Mechanism and clinical significance of precordial ST depression in inferior myocardial infarction: Evaluation by contrast-enhanced dynamic myocardial perfusion magnetic resonance imaging

We elucidated the mechanism and clinical significance of precordial ST depression in patients with an inferior myocardial infarction using first-pass, contrast-enhanced, myocardial perfusion magnetic resonance imaging (MRI). Forty-seven patients with acute inferior myocardial infarction underwent first-pass contrast-enhanced MR studies within 2-6 days postinfarction. Patients were followed-lip for a minimum of I year after infarct (range, 12-32 months). Total perfusion deficit scores derived qualitatively from MRIs were compared in patients with (group I, n = 30) and without (group 2, n = 17) ST depression precordially. Perfusion remote from the infarct zone was also compared. The combined end points of adverse clinical events and/or the need for further intervention were assessed for each group. Total perfusion deficit scores were significantly higher in group 1 than group 2 (medians 9.7 versus 4.5, p < 0.005). Posterolateral basal extension of hyperfusion was greater in group 1 versus group 2 (1.23 versus 0.42, p < 0.02), with no evidence of remote anterior perfusion abnormalities. They were more patients with art adverse clinical end point in group 1 versus group 2 (18 versus 1, p < 0.01). Furthermore, in patients with ST depression (group 1), there,vas a significant increase in number of adverse clinical end points in patients with a global deficit score > 15 versus 0-5 (7/7 versus 1/7, p < 0.01). MRI shows that precordial ST depression in inferior myocardial infarction is a market for a larger global perfusion abnormality with posterolateral basal extension and all increase in adverse clinical end points. Furthermore, the magnitude of the perfusion deficit correlates with an increase in the number of adverse clinical end Points, highlighting the potential of MRI perfusion studies as a research and clinical tool in myocardial infarction.