Evaluation of Acute Coronary Syndromes by Cardiac Magnetic Resonance Imaging

Abstract

The use of cardiovascular magnetic resonance (CMR) imaging for the evaluation of patients with acute chest pain and acute coronary syndromes has great potential. The strength of CMR relies on its ability to provide information on anatomy, physiology, and function in a single scanning session in a noninvasive manner without the need for iodinated contrast, radiation, or the need to undergo invasive procedures. Specifically, with regard to imaging patients with acute chest pain and/or myocardial infarction (MI), CMR has the ability to qualitatively and quantitatively evaluate global and regional right and left ventricular systolic functions, myocardial edema, myocardial perfusion, and myocardial infarct size and transmurality/viability. This review will focus on CMR imaging for the following applications: (1) imaging for the evaluation of ventricular function and infarct size in patients with acute chest pain and/or acute MI, (2) for triage and prognosis of patients presenting to the emergency department with acute chest pain, (3) for evaluating patients after sustaining an acute MI, and (4) for stem cell research.

The use of cardiovascular magnetic resonance (CMR) imaging for the evaluation of patients with acute chest pain and acute coronary syndromes (ACSs) has great potential. The strength of CMR relies on its ability to provide information on anatomy, physiology, and function in a single scanning session in a noninvasive manner without the need for iodinated contrast, radiation, or the need to undergo invasive procedures. Specifically, with regard to imaging patients with acute chest pain and/or myocardial infarction (MI), CMR has the ability to qualitatively and quantitatively evaluate global and regional right and left ventricular (LV) systolic function, myocardial edema, myocardial perfusion, and myocardial infarct size and transmurality/viability. This review will focus on CMR imaging for the following applications: (1) imaging for evaluation of ventricular function and infarct size in patients with acute chest pain and/or acute MI, (2) for triage and prognosis of patients presenting to the emergency department (ED) with acute chest pain, (3) for evaluating patients after sustaining an acute MI, and (4) for stem cell research.

CMR FOR THE EVALUATION OF VENTRICULAR FUNCTION AND INFARCT SIZE

Cardiovascular magnetic resonance imaging is a powerful technique in studying patients who present with acute chest pain and those who have actually sustained an acute MI. There is a wide variety of pulse sequences available, and many protocols exist to provide useful diagnostic and prognostic information. The common denominator in all CMR protocols used in these patient populations, however, involves evaluating global and regional LV function with the steady-state free precession cine technique and myocardial infarct size and transmurality with the delayed enhancement magnetic resonance imaging (DE-MRI) technique. Additional pulse sequences that may be added include those for evaluating myocardial perfusion at rest and/or stress and myocardial edema ("area at risk"). These additional techniques will be elaborated later in the paper.

Assessment of Global and Regional LV Volumes and Systolic Function

Cardiac magnetic resonance imaging is an accurate and reproducible technique for the evaluation of ventricular volumes and function. It provides cardiac views at any desired plane during multiple phases of the cardiac cycle that can be prospectively prescribed with high temporal and spatial resolution. Moreover, the excellent tissue contrast characteristics and favorable signal-to-noise ratio allow for superb delineation of the endocardial and epicardial borders, allowing for easy, semiautomatic contour detection. Because of these characteristics, it is considered the reference standard for the evaluation of global and regional ventricular function and ventricular volumes.

Cardiac magnetic resonance imaging techniques used for quantifying LV volumes involve segmentation of the ventricle in to several short-axis slices. Short-axis slices provide the most reliable imaging plane for the determination of ventricular volumes and myocardial mass.¹ After segmentation, contours are drawn along the endocardial border of the ventricular wall, and the Simpson rule is used to calculate the end-diastolic volume, end-systolic volume, stroke volume, and ejection fraction (Fig. 1).

FIGURE 1: Assessment of LV function using the steady-state free precession cine technique is important when evaluating patients with acute chest pain and/or MI. This patient sustained an acute MI in the left anterior descending coronary artery territory and was treated with primary PCI. End-diastolic (A) and end-systolic (B) phases in the short-axis view demonstrate akinesis of the anterior and anterolateral walls (arrow) of the left ventricle. The anterior wall motion abnormality (arrow) can also be appreciated in the vertical long-axis view by comparing regional wall motion thickening in end-diastole (C) and end-systole (D).

