STATE-OF-THE-ART PAPER
The quantification of infarct size
Raymond J. Gibbons, MD*,*,
Uma S. Valeti, MD*,
Philip A. Araoz, MD and
Allan S. Jaffe, MD*
* Division of Cardiovascular Diseases and Internal Medicine, Mayo Clinic and Foundation, Rochester, Minnesota
Department of Radiology, Mayo Clinic and Foundation, Rochester, Minnesota
Manuscript received January 22, 2004;
revised manuscript received June 7, 2004,
accepted June 14, 2004.
* Reprint requests and correspondence: Dr. Raymond J. Gibbons, Mayo Clinic, Gonda 5, 200 First Street, SW, Rochester, Minnesota 55905 (Email: gibbons.raymond{at}mayo.edu).
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Abstract
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We sought to summarize the published evidence regarding the measurement of infarct size by serum markers, technetium-99m sestamibi single-photon emission computed tomography (SPECT) myocardial perfusion imaging, and magnetic resonance imaging. The measurement of infarct size is an attractive surrogate end point for the early assessment of new therapies for acute myocardial infarction. For each of these three approaches, we reviewed reports published in English providing the clinical validation for the measurement of infarct size and the relevant clinical trial experience. The measurement of infarct size by serum markers has multiple theoretical and practical limitations. The measurement of troponin is promising, but the available data validating this marker are limited. Sestamibi SPECT imaging has five separate lines of published evidence supporting its validity and has received extensive study in multicenter trials. Magnetic resonance imaging has great promise but has less clinical validation and no multicenter trial experience. Therefore, SPECT sestamibi imaging is currently the best available technique for the quantitation of infarct size to assess the incremental treatment benefit of new therapies in multicenter trials of acute myocardial infarction.
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Abbreviations and Acronyms
| | CK = creatine kinase | | CK-MB = creatine kinase-MB fraction | | HBDH = hydroxybutyrate dehydrogenase | | MI = myocardial infarction | | MRI = magnetic resonance imaging | | SPECT = single-photon emission computed tomography | | Tc = technetium |
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Multiple end points have been used to assess the efficacy of reperfusion therapy in dozens of randomized trials (1). The measurement of infarct size has several advantages: 1) it permits early pilot studies to test the potential efficacy of new approaches, 2) it can serve as an end point for dose-ranging studies to select the most appropriate dose of a new drug for larger studies, and 3) it can potentially demonstrate the efficacy of a new therapy that is equivalent to an existing therapy with respect to early mortality but may still have a favorable impact on long-term mortality.
This review will focus on three approaches that are potentially available for the measurement of infarct size: serum (biochemical) markers, technetium (Tc)-99m sestamibi single-photon emission computed tomography (SPECT) myocardial perfusion imaging, and magnetic resonance imaging (MRI). Although measurements of global and regional left ventricular function often are used clinically in the estimation of infarct size, these measurements are less direct and are influenced by the presence of arrhythmias, cardiomyopathies, valvular heart disease, and ventricular loading (2). Electrocardiographic assessment of infarct size also is useful clinically; however, even when carefully analyzed and expressed on an ordinal scale, it has limited ability to resolve small differences in infarct size.
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Serum (biochemical) markers
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Pathophysiologic principles.
Once experimental data confirmed that the evolution of acute myocardial infarction (MI) was dynamic and could potentially be modified, researchers began to quantitate infarct size using biochemical markers (3). The initial marker of interest was total creatine kinase (CK) (3), which evolved to CK-MB fraction (CK-MB) when practical assays for the isoenzyme became available (4). The critical parameters needed to estimate infarct size in this manner were defined in a series of rigorous experimental studies (5). These included: 1) The quantity of CK that was released into the plasma compared with that depleted from the myocardium. This is known as the release ratio. 2) The optimal sampling intervals to provide an accurate area under the time activity (or time concentration) curve so that the total amount released could be determined. 3) Sufficient information on the clearance and compartmentalization of the marker so that one could calculate the clearance rate. 4) The relationship between infarct size measured in this manner and pathologically and electrocardiographically determined infarct size, measures of left ventricular function, and arrhythmias.
