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editorial
. 2026 Aug 12;31(32):109318. doi: 10.1016/j.jaccas.2026.109318

Beyond Aortic Sealing

Integrating Anatomy and Physiology in Type B Aortic Dissection

Pedro Castilhos de Freitas Crivelaro a, Rodrigo Petersen Saadi b,∗
PMCID: PMC13480263  PMID: 42593022

Corresponding Author

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Key Words: atherosclerosis, dissection, hypertension


The management of Stanford type B aortic dissection (TBAD) extends far beyond the technical success of sealing an intimal tear. Although thoracic endovascular aortic repair (TEVAR) has transformed the treatment of complicated TBAD by promoting favorable aortic remodeling and reducing aortic-related mortality, long-term prognosis remains critically dependent on sustained blood pressure control.1 In many patients, refractory hypertension perpetuates wall stress, false-lumen pressurization, and progressive aortic degeneration, sustaining a dangerous cycle.

In this issue of JACC: Case Reports, Chen et al2 present a compelling example of how this cycle may be disrupted through a “one-stop” strategy integrating TEVAR with bilateral renal denervation (RDN) in a patient with TBAD complicated by severe uncontrolled hypertension and complex renal artery involvement. Rather than approaching dissection as a purely structural disease, the authors simultaneously targeted both the anatomical substrate and the physiological mechanisms sustaining hypertensive burden—a “dual anatomical and physiological intervention” that represents the most important contribution of the report.

The case is particularly noteworthy because the right renal artery exhibited mixed true- and false-lumen perfusion (Nagamine subtype III-a),3 yet bilateral RDN was completed without vascular complications. The Nagamine classification was not merely descriptive; it directly informed feasibility, risk stratification, and procedural strategy—a reminder that in complex structural interventions, imaging is not simply a diagnostic step but the foundation on which the therapeutic plan is built.

The role of catheter-based RDN in resistant hypertension has undergone substantial re-evaluation since the neutral SYMPLICITY HTN-3 (A Controlled Trial of Renal Denervation for Resistant Hypertension) result.4 Sham-controlled trials—including SPYRAL HTN-ON MED5 (Global Clinical Study of Renal Denervation With the Symplicity Spyral™ Multi-electrode Renal Denervation System in Patients With Uncontrolled Hypertension on Standard Medical Therapy) and RADIANCE II6 (The RADIANCE II Pivotal Study: A Study of the ReCor Medical Paradise System in Stage II Hypertension)—demonstrated meaningful ambulatory blood pressure reductions independent of pharmacological background. The 2025 American Heart Association/American College of Cardiology Hypertension Guideline considers renal denervation a reasonable adjunctive therapy (Class IIb, Level of Evidence B-R) for carefully selected patients with resistant hypertension despite optimal medical treatment.7 In aortic dissection, the rationale is especially compelling: renal malperfusion activates the renin-angiotensin-aldosterone system, dissection-related pain amplifies central sympathetic drive, and progressive wall stress sustains a self-perpetuating hypertensive cycle. In this context, RDN is not merely an add-on antihypertensive maneuver—it targets the mechanism perpetuating the disease.

The present case also raises a key question about the role of intravascular imaging. Intravascular ultrasound has demonstrated utility during TEVAR by improving true- and false-lumen discrimination, facilitating landing zone assessment, and reducing contrast utilization.8 In dissections involving branch vessels, intravascular ultrasound–guided navigation may reduce the risk of iatrogenic dissection extension from forceful contrast injection within fragile segments, and may become an important adjunct as combined TEVAR-RDN strategies evolve.

Although innovative, this combined concept is not entirely unprecedented. Prior reports in JACC: Case Reports have demonstrated the feasibility of RDN concomitant with TEVAR for acute aortic syndromes.9 The present report substantially extends this experience by addressing a more complex anatomical scenario and introducing a reproducible classification framework for candidate selection, suggesting that RDN may evolve from an anecdotal rescue strategy into a structured adjunctive therapy.

The report also invites critical reflection on procedural proportionality. Whether bilateral RDN was truly necessary remains an open question: the right renal artery represented the highest-risk component of the procedure, and prior literature has shown that unilateral ablation can achieve meaningful blood pressure reduction in patients with chronic aortic dissection and prohibitive contralateral anatomy.10 A related concern is whether the independent antihypertensive contribution of RDN can be separated from the improvement that frequently follows TEVAR itself, through true lumen restoration and reduction of renal malperfusion. These uncertainties raise the question of whether a staged approach—TEVAR first, RDN reserved for persistent hypertension—might have been equally effective while reducing procedural duration, contrast exposure, and radiofrequency manipulation within actively dissected territories.

Despite these considerations, the report by Chen et al2 should be viewed as an important proof-of-concept, demonstrating that RDN in complex dissected renal artery anatomy is technically feasible when meticulous anatomical assessment, procedural planning, and multidisciplinary collaboration are combined. Future endovascular therapies may increasingly integrate structural repair with targeted modulation of the physiological pathways driving disease progression.

Ultimately, this case reminds us that successful treatment of TBAD may require more than sealing the dissection. It may require treating the biological forces that continue to pressurize it (Figure 1).

Figure 1.

Figure 1

The Pathophysiological Rationale for Combined “One-Stop” TEVAR and Renal Denervation in Stanford Type B Aortic Dissection

BP = blood pressure; ESH = European Society of Hypertension; RAAS = renin-angiotensin-aldosterone system; RDN = renal denervation; SNS = sympathetic nervous system; TEVAR = thoracic endovascular aortic repair.

Funding Support and Author Disclosures

This editorial received no specific funding from any agency in the public, commercial, or not-for-profit sectors. The authors have reported that they have no relationships relevant to the contents of this paper to disclose.

Footnotes

The authors attest they are in compliance with human studies committees and animal welfare regulations of the authors’ institutions and Food and Drug Administration guidelines, including patient consent where appropriate. For more information, visit the Author Center.

References

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