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Research Snapshot Theater: Cardiovascular/Shock, Adult II

Is Lipoprotein (a) an Independent Predictor for Cardiogenic Shock?

Sunday, March 22, 2026
9:45 AM - 10:45 AM Central Time
Location: Connections Central - RST 03

  • Arnaldo Lopez-Ruiz, MD (he/him/his)

    null
    null, Florida

    Disclosure(s): BioPorto: Speaker/Honoraria (includes speakers bureau, symposia, and expert witness) (Ongoing); MicroGenDx: Consulting fees or other remuneration (Ongoing)

  • MQ

    Miguel A. Quintana Da Silva, MD, FACC

    Medical Director
    Cardiovascular & Pulmonary Institute ICAP-LW, Paraguay

    Disclosure information not submitted.

  • MP

    Mehul Patel, MD

    Medical Director Cardiac ICU
    Advent Health Orlando, Florida

    Disclosure information not submitted.

  • DG

    David D. Goldenberg, DO

    Assistant Professor - Department of Anesthesiology & Critical Care
    Moffitt Cancer Center, Florida

    Disclosure information not submitted.

  • AG

    Andrew Gabanic, MD

    Critical Care Fellow
    Advent Health Orlando, Florida

    Disclosure information not submitted.

  • DO

    Denny Oliveira, N/A

    Graduate Student
    Florida State University, Florida

    Disclosure information not submitted.

  • MC

    Maria C. Carrillo, MD

    Associate Executive Medical Director - Department of Critical Care
    Advent Health Orlando, Florida

    Disclosure information not submitted.

  • LJ

    Luis A. Juncos, MD, FASN

    Adjunctive Professor of Medicine - Department of Internal Medicine - Division of Nephrology
    University of Arkansas for Medical Sciences, Massachusetts

    Disclosure information not submitted.

  • EO

    Eduardo Oliveira, MD, MBA

    Executive Medical Director - Department of Critical Care
    Advent Health Orlando, Florida

    Disclosure information not submitted.

Introduction: Lipoprotein(a) [Lp(a)] has emerged as an independent cardiovascular risk factor, but its prognostic significance in acute myocardial infarction (MI), particularly regarding multivessel involvement, cardiogenic shock severity, and renal complications, remains under investigation. This study evaluates the clinical outcomes associated with elevated Lp(a) in acute MI patients.


Methods: We conducted a retrospective cohort study of 97 patients admitted with acute MI (56% STEMI, 44% NSTEMI) from 2023-2025. Patients were stratified into two groups based on Lp(a) levels: elevated Lp(a) >50 mg/dL (n=49, mean 74 mg/dL, SD 12) and normal Lp(a) ≤50 mg/dL (n=48). Baseline characteristics, including type 2 diabetes prevalence (42% vs. 44%), LDL, and HDL levels and eGFR were comparable between groups. We assessed the incidence of multivessel MI, severity of cardiogenic shock (using SCAI classification), and renal complications including acute kidney injury (AKI) and the need for continuous renal replacement therapy (CRRT).


Results: Patients with elevated Lp(a) had a significantly higher incidence of multivessel MI requiring percutaneous intervention (85% vs 23%, p< 0.05) and a markedly increased risk of developing cardiogenic shock (OR 5.44; 95% CI: 3.5–8.1). SCAI stage D shock occurred in 48.9% of patients with high Lp(a), compared to 25% in the normal Lp(a) group (p < 0.05). Elevated Lp(a) was also associated with a higher risk of severe AKI (OR 6.2; 95% CI: 3.4–8.3), reflected by significantly elevated urine neutrophil gelatinase-associated lipocalin (NGAL) levels (5880 U/mL [SD 210] vs. 1970 U/mL [SD 120]). Furthermore, 44.8% of patients with high Lp(a) required CRRT compared to 18.7% in the control group (p < 0.05).


Conclusions: Elevated Lp(a) levels in acute MI patients is independently associated with multivessel coronary involvement, more severe cardiogenic shock, and increased risk of AKI requiring CRRT. These findings support the growing recognition of Lp(a) as a key biomarker for cardiovascular and systemic complications during acute MI and suggest the need for early risk stratification in patients with elevated Lp(a).