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Percutaneous Creation of a Central Iliac Arteriovenous Anastomosis for the Treatment of Arterial Hypertension

  • Mechanisms of Hypertension (M Weir, Section Editor)
  • Published:
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A Correction to this article was published on 01 March 2018

This article has been updated

Abstract

Purpose of Review

Provision of a summary on the physiologic effects of arteriovenous fistula creation and description of previously published human data on the efficacy of a percutaneously implanted device creating an arteriovenous fistula. Though antihypertensive therapy is effective, some patient’s blood pressure remains poorly controlled despite adherence to optimal medical therapy. Moreover, some patients are not compliant with recommended medical therapy due to side effects or personal decision. This has prompted exploration of alternative, device-based antihypertensive therapies including, among others, the percutaneous creation of an arteriovenous fistula. An arteriovenous fistula is accompanied by a number of favorable physiologic changes that may lower blood pressure. These physiologic changes, conduction of the procedure, and previously published human experience are summarized in this review article.

Recent Findings

The results of a recently published trial comparing arteriovenous fistula creation and standard antihypertensive therapy versus standard antihypertensive therapy alone are summarized.

Summary

Creation of an arteriovenous fistula is accompanied by a significant blood pressure reduction likely related to a reduction in total arterial resistance, perhaps blood volume reduction, inhibition of the baroreceptor reflex, and release of natriuretic peptides. These findings foster further interest in studying the impact of an arteriovenous fistula and arterial blood pressure. The design of a large randomized trial comparing arteriovenous fistula creation to sham control is outlined.

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Change history

  • 09 April 2018

    In the March 2018 issue of Current Hypertension Reports, the second author’s name Nathan A. Sobotka was inadvertently left out of the byline. Also, the author names were changed from initials to spelled out. The corrected author list is given above. The original article has been corrected.

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Authors and Affiliations

Authors

Corresponding author

Correspondence to Roland E. Schmieder.

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Conflict of Interest

Dr. Stefan Bertog has received reimbursement for travel expenses or study honoraria from Ablative Solutions, Johnson and Johnson, and Medtronic.

Nathan Sobotka is a member of Paul Sobotka’s immediate family.

Dr. Paul Sobotka is chief medical officer of ROX Medical Inc. with both salary and stock.

Dr. Melvin Lobo reports personal fees from ROX Medical during the conduct of the study and personal fees from CVRx, personal fees from Cardiosonic, personal fees from St Jude Medical, and personal fees from KONA Medical, outside the submitted work.

Dr. Kolja Sievert has nothing to disclose.

Laura Vaskelyte has nothing to disclose.

Dr. Horst Sievert has received consulting fees, reimbursement for travel expenses or study honoraria from the following companies: Abbott, Ablative Solutions, Ancona Heart, Bioventrix, Boston Scientific, Carag, Cardiac Dimensions, Celonova, Cibiem, CGuard, Comed B.V., Contego, CVRx, Edwards, Gardia, Hemoteq, InspireMD, Kona Medical, Lifetech, Maquet Getinge Group, Medtronic, Occlutech, pfm Medical, Recor, St. Jude Medical, Terumo, Trivascular, Vascular Dynamics, Venus, and Veryan.

Schmieder RE reports grants from Rox Medical to the institution, outside the submitted work.

Human and Animal Rights and Informed Consent

All reported studies/experiments with human or animal subjects performed by the authors have been previously published and complied with all applicable ethical standards (including the Helsinki declaration and its amendments, institutional/national research committee standards, and international/national/institutional guidelines).

Additional information

Key Learning Points

• Older age is the strongest predictor of resistant hypertension which is likely to be driven by arterial (and in particular aortic) stiffening leading to the structural hypertension phenotype characterized by increased pulse pressure and isolated systolic hypertension

• Responses to devices such as RDN and BAT have been shown to be significantly attenuated in patients with ISH suggesting that sympathomodulation alone is insufficient to target arterial hypertension with advanced stiffening of large arteries.

• A novel approach with a cAV anastomosis appears to effectively target both structural and systo-/diastolic hypertension producing significant and sustained reduction in ambulatory BP

• Additional effects of the cAV anastomosis are likely to include increase in ANP/BNP and engagement of low-pressure baroreceptors to suppress the high-pressure baroreflex-mediated increase in sympathetic tone that usually accompanies BP lowering

• Future iterations of the coupler will aim at improving the ease of implantation as well as reducing the incidence of ipsilateral venous stenosis and cardiovascular efficacy and safety

The original version of this article was revised: The second author’s name Nathan A. Sobotka was inadvertently left out of the byline. Also, the author names were changed from initials to spelled out.

This article is part of the Topical Collection on Mechanisms of Hypertension

Electronic supplementary material

Video 1

Crossing from the external iliac vein into the external iliac artery via a curved needle and advancement of a 0.018-in. wire into the external iliac artery. (MOV 15705 kb)

Video 2

Deployment of the arterial portion of the ROX coupler. (MOV 7708 kb)

Video 3

Deployment of the venous portion of the ROX coupler. (MOV 9652 kb)

Video 4

Balloon dilatation with a 4-mm balloon to establish flow. (MOV 4001 kb)

Video 5

Final angiography demonstrating a fistulous connection between the external iliac artery and vein. (MOV 1698 kb)

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Bertog, S.C., Sobotka, N.A., Sobotka, P.A. et al. Percutaneous Creation of a Central Iliac Arteriovenous Anastomosis for the Treatment of Arterial Hypertension. Curr Hypertens Rep 20, 18 (2018). https://doi.org/10.1007/s11906-018-0816-8

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