Systemic inflammation in the acute myocardial infarction can predict early negative left ventricular remodeling assessed by myocardial work analysis

Abstract

Abstract Funding Acknowledgements Type of funding sources: Public grant(s) – EU funding. Main funding source(s): UEFISCDI Background. Left ventricular (LV) remodeling after acute myocardial infarction (AMI) is an important predictor of heart failure (HF). Systemic inflammatory response in the acute phase of AMI is of particular interest, while the relation to the remodeling process is still under debate. New imaging techniques derived from speckle tracking echocardiography (STE), such as myocardial work (MW), are attractive tools since they can detect myocardial remodeling before decrease of global LVEF. However, there is insufficient data regarding MW in AMI patients, and its relation to the inflammatory process. Methods. We assessed 57 patients (53 ± 9 years, 45 men, 64% smokers, 59% hypertensive, 54% with type 2 diabetes) with AMI, by clinical, 2D echo, and STE. Biomarkers panel was evaluated within the first 24 hours from admission: hsTpI and CRP. A second visit with clinical and echo assessment was performed at 6-8 weeks from the baseline visit. Exclusion criteria were unstable patients, non-sinus rhythm, significant valvular disease (>grade 2), other significant pathologies leading to decreased life expectancy, and low quality 2DE. At both visits, global longitudinal stain (GLS) and MW by 2DSTE were measured, on top of conventional echo parameters: global work index (GWI), global constructive work (GCW), global wasted work (GWW), global work efficiency (GWE) (Figure 1: upper panel - an example of a patient with increase of GWE from baseline to visit 2 ; lower panel - an example of a patient with decrease of the GWE from baseline to visit 2). Results. At baseline, myocardial necrosis by hsTpI significantly corelated with GLS (r = 0.44, p = 0.001) and MW (GWI: r=-0.44, p = 0.001; GCW: r=-0.40, p = 0.002), but not with LVEF. However, systemic inflammation by CRP did not correlate with LVEF or any of the STE parameters. Interestingly, systemic inflammation by CRP significantly correlated with changes of MW between the two visits: for GWE r=-0.53, p < 0.001; and for GWW r = 0.48, p < 0.001 (Figure 2). A CRP level >28 mg/l was able to predict decrease of GWE from baseline to visit 2. Conclusions. Magnitude of necrosis, expressed by hsTpI, corelates only with GLS and MW parameters, but not with LVEF. CRP level in the acute phase of AMI correlates with myocardial work changes, as an early marker of negative LV remodeling. Abstract Figure 1 Abstract Figure 2