In canine models without reperfusion, approximately 85% of the CK found in the myocardium (dogs have very little CK-MB) is depleted in response to ischemic-induced myocardial injury (4,5). Fifteen percent remains in the Z band. The amount of enzyme depleted from the heart is proportional to the size of the infarction. However, of the 85% depleted, only 15% reaches the circulation in the absence of coronary recanalization. The remainder is hydrolyzed either locally or in lymph (5). As long as a predictable relationship exists between the amount of CK depleted and the amount that reaches the circulation, serial samples permit a mathematic model of the amount depleted and, therefore, an estimate of infarct size. Such a model requires estimation of both the volume of distribution and the clearance of CK so that the model can be corrected to reflect the amount of CK released. The use of serial values on the downslope of the time activity curves to calculate a specific clearance rate (kd) is equivalent in most cases to using a mean clearance rate. With sufficient samples, there is an excellent correlation between enzymatic and pathologic infarct size in animals (4,5).
Effects of reperfusion.
In the presence of coronary reperfusion, enzyme kinetics are altered in several ways. The amount of marker released into the plasma relative to the amount depleted from the myocardium increases substantially. In animals with reperfusion within 2 h after coronary occlusion, the release ratio (the amount of enzyme that is in the plasma compared with that depleted from myocardium) doubles (6). The release ratio is likely a continuous function depending upon the time from the onset of the coronary occlusion to recanalization and the abruptness of the reperfusion because the washout of marker is flow-dependent. The ability to model this system becomes problematic once one recognizes the range of release ratios related to these parameters. The kinetics of release are also altered with a much more rapid peak and consequently a much faster decline. Thus, comparisons between reperfused and non-reperfused patients are problematic because a different amount of enzyme per gram of myocardium destroyed is released into the blood. Even within the reperfused group, given the known marked differences in the rapidity and magnitude of reflow and therefore the release ratio as well as the time of peak CK, CK-MB, or troponin, meaningful comparisons between areas under the curve and infarct size are difficult. The ability to determine peak values also is more difficult because the peak is much earlier and, therefore, much more easily missed. However, some groups have attempted, in a series of studies in animals, to account for all of the markers that can be lost from myocardium with and without reperfusion (7). This has been attempted for both hydroxybutyrate dehydrogenase (HBDH; LDH1 and LDH2) and total CK. With corrections, it was suggested that one could account for nearly all the marker depleted from the myocardium. However, these results depend heavily on an assumed disappearance rate derived from multicompartmental modeling and the corrections, which are not accepted universally. In addition, there is a very large amount of HBDHin red cells (8); hemorrhagic infarcts may elaborate more HBDH than bland infarcts. This is an even greater problem if there is any hemolysis (9) or if there is bleeding during/after intervention with breakdown of red cells.
Clinical studies: no reperfusion.
In patients, in the absence of reperfusion, enzymatic estimates of infarct size correlate with the ejection fraction, hemodynamics, arrhythmias, and prognosis (10,11). Hackel et al. (12) reported an excellent correlation (Spearman r = 0.87) between the enzymatic estimates based on CK-MB and pathologic measurements. There was slight underestimation of infarct size using enzymatic measurements.
Peak CK-MB can be used as a substitute for the area under the curve if one has a sufficient number of samples to detect true peak values. Smith et al. (13) found that the degree of underestimation of infarct size ranged from 14% to 47% when the data from the upslope of the CK-MB time activity curves were missing. The correlations were good for both Q-wave and non–Q-wave MI when peak values were ascertained (13). However, without sufficient samples, the likelihood of missing the peak enzyme concentration is high. This is particularly true if the study group includes both ST-segment and non–ST-segment elevation MIs because the enzyme peaks occur earlier with non–Q-wave MI.Thus, it would be easy to miss the peak without multiple samples (14). Peak values may permit gross classification of patient risk but that is substantially different from quantification of the amount of myocardial damage to permit individual or group comparisons. Total CK and CK-MB infarct sizing were used to evaluate many (pre-reperfusion) interventions that were thought to reduce infarct size. The effects often were modest (15).
