Myocardium at Risk After Acute Infarction in Humans on Cardiac Magnetic ResonanceQuantitative Assessment During Follow-Up and Validation With Single-Photon Emission Computed Tomography
Marcus Carlsson, MD, PhD*,
Joey F.A. Ubachs, MD*,
Erik Hedström, MD, PhD*,
Einar Heiberg, PhD*,
Stefan Jovinge, MD, PhD ,
Håkan Arheden, MD, PhD*,*
* Cardiac MR Group, Department of Clinical Physiology, Lund University Hospital, Lund, Sweden
Department of Cardiology, Lund University Hospital, Lund, Sweden
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Abstract
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Objectives: Our goal was to validate myocardium at risk on T2-weighted short tau inversion recovery (T2-STIR) cardiac magnetic resonance (CMR) over time, compared with that seen with perfusion single-photon emission computed tomography (SPECT) in patients with ST-segment elevation myocardial infarction, and to assess the amount of salvaged myocardium after 1 week.
Background: To assess reperfusion therapy, it is necessary to determine how much myocardium is salvaged by measuring the final infarct size in relation to the initial myocardium at risk of the left ventricle (LV).
Methods: Sixteen patients with first-time ST-segment elevation myocardial infarction received 99mTc tetrofosmin before primary percutaneous coronary intervention. SPECT was performed within 4 h and T2-STIR CMR within 1 day, 1 week, 6 weeks, and 6 months. At 1 week, patients were injected with a gadolinium-based contrast agent for quantification of infarct size.
Results: Myocardium at risk at occlusion on SPECT was 33 ± 10% of the LV. Myocardium at risk on T2-STIR did not differ from SPECT, at day 1 (29 ± 7%, p = 0.49) or week 1 (31 ± 6%, p = 0.16) but declined at week 6 (10 ± 12%, p = 0.0096 vs. 1 week) and month 6 (4 ± 11%, p = 0.0013 vs. 1 week). There was a correlation between myocardium at risk demonstrated by T2-STIR at week 1 and myocardium at risk by SPECT (r2 = 0.70, p < 0.001), and the difference between the methods on Bland-Altman analysis was not significant (–2.3 ± 5.7%, p = 0.16). Both modalities identified myocardium at risk in the same perfusion territory and in concordance with angiography. Final infarct size was 8 ± 7%, and salvage was 75 ± 19% of myocardium at risk.
Conclusions: This study demonstrates that T2-STIR performed up to 1 week after reperfusion can accurately determine myocardium at risk as it was before opening of the occluded artery. CMR can also quantify salvaged myocardium as myocardium at risk minus final infarct size.
Key Words: myocardium at risk • T2-STIR • CMR • salvaged myocardium
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Abbreviations and Acronyms
| | CMR = cardiac magnetic resonance | | DE = delayed enhanced | | LV = left ventricle/ventricular | | MI = myocardial infarction | | PCI = percutaneous coronary intervention | | SPECT = single-photon emission computed tomography | | STEMI = ST-segment elevation myocardial infarction | | T2-STIR = T2-weighted short tau inversion recovery |
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Myocardial infarction (MI) size depends heavily on duration of occlusion, collateral flow, and size of the initial myocardium at risk (1–3). Therefore, ST-segment elevation myocardial infarction (STEMI) is treated with reperfusion therapy as soon as possible. The myocardium at risk, defined as the hypoperfused myocardium during acute coronary occlusion, is an important measure, since a variable amount of this area will become infarcted (4). Therefore, to assess the efficacy of reperfusion therapy, it is necessary to determine how much myocardium is salvaged by measuring the final infarct size in relation to the initial myocardium at risk.
MI size has earlier been quantified by single-photon emission computed tomography (SPECT) after injection of a technetium-labeled perfusion tracer at rest (5), where MI is indirectly detected as a region with decreased myocardial perfusion. More recently, contrast delayed enhancement (DE) cardiac magnetic resonance (CMR) has emerged as the new reference method for infarct localization and quantification (6–8).
