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. 2024 Dec 31:9:e217-e225.
doi: 10.5114/amsad/196826. eCollection 2024.

Cardiac complications of arteriovenous access: a narrative review from a multidisciplinary team perspective

Affiliations

Cardiac complications of arteriovenous access: a narrative review from a multidisciplinary team perspective

Melina Stathopoulou et al. Arch Med Sci Atheroscler Dis. .

Abstract

Although cardiovascular disease is common among hemodialysis patients, arteriovenous access creation has been invariably implicated in the evolution of adverse cardiac outcomes or deterioration of pre-existing cardiovascular disease. In most cases, these effects are subclinical but with potential underlying echocardiographic findings. Compared with grafts, arteriovenous fistulas are implicated more often, due to the progressively increased flow from the continuous dilatation of the venous outflow tract in the long term. The increasing flow is in the majority of patients well tolerated by cardiac adaptive alterations. However, the clinical impact is based on the balance between the amount of flow volume and the patient's cardiac reserves. Having extensively reviewed the existing English literature, we present the pathophysiology and the different types of cardiovascular complications, the indications, types, and efficacy of flow-restrictive procedures in the context of a high-flow AVF, as well as some precautions and considerations for AVF creation in high-risk patients.

Keywords: arteriovenous fistula; end stage renal disease; flow-restrictive procedures; heart failure; high flow vascular access.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
AV access forms a parallel circuit to the systemic circulation leading postoperatively to lower peripheral resistance, increase in CO, contractility, stroke volume and heart rate SVC – superior vena cava, LPA – left pulmonary artery, RPA – right pulmonary artery, IVC – inferior vena cava, MAP – mean arterial pressure, CO – cardiac output, Qa – AVF flow rate, AR – AVF resistance, SVR – systemic vascular resistance, TPVR – total peripheral vascular resistance (TPVR = PVR + AR).
Figure 2
Figure 2
Emerging clinical symptoms are the result of the balance between the magnitude of the AVF flow and the amount of cardiac reserves
Figure 3
Figure 3
Upper arm AVF in a 55-year-old male patient with severely dilated superficial venous system (purple arrows: cephalic vein, green arrow: basilica vein, orange arrow: site of AVF anastomosis). Upper arm arteries were also severely dilated. AVF flow was 3.7 l/min. AVF was ligated
Figure 4
Figure 4
An asymptomatic patient with a well-tolerated high-flow AVF (transposed basilic vein). A – A flow volume > 3 l/min was measured at the brachial artery. B – Echocardiography depicted mild dilated and hypertrophied LV due to volume overload (green arrow: myocardial wall thickness, red arrow: myocardial septal thickness, purple arrow: LV diameter) with systolic indices (LV ejection fraction and global longitudinal strain) in the upper normal range. C – Global longitudinal strain: –19% (green-yellow arrow). D – LVEF: 64% (gray-blue arrow: LV diastole, white-green arrow: LV systole)
Figure 5
Figure 5
Heart failure classification of the New York Heart Association (NYHA)

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