Clinical, Laboratory and Echocardiographic Features in Severe Acute Myocardial Infarction Complicated by Acute Heart Failure

Abstract

Aim. To determine the clinical, laboratory, and instrumental characteristics of acute myocardial infarction (AMI) complicated by severe acute heart failure (AHF).Materials and methods. This single-center prospective observational cohort study included 137 patients with AMI complicated by AHF who underwent percutaneous coronary intervention (PCI). According to the Killip classification, patients were divided into three groups: class II (n=46), class III (n=43), and cardiogenic shock (class IV, n=48). Laboratory tests included complete blood count, creatinine, NT-proBNP, troponin I, CK-MB, D-dimer, and C-reactive protein. All patients underwent echocardiography and coronary angiography. Statistical analysis included parametric and nonparametric tests, correlation analysis, and multivariate logistic regression.Results. Increasing AHF severity was associated with lower hemoglobin levels (p<0.001) and higher levels of NT-proBNP (p<0.001), C-reactive protein (p<0.001), creatinine (p<0.05), and CK-MB (p<0.05). Progressive reduction in left ventricular ejection fraction (LVEF) was observed with increasing AHF severity (52.4±0.8% in Killip class II vs. 35.6±1.1% in Killip class IV; p<0.0001), accompanied by increased left ventricular volumes (p<0.001) and signs of adverse myocardial remodeling. Patients with severe AHF more frequently had multivessel coronary artery disease and less favorable restoration of coronary blood flow after PCI. NT-proBNP levels correlated with left ventricular end-diastolic volume both at admission and discharge, suggesting its potential role as a marker of left ventricular remodeling. Multivariate analysis identified elevated NT-proBNP (OR=1.42; p<0.001), LVEF <40% (OR=2.86; p<0.001), multivessel coronary artery disease (OR=2.11; p<0.01), C-reactive protein >10 mg/L (OR=1.78; p<0.05), and glomerular filtration rate <60 mL/min (OR=1.95; p<0.01) as independent predictors of cardiogenic shock. These findings allowed identification of a “high-risk phenotype” of severe AHF characterized by neurohumoral activation, elevated LV filling pressure reflected by increased E/e′, systemic inflammation, LV systolic dysfunction, multivessel coronary artery disease, and renal dysfunction.Conclusions. Severe AHF in patients with AMI is characterized by pronounced laboratory abnormalities and structural and functional myocardial changes, highlighting the importance of comprehensive assessment for early risk stratification and optimization of treatment strategies.