Evidence map›Paper›PMID 42380766›Full record

ArticleBMC cardiovascular disorders2026

Fulminant cholesterol crystal embolism syndrome triggered by Vein of Marshall ethanol infusion: a case report.

Bingquan Yu, Jikang Tang, Jing Zhang

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Article in BMC cardiovascular disorders, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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2 · The registry

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4 · The record

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5 · Who and what money

Authors and funding

3 authors.

Bingquan YuGuangxi Medical University, Nanning, Guangxi Autonomous Region, China.ORCID http://orcid.org/0009-0008-2460-5828
Jikang TangDepartment of Cardiology, Liuzhou Municipal Liutie Central Hospital, No. 14 Limin District, Fei'e Road, Liuzhou, Guangxi Autonomous Region, 545007, China.ORCID http://orcid.org/0009-0006-3544-1297
Jing ZhangDepartment of Cardiology, Liuzhou Municipal Liutie Central Hospital, No. 14 Limin District, Fei'e Road, Liuzhou, Guangxi Autonomous Region, 545007, China. zj19780809@163.com.ORCID http://orcid.org/0009-0001-3435-3109

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCholesterol crystal embolism syndrome (CCES) represents a catastrophic complication of endovascular procedures. While mechanical trauma during left atrial catheter ablation acts as a known trigger, the specific embolic risks associated with Vein of Marshall ethanol infusion (VOM-EI) remain unexplored. CASE PRESENTATION: A 66-year-old male with severe atherosclerosis and chronic kidney disease underwent persistent atrial fibrillation ablation involving VOM-EI (8 mL of ≥ 99.7% dehydrated ethanol). Six hours post-procedure, he developed extensive, non-pruritic livedo reticularis. He remained hemodynamically stable (lowest blood pressure 111/78 mmHg) but rapidly progressed to anuric acute kidney injury (creatinine peaking at 542 µmol/L) and severe systemic inflammation. Diagnostic evaluation effectively ruled out contrast-induced nephropathy, hypotensive acute tubular necrosis, and autoimmune vasculitis. Given the rapid deterioration, specific eosinophiluria testing and renal biopsy were deferred; however, sterile pyuria, classic skin lesions, and recent vascular intervention established a highly probable clinical diagnosis of CCES. Treatment with intermittent hemodialysis and high-dose intravenous methylprednisolone (40 mg/day) rapidly suppressed the inflammatory storm and facilitated substantial renal recovery.

conclusionsIn patients with severe aortic plaque burden, VOM-EI, alongside established factors like transseptal catheter manipulation and systemic anticoagulation, may act as a potential trigger for CCES. Although a definitive diagnosis via biopsy was not feasible, we believe that early recognition and prompt corticosteroid therapy contributed substantially to the patient's clinical recovery.

Indexed as

Acute Kidney InjuryAtherosclerosisAtrial FibrillationCatheter AblationEmbolism, CholesterolEthanolAgedHumansInfusions, IntravenousMaleMethylprednisoloneRenal DialysisSyndromeTreatment OutcomeEthanolMethylprednisoloneAcute kidney injuryAtrial fibrillationCatheter ablationCholesterol embolismMethylprednisolone

Identifiers

PMID42380766
PMCPMC13560109

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.