Reperfusion.
In the reperfusion era, the most extensive work has been done with lactic dehydrogenaseisoenzymes 1 and 2 (known also as HBDH). The potential problems with that approach were discussed earlier. These problems are confounded if only peak values are used, although some have claimed that one properly timed sample at 72 h is adequate (16). However, the release of HBDH can continue beyond 72 h, although the error induced by the absence of later samples is thought to be modest (17). It is often difficult to time the onset of the infarction and thus obtain the requisite sample at the proper time. In tightly controlled studies, infarct size calculated from HBDH release does correlate with ejection fraction in patients with first infarction (Fig. 1) (18).
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Figure 1 Relationship between commutative release of hydroxybutyrate dehydrogenase (HBDH) during the course of 120 h and ejection fraction in 54 patients. Although there was a highly significant correlation, there is considerable scatter in data with a wide range of enzyme release for ejection fraction between 50% and 55% and a wide range in ejection fraction for cumulative enzyme release of between 1,500 and 2,000. Reprinted, with permission, from Dissman et al. (17).
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These issues, especially those related to bleeding/hemolysis and release of red cell HBDH, may help explain some of the reported results where infarct size was estimated by HBDH. When streptokinase was compared with acute percutaneous transluminal coronary angioplasty (19), there were significant differences in ejection fraction between the treatment groups in both anterior MI and non-anterior MI. However, the differences in HBDH release between treatment groups were modest in anterior MI and insignificant in inferior MI. There was no association between HBDH and ejection fraction in the group undergoing percutaneous transluminal coronary angioplasty. In a randomized trial evaluating eniporide, the pilot phase showed a significant reduction in HBDH release with two different doses of the drug, which was not confirmed in the larger definitive trial (20).
Will troponin measurements permit more accurate determination of infarct sizes? The kinetics and release ratio of the troponins are not well defined. The depletion of troponin T but not troponin I has been reported to correlate with pathologic infarct size in dogs (21). However, the release ratio is unclear and could be different for the cytosolic and structural pools. Given its improved specificity, troponin should be a more accurate way to assess infarct size. Ideally, one would like to measure all the troponin released and then correct for clearance to determine release and infarct size. Unfortunately, troponin values remain elevated for up to two weeks. Serial sampling for this time is difficult if not impossible. Thus, experiments have been performed exploring values at fixed time points, recognizing the potential timing difficulties. Seventy-two-hour troponin T measurements correlate best with scintigraphically determined infarct size in animals and patients (Fig. 2) (22,23). However, none of the patient studies has pathologic confirmation. In each of the studies, the correlation with and without reperfusion has been superiorfor troponin rather than for CK-MB. Most of these studies have been conducted with troponin T. Thus, the applicability of these findings to troponin I is uncertain. Troponin I must be validated separately, both experimentally and clinically, given the heterogenicity among troponin assays and potentially different clearance. Initial data are promising (24).
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Figure 2 Association between single troponin T (TnT) measurement at 72 h and peak creatine kinase (CK) with estimated thallium infarct size in non-reperfused (A) and reperfused (B) patients. Reprinted, with permission, from Licka et al. (23).
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Tc-99m sestamibi SPECT imaging
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Multiple animal studies demonstrated the potential value of Tc-99m sestamibi in the assessment of reperfusion therapy. Detailed reviews are available (25). The efficacy of reperfusion therapy can be assessed either by using both the acute and final perfusion defect to measure myocardial salvage or more simply by using the final defect to measure infarct size. The latter approach, which has been increasingly favored for logistical reasons, is summarized here.
Clinical validation of the measurement.
