Detection of viable myocardium in segments with fixed defects on thallium-201 scintigraphy: Usefulness of magnetic resonance imaging early after acute myocardial infarction

hfognelic Resonance Imaging, Vol. I I, pp. 949-956. 1993 Printed in the USA. All rights reserved.

0730-725X/93 $6.00 + .Cil Copyright 0 1993 Pergamon Press Ltd.

l Original Contribution

DETECTION OF VIABLE MYOCARDIUM IN SEGMENTS WITH FIXED DEFECTS ON THALLIUM-201 SCINTIGRAPHY: USEFULNESS OF MAGNETIC RESONANCE IMAGING EARLY AFTER ACUTE MYOCARDIAL INFARCTION

DONALD L. JOHNSTON,* VINOD K. GUPTA,* RICHARD E. WENDT,~

JOHN J. MAHMARLAN,* AND MARIO S. VERANI*

*Section of Cardiology, Department of Medicine and the TDepartment of Radiology, Baylor College of Medicine, The Methodist Hospital, Houston, TX, USA

To determine if magnetic resonance imaging (MRI) can be used to detect tissue viability in segments with persistent ZOIT1 defects early following acute myocardial infarction, 24 patients underwent MRI and adenosine ZO’T1 single photon emission computed tomography (SPECT) imaging at approximately 6 days. Infarction was demonstrated on MRI using a velocity-compensated, &weighted spin-echo pulse sequence. Wall thickening was assessed using a gradient-echo pulse sequence obtained in the same anatomic position. Viable myocardium was defined by MRI as a segment with increased signal intensity and preserved wall thickening. A fixed defect on the *“Tl SPECT images was defined as the absence of any redistribution 4 hours after the *‘lTl infusion. Of 11 patients with redistribution on the *‘lTl images in the infarction region, 10 (91%) had preserved wall thickening by MRI. Of 13 patients with fixed defects on the ZOIT1 images in the infarction region, 6 (46%) had preserved wall thickening by MRI. Of 7 patients with absent thickening, all had one or more segments with absent perfusion on redistribution imaging. Wall thickening tended to occur in patients who received thrombolytic therapy or who underwent revascularization procedures prior to imaging. The results of the present study suggest that spin-echo MRI with motion compensation can be used to identify viable myocardium in patients with fixed defects on *‘lTl SPECT following acute myocardial infarction.

Keywords: Myocardial viability; Adenosine thallium scintigraphy; Magnetic resonance imaging.

INTRODUCTION

The ability to differentiate necrosis from reversible tissue injury following acute myocardial infarction has assumed considerable clinical significance as aggressive interventional techniques for recanalization of infarction-related coronary arteries are increasingly utilized. Stress thallium-201 (‘OlTl) scintigraphy has been pro- posed as a method of assessing myocardial viability. Diminished uptake of 201T1 with stress and absent redistribution at 4 hr (fixed defect) has usually been called scar ’ while a reduction in 20’T1 uptake followed by rediitribution is considered a marker of tissue viability. Recently, however, it has been shown that some fixed defects, when imaged with positron emission tomography and isfluorine deoxyglucose, contain viable myocardium rather than scar tissue.2y3 18Fluorine deoxyglucose uptake has also been reported in established

myocardial infarction (as defined by ECG), suggesting that areas of viable tissue may coexist with completed infarction.4 Repeat resting 201T1 imaging at 24 hr or reimaging after reinjection of 20’T1 at 4 hr have also demonstrated tissue viability.5s6

In the present study, it was hypothesized that magnetic resonance imaging (MRI), by detecting wall thickening in the acute infarction region (defined as the area of increased signal intensity on MRI), could be used to identify viable tissue in segments with fixed defects on stress 20’T1 scintigraphy. Wall thickening, detected by MRI, has previously been used as a “gold standard” for tissue viability in patients with stable angina.5

METHODS

Patient Population Twenty-four patients (mean age 65 + 9 years; 21

males, 3 females) were entered into the study. Eleven

RECEIVED 12/18/93; ACCEPTED 5/10/93. Division of Cardiovascular Diseases, Mayo Clinic, 200 First Address correspondence to Donald L. Johnston, MD, Street, SW, Rochester, MN 55905, USA.

