Quantitative assessment of myocardial viability after infarction by dobutamine magnetic resonance tagging

Abstract

Background - The assessment of return of function within dysfunctional myocardium after acute myocardial infarction (MI) using contractile reserve has been primarily qualitative. Magnetic resonance (MR) myocardial tagging is a novel noninvasive method that measures intramyocardial function. We hypothesized that MR tagging could be used to quantify the intramyocardial response to low-dose dobutamine and relate this response to return of function in patients after first MI. Methods and Results - Twenty patients with a first reperfused MI (age, 53±12 years; 16 male; 11 inferior MIs) were studied. Patients underwent breath-hold MR-tagged short-axis imaging on day 4±2 after MI at baseline and during dobutamine infusion at 5 and 10 μg·kg-1·min-1. At 8±1 weeks after MI, patients returned for a follow- up MR tagging study without dobutamine. Quantification of percent intramyocardial circumferential segment shortening (%S) was performed. Low- dose dobutamine MRI was well tolerated. Overall, mean %S was 15±11% at baseline (n=227 segments), increased to 16±10% at 5 μg·kg-1·min-1 dobutamine (P=NS), 21±10% at peak (P<0.0001 versus baseline and 5 μg·kg-1·min-1), and 18±10% at 8 weeks (P<0.004 versus baseline and peak). The increase in %S with peak dobutamine was greater in dysfunctional myocardium (103 segments, +9±10%) than in normal tissue (124 segments, +4±12%, P<0.0001). In dysfunctional regions, %S also increased from 6±7% at baseline to 14±10% at 8 weeks after MI (P<0.0001). In dysfunctional regions that responded normally to peak dobutamine (≤5% increase in %S), the increase in %S from baseline to 8 weeks after MI (+9±9%) was greater than in those regions that did not respond normally (+5±9%, P<0.04). Midmyocardial and subepicardial response to dobutamine were predictive of functional recovery, but the subendocardial response was not. Conclusions - The response of intramyocardial function to low-dose dobutamine after reperfused MI can be quantified with MR tagging. Dysfunctional tissue after MI demonstrates a larger contractile response to dobutamine than normal myocardium. A normal increase in shortening elicited by dobutamine within dysfunctional midwall and subepicardium predicts greater functional recovery at 8 weeks after MI, but the response within the subendocardium is not predictive.