Abstract: TH-OR19
High-Flow Arteriovenous Fistula and Myocardial Fibrosis in Hemodialysis Patients With Non-Contrast Cardiac Magnetic Resonance Imaging
Session Information
- Dialysis: Patient-Centered Interventions and Outcomes
November 03, 2022 | Location: W414, Orange County Convention Center‚ West Building
Abstract Time: 05:42 PM - 05:51 PM
Category: Dialysis
- 703 Dialysis: Vascular Access
Authors
- Kim, Jwa-kyung, Hallym University Sacred Heart Hospital, Anyang, Gyeonggi-do, Korea (the Republic of)
- Moon, Sung Jin, Catholic Kwandong University International Saint Mary's Hospital, Incheon, Korea (the Republic of)
- Kim, Sungmin, Hallym University Sacred Heart Hospital, Anyang, Gyeonggi-do, Korea (the Republic of)
- Lee, Dong Hee, Hallym University Sacred Heart Hospital, Anyang, Gyeonggi-do, Korea (the Republic of)
- Kim, Sung Gyun, Hallym University Sacred Heart Hospital, Anyang, Gyeonggi-do, Korea (the Republic of)
Background
Myocardial fibrosis is a critical part of maladaptive cardiac remodeling that leads to heart failure (HF). In patients with chronic kidney disease, diffuse myocardial fibrosis is a typical uremic cardiomyopathy characteristic unrelated to ischemic heart disease. The role of high-flow arteriovenous fistula (AVF) in myocardial fibrosis in hemodialysis (HD) patients is very likely under-recognized.
Methods
Markers of myocardial damage, galectin-3 and N-terminal pro B-type natriuretic peptide (NT-proBNP), were measured in 101 HD patients who underwent regular monitoring of intra-access Qa. AVF with Qa >2 L/min was considered a high-flow AVF. The degree of myocardial fibrosis according to intra-access Qa was assessed by native T1 relaxation times on cardiac MRI and serum galectin-3.
Results
Compared to HV, HD patients showed a significantly higher galectin-3 value and increased T1 relaxation time, suggesting increased myocardial fibrosis in uremic conditions. In HD patients, 20 (19.8%) had a Qa >2 L/min, and they had significantly higher cardiac output, cardiac index, left ventricular mass, as well as increased T1 relaxation times than those with a Qa ≤2 L/min. Also, galectin-3 value and NT-proBNP levels were much higher in these patients with a high Qa, indicating a close relationship between increased Qa, myocardial fibrosis, and increased risk of HF. Notably, the association between higher Qa and myocardial fibrosis was independent of traditional risk factors as well as serum NT-proBNP and inflammatory marker, monocyte chemoattractant protein-1.
Conclusion
A supra-physiologically high Qa can be related to increased myocardial fibrosis and remodeling in HD patients. Regular Qa monitoring and early detection of myocardial fibrosis could be helpful for preventing further cardiac damage.