Myocardium at risk can be measured on SPECT by injection of a technetium-based tracer before opening of the occluded vessel and is currently the most widely practiced technique to determine myocardium at risk (9–11). However, drawbacks in the use of SPECT to estimate myocardium at risk are the availability of a technetium-based tracer, the need for injection of the isotope in the acute setting of coronary occlusion, and scanning with a gamma camera after completion of primary percutaneous coronary intervention (PCI), which could interfere with patient care in the acute setting. These factors have limited the applicability of SPECT in measurement of myocardium at risk. Therefore, new clinical methods to quantify myocardium at risk need to be developed.
T2-weighted short tau inversion recovery (T2-STIR) highlights myocardial edema (12) present after MI (13) without the need of tracer administration. Moreover, CMR with T2-STIR allows the detection of the ischemic zone several days after the occluded coronary artery is opened (14,15). Therefore, CMR with T2-STIR can potentially be used for quantification of myocardium at risk. Previous studies have shown the use of T2-STIR imaging for acute infarction in both reperfused and nonreperfused infarcts (12,14–17) and validated T2-STIR for myocardium at risk in animals (14). There are, however, no validation studies in humans for the quantification of myocardium at risk using T2-STIR CMR. Hence, the purpose of this study was to validate the measurement of the myocardium at risk on T2-STIR over time, in comparison with SPECT in humans with acute MI, and to assess the amount of salvaged myocardium after 1 week.
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Methods
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Study population and design.
The study was approved by the local ethics committee, and all patients gave their written informed consent. Sixteen patients (age 64 ± 12 years, 14 men) with no history of MI, presenting with acute STEMI due to an occluded coronary artery, were included in the study. All patients were treated by primary PCI with coronary stents, resulting in Thrombolysis In Myocardial Infarction flow grade 3 in the opened artery and received glycoprotein IIb/IIIa inhibitor.
Before primary PCI, 99mTc tetrofosmin was administered intravenously, and myocardial perfusion SPECT was performed 3 to 4 h after primary PCI for determination of myocardium at risk. CMR with T2-STIR was undertaken 1 week after revascularization. In 1 patient, adequate T2-STIR images at 1 week were not obtained. To determine the time evolution of the increase in T2-STIR signal, early imaging was performed at 1 day in 8 patients and within 2 days in 2 patients (hereafter described as day 1), and 9 patients underwent CMR follow-up at 6 weeks and 6 months. For comparison, all patients underwent DE-CMR with administration of gadolinium at 1 week. The culprit vessel was identified on angiography by 2 observers in consensus.
Myocardial perfusion SPECT.
Patients were injected with 500 to 700 MBq 99mTc tetrofosmin (Amersham Health, Buckinghamshire, United Kingdom), depending on body weight. Myocardial perfusion electrocardiogram-gated SPECT was performed according to the standard clinical protocol at rest, using a dual-head camera. Nine patients were imaged using an ADAC Vertex camera (Milpitas, California), 7 patients with a cardiac dedicated GE Ventri camera (GE Healthcare, Buckinghamshire, United Kingdom). The patients were placed in a supine position and imaged in steps of 5.6° using a 64 x 64 matrix with a pixel size of 5.02 mm for the ADAC camera and a pixel size of 6.4 mm for the GE Ventri camera. Image acquisition time was approximately 15 min, but was extended to 25 min when imaging was performed after 3 h. Short- and long-axis images covering the left ventricle (LV) were reconstructed. Myocardium at risk was determined using an in-house developed segmentation software (segment version 1.702) (18). The automatic segmentation finds the centerline through the LV wall and identifies the endocardium and epicardium based on an individually estimated wall thickness and signal intensity values within the image. Manual adjustment of the automatic delineation was sometimes required in the LV outflow region.
CMR.
CMR was performed on either of 2 1.5-T systems: Magnetom Vision (Siemens, Erlangen, Germany) with a CP body array coil, or Philips Intera CV (Philips, Best, the Netherlands) with a cardiac synergy coil. All subjects were placed in a supine position, and images were acquired at end-expiratory breath hold with electrocardiogram gating. Initial scout images were acquired to locate the heart, and a T2-weighted double inversion blood suppressed turbo spin echo sequence (T2-STIR) was employed to depict myocardium at risk. T2-STIR images were acquired in the short-axis view, covering the LV from the base to apex. Image parameters for T2-STIR were: echo time, 43 ms (Siemens), or 100 ms (Philips); repetition time, 2 heart beats; number of averages, 2; inversion time, 180 ms; image resolution, 1.5 x 1.5 mm; slice thickness, 10 mm (Siemens), or 8 mm with a slice gap of 2 mm (Philips). When acquiring images with the cardiac synergy coil, parallel imaging with SENSE = 1 was used to minimize signal inhomogeneities due to differences in coil sensitivity.