Five separate lines of clinical evidence have validated the use of SPECT sestamibi imaging for the measurement of infarct size:
- 1 There is a close association between sestamibi infarct size and measurements that have been traditionally used to assess infarct size in clinical medicine, including ejection fraction, end-systolic volume, regional wall motion, enzyme release, and resting thallium-201 myocardial perfusion imaging (Table 1) (26–31).
- 2 There is a close association between fibrosis in human hearts and infarct size assessed by sestamibi (32–34). The defect measured by ex vivo sestamibi imaging of myocardial slices from explanted human hearts at the time of cardiac transplantation is closely associated with the quantitation of fibrosis by pathology (Fig. 3). Two subsequent studies (33,34) showed a similar close association between in vivo sestamibi defect size and the amount of fibrosis on surgical myocardial biopsies.
- 3 The magnitude of sestamibi uptake predicts the response of myocardium with abnormal function to subsequent revascularization in chronic coronary artery disease, and the recovery of myocardium after reperfusion therapy for acute MI. Sestamibi uptake correlates closely with the uptake of thallium on a resting redistribution scan (35) and predicts improvement in function after revascularization (33,35). The mismatch between infarct size and ventricular function after reperfusion therapy in acute MI identified myocardial stunning in both retrospective (28) and prospective (36) studies.
- 4 Sestamibi infarct size measured at discharge predicts short-term patient mortality in both single-center (37) and multicenter (38) studies. In the largest series of 1,181 patients (39), there was a significant linear association between infarct size and six-month mortality (Fig. 4).
- 5 Most importantly, two separate randomized trials (40,41) have now shown a corresponding improvement in clinical outcome in association with a therapy that reduces infarct size. This is an important requirement from a regulatory standpoint to make certain that a "surrogate" end point does not show benefit when there is in fact clinical harm. A randomized trial (40) showed that the use of stenting and a glycoprotein IIb/IIIa inhibitor was associated with smaller infarct size and a lower incidence of death, reinfarction, or stroke compared with therapy with tissue plasminogen activator (Figs. 5 and 6). In a second randomized trial (41), stenting and thrombolysis were both combined with abciximab. Stenting was associated with a smaller infarct size and better outcomes.
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Figure 3 Relationship between the perfusion defect measured by single-photon emission computed tomography and the amount of scarring measured by pathology in human hearts explanted at the time of cardiac transplantation. Reprinted, with permission, from Medrano et al. (32).
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Figure 4 Six-month mortality in 1,122 patients in the Collaborative Organization for RheothRX Evaluation (CORE)trial, according to the single-photon emission computed tomography infarct size measured at discharge. The groupings of infarct size were chosen on the basis of previous studies. LV = left ventricle. Modified from Burns et al. (39).
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Figure 5 Infarct size and myocardial salvage measured by single-photon emission computed tomography sestamibi imaging in patients treated with tissue plasminogen activator (tPA) and patients treated with stenting and a glycoprotein IIb/IIIa inhibitor. The stent group had a smaller infarct size and greater myocardial salvage. LV = left ventricle. Based on data from Schomig et al. (40).
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Figure 6 Clinical outcome in patients from the same randomized trial shown in Figure 5. The cumulative incidence of death, infarction, and stroke was significantly lower in the stent group compared with the tissue plasminogen activator group. Reprinted, with permission, from Schomig et al. (40).
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Quantitative approach.
Sestamibi infarct size has been quantitated using a standardized approach (26) based on cardiac phantom studies (42).
Comparability of data from multiple centers.
The feasibility of performing multicenter trials using SPECT sestamibi imaging was first demonstrated using a phantom experiment (43). The measured "infarct" size closely correlates with the actual defect size in the phantom with an average absolute error of <3% of the left ventricle (43). The quantitation is insensitive to differences in camera, collimator, or imaging routine. More than 600 centers in 19 countries on 6 continents have successfully completed this phantom validation to ensure useful data in multicenter trials. In one large trial(44), 98% of 1,184 studies provided analyzable end point data.
Randomized clinical trial experience.