In addition to being highly accurate as a tool to measure global ventricular function, CMR is also useful in the evaluation of regional ventricular function. Assessment of regional function can be performed by evaluating wall thickening and wall motion. Regional LV function is typically evaluated on a qualitative basis by visually assessing segmental LV thickening and motion of the 17 LV segments. The 17-segment model used in CMR is based on the criteria set forth by a consensus statement of the American Heart Association/American College of Cardiology.² Typically, segments will be scored as normal, hypokinetic, akinetic, or dyskinetic. Some clinicians use a semiquantitative scale, whereby the regional wall motion of individual segments is graded as follows: normal, 0; hypokinesia, 1; akinesia, 2; and dyskinesia, 3. Hypokinesia is defined as impaired thickening and motion, akinesia is defined by absent thickening and motion, and dyskinesia is defined as a paradoxical outward motion of the segment during systole. A global wall motion score can be calculated by dividing the total score of each segment by the number of segments that is evaluable.³

Left ventricular global and regional function is integral for determining prognosis, designing therapeutic strategies, and identifying the efficacy of pharmacologic and mechanical efforts in patients after MI. As such, an accurate assessment of LV function not only dictates which medications or mechanical devices to use for patient management but also provides a means for evaluating therapeutic benefits from the maneuver (for improvement in function). Furthermore, LV function also confers a significant independent prognostic value. Recently, Thune et al⁴ evaluated wall motion index (a surrogate for regional wall motion) in patients with MI who were enrolled in the Valsartan in Acute Myocardial Infarction trial in an attempt to determine whether regional function or global function was more important for prognosis. Of 502 patients who were assessed for both wall motion index and LV ejection fraction (LVEF), they found that the wall motion index and the total number of affected wall segments were stronger predictors of cardiovascular mortality than global LVEF.

Assessment of Microvascular Obstruction and Infarct Size/Transmurality

Cardiac magnetic resonance imaging allows for precise evaluation of myocardial infarct size and transmurality by means of the DE-MRI technique (Fig. 2). Ten minutes after the administration of intravenous gadolinium (0.1-0.2 mmol/kg), an inversion recovery pulse sequence is performed with an inversion time optimized to null the normal myocardium (Fig. 3). This takes advantage of gadolinium's unique properties to concentrate in areas of nonviable myocardial tissue. Gadolinium is a metabolically inert paramagnetic molecule that is distributed in the extracellular compartment. Most notably, it accentuates the difference in relaxation characteristics between normal tissue and infarcted myocardium. There is increased gadolinium accumulation in acute infarction likely due to an increased volume of distribution created by myocyte membrane rupture.⁵ In the setting of chronic MI, however, the proposed mechanism of increased gadolinium concentration is likely due to the larger extracellular compartment created by a collagenous scar.⁶ With the selection of an appropriate inversion time, normal myocardium will be devoid of signal, whereas the infarct will demonstrate signal hyperintensity.

FIGURE 2: The delayed enhancement technique is useful in quantifying infarct size and transmurality and ultimately myocardial viability. The delayed enhancement image in (A) demonstrates a subendocardial MI of the anterior and anteroseptal walls (arrow) of the left ventricle. The transmurality of this infarct is less than 25% and is associated with myocardial viability. In (B), the delayed enhancement images demonstrate a near transmural infarct (>75% transmurality) which would not be associated with myocardial viability.

FIGURE 3: Perfusion imaging during the first pass of gadolinium is often added to a CMR protocol that includes assessment of LV function and infarct size/transmurality. The patient in (A) sustained an infarct of the right coronary artery with resultant myocardial perfusion defect in the inferior and inferoseptal walls (arrow) of the left ventricle. The patient in (B) sustained an infarct of the left anterior descending coronary artery with a perfusion defect noted in the apical anterior and septal walls (arrow) of the left ventricle.

