Background: The aim of this study was to investigate the correlation between serum biomarkers of left ventricular dysfunction and systemic inflammation in the first days after the acute episode, and to investigate their role for early identification of patients at high risk for post-infarction heart failure. Materials and methods: In total, 123 subjects admitted to the Intensive Cardiovascular Care Unit of the Cardiology Clinic of the Târgu Mureș County Clinical Emergency Hospital, Romania, with acute myocardial infarction were retrospectively analyzed in this study. Based on the level of NT-proBNP, the study population was divided into 2 groups: Group 1 (n = 92), with NT-proBNP <3,000 pg/mL, and Group 2 (n = 31), with NT-proBNP >3,000 pg/mL. Results: Biomarkers reflecting systemic inflammation presented significantly higher values in patients with elevated NT-proBNP (hs-CRP – 12.3 ± 8.9 mg/L vs. 3.6 ± 6.7 mg/L, p <0.0001, and interleukin 6 – 27.6 ± 30.7 pg/mL vs. 8.6 ± 6.2 pg/mL, p <0.0001). However, cell adhesion molecules VCAM and ICAM were not significantly different between the groups. Patients in Group 2 presented significantly higher rates of major cardiovascular events and rehospitalizations in the first year after the acute coronary event, with 13.33% event rate for patients in Group 2 compared to 8.7% in Group 1 (p <0.05). Conclusions: Serum biomarkers of ventricular dysfunction are strongly associated with systemic inflammation and ventricular impairment in the immediate phase after an acute myocardial infarction. Systemic inflammation has a higher impact on the clinical outcomes and progression to heart failure than the local coronary inflammation expressed by cell adhesion molecules.
Introduction: Systemic inflammation plays a key role in the pathophysiology of acute coronary syndrome (ACS), having a direct effect in promoting the progression and rupture of vulnerable coronary plaques. The aim of this study was to investigate the association between inflammatory biomarkers and the type of ACS (ST-elevation myocardial infarction – STEMI, non-ST-elevation myocardial infarction – NSTEMI, or unstable angina – UA) in patients with confirmed heart failure. Material and Methods: This study included a total of 266 patients admitted to the Clinical Department of Cardiology of the County Emergency Clinical Hospital of Târgu Mureș – Cardiac Intensive Care Unit (CICU) for ACS of various types (UA, NSTEMI or STEMI) between January 1, 2017 and December 31, 2020, in whom the diagnosis of heart failure was established based on clinical and paraclinical data. From the total number of patients, 36 were hospitalized for UA and 230 for MI, of which 165 were STEMI and 65 were NSTEMI. Results: Only hs-CRP and IL-6 were significantly higher in MI compared to UA. Mean hs-CRP was 4.9 ± 4.5 mg/mL in patients with UA vs. 20.4 ± 42.2 mg/mL in patients with MI (p = 0.001), and mean IL-6 was 7.2 ± 13.8 pg/mL in UA vs. 31.6 ± 129.2 pg/mL in MI (p <0.0001). ICAM seems to have had a greater discriminating power between STEMI and other types of ACS in those with heart failure, having a value more than double in those with STEMI (216.1 ± 149.6 ng/mL vs. 448.2 ± 754.4 ng/mL, p <0.0001). Conclusions: In patients with heart failure, the increase of inflammatory biomarkers such as hs-CRP is associated with the development of an acute myocardial infarction but not with its type. Adhesion molecules, especially ICAM, are elevated in patients with STEMI compared to other types of ACS, indicating a potential role of endothelial alteration in the development of an ACS when it adds to systemic inflammation linked to heart failure.
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