Abstract
To assess the joint prognostic value of periprocedural dynamics of the left ventricular ejection fraction (PPD of LVEF) and subclinical pulmonary congestion during lung stress ultrasound in patients with first acute myocardial infarction (AMI) and percutaneous coronary intervention (PCI) in relation to the development of heart failure (HF) in the postinfarction period. Our prospective, single-centre, observational study included 105 patients with a first MI with no HF in the anamnesis and successful PCI. All patients underwent standard clinical and laboratory tests, NT-proBNP level assessment, echocardiography, lung stress ultrasound with a 6-minute walk test. All patients had no clinical signs of heart failure at admission and at discharge. Criteria for PPD of LV EF: improvement in LV EF≥50%; ∆LV EF more than 5%, but LV EF<50%. According to the results of lung stress ultrasound, pulmonary congestion was diagnosed: mild (2-4 B-lines), moderate (5-9 B-lines) and severe (≥10 B-lines). The end point was hospitalization for HF for 2.5 years. Upon admission, LV EF of 50% or more was registered in 45 patients (42.9%). Positive PPD was registered in 31 (29.5%) patients. After stress ultrasound of the lungs, 20 (19%) patients had mild subclinical pulmonary congestion, 38 (36%) moderate and 47 (45%) severe according to the criteria presented. During the observation period, patients with no PPD of LVEF were significantly more likely to be hospitalized for the development of HF (in 44.4% of cases) compared with patients with positive PPD (in 15.2% of cases) and with initial LV EF≥50% (in 13.4% of cases; p=0.005). When performing logistic regression analysis, the best predictive ability was found in the combination of the absence of PPD of LV EF and the sum of B-lines ≥10 on exercise (relative risk 7.45; 95% confidence interval 2.55-21.79; p<0.000). Evaluation of the combination of PPD of LV EF and the results of stress lung ultrasound at discharge in patients with first AMI and successful PCI with no HF in anamnesis allows us to identify a high-risk group for the development of HF in the postinfarction period.
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