Identification of microvascular obstruction (MVO) during and after MI also has prognostic implications. Accumulation of atheromatous, cellular debris, inflammatory cells, and platelets in the microvasculature activates complement and free radical formation. This cascade of events results in a "no-reflow" phenomenon.^7,8 This no-reflow zone, which is the result of MVO within the infarcted myocardium, represents an area lacking adequate tissue perfusion.⁹ Even with the restoration of normal epicardial coronary blood flow, which has been shown to improve overall morbidity and mortality, the no-reflow zone often remains obstructed. Contrast-enhanced CMR correlates well with histopathology (criterion standard) when assessing the degree of MVO. Areas of MVO appear dark (hypoenhanced) when imaged with DE-MRI. This is likely due to the inadequate contrast penetration into the core of the MVO. Several groups have identified a direct relationship between MVO and adverse clinical outcomes.^10-15 Wu et al¹⁶ studied 44 patients with DE-MRI who were reperfused after AMI. Microvascular obstruction was predictive of increased complication rates, including recurrent MI, congestive heart failure, cardiovascular death, and stroke, 16 months (SD, 5 months) after the index event. Furthermore, when a subset of these patients was reimaged 6 months later, patients with MVO had higher rates of myocardial scar formation.¹⁶ Additionally, MVO has been shown to initiate adverse LV remodeling. Some hypothesize that as MVO increases, there are concomitant alterations in the regional myocardial function not only in the infarcted tissue but also in adjacent noninfarcted myocardium.⁸ This phenomenon may be due to the increased wall stiffness or wall stress at the border between infarcted and noninfarcted myocardium.⁸

Although other techniques such as positron emission tomography, dobutamine stress echocardiography, and thallium single-photon emission computed tomography (SPECT) can evaluate myocardial viability, CMR has the unique ability to define the extent of transmural necrosis. Comparison of CMR with other well-studied modalities, including SPECT and positron emission tomography, for the detection of infarct size favors the use of CMR. Recent studies in both animal and patient models reveal an advantage of CMR, particularly in detecting smaller infarcts.^17-19 One such study found that SPECT, despite its high specificity, routinely missed subendocardial infarcts that were detected with CMR.^19,20 This finding is related to the higher spatial resolution of CMR compared to other imaging modalities. A study by Lund et al⁷ compared CMR with first pass and delayed enhancement to thallium SPECT in patients who had a recent MI. In 60 consecutive patients, CMR and SPECT images were obtained at 3 to 9 days after reperfused first MI. Mean infarct size was not significantly different between CMR imaging and thallium SPECT. However, SPECT failed to depict infarct in 6 of 30 patients with inferior MI (mean [SD] size of LV area on DE-MRI scans, 6.4% [5.7%]), whereas DE-MRI scans revealed the infarct in all patients. The ability of CMR to precisely evaluate infarct size, transmurality, and MVO coupled with its ability to assess global and regional systolic function allow for its higher accuracy to predict coronary artery disease (CAD), myocardial viability, and future cardiovascular events.

CMR FOR TRIAGE AND PROGNOSIS OF PATIENTS PRESENTING TO THE ED WITH ACUTE CHEST PAIN

In the US, more than 5 million patients per year are evaluated in the ED setting for chest pain or other symptoms suggestive of ACS.⁵ A small number of these patients will present with ST segment elevations on their initial electrocardiogram (ECG) and go on to immediate thrombolysis or percutaneous coronary intervention (PCI). A much larger subset of these patients presenting to the ED with chest pain will ultimately be found to have an alternative diagnosis other than cardiac ischemic chest pain. Some of these patients will be assessed as having a very low probability of ACS and will be discharged expeditiously from the ED. A larger number of these patients, however, will be determined to have a nonnegligible risk for an ischemic etiology of their symptoms. In this group, initial serologic markers of cardiac injury and electrocardiographic changes are nondiagnostic. Indeed, the sensitivity of initial biochemical markers (creatine kinase-MB and troponin T) and electrocardiographic changes in patients with suspected acute ischemia obtained at arrival to the ED is low (approximately 20% and 50%, respectively).^6,17 Emergency department physicians thus routinely face the question of how to manage patients who are at risk for ACS but have no certain diagnostic indications of ACS on presentation to the ED.

