BACKGROUND: The amount of myocardial scar measured by late gadolinium enhancement (LGE) cardiovascular magnetic resonance (CMR) imaging predicts regional recovery in wall motion following revascularization. Previous studies have been conducted in patients with a relatively recent myocardial insult and relatively preserved left ventricular (LV) function. In this sub-study of a clinical trial, the predictive value of LGE, and other CMR-derived data, for myocardial recovery in patients with chronic severe ischaemic cardiomyopathy was assessed. METHODS:Twenty-two patients with severe LV impairment of ischaemic origin were enrolled as a sub-study of a trial that randomly assigned patients to revascularization or not in addition to guideline-indicated pharmacological therapy. Patients underwent a CMR study at baseline and 6 months. Scans were qualitatively and quantitatively assessed for wall motion, rest/stress myocardial perfusion, and LGE. RESULTS: The median duration of heart failure was 13 (inter-quartile range 5-21) months. Patients had severe LV dilatation [end-diastolic volume (EDV) 280 ± 77 mL] and reduction in LV ejection fraction (LVEF) (29 ± 10%). The percentage scar burden by LGE was 17 ± 9%. Patient characteristics of those undergoing revascularization (n = 7) or not (n = 14) were similar. Myocardial perfusion reserve index (MPRI) improved following revascularization (MPRI 1.17 vs. 1.57, P < 0.0001) but not following medical therapy (1.39 vs. 1.32, P = 0.54). However, LVEF improved in patients whether or not they had revascularization. In the revascularization group, 14% of dysfunctional segments with LGE <25% and 22% of dysfunctional segments with LGE <50% had improved contractile function. However, the transmural extent of LGE did not predict contractile recovery following revascularization or pharmacological therapy (P = 0.19, P = 0.42). LVEDV improved overall (280 ± 77 to 269 ± 83 mL, P = 0.05); improvement was associated with heart failure duration (P = 0.04). CONCLUSIONS: In patients with chronic severe LV impairment of ischaemic origin, duration of heart failure is a better predictor of recovery than transmural extent of LGE, following medical therapy or successful revascularization. This suggests that the extent of myocardial remodelling is more important for LV recovery than the presence and extent of prior infarction alone and that LGE should not be the sole determinant of treatment method in severe LV systolic dysfunction of ischaemic origin.
RCT Entities:
BACKGROUND: The amount of myocardial scar measured by late gadolinium enhancement (LGE) cardiovascular magnetic resonance (CMR) imaging predicts regional recovery in wall motion following revascularization. Previous studies have been conducted in patients with a relatively recent myocardial insult and relatively preserved left ventricular (LV) function. In this sub-study of a clinical trial, the predictive value of LGE, and other CMR-derived data, for myocardial recovery in patients with chronic severe ischaemic cardiomyopathy was assessed. METHODS: Twenty-two patients with severe LV impairment of ischaemic origin were enrolled as a sub-study of a trial that randomly assigned patients to revascularization or not in addition to guideline-indicated pharmacological therapy. Patients underwent a CMR study at baseline and 6 months. Scans were qualitatively and quantitatively assessed for wall motion, rest/stress myocardial perfusion, and LGE. RESULTS: The median duration of heart failure was 13 (inter-quartile range 5-21) months. Patients had severe LV dilatation [end-diastolic volume (EDV) 280 ± 77 mL] and reduction in LV ejection fraction (LVEF) (29 ± 10%). The percentage scar burden by LGE was 17 ± 9%. Patient characteristics of those undergoing revascularization (n = 7) or not (n = 14) were similar. Myocardial perfusion reserve index (MPRI) improved following revascularization (MPRI 1.17 vs. 1.57, P < 0.0001) but not following medical therapy (1.39 vs. 1.32, P = 0.54). However, LVEF improved in patients whether or not they had revascularization. In the revascularization group, 14% of dysfunctional segments with LGE <25% and 22% of dysfunctional segments with LGE <50% had improved contractile function. However, the transmural extent of LGE did not predict contractile recovery following revascularization or pharmacological therapy (P = 0.19, P = 0.42). LVEDV improved overall (280 ± 77 to 269 ± 83 mL, P = 0.05); improvement was associated with heart failure duration (P = 0.04). CONCLUSIONS: In patients with chronic severe LV impairment of ischaemic origin, duration of heart failure is a better predictor of recovery than transmural extent of LGE, following medical therapy or successful revascularization. This suggests that the extent of myocardial remodelling is more important for LV recovery than the presence and extent of prior infarction alone and that LGE should not be the sole determinant of treatment method in severe LV systolic dysfunction of ischaemic origin.