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950 Magnetic Resonance Imaging 0 Volume 11, Number 7, 1993

patients had an anterior myocardial infarction, 10 had an inferior wall myocardial infarction, and 3 had a lateral myocardial infarction. According to ECG cri- teria, 20 patients had a Q-wave infarction and 4 had a non-Q-wave infarction. Peak CK was 722 + 505 IU and CK-MB was 70 f 56 IU. Eleven patients received tissue-type plasminogen activator upon admission, and 10 patients had percutaneous transluminal coronary an- giography performed early during the hospitalization period (4 within 48 hr of chest pain onset). Coronary arteriography was performed on all patients at a mean time of 2.1 f 2.4 days after infarction. Magnetic resonance imaging was obtained 5.7 f 2.3 days following the acute infarction and the adenosine 20’T1 SPECT study was obtained 6.1 f 2.6 days following the infarction. Seventeen patients had the two studies performed within 24 hr of each other.

Magnetic Resonance Imaging A Magnetom 42 (1 T) Siemens MRI system equipped

with a quadrature body radiofrequency (RF) coil was used for all studies. ECG gating was accomplished with a Sirecust 404-l device. The short axis of the left ventricle was determined from a scout coronal spin-echo image. A multi-slice short axis spin-echo acquisition was used to identify the base, mid-and distal portion of the left ventricle. A single-slice, velocity-compensated, spin-echo pulse sequence with an echo time (TE) of 90 ms was obtained at each of these levels to identify the region of ischemic injury.’ A gradient-echo, multiphase, fast imaging with steady precession (FISP) pulse sequence was used to assess wall thickening in the anatomic position imaged with the spin-echo pulse sequence.

Study Protocol Patients were placed in a 30” right anterior oblique

position with the heart in the center of the magnet. Nonmagnetic electrodes and leads were placed over the left anterior thorax in the shape of a triangle. The leads were braided to reduce induction of magnetic gradient switching artifacts in the ECG signal. All patients were imaged using a standard imaging protocol previously devised in our laboratory.* Briefly, three short axis positions were chosen from the initial scout coronal image to represent the basilar, mid, and distal (apical) left ventricle. The T2-weighted images were acquired at each of the three anatomical positions, followed by acquisition of FISP images. Pulse repetition time for both sequences was dependent on heart rate (mean 76 beats per minute). All spin-echo images were obtained at 250 ms after the QRS complex of the ECG to approximate end-systole. MRI wall motion studies using the FISP sequence were obtained with TE =

10 ms or 7 ms. The repetition time was set to 100 ms less than the R-R interval to prevent data acquisition in the next cardiac cycle if heart rate varied.

MR Data Analysis Magnetic resonance images were evaluated without

previous knowledge of the 201T1 SPECT data. Each slice of the left ventricle was divided into anterior, lateral, inferior, and septal segments on the short-axis magnetic resonance images. These segments were compared to equivalent slices and segments on the 201T1 images. The spin-echo images were assessed visually for changes in regional myocardial signal intensity. Signal intensity was also quantitatively measured by placing a region of interest over the myocardial segment and registering an arbitrary signal intensity value. The mea- surements were repeated at several locations in that segment and a mean signal intensity value was calculated. The percent change in signal intensity of the segment with the greatest increase visually was compared with a remote segment [(infarction) - (normal/normal) x lOO%)]. The equivalent segment on the FISP image was examined and wall thickening was visually determined. Wall thickening was classified as normal, hypokinetic, akinetic,or dyskinetic. Since tissue viability was classified according to the presence or absence of wall thickening, a qualitative approach to the measurement of contraction was considered reasonable for this study. It was necessary to separate the endocardial border on the spin-echo image from the intraventricular flow signal by overlaying a FISP image obtained at the iden- tical ECG-gate delay time onto the T2-weighted spin- echo image.

