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Non-ischemic myocardial injury in heart failure is significantly associated with a higher symptomatic burden and higher circulating levels of sST2, inflammation mediators and natriuretic peptides

Session HFA Discoveries - ePosters

Speaker Doctor Josip Andjelo Borovac

Event : HFA Discoveries 2020

  • Topic : heart failure
  • Sub-topic : Biomarkers
  • Session type : ePosters

Authors : JA Borovac (Split,HR), D Glavas (Split,HR), Z Susilovic Grabovac (Split,HR), A Bradaric (Split,HR), D Supe Domic (Split,HR), D Duplancic (Split,HR), J Bozic (Split,HR)

JA Borovac1 , D Glavas1 , Z Susilovic Grabovac1 , A Bradaric1 , D Supe Domic2 , D Duplancic1 , J Bozic3 , 1University Hospital Center Split, Clinic for Cardiovascular Diseases - Split - Croatia , 2University Hospital Center Split, Department of Medical Laboratory Diagnostics - Split - Croatia , 3University of Split School of Medicine, Department of Pathophysiology - Split - Croatia ,

On behalf: CATSTAT-HF

Acute Heart Failure: Biomarkers

Background: Myocardial injury (MI) defined as an elevation of cardiac troponins beyond a certain threshold is frequently encountered during the acute worsening of heart failure (AWHF) and is associated with an adverse prognosis. The MI has many potential causes other than myocardial ischemia and underlying etiology must be carefully investigated. In this study, we aimed to assess whether the symptomatic burden of the disease as assessed with the New York Heart Association (NYHA) classification will differ between AWHF patients with and without MI of non-ischemic etiology. Furthermore, we sought to assess potential difference between those two groups in terms of circulating levels of soluble suppressor of tumorigenicity 2 (sST2) reflecting adverse myocardial remodeling under stressed conditions and biomarkers reflecting inflammatory response (C-reactive protein, CRP and neutrophil-to-lymphocyte ratio, NLR) and ventricular overload (N-terminal pro b-type natriuretic peptide, NT-proBNP).

Methods: A total of 85 consecutive patients with AWHF, NYHA class II-IV, and without acute coronary syndrome (ACS) as an underlying cause of hospitalization were examined at our Cardiology Department. ACS was ruled out in all patients based on serial 12-lead electrocardiography tracings, clinical evaluation of symptoms/medical history and/or by diagnostic coronary angiography. All patients had their peripheral blood sampled within 24 hours of index hospitalization. The MI was defined as an elevation of high-sensitivity cardiac troponin I (hs-cTnI) beyond the upper limit of the 99th percentile, adjusted for sex, as following: >34.2 ng/L for men and >15.6 ng/L for women. All variables had normal distribution.

Results: Patients were on average 71.7±9.1 years old, with predominance of women (51.8%) and with a mean left ventricular ejection fraction (LVEF) of 44.1±16.8 %. Most of the patients had reduced LVEF (43.5%), followed by preserved LVEF (38.8%) while 17.6% of patients had midrange LVEF. The mean hs-cTnI value was 68.9±101 ng/L. Slightly less than half of the patients (48.2%, N=41) had a myocardial injury with a mean hs-cTnI value of 132±108 ng/L, while 51.8% (N=44) of patients did not have a myocardial injury with mean hs-cTnI value of 14±8 ng/L. Both compared groups did not differ significantly in terms of age (p=0.952), body mass index (p=0.947) and estimated glomerular filtration rate (p=0.288). Patients with AWHF and with myocardial injury, compared to those without, had significantly higher NYHA class (3.2 vs. 2.8, p=0.017) and higher levels of circulating sST2 (62.1±45.2 vs. 40.2±32.5 ng/mL, p=0.018), CRP (26.9±29.6 vs. 11.4±14.0 mg/L, p=0.002), NLR (5.6±3.6 vs. 3.7±2.2, p=0.005) and NT-proBNP (9763±10319 vs. 4825±7821 pg/mL, p=0.023) (Figure 1).

Conclusion: A presence of non-ischemic MI in AWHF is significantly associated with a higher symptomatic burden and an increase in adverse laboratory biomarkers that are historically associated with poor prognosis.

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