Admission heart failure and coronary perfusion in ST-elevation myocardial infarction patients undergoing primary percutaneous coronary intervention

Abstract

Funding Acknowledgements Type of funding sources: None. Introduction Studies demonstrated a link between the presence of HF on the admission of ACS patients and increased in-hospital morbidity and mortality. However, the literature did not establish the connection between the admission HF and the angiographic burden and the coronary vessel perfusion post-PPCI. Purpose To establish the correlation between acute HF on admission of STEMI patients, the coronary thrombus burden and the final coronary perfusion post PPCI. Methods We retrospectively studied 210 STEMI patients who presented to a single PPCI centre. We excluded post-fibrinolysis patients, patients with old stents and those who presented more than 24 hours after the onset of pain. We divided the studied cohort into two subgroups based on the presence of HF on presentation to the emergency department. We obtained Informed consent from all patients, and all procedures were done in compliance with the Helsinki declaration for research on human beings. Two blinded interventional cardiology consultants assessed the thrombus burden and coronary flow using TIMI grades of both variables. Results 20 patients (10%) of the studied group had HF on admission. There was no significant difference between the two subgroups regarding other cardiovascular risk factors (figure 1). The coronary thrombus burden did not differ significantly between the HF and no HF subgroups (50% vs 43.16%, respectively, p=0.557). However, the incidence of impaired coronary flow post-PPCI was significantly higher in the HF group (25% vs 8.4%, p=0.019) (figure 2). Multivariate logistic regression analysis showed that admission HF is an independent predictor of impaired perfusion post-PPCI ( OR= 5.49, 95% CI=1.54-19.49, p=0.01). Our study demonstrates the association between admission HF in STEMI patients undergoing PPCI and increased incidence of impaired coronary flow after PPCI. This finding was independent of the heavy coronary thrombus burden on angiography. Animal studies have demonstrated impaired coronary flow even in HF secondary to non-ischaemic causes.1,2 Possible mechanisms include impaired nitric oxide-mediated endothelium-dependent vasodilatation and enhanced vasoconstriction to mediators of neurohumoral activation.3 These mechanisms can explain our study's impaired coronary flow in HF patients. Conclusion Admission HF is an independent predictor of reduced coronary blood flow after PPCI. Timely treatment of STEMI patients can prevent HF development and improve their prognosis.