In practice, the determination of ischemic chest pain in the ED population is difficult, and errors are common. Because the consequences of premature discharge of patients at high risk for adverse coronary events can be catastrophic, physicians tend to be conservative, with the result that there are many unnecessary admissions of patients without ACS.¹⁸ Only approximately 30% of patients admitted for suspected MI are eventually diagnosed with ischemic heart disease.¹⁹ On the other hand, up to 4% of patients with chest pain discharged from hospital EDs experience an MI within 30 days.^21,22

Various strategies have been proposed to manage this group of patients who are found to be at risk for ACS but without initial laboratory or ECG confirmation. Some have proposed admitting such patients to dedicated short-stay "chest pain units" to obtain serial serum cardiac enzymes and monitor for electrocardiographic changes. The use of nuclear imaging in the ED setting has been advocated as a means to rapidly risk-stratify such patients. In many centers, patients are admitted to the hospital for a "rule out MI" protocol involving 24 hours of serum marker evaluation and repeated electrocardiograph scans. If serial serum markers demonstrate no evidence of cardiac injury, many patients undergo a functional study, usually an exercise or pharmacological stress test with or without myocardial perfusion imaging. Physiological assessment allows for risk stratification and prognostication for an adverse coronary event. Patients determined to be at higher risk are often referred to invasive coronary angiography. Although this strategy is reasonable, it involves admission to either a chest pain unit or a hospital ward, with its associated costs of both time and financial expense. Cardiac magnetic resonance imaging may offer the ability to improve the triage of patients presenting to the ED with acute chest pain and effectively reduce hospital admissions and costs.

Cardiac magnetic resonance imaging has been demonstrated to have diagnostic capabilities suitable for triage of patients with chest pain in the ED. The study reported by Kwong et al²³ not only demonstrated the feasibility of performing CMR in patients with acute chest pain in a timely fashion (mean scan time, 38 minutes) but also reported CMR to be the strongest predictor for the diagnosis of ACS, compared to a standard workup. In this study, the performance of CMR as a diagnostic tool was prospectively tested in 161 consecutive patients with acute chest pain. Cardiac magnetic resonance imaging was performed at rest within 12 hours of presentation and included assessment of LV function, myocardial perfusion, and infarct size and transmurality using DE-MRI. The sensitivity and specificity of CMR for detecting ACS was 84% and 85%, respectively. Cardiac magnetic resonance imaging performed better than conventional clinical assessment and diagnostic testing. Moreover, multiple logistic regression analysis revealed that CMR had independent diagnostic value over clinical parameters, including ECG, initial troponin I, and the Thrombolysis in Myocardial Infarction risk score.

A more recent prospective cohort observational study enrolled patients presenting to the ED with acute chest pain, negative cardiac biomarkers, and no electro cardiographic changes indicative of acute ischemia (R. C. Cury, MD, et al, unpublished data, September 2007). The CMR protocol was composed of T2-weighted imaging, resting first-pass perfusion, cine function, DE-MRI, and assessment of LV wall thickness (LVWT). Of 62 patients, 13 developed ACS during index hospitalization. The new CMR protocol (adding T2-weighted imaging and LVWT) increased the specificity, positive predictive value, and overall accuracy from 84% to 96%, 55% to 85%, and 84% to 93%, respectively, compared with the conventional CMR protocol (cine, perfusion, and DE-MRI) as described in the previous paragraphs. The new CMR protocol improved the detection of patients with ACS in the ED and added significant value over clinical assessment and traditional cardiac risk factors. In the study by Kwong et al,²³ the performance of CMR was limited by its inability to differentiate prior MI from new ACS. The more recent study addressed this inherent difficulty by adding an additional pulse sequence (T2-weighted imaging) that allows for the imaging of myocardial edema, the hallmark of acute injury, and assessment of LVWT to identify patients with chronic infarct. