Progressive left ventricular post-infarction remodelling: impact on outcome

Abstract

Abstract Background While the presence left ventricular (LV) remodelling after ST-segment elevation myocardial infarction (STEMI) is known to worsen prognosis, the impact of progressive vs. stable LV remodelling on outcome has not been established. Purpose To investigate the impact of progressive LV remodelling on outcome in STEMI patients who were treated with primary percutaneous coronary intervention (PCI) and optimal pharmacotherapy. Methods Baseline, 3-, 6- and 12-month echocardiograms were analysed. Early LV remodelling (ER) was defined as a ≥20% increase in LV end-diastolic volume (EDV) during the first 3 months post-STEMI, and mid-term remodelling (MTR) as ≥20% LVEDV change by 6 months. Progressive LV remodelling was defined according to spline curve analyses: ≥0% LVEDV increase by 6 months (i.e. further increase after 3 months) for ER, and ≥20% by 12 months (i.e. an additional increase after 6 months) for MTR. The impact of progressive LV remodelling on outcome was evaluated with a Log rank test. Results 589 STEMI patients (mean age 61±12 years, 78% male) who demonstrated LV remodelling in the first 6 months post-infarct, were analysed: 408 (69%) ER and 181 (31%) MTR. Progressive LV remodelling occurred in 146 (36%) ER and in 12 (7%) MTR. After a median follow-up of 90 (IQR 64–117) months, 39 (10%) ER were hospitalised for heart failure. 25 (14%) MTR remodellers died after a median follow-up of 86 (IQR 66–112) months. Progressive LV remodelling in ER led to a higher rate of heart failure hospitalisation (P=0.017 vs. non-progressive ER, Fig. 1A) but no mortality difference (P=0.10 vs. non-progressive ER). In contrast, MTR with progressive LV remodelling experienced worse survival (P=0.01 vs. non-progressive MTR, Fig. 1B) but no increase in heart failure hospitalisation (P=0.65 vs. non-progressive MTR). Conclusions Progressive LV remodelling causes an increased risk of heart failure in ER post-infarct, vs. higher mortality in MTR. These two patterns of progressive, post-infarct LV remodelling possibly represent different underlying pathophysiological mechanisms: i.e. evolution of true post-infarct remodelling in ER, vs. natural history of established heart failure in MTR. Figure 1 Funding Acknowledgement Type of funding source: None