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. 2024 Feb 29;11(3):1810–1811. doi: 10.1002/ehf2.14735

Reply to: ‘Non‐invasively assessed hemodynamics in patients with high flow arteriovenous fistula and high output cardiac failure’

Dan‐Ying Lee 1,2, Wei‐Chieh Huang 1,✉, Cheng‐Hsueh Wu 1,✉, Chih‐Yu Yang 3,✉
PMCID: PMC11098621  PMID: 38424001

In response:

We would like to thank Dr Kristína Burýšková Salajová et al. for their comments on our article. We have carefully read through all suggestions and made necessary responses based on these comments.

In the method section, high output cardiac failure (HOCF) hospitalization was defined as symptomatic HF (stage C or D) with a high output status [cardiac output (CO) value > 8 or cardiac index (CI) > 4]. In 19 patients with HOCF hospitalization, all patients receive more frequent haemodialysis or haemodialysis with a lower dry weight setting to treat fluid overload. Six of the HOCF patients with residual urine output received diuretics. Other medications included nitrates (n = 6, 31.5%), angiotensin‐converting enzyme inhibitors or angiotensin receptor blockers (n = 10, 52.6%), beta‐blockers (n = 13, 68.4%), and calcium channel blockers (n = 7, 36.8%). And nearly half of HOCF patients received banding surgery for Qa reduction (n = 9, 47.3%).

We re‐collected and re‐analysed our data at the index visit. The majority of the patients included in this study were free of HF symptoms when they received follow‐up echocardiography (n = 100, 91.7%). Two of nine patients with HF symptoms had high output status (CO value > 8 or CI > 4) and received banding surgery for flow reduction (2/9, 22%). In the remaining 100 patients without HF symptoms at the index visit, 7 patients received banding surgery (n = 7/100, 7%). All patients who received banding surgery in this study fulfilled the criteria of HOCF and were included in the HOCF group.

There is no consensus on the definition of a high‐flow arteriovenous fistula (AVF) currently. Based on the guidelines of the Vascular Access Society, an arteriovenous access flow rate (Qa) of 1–1.5 L/min or a Qa of >20% of the CO (Qa/CO) has been suggested as the criteria to define high‐flow AVF. 1 Generally, the access flow is lower in the forearm and higher in the upper arm AVF (500–900 vs. 900–1500 mL/min). 2 , 3 In our study, 27.5% of patients had brachiocephalic AVF, so we chose the upper limit of the access flow in the upper arm. In the landmark study conducted by Basile et al., a threshold of Qa value ≥ 2000 mL/min was first introduced to predict HOCF in patients undergoing haemodialysis with excellent predictive performance. 4 However, the HOCF group had a higher Qa value (P = 0.045), but the percentage of Qa > 2000 L/min is not significantly different between the HOCF group and the non‐HOCF group (P = 0.094) in our study. 5 This result could be interpreted as the patient with Qa between 1500 and 2000 L/min also having a chance to develop HOCF if the estimated vascular resistance is low. The important concept we want to illustrate is that the high‐flow AVF is associated with but not equal to the development of HOCF. Lowering the Qa threshold to recruit the study population also helps us evaluate the relationship between vascular resistance and HOCF more comprehensively. Further recruiting relative normal access flow as a control group is required to assess the potential predictive value of estimated systemic vascular resistance (SVR) in haemodialysis patients with AVF.

The main reason we did not use the following formula [mean arterial pressure (MAP) − central venous pressure (CVP)]/CO to calculate vascular resistance is that the echocardiography‐derived CVP level has limitations in determining the exact value. First, CVP is identical to right atrial pressure (RAP) under the premise of the absence of vena cava obstruction. Second, the echocardiography‐derived CVP level could be classified only into three categories: normal (mean RAP 3 mmHg, range 0–5 mmHg), intermediate (mean RAP 8 mmHg, range 5–10 mmHg), and high (mean RAP 15 mmHg, range 10–20 mmHg). Applying the mean CVP level to the formula may cause absolute errors. In addition, a previous study reported that the approach of estimating CVP using two‐dimensional echocardiography (2DE) by assessing inferior vena cava (IVC) size in the subcostal view has high interobserver variability, and the agreement with invasive measurement is poor. 6 Three‐dimensional echocardiography may be a better choice to evaluate IVC geometry, allowing a more accurate correlation with invasively measured CVP. 7 We also agreed that the concept of effective CO (the difference between the total CO and AVF flow) comes with the SVR [total vascular resistance (TVR)–AVF resistance] and is more specific. We used the term SVR based on the study of Reddy et al., in which the SVR was calculated from the pressure drop across the systemic circulations (MAP–RAP) multiplied by 80, divided by CO via invasive right heart catheterization. Therefore, Reddy et al. also estimated TVR according to the definition in the study of Malik et al., 8 and the TVR was still lower in the HOCF group than in the control group (8.5 ± 3.0 vs. 18.3 ± 5.9 wood units; P < 0.0001). In the shunt‐related HOCF in the study of Reddy et al., the TVR was 9.8 (6.8–12.4) wood units, which is lower than the symptomatic HF patient in the study of Malik et al. (12 ± 4 wood units) and HOCF patients in our study (14.4 ± 3.5 wood units), which may be due to systematic underestimation of 2DE‐derived CVP level and overestimation of routine predialysis and post‐dialysis systolic blood pressure. 6 , 9 , 10 We also re‐collected and re‐analysed our data based on your suggestion, and the result still showed a statistically significant difference between the non‐HOCF and HOCF groups in SVR (21.6 ± 6.3 vs. 26.2 ± 13.1 wood units; P = 0.02) and a trend for lower TVR in the HOCF group (14.4 ± 3.5 vs. 16.9 ± 6.0 wood units; P = 0.07). It would be interesting to analyse the post‐banding surgery resistance change of the nine patients in our study to see the change in SVR and TVR. Finally, I would like to restate that our study is a retrospective study with a small sample size and several limitations. Additional high‐quality studies with invasive haemodynamic examinations are required to validate the non‐invasive estimated SVR.

Lee, D.‐Y. , Huang, W.‐C. , Wu, C.‐H. , and Yang, C.‐Y. (2024) Reply to: ‘Non‐invasively assessed hemodynamics in patients with high flow arteriovenous fistula and high output cardiac failure’. ESC Heart Failure, 11: 1810–1811. 10.1002/ehf2.14735.

Contributor Information

Wei‐Chieh Huang, Email: chwu6@vghtpe.gov.tw, Email: hwcc0314@gmail.com.

Cheng‐Hsueh Wu, Email: chwu6@vghtpe.gov.tw.

Chih‐Yu Yang, Email: cyyang3@vghtpe.gov.tw.

References

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