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Release of mitochondrial DNA is associated with mortality in severe acute heart failure

Session Poster Session 2

Speaker Konstantin A Krychtiuk

Event : Acute Cardiovascular Care 2019

  • Topic : heart failure
  • Sub-topic : Acute Heart Failure: Biomarkers
  • Session type : Poster Session

Authors : KA Krychtiuk (Vienna,AT), R Wurm (Vienna,AT), M Lenz (Vienna,AT), K Huber (Vienna,AT), J Wojta (Vienna,AT), G Heinz (Vienna,AT), M Huelsmann (Vienna,AT), WS Speidl (Vienna,AT)

KA Krychtiuk1 , R Wurm1 , M Lenz1 , K Huber2 , J Wojta1 , G Heinz1 , M Huelsmann1 , WS Speidl1 , 1Medical University of Vienna, Department of Internal Medicine II, Division of Cardiology - Vienna - Austria , 2Wilhelminen Hospital, 3rd Department of Internal Medicine, Cardiology and Emergency Medicine - Vienna - Austria ,


Inflammation is regarded as an important trigger for disease progression in heart failure (HF). Particularly in severe acute heart failure (AHF), tissue hypoxia may lead to cellular damage and the release of intracellular mitochondrial DNA (mtDNA), which acts as an activator of the immune system due to its resemblance to bacterial DNA. It therefore may serve as a mediator of disease progression. The aim of this study was to determine circulating levels of mtDNA and its association with mortality in patients with HF in different presentations.

Plasma levels of circulating mtDNA were measured in 90 consecutive patients with severe AHF admitted to our medical ICU as well as 109 consecutive chronic heart failure (CHF) patients.

In patients admitted to our medical ICU (median age 64 (49-74) years, median NT-proBNP 4986 (1525 – 23842) pg/mL, 30-day survival 64.4%), mtDNA levels were significantly higher in patients that died within 30 days after ICU admission and patients with plasma levels of mtDNA in the highest quartile had a 3.4-fold increased risk (p=0.002) of dying independent from renal function, vasopressor use and NT-proBNP, TnT, lactate levels or CardShock and APACHE II score. Patients with severe AHF showed significantly higher mtDNA levels (p<0.005) as compared to patients with CHF. In these patients, mtDNA levels were associated with NYHA functional class but were not associated with outcome.

mtDNA release into the circulation is associated with mortality in patients with severe AHF but not in patients with CHF. Release of mtDNA may therefore play a role within the pathophysiology of AHF.

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