If wall thickening of a segment with increased signal intensity was normal or hypokinetic, the segment was considered to contain reversibly injured, or viable myocardium. Segments that were severely akinetic or dyskinetic were considered to be irreversibly injured.

Adenosine “IT1 SPECT Ten vials (12 mg/vial) of adenosine were diluted into

30 ml of normal saline and infused intravenously using a computer-controlled pump infusion system? Infu- sion rates were as follows: minute 1: 50 g/kg; minute 2: 75 g/kg; minute 3: 100 g/kg; minute 4: 140 g/kg. In patients who could not tolerate the 140 g/kg/min dose, the infusion rate was decreased to the previous infusion rate. After 1 min at the highest dose, 3 mCi of 201T1 were injected as a bolus into the contralateral vein and flushed with saline. The adenosine infusion was maintained at the highest dose for 2 (modified dose) or 3 (full dose) additional minutes after the 201T1 injection.

Thallium-201 myocardial perfusion scintigraphy was

Detection of viable myocardium 0 D.L. JOHNSTON ET AL. 951

performed as previously described.’ Briefly, images were acquired with a large field-of-view rotating gamma camera (ARC 3000, ADAC Laboratories, Milpitas, CA) equipped with a low energy, high-resolution col- limator interfaced to a ADAC 3300 computer. Thirty- two images were obtained over a 1 BO-degree arc from the 60-degree left posterior oblique to the 30-degree right anterior oblique position for 40 s per image. Im- aging began 5 min after completion of the 201T1 infusion and was repeated 4 hr later.

A 201T1 image was considered abnormal if there was a visually obvious decrease of 201T1 uptake in any myocardial segments. Perfusion defects were graded in the following manner: 3 = normal uptake, 2 = mildly diminished uptake, 1 = moderately diminished uptake, and 0 = severely diminished or absent uptake. The presence or absence of redistribution was visually determined at 4 hr. Such a qualitative analysis of 201T1 images is widespread and the clinical significance of this method is readily acknowledged. All images were in- terpreted without previous knowledge of the magnetic resonance images. Segments in the zone of infarction that had any amount of 201T1 redistribution were considered to contain viable myocardium. Defects without any redistribution at 4 hr were called fixed defects. Two patients with fixed defects had repeat redistribution imaging at 24 hr.

RESULTS

Signal Intensity All patients had at least one segment with increased

signal intensity in the infarction zone (identified from the ECG and location of the infarction-related coronary artery) on MRI. The change in signal intensity measured in the segment with the greatest increase in signal compared to the opposite cardiac wall was 65 + 28%. There was no correlation between the amount of increase in signal intensity and the degree of wall thickening. Most patients had segments with combined transmural and nontransmural (endocardial) signal increase.

Perfusion vs. Wall Thickening Eleven patients (46%) had evidence of “IT1 redis-

tribution or had no hypoperfusion in the infarction region (7 partial redistribution; 3 complete redistribution; 1 normal study) (Fig. 1, Table 1). Ten (91Vo) of these patients had preserved wall thickening (2 normal; 8 hypokinesis) in at least one segment on MRI. Thirteen patients had fixed defects by “‘Tl. Six (46%) of these patients had preserved wall thickening of one or more segments on MRI. All 7 patients with absent wall thickening by MRI had fixed defects by 20’T1 scintigraphy

Table 1. Comparison of ‘O’Tl perfusion and MRI wall thickening

*‘IT1 (number of patients)

Redistribution Fixed Defect

MRI Wall thickening 10 6 No wall thickening 0 I

and had at least one segment with no perfusion on the redistribution 201T1 images (Figs. 2-4).

24-Hour 20’TI Reimaging Two of the patients with fixed defects at 4 hr had

a repeat “‘Tl redistribution study performed at 24 hr. In one, mild redistribution occurred and the MRI showed two segments in the infarction zone with hypokinesis and one segment with akinesis. In the other, there was no redistribution and the MRI showed one segment in the infarction zone with hypokinesis and one with akinesis.