There is considerable randomized clinical trial experience (40–41,44–60)using sestamibi infarct size as an end point (Table 2). Five single-center trials and 16 multicenter-randomized trials have been completed using sestamibi infarct size as an end point in 5,401 patients. Multiple additional trials are ongoing.
Most trials have performed sestamibi imaging at 120 to 216 h after reperfusion, which was the time interval used in many of the validation studies. Imaging at 30 days has been performed in two recent trials (51,52) in an effortto detect later cellular recovery.
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MRI
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The basics of the technique.
Infarct imaging by MRI uses delayed contrast-enhanced imaging. A paramagnetic contrast agent such as gadolinium is first injected intravenously (61). Infarcted myocardium appears hyperenhanced relative to normal myocardium when imaged 5 to 30 min later (62–66). The hyperenhancement of infarcted myocardium appears to be related to altered myocardial kinetics of gadolinium, resulting in its accumulation and prolonged presence in the infarct (67–69).
Early studies of this delayed hyperenhancement had limitations. In some animal studies using older sequences, there was an overestimation of infarct size (67,68,70–72), suggesting that the enhanced area represented both reversible and irreversible myocardial injury. In addition to technical limitations, these earlier studies frequently did not account for the transmural extent of hyperenhancement before labeling a segment as infarcted or stunned. This may have led to the conflicting reports that hyperenhanced myocardium was viable (73).
Technical advances (reviewed elsewhere) (74) have contributed to the more accurate estimation of infarct size. The remainder of this section is based primarily on modern imaging sequences.
Validation of infarct size measurement by MRI in animal studies.
Several animal studies have validated the measurement of infarct size by contrast-enhanced MRI. In a canine model of acute and chronic infarction (63), infarct size by ex vivo contrast-enhanced MRI correlated closely (r = 0.99) with triphenyltetrazolium chloride staining. Other studies confirmed these findings in both canine (64) and rabbit (75) models. In a canine model (76), the transmural extent of hyperenhancement 3 days after an acute infarct predicted functional improvement by 28 days.
Clinical validation of MRI measurements.
Several different lines of evidence provide clinical validation for the use of MRI using segmented inversion recovery for the measurement of infarct size.
- 1 There is a close association between MRI infarct size and measurements that have been used clinically to assess infarct size, including ejection fraction, regional wall motion enzyme release, and positron emission tomography imaging (Table 3) (77–83).
- 2 The MRI infarct sizepredicts recovery of function after revascularization (81,84–86) and after MI (Table 4) (78,87–89). The transmural extent of the infarct appears to delineate viable and nonviable myocardium and the recovery of function after revascularization (Fig. 7). The extent of transmural enhancement also predicts recovery of function after MI (78,87).
- 3 In one small study of 44 patients (90), MRI infarct size was significantly associated with cardiovascular events (Fig. 8).
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Table 4. Magnetic Resonance Imaging for Prediction of Functional Recovery After Revascularization of Chronic CAD or Reperfusion of Acute MI
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Figure 7 Relationship between the transmural extent of hyperenhancement by magnetic resonance imaging before revascularization and the likelihood of improved function after revascularization in 804 dysfunctional segments in 41 patients. There was a clear inverse relationship between the transmural extent of hyperenhancement and the likelihood of improved function. Reprinted, with permission, from Kim et al. (85).
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Figure 8 Survival free of reinfarction, congestive heart failure, stroke, or unstable angina requiring hospitalization for 43 patients grouped by infarct size obtained by magnetic resonance imaging. There was a significant association of infarct size with subsequent outcome.However, if unstable angina was removed from the definition of events, the relationship was no longer significant. Reprinted, with permission, from Wu et al. (90).
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Quantitative approach.
Infarct size volume by MRI generally is measured by computer-assisted planimetry of the hyperenhanced myocardium. The area of hyperenhanced myocardium is traced in each slice and multiplied by the slice thickness and the myocardial density of 1.05 g/ml to obtain the infarct mass. A second method to quantify infarct size determines the enhancement score (0 to 4) for each segment, sums these scores over all segments, and then divides this sum by the maximal possible score (total number of segments x 4).