Infarct quantification was performed on DE-CMR 30 ± 9 min after intravenous administration of 0.2 mmol/kg extracellular gadolinium-based contrast agent (gadoteric acid, Gd-DOTA; Guerbet, Gothia Medical AB, Billdal, Sweden). DE-CMR with an inversion-recovery turbo fast low-angle shot sequence (Siemens) (slice thickness 10 mm, field of view 380 mm, matrix 126 x 256, flip angle 25°, repetition time 100 ms, echo time 4.8 ms) or an inversion-recovery balanced turbo field echo sequence (Philips) (slice thickness 8 mm, field of view 340 mm, repetition time 3.14 ms, echo time 1.58 ms) was performed, covering the LV.
The CMR images were analyzed using the same software as for the SPECT images (segment version 1.702) (19). Observers were blinded to patient data and time of acquisition after infarction. The myocardium in each LV short-axis slice was manually segmented by tracing the endocardial and epicardial borders. Regions of myocardium at risk and MI were identified as hyperenhanced regions, within the T2-STIR images and DE-CMR images, respectively. The myocardium at risk region was delineated manually by independent and blinded observers, and the infarcted region was delineated automatically as previously described with manual adjustment when needed (19). Myocardium at risk size and MI size were defined as the total amount of myocardium at risk/MI in all short-axis slices and expressed as percentage of LV mass.
Statistical methods.
Continuous variables are presented as mean ± SD. Pearson's correlation was used to determine the relationship between T2-STIR and SPECT. Two-tailed paired t test was used to detect differences in myocardium at risk between techniques, differences in myocardium at risk on T2-STIR at different time points, and the final infarct size compared with myocardium at risk on T2-STIR. A p value <0.05 was considered significant. Agreement between methods was expressed as mean difference ± SD, and the limits of agreement were shown in a Bland-Altman graph as mean difference ± 2 SD.
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Results
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Myocardium at risk.
Table 1
shows the patient characteristics for all 16 patients included in this study. Figure 1
shows multislice images from base to apex from T2-STIR at week 1, SPECT at day 1, and DE-CMR at week 1 from 1 patient. Myocardium at risk presented as a perfusion defect on SPECT and hyperenhanced regions on T2-STIR. In all patients, T2-STIR and SPECT identified myocardium at risk in the same perfusion territory and in concordance with angiography. The resulting infarction on DE-CMR was present in the same region in all patients.
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Figure 1 Myocardium at Risk by SPECT and T2-STIR CMR and Final Infarct Size by DE-CMR in 1 Typical Patient
Short-axis slices at the same ventricular level of single-photon emission computed tomography (SPECT) day 1, T2-weighted short tau inversion recovery (T2-STIR) week 1, and delayed enhanced-cardiac magnetic resonance (DE-CMR) week 1 in a patient with reperfused right coronary occlusion resulting in an inferior infarct. The epicardium is traced in green, the endocardium is traced in red, and the affected region is traced in yellow. Note the similarity in size of the affected region between perfusion defect size during coronary occlusion by SPECT and T2-STIR CMR 1 week later, showing that T2-STIR at week 1 can be used to quantify myocardium at risk.
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Myocardium at risk on SPECT was 33 ± 10% of the LV and on T2-STIR at day 1 it was 29 ± 7% (p = 0.49 compared with SPECT). Myocardium at risk on week 1 was 31 ± 6% (p = 0.16 compared with SPECT) (Table 2). Myocardium at risk on T2-STIR at day 1 and week 1 did not differ (p = 1.00). Over time, myocardium at risk declined to 10 ± 12% at week 6 (p = 0.0096 vs. T2-STIR at 1 week and p = 0.0026 vs. SPECT) and 4 ± 11% at month 6 (p = 0.0013 vs. T2-STIR at 1 week and p = 0.001 vs. SPECT). In patient 5, the observers were unable to designate the culprit vessel within the T2-STIR images at day 1; however, at week 1 the myocardium at risk could be identified. Figure 2A shows the relationship between myocardium at risk demonstrated on T2-STIR at week 1 and SPECT (r2 = 0.70, p < 0.001). There was no statistical significant difference between myocardium at risk on T2-STIR compared with that of SPECT on Bland-Altman analysis (–2.3 ± 5.7, p = 0.16) (Fig. 2B).
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Figure 2 Agreement Between T2-STIR and SPECT
(A) T2-STIR at week 1 versus perfusion defect during coronary occlusion by SPECT (r2 = 0.70, p < 0.001) with the line of identity. (B) Bland-Altman graph showing the difference between myocardium at risk quantified on T2-STIR (week 1) and SPECT versus the reference method SPECT. The difference between T2-STIR and SPECT was –2.3 ± 5.7%. Solid lines = mean of T2-STIR – SPECT; dotted lines = ±2 SD. LVM = left ventricular mass; other abbreviations as in Figure 1.
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The evolution of myocardial edema in a patient with left anterior descending artery occlusion is shown in Figure 3; SPECT is shown for comparison. The size of the affected region is similar at day 1 and week 1 on T2-STIR, but cannot be detected at week 6 in this patient. Figure 4
displays the ratio between T2-STIR and SPECT at the different acquisition times, day 1 (0.97 ± 0.20), week 1 (0.97 ± 0.18), week 6 (0.35 ± 0.40), and month 6 (0.11 ± 0.27).
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Figure 3 T2-STIR Over Time in 1 Typical Patient
Midventricular short-axis slices of automatically delineated perfusion defect during coronary occlusion by SPECT and blinded manual delineation of T2-STIR over time, in the same patient with a left anterior descending occlusion. The epicardium is traced in green; the endocardium is traced in red. The myocardium at risk is delineated in yellow. Note that the signal of the affected region on T2-STIR imaging is similar at day 1 and week 1, but disappears at week 6. Abbreviations as in Figure 1.
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Figure 4 T2-STIR Over Time in All Patients in Relation to Perfusion Defect at Occlusion by SPECT Imaging
Ratio between T2-STIR and SPECT at day 1, week 1, week 6, and month 6 were 0.97 ± 0.20; 0.97 ± 0.18; 0.35 ± 0.40; and 0.11 ± 0.27, respectively, showing that the T2-STIR signal at day 1 and week 1 agree with perfusion defect at occlusion by SPECT imaging. The presence of edema at 6 months was found in 2 of 9 patients. CMR = cardiac magnetic resonance; other abbreviations as in Figure 1.
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Myocardial salvage.
The mean infarct size at week 1 was 8 ± 7% LV (range 0% to 19%), significantly smaller than myocardium at risk (p < 0.001) (Table 2). Myocardial salvage, calculated as the difference of T2-STIR and DE-CMR at week 1 was, on average, 75 ± 19% (range 41% to 100%). One patient did not have any infarcted myocardium on DE-CMR after the acute revascularization, meaning that all myocardium was salvaged by primary PCI; salvage in this patient was therefore 100%. This patient underwent revascularization within 1 h after pain onset. In patient 1, infarct size by DE-CMR was compared with that of T2-STIR at day 1 in absence of T2-STIR data at week 1. The amount of salvaged myocardium is exemplified in 1 patient in Figure 5. Note that the salvage occurs in the subepicardial layers of the myocardium.
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Figure 5 Myocardial Salvage by CMR
Midventricular short-axis slices in a patient with a left circumflex artery occlusion. The epicardium is traced in green; the endocardium is traced in red. (Left) T2-STIR image showing the myocardium at risk (delineated in yellow). (Middle) DE-CMR showing myocardial infarction (delineated in yellow). (Right) T2-STIR image with inclusion of infarcted region showing the amount of salvaged myocardium (blue area). Abbreviations as in Figure 1.
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Discussion
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This study is the first to validate the quantification of myocardium at risk on T2-STIR over time in comparison with that of SPECT, in patients with STEMI. The main finding is that T2-STIR accurately identifies and quantifies myocardium at risk up to 1 week after opening of the occluded coronary artery. Thus, the success of reperfusion therapy can be assessed on CMR within 1 image session utilizing the combination of DE and T2-STIR to measure final infarct size and myocardium at risk, respectively, and thereby measuring myocardial salvage.
Myocardium at risk.
