| Literature DB >> 33556504 |
Syeda Anum Zahra1, Rozina Yasmin Choudhury1, Kamran Basharat1, Tien Tran1, Munira Begum1, Ahmed Abotabekh1, Fatemeh Hedayat2, Lara Rimmer3, Amer Harky4, Mohamad Bashir5.
Abstract
High-output cardiac failure is a rare form of heart failure associated with the formation of arteriovenous fistula (AVF) in hemodialysis patients. The pathophysiology underlying the HOCF is complex and multifactorial. Presence of AVF can cause long term hemodynamic changes that ultimately lead to increased cardiac output and consequently cardiac failure. A number of risk factors have been associated with the development of HOCF post-AVF construction, including male sex, a proximally located AVF and a state of volume overload. Dysregulation of tissue inhibitor of matrix metalloproteinase 4, Sirtuin-1 and Sirtuin-3 gene expression have been associated with the development of heart failure. The differences observed between genders have been attributed to altered activity of the β-adrenoceptor system. Numerous biomarkers including cardiac troponin T and I, atrial natriuretic peptide, brain natriuretic peptide among others have shown both prognostic and diagnostic potential; however further research is needed to establish their utility in clinical practice for patients with AVF associated HOCF. In recent years risk stratification models have been developed to help identify patients at the highest risk of developing HOCF post AVF which could be revolutionary in its identification and management. Potential options for managing HOCF post-AVF include AVF ligation, banding and anastoplasty however these procedures are not without their own associated risks. In this review, we discuss the pathophysiology, risk stratification and management of patients with AVF associated HOCF.Entities:
Mesh:
Substances:
Year: 2021 PMID: 33556504 DOI: 10.1016/j.avsg.2021.01.071
Source DB: PubMed Journal: Ann Vasc Surg ISSN: 0890-5096 Impact factor: 1.466