Comparability of images from multiple centers.
There are no published studies to date evaluating the capability and comparability of studies from multiple centers.
Use of MRI in clinical trials.
There has been very limited experience to date with the use of MRI for infarct sizing in clinical trials. An early observational study (91) reported that MRI infarct size eight days after infarction was significantly smaller in patients who received reperfusion therapy. In a substudy of 40 patients in a randomized trial (92), MRI showed a smaller infarct size with streptokinase compared with placebo. Both of these studies used older imaging sequences. There are no published randomized trials using the current inversion recovery fast gradient technique. There are no published data regarding the correct timing of MRI images after reperfusion.
Comparison of SPECT and MRI.
The limited available data suggest that MRI can detect smaller infarctions than SPECT and is more reproducible. Wagner et al. (93) found that SPECT thallium and MRI were highly specific for infarction and had similar sensitivity for transmural infarction. However, 47% of the segments identified as having subendocardial infarction by MRI were not detected by SPECT. In a second study (94) comparing resting SPECT thallium to MRI, MRI was superior in predicting myocardial viability.
A single study (66) compared the reproducibility of infarct size determination by SPECT sestamibi and MRI and found that MRI infarct size was more reproducible. The authors concluded that the numbers of patients needed for clinical trials using MRI would be much smaller. However, this would be true only if paired imaging was performed to detect a change in infarct size over the course of time. As reported by the authors, the standard deviation of infarct size in their population of 15 patients was 6% for MRI and 7% for SPECT. These standard deviations would lead to very similar sample size estimates for single (unpaired) images comparing different treatments. Table 5 summarizes the comparison of SPECT and MRI.
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The future challenge
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During the past decade, multiple randomized trials have studied an array of adjuvant therapies used with reperfusion in acute MI. The results have been generally negative. However, there have been exceptions; in three separate randomized trials using poloxamer 188 (54) and adenosine (47,56), SPECT sestamibi has shown treatment efficacy in relatively modest numbers of patients.
The challenge of demonstrating incremental treatment benefit with reperfusion therapy in acute MI is usually underestimated. The variability in infarct size in patients is substantial, reflecting the known variability in the important parameters of myocardium at risk, residual flow to the infarct zone (via collaterals or intermittent antegrade flow), and time to reperfusion (95). Current reperfusion therapy is highly effective. Nearly 50% of patients will have infarcts of <10% of the left ventricle with current therapy (37). The incremental benefit of ancillary therapy will be small in these patients. Sizable treatment benefit will be restricted to the 50% of patients with infarcts of >10% of the left ventricle. The overall incremental benefit of ancillary therapy, therefore, will be modest and difficult to measure against the background of the tremendous variability in infarct size. The measurement of troponin is promising, but the available data validating this marker are limited. Magnetic resonance imaging has definite technical advantages and great promise, but there are as yet no multicenter trial data to confirm this. On the basis of existing evidence, SPECT sestamibi imaging currently is the best technique available to meet this challenge.
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Acknowledgments
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The authors would like to acknowledge the careful review of the manuscript by Dr. Ernst van der Waal.
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Footnotes
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Dr. Gibbons has received research grants from Medtronic, King Pharm, Wyeth-Ayerst, Radiant Medical, Alsius Corp., Ther Ox, Innercool Therapies, Boston Scientific, Spectranectics, KAI Pharmaceuticals, and Boehringer Ingelheim and is a consultant for CV Therapeutics, DOV Pharmaceuticals, King Pharm, Medicure, Hawaii Biotech, Glaxo Smith Kline, Molecular Insight Pharm, Ther Ox, and TargeGen. Dr. Jaffe’s potential conflicts include Roche, Dade-Behring, and Beckman Coulter (consulting and research funds) and Pfizer, Abbott, and Sensera (consulting).
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Top
Abstract
Serum (biochemical) markers