Early contrast-enhanced MRI predicts late functional recovery after reperfused myocardial infarction.

BACKGROUND: We have observed 3 abnormal patterns on contrast-enhanced MRI early after reperfused myocardial infarction (MI): (1) absence of normal first-pass signal enhancement (HYPO), (2) normal first pass signal followed by hyperenhanced signal on delayed images (HYPER), or (3) both absence of normal first-pass enhancement and delayed hyperenhancement (COMB). This study examines the association between these patterns in the first week after MI and late recovery of myocardial contractile function by use of magnetic resonance myocardial tissue tagging. METHODS AND RESULTS: Seventeen patients (14 men) with a mean age of 53+/-12 years were studied after a reperfused first MI. Contrast-enhanced images were acquired immediately after bolus administration of gadolinium and 7+/-2 minutes later. Tagged images were acquired at weeks 1 and 7. Circumferential segment shortening (%S) was measured in regions displaying HYPER, COMB, or HYPO contrast patterns and in remote regions (REMOTE) at weeks 1 and 7. At week 1, %S was depressed in HYPER, COMB, and HYPO (9+/-8%, 7+/-6%, and 5+/-4%, respectively) and were less than REMOTE (18+/-6%, P<0.003). However, in HYPER, %S improved at week 7 from 9+/-8% to 18+/-5% (P<0.001 versus week 1). In contrast, HYPO did not improve significantly (5+/-4% to 6+/-3%, P=NS) and COMB tended to improve 7+/-6% to 11+/-6% (P=0.06). CONCLUSIONS: HYPER has partially reversible dysfunction and represents predominantly viable myocardium. COMB shows borderline improvement and likely contains an admixture of viable and necrotic myocardium. HYPO shows little functional improvement at 7 weeks, presumably because of irreversible myocardial damage.

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

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 microg x kg(-1) x 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 microg x kg(-1) x min(-1) dobutamine (P=NS), 21+/-10% at peak (P<0.0001 versus baseline and 5 microg x kg(-1) x 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 (> or =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.

Dissociation between changes in intramyocardial function and left ventricular volumes in the eight weeks after first anterior myocardial infarction.

OBJECTIVES: We sought to examine the relation between regional changes in intramyocardial function and global left ventricular (LV) remodeling in the first 8 weeks after reperfused first anterior myocardial infarction (MI). BACKGROUND: Because of limitations in imaging methods used to date, this relation has not been thoroughly evaluated. METHODS: We studied 26 patients (21 men, 5 women; mean age 51 years) by magnetic resonance imaging (MRI) on day 5 +/- 2 (mean +/- SD) and week 8 +/- 1 after their first anterior MI. All patients had single-vessel left anterior descending coronary artery disease and although they had received reperfusion therapy, all had regional LV dysfunction and an initial ejection fraction (EF) < or = 50%. Short-axis magnetic resonance tagging was performed spanning the LV. Percent intramyocardial circumferential shortening (%S) on a topographic basis, LV mass index, LV end-diastolic volume index (LVEDVI), LV end-systolic volume index and LV ejection fraction (LVEF) were measured. RESULTS: Left ventricular mass index tended to decrease, whereas the LVEDVI increased from 82 +/- 24 to 96 +/- 27 ml/m2 (p = 0.002). Left ventricular end-systolic volume index remained unchanged, whereas LVEF increased from 39 +/- 12% to 45 +/- 14% (p = 0.002). Apical %S improved from 9 +/- 6% to 13 +/- 5% (p < 0.0001), as it did in the midanterior (6 +/- 6% to 10 +/- 7%, p < 0.02) and midseptal regions (8 +/- 7% to 12 +/- 6%, p < 0.02). Early dysfunction in remote midinferior and basal lateral regions resolved by 8 weeks. By multivariate analysis, the only significant predictor of an increase in LVEDVI over the study period was peak creatine kinase (p = 0.04). CONCLUSIONS: In the first 8 weeks after a large, reperfused anterior MI, %S improved in the apex, midanterior and midseptal regions and normalized in remote noninfarct-related regions, but LV end-diastolic volumes also increased. This increased LVEDVI correlated with infarct size by peak creatine kinase and was not related to changes in global and regional LV function.