Interventional Therapy Preserved wall thickening was more commonly

found in the patients who received thrombolytic therapy (9 of 10 patients; 9OVo) compared with the patients not receiving thrombolysis (6 of 14; 43%). Five of the 10 patients receiving thrombolytic therapy had fixed 201T1 defects compared with 8 of 14 not receiving thrombolysis. Also, 9 of 10 patients having percutaneous transluminal coronary angioplasty or coronary artery bypass during hospitalization had preserved wall thickening; 4 had fixed 201T1 defects.

25

20

5 Redistribution

0 MRI TI-201 SPECT

Fig. 1. Number of patients with normal studies, fried defects or absent wall thickening, and radionuclide redistribution or residual wall thickening.

952 Magnetic Resonance Imaging 0 Volume I I, Number 7, 1993

4 - HOUR REDISTRIBUTION

(A)

(Cl

DISCUSSION

The present study examines myocardial viability with MRI in humans immediately following acute myo-

cardial infarction. Overall, 17 of 24 patients (71%) had partial or complete preservation of wall thickening (an indication of tissue viability), a finding that may have been due to the aggressive interventional therapy received by the patients at the time of presentation. Of the 11 patients with 20’T1 redistribution (a marker of myocardial viability) in the infarction segment, 10

patients had preserved wall thickening in the same segment. The presence of wall thickening in 6 of 13 patients (46%) without 201T1 redistribution at 4 hr would

Fig. 2. Agreement between MRI and “‘Tl scintigraphy on the extent of tissue viability. (A) There is an anterior and apical wall defect (arrows) on the 20’T1 images. Complete redistribution occurs in the short axis; redistribution is partial in the horizontal and vertical views. (B) Signal intensity is increased in the anterior segment on MRI at the mid-left ventricle (arrow). (C) Images obtained at 13 phases of the cardiac cycle at the same anatomic position as (B) show wall thickening in the anterior segment (arrows).

suggest that assessment of early 201T1 redistribution is a poor indicator of tissue viability in patients with acute myocardial infarction. Similar observations in patients with stable coronary artery disease have been reported

by other investigators using different techniques?*3J0J1 It has also been shown that lack of redistribution following rest or stress 201T1 injection does not preclude the possibility of functional recovery of segments sup- plied by critically stenosed coronary arteries following revascularization.‘2-14 In the present study, patients with no wall thickening had no perfusion in at least one segment on redistribution “IT1 imaging. Absent perfusion at rest strongly implies the presence of irre- versible injury and is consistent with other studies in


ADENOSINE STRESS

4 - HOUR REDISTRIBUTION

(A)

which the amount of radionuclide uptake or echo- cardiographic contrast have been shown to be related to myocardial viability.‘5-17

We previously found that in a dog model of ischemia/ reperfusion, reperfusion of an endocardial infarction (defined as negative TTC staining in the endocardium) produced a transmural increase in signal intensity.‘*,19 This suggested that MRI signal increases in reversibly injured myocardium (i.e., epicardium) when the isch- emit injury is severe enough, and would account for those instances in the present study in which wall thickening was preserved despite a transmural increase in signal intensity.

A potential problem with the present study was that only three anatomical slices were imaged along the short axis of the left ventricle. Some additional wall thickening might be found if more slices were obtained. Development of rapid imaging methods that allow acquisition of a set of data to include the entire left ven-

(B)

Fig. 3. Agreement between MRI and 201T1 scintigraphy on the absence of tissue viability. (A) The adenosine stress and redistribution 201T1 images show an anterior and apical wall defect in which perfusion is absent (arrows). (B) Signal intensity is increased in the anterior and anteroseptal segments on MRI (arrows). (C) Images obtained at 11 phases of the cardiac cycle at the same anatomic position as (B) show akinesis in the anterior segment (arrows).

