Vascular Surgery

Three-branched in-situ laser fenestration TEVAR provides durable 5-year repair for zone-0 acute type A dissection

In 152 patients with zone-0 acute type A dissection, triple-branch in-situ laser fenestration TEVAR achieved 95.4% immediate technical success. Thirty-day events included 3.9% mortality, 7.2% stroke, 3.3% spinal cord ischemia, and 2.6% proximal stent-induced dissection, with no distal SINE. At roughly 5 years, branch-stent patency exceeded 94% and complete false-lumen thrombosis in the covered segment exceeded 80%. All-cause 5-year mortality was 7.9% and reintervention 12.5%, indicating acceptable durability in this high-risk arch cohort. 1

Infrainguinal interventions for claudication in ESRD show poor 1-year limb and survival outcomes

Among 83,698 PVIs for claudication, only 2% involved ESRD patients, who more often underwent femoropopliteal and infrapopliteal interventions. ESRD patients had higher 30-day mortality after PVI (2.2% vs 0.4%) despite similar access complications. At 1 year post-PVI, ESRD patients had substantially lower freedom from reintervention/major amputation/death and lower overall survival than non-ESRD patients. Similar patterns were seen after infrainguinal bypass, with ESRD independently predicting reintervention/major amputation/death and mortality. 2

Type III and mixed II/III endoleaks after complex EVAR often resolve under CTA surveillance without sac growth

In 230 patients after complex EVAR, predischarge CTA showed endoleaks in 75%, with reintervention reserved for sac enlargement thresholds. Type I endoleaks did not resolve spontaneously and therefore merit proactive management even when the sac is initially stable. Type III endoleaks resolved spontaneously in 83% by 24 months, mostly within 12 months, when the aneurysm sac remained stable. Mixed type II/III endoleaks had about 50% spontaneous resolution at 12 months, supporting conservative CTA surveillance in selected cases. 3

Calcium channel blocker use associates with higher aortic aneurysm and dissection risk

In 501,878 UK Biobank participants, calcium channel blocker users had a 31% higher aortic aneurysm or dissection risk than untreated hypertensive patients. In mouse models, calcium channel blockers increased aortic stiffness and aggravated aneurysm and dissection development. Among type B dissection patients after endovascular repair, calcium channel blocker therapy limited aortic regression versus other antihypertensives. Silencing PRKG1 mitigated calcium channel blocker–driven worsening of aortic disease in experimental models. 4