Relation of changes in left ventricular peak filling rate during exercise to exercise performance in systemic hypertension and in healed myocardial infarction.

Patients with systemic hypertension and coronary artery disease (CAD) often manifest abnormalities at rest in left ventricular (LV) diastolic function and reduced exercise tolerance. It is possible that abnormalities in filling persist during exercise and are partially related to abnormal exercise tolerance. We examined rest and exercise peak filling rate (PFR) to determine if changes in PFR during exercise influence exercise performance. We studied 20 patients with systemic hypertension who had no evidence of CAD (negative thallium-201 stress imaging) and 15 patients with prior myocardial infarction, preserved ejection fraction, and no ischemia by thallium-201 stress imaging. Results were compared with 20 normal subjects. All 55 subjects had rest and exercise radionuclide angiograms Peak workload, exercise time, and LV ejection fraction were reduced in subjects with CAD (57 +/- 24 W, 7.41 +/- 2.91 min, and 60 +/- 9%) compared with subjects with hypertension (72 +/- 21 W, 9.69 +/- 3.03 min, and 70 +/- 6%, p <0.05) and controls (80 +/- 30 W, 10.82 +/- 3.50 min, and 67 +/- 6%, p <0.05). PFR at rest was reduced in CAD subjects (2.40 +/- 0.70 end-diastolic volume per second [EDV/s]) compared with those with hypertension (2.89 +/- 0.70 EDV/s, p <0.02) and controls (3.23 +/- 0.52 EDV/s, p <0.0002). The increments in PFR during exercise were reduced in CAD patients (+1.76 +/- 0.95 EDV/s) compared with hypertensive subjects (+2.93 +/- 1.7 EDV/s) and controls (+3.22 +/- 1.4 EDV/s, p <0.05). The increment in PFR during exercise was related to exercise performance (r = 0.49, p <0.0002). These findings suggest that alterations in LV diastolic filling during exercise are important determinants of exercise performance.

Usefulness of magnetic resonance imaging early after acute myocardial infarction.

In patients, early after acute myocardial infarction (AMI), rapid magnetic resonance imaging (MRI) techniques have been used to assess left ventricular (LV) structure, global and regional function, infarct artery patency, or contrast uptake individually. We hypothesized that MRI could be used as a comprehensive evaluation of the post-AMI patient, studying all of these parameters in < 1 hour. Twenty-seven patients were studied after first AMI. Complete examinations were performed in 23 patients, 16 with anterior and 7 with inferior wall myocardial infarction, on day 5 +/- 2 after the event. For measurement of LV structure and regional function, a breath-hold segmented k-space gradient echo tagging sequence was used. A fat-suppressed segmented k-space breath-hold sequence was used for coronary artery imaging. MRI contrast-enhanced images during bolus gadoteridol transit through the myocardium were obtained to assess first-pass contrast uptake. No adverse events were noted during the MRI scanning, which was completed in 46 +/- 5 minutes. The LV mass index, end-diastolic and end-systolic volume indexes, and ejection fraction were (mean +/- SD) 107 +/- 13 g/m2, 87 +/- 23 ml/m2, 54 +/- 20 ml/m2, and 39 +/- 12%, respectively. Intramyocardial percent circumferential shortening was 11 +/- 6% at the apex, 14 +/- 4% in the midventricle, and 15 +/- 4% at the base. Flow within all infarct arteries was visualized. Seventeen of 23 patients had regions of reduced contrast uptake on first-pass imaging with mean signal intensity of 47 +/- 24% that of remote regions. In patients with recent AMI, comprehensive assessment of LV structure and function, infarct artery patency, and regional myocardial contrast uptake was safe and feasible with MRI of < 1 hour.