tricle would eliminate errors caused by inadequate sampling of the infarction. Alternatively, wall thickening may have been falsely enhanced due to a partial volume effect potentially present with all tomographic imaging techniques. Careful attention to the orienta- tion of the image plane in the true short axis and the use of thin slices reduces the effects of partial volume imaging. Through-plane motion has been shown to un- derestimate true contraction by 16-20’70 at the base and midventricle, respectively. 2o Another limitation to the use of noninvasive imaging methods to detect viability is that the basic abnormality resulting in loss of viability is not primarily identified. Thallium-201, echocardiography, PET, and MRI reflect only secondary changes that act as markers of impaired cell function. Despite the limitations of tomographic imaging, previous studies have shown these methods to be useful for the assessment of tissue viability.5,15,21,22

Myocardial metabolic abnormalities associated with

24-Hour Redistribution


Fig. 4. Disagreement between MRI and *‘IT1 scintigraphy on the extent of tissue viability. (A) *OIT1 views show no sig- nificant redistribution in the septum and inferior wall at 4 hr. At 24 hr, slight redistribution is noted in the inferior and posterior walls (arrows). (B) Signal intensity was increased in the inferior septal and inferior segments on MRI (arrows). (C) Images obtained at 14 phases of the cardiac cycle at the same anatomic position as (B) show near-normal wall thickening of the inferior segment (arrows).

m

stunning result in loss of wall thickening. However, it has been shown that wall motion improves within 3 days following reperfusion.23 In the present study, MRI was completed at an average of 5.7 days following myocardial infarction. Similarly, wall thickening may be absent in hibernating myocardium. it is possible that some infarct-related segments were hypoperfused at rest despite the policy of aggressive revascularization used in this study. Perrone-Filardi et a1.24 have shown that absent wall thickening, as assessed by MRI in pa-

tients with stable angina, may be associated with via-

bility determined by uptake of *“Tl measured from redistribution/reinjection images and “flourine de-

oxyglucose uptake. The scintigraphic findings of the present study ap-

ply only to the use of standard *OlTl imaging techniques. Patients did not have “‘Tl reinjection at 4 hr in this study, as recommended by Dilsizian et al.,” be-

cause our study was in progress before this report ap- peared. Only two patients had repeat redistribution images at 24 hr. Reinjection of “‘Tl at 4 hr, or 24 hr imaging in all patients may have reduced the number


of patients who had wall thickening by MRI and no and thallium-201 scintigraphy in patients unable to ex- **IT1 redistribution. ercise. Circulation 82:80-87; 1990.

In summary, MRI detects wall thickening in the

infarction zone early following acute myocardial infarction in 46% of patients who fail to demonstrate redistribution at 4 hr on **IT1 scintigraphy. These findings indicate that patients often have viable myo-

cardium present in the region of acute myocardial infarction and detection is possible within a few days of presentation using MRI.

10. Dilsizian, V.; Rocco, T.P.; Freedman, M.T.; Leon, M.B.; Bonow, R.O. Enhanced detection of ischemic but viable myocardium by the reinjection of thallium after stress-redistribution imaging. N. Engl. J. Med. 323: 141- 146; 1990.

11. Kiat , H .; Berman, D.S.; Maddahi, 3. ; Yang, L.D.; Van Train, K.; Rozanski, A.; Friedman, J. Late reversibility of tomographic myocardial thallium-201 defects: An ac- curate marker of myocardial viability. J. Am. COIL Car- dial. 12:1456-1463; 1988. Liu, P.; Kiess, M.C.; Okada, R.D.; Block, P.F.; Strauss, H.W.; Pohost, G.M.; Boucher, C.A. The persistent defect on exercise thallium imaging and its fate after myocardial revascularization: Does it represent scar or ischemia? Am. Heart .T. 110:996-1001; 1985. Tillisch, J.; Brunken, R.; Marshall, R.; Schwaiger, M.; Mandelkern, M.; Phelps, M.; Schelbert, H. Reversibil- ity of cardiac wall-motion abnormalities predicted by positron tomography. N. Engl. J. Med. 314:884-888; 1986.

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Detection of viable myocardium in segments with fixed defects on thallium-201 scintigraphy: Usefulness of magnetic resonance imaging early after acute myocardial infarction