Earlier studies (12,14–17,20) have demonstrated the use of T2-weighted imaging for acute infarction, in both reperfused and nonreperfused infarcts. The current study showed that T2-STIR accurately assessed myocardium at risk in reperfused infarcts in patients using SPECT at the time of coronary occlusion as the reference method. In agreement with studies on humans (21,22) and animals (12,14,23), the area with high T2 signal exceeded that of irreversible injury in acute MI. Pathology studies in humans have shown complete resorption of edema after acute MI within 5 weeks (13), and Aletras et al. (14) showed that edema was still present at the 2-month follow-up CMR in a canine model. No evidence of edema was found on T2-STIR in 7 of the 9 patients at 6 months after the acute coronary occlusion in the present study. One may hypothesize that these 2 patients may have had residual or recurring ischemia within the same myocardial region.
Myocardial ischemia increases cellular and extracellular osmolarity, alters plasma membrane permeability, causes cell swelling and interstitial edema (24). Quantification of interstitial edema has been demonstrated in experimental studies of myocardium at risk after reperfusion by light microscopy, autoradiography, and contrast-enhanced inversion recovery echo-planar CMR (25). Once reperfusion is established, an inflammatory reaction within the perfusion bed of the culprit vessel takes place, which significantly increases tissue edema. Myocardial edema is therefore a consistent feature of acute ischemia (26), which can be demonstrated on T2-STIR (12) although the myocardium is reperfused (14,15). The results of the present study showed that the amount of edema present after 1 week was similar to the amount of edema at 1 day after reperfusion.
Advantages of T2-STIR over SPECT in assessing myocardium at risk are: 1) no need of tracer administration; 2) no complicated imaging interfering with patient care in the acute setting; 3) no radiation dose; and 4) higher spatial resolution. Although quantification of myocardium at risk by T2-STIR at day 1 and week 1 did not show any significant difference, image quality was in favor to T2-STIR imaging at week 1.
Myocardial salvage.
The clinical usefulness of the present study is mainly that the size of myocardium at risk and MI, and therefore myocardial salvage, can be assessed at the same image session within 1 week after acute coronary occlusion, without interfering with patient care in the acute setting. In acute infarcts, the necrotic region is surrounded by a region of reversible injury, characterized by edema, and consists of myocardial tissue that has not undergone irreversible injury. This region is referred to as the salvageable myocardium at risk, and the region of irreversible injury, if left untreated, will expand in the first hours after acute MI in accordance with the wavefront phenomena described by Reimer et al. (27). To assess reperfusion therapy, it is necessary to determine how much myocardium is salvaged by measuring final infarct size in relation to the initial myocardium at risk. DE-CMR has the ability to quantify final infarct size (6,7), and, as shown in this study, T2-STIR accurately quantifies myocardium at risk. Therefore, CMR has the ability to calculate salvaged myocardium within the same imaging acquisition session (21). This can be used to evaluate new drugs and therapeutic procedures aimed at reducing infarct size without interfering with patient care in the acute setting. Indeed, Ibanez et al. (28) recently showed that metoprolol administered before revascularization increased myocardial salvage in a pig model where myocardium at risk and final infarct size were assessed with T2-STIR and DE-CMR. The results of the current study in patients with primary PCI showed that 75% (range 41% to 100%) of the initial myocardium, on average, was salvaged. Hence, this line of research can be applied in patient populations providing a salvageable index for each patient undergoing primary PCI after acute MI and would potentially increase the knowledge on infarct-related tissue injury.
Study limitations.
The present study was performed on a limited number of patients, all presenting with first-time STEMI and undergoing successful reperfusion. Thus, how this would translate to other populations, for example unsuccessful revascularization, patients treated with thrombolytic therapy, or patients with previous MIs, is not known (15). Only 2 women were included in this study, and more data on female subjects are, therefore, needed. However, T2-STIR images from the 2 female subjects showed similar enhancement as the 14 male patients, and there is no a priori reason to expect a gender difference in edema formation after acute MI. Quantification of myocardium at risk by SPECT has previously been performed using sestamibi tracers. In the present study, tetrofosmin was used; however, sestamibi and tetrofosmin are used interchangeably in patient studies (29). Image quality can be a limitation in assessing myocardium at risk by T2-STIR, and the image quality of the present study did not allow for automated segmentation. New sequences, however, are continuously developed to overcome this problem (30,31). Images were acquired using a body array coil with the Siemens scanner and a cardiac surface coil with the Philips scanner. It has been suggested that a body coil has a more homogenous reception whereas the surface coil has an inherent signal intensity gradient (21). However, image reconstruction with parallel imaging techniques uses differences in coil sensitivity and, therefore, compensates inhomogenous reception. Thus, the images obtained with the surface coil in the present study was acquired using a parallel imaging factor (SENSE factor) of 1 to minimize this effect.
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Conclusions
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This is the first study to validate T2-STIR for quantification of myocardium at risk against an independent method (SPECT) in patients with acute MI after reperfusion therapy. The results demonstrate that T2-STIR performed up to 1 week after reperfusion can accurately determine myocardium at risk as it was before opening of the occluded artery. The result of reperfusion therapy can, therefore, be assessed clinically by calculating myocardial salvage as the difference between myocardium at risk and final infarct size using CMR.
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Acknowledgments
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The authors would like to acknowledge Ann-Helen Arvidsson and Christel Carlander, both with the Lund Cardiac MR Group, for their skillful assistance with image acquisition.
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Footnotes
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This study has been funded by the Swedish Research Council, the Swedish Heart and Lung Foundation, the Medical Faculty at Lund University, Sweden, and the region of Scania, Sweden.
* Reprint requests and correspondence: Dr. Håkan Arheden, Department of Clinical Physiology, Lund University Hospital, Lund SE-22185, Sweden (Email: hakan.arheden{at}med.lu.se).
Manuscript received July 23, 2008;
revised manuscript received October 17, 2008,
accepted November 21, 2008.
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C. Delhaye, M. Mahmoudi, and R. Waksman
Hypothermia Therapy: Neurological and Cardiac Benefits
J. Am. Coll. Cardiol.,
January 17, 2012;
59(3):
197 - 210.
[Abstract]
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G. Fuernau, I. Eitel, V. Franke, L. Hildebrandt, J. Meissner, S. de Waha, P. Lurz, M. Gutberlet, S. Desch, G. Schuler, et al.
Myocardium at Risk in ST-Segment Elevation Myocardial Infarction: Comparison of T2-Weighted Edema Imaging With the MR-Assessed Endocardial Surface Area and Validation Against Angiographic Scoring
J. Am. Coll. Cardiol. Img.,
September 1, 2011;
4(9):
967 - 976.
[Abstract]
[Full Text]
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A. E. Arai
Gadolinium Can Depict Area at Risk and Myocardial Infarction: A Double-Edged Sword?
J. Am. Coll. Cardiol. Img.,
June 1, 2011;
4(6):
619 - 621.
[Full Text]
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G. A. Figtree, J. Lonborg, S. M. Grieve, M. R. Ward, and R. Bhindi
Cardiac Magnetic Resonance Imaging for the Interventional Cardiologist
J. Am. Coll. Cardiol. Intv.,
February 1, 2011;
4(2):
137 - 148.
[Abstract]
[Full Text]
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I. Eitel, S. Desch, G. Fuernau, L. Hildebrand, M. Gutberlet, G. Schuler, and H. Thiele
Prognostic Significance and Determinants of Myocardial Salvage Assessed by Cardiovascular Magnetic Resonance in Acute Reperfused Myocardial Infarction
J. Am. Coll. Cardiol.,
June 1, 2010;
55(22):
2470 - 2479.
[Abstract]
[Full Text]
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J. T. Ortiz-Perez, D. C. Lee, S. N. Meyers, C. J. Davidson, R. O. Bonow, and E. Wu
Determinants of Myocardial Salvage During Acute Myocardial Infarction: Evaluation With a Combined Angiographic and CMR Myocardial Salvage Index
J. Am. Coll. Cardiol. Img.,
May 1, 2010;
3(5):
491 - 500.
[Abstract]
[Full Text]
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R. J. Gibbons, P. A. Araoz, and E. E. Williamson
The Year in Cardiac Imaging
J. Am. Coll. Cardiol.,
February 2, 2010;
55(5):
483 - 495.
[Full Text]
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M. G. Friedrich
A closer look on the battlefield the salvaged area at risk as an outcome marker for myocardial reperfusion.
J. Am. Coll. Cardiol. Img.,
May 1, 2009;
2(5):
577 - 579.
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Abstract
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