up.

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Changes in Noninvasive Arterial Stiffness and Central Blood Pressure After Endovascular Abdominal Aneurysm Repair

Journal of Endovascular Therapy ◽

10.1177/15266028211007460 ◽

2021 ◽

pp. 152660282110074

Author(s):

Suzanne Holewijn ◽

Jenske J. M. Vermeulen ◽

Majorie van Helvert ◽

Lennart van de Velde ◽

Michel M. P. J. Reijnen

Keyword(s):

Aortic Aneurysm ◽

Pulse Wave Velocity ◽

Wave Velocity ◽

Pulse Wave ◽

Augmentation Index ◽

Central Pressure ◽

Pressure Waveform ◽

Aneurysm Repair ◽

The Impact

Purpose: To evaluate the impact of elective endovascular aneurysm repair (EVAR) on the carotid-femoral pulse wave velocity (cfPWV) and central pressure waveform, through 1-year follow-up. Materials and Methods: A tonometric device was used to measure cfPWV and estimate the central pressure waveform in 20 patients with an infrarenal abdominal aortic aneurysm scheduled for elective EVAR. The evaluated central hemodynamic parameters included the central pressures, the augmentation index (AIx), and the subendocardial viability ratio (SEVR). AIx quantifies the contribution of reflected wave to the central systolic pressure, whereas SEVR describes the myocardial perfusion relative to the cardiac workload. Measurements were performed before EVAR, at discharge, and 6 weeks and 1 year after EVAR. Results: CfPWV was increased at discharge (12.4±0.4 vs 11.3±0.5 m/s at baseline; p=0.005) and remained elevated over the course of 1-year follow-up (6 weeks: cfPWV = 12.2±0.5 m/s; 1 year: cfPWV = 12.2±0.7 m/s, p<0.05). After an initial drop in systolic central pressure at discharge, all the central pressures increased thereafter up to 1 year, without significant differences compared with baseline. The same was observed for the AIx and SEVR. Conclusion: Endovascular aortic aneurysm repair caused an increase in pulse wave velocity compared with baseline, which remained elevated through 1 year follow-up, which may be related to an increased cardiovascular risk. However, no differences in central pressure, augmentation index, and subendocardial viability ration were observed during follow-up.

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