Predictors of acute heart failure in patients with ST-segment elevation myocardial infarction of the electrocardiogram after PCI

Background. Despite the PCI in patients with ST-segment elevation myocardial infarction (STEMI) the development of acute heart failure (AHF) Killip ≥II is associated with a poor prognosis. Aim. To identify predictors of the development of AHF and the prognostic value of AHF in patients with STEMI after PCI. Materials and methods. In a prospective study, which lasted 6 months, included 233 patients (average age of 62.1±10.89 years, 73.4% of men) admitted to the hospital due to the development of STEMI who underwent PCI. The endpoint was defined as the death from cardiovascular causes. Statistical processing of the results was carried out using the statistical packages of the programs “SPSS Statistics 17.0" Result. During the follow-up observation from 1 day to 6 months (median follow-up of 5.2 months), 25 patients (10.7%) reported the onset of the endpoint, including 20 cases during the index hospitalization. AHF Killip ≥II during indexed hospitalization developed in 25 patients (10.7%). Independent predictors of Killip >II were: GFR<60 ml/min initially on admission to hospital (OR 95% 5.690 (2.082-15.551), p=0.001), anemia (OR 95% 5.317 (1.957-14.448), p=0.001), EF<40% (OR 95% 6.686 (1.291-34.628), p=0.024). OR of the development of Killip ≥II increased with a decrease in GFR initially when admitted to the hospital: GFR 45-59 ml/min (OR 95% 6.167 (1.432-26.563), p=0.015), GFR 30-44 ml/min (OR 95% 13.704 (2.795-67.187), p=0.001), GFR 15-29 ml/min (OR 95% 32.889 (4.967-217.770), p<0.001). The development of AHF Killip ≥II was associated with an increase in the frequency of the onset of the endpoint (7.2% and 40%, respectively, p<0.001), increasing with the increase in the class Killip (I 7.2%, II 0%, III 55.6%, IV 83.3%, p<0.001). In patients with AHF Killip ≥II, the incidence of acute kidney injury (AKI) increased (20.2% and 40%, respectively, p=0.025). Killip ≥II increases the OR of development of AKI by 2.6 times (OR 95% 2.635 (1.105-6.282), p=0.029). In the case of the development of both the AHF Killip ≥II and AKI, the OR of the onset of the endpoint increased many times (OR 95% 40.704 (8.990-184.283), p<0.001), while the AHF Killip ≥II without AKI increased the OR fourfold (OR 95% 4.361 (1.041-18.268), p=0.044). Conclusion. In patients with STEMI the development of the AHF Killip ≥II is associated with a poor prognosis, the development of AKI in patients with AHF Killip ≥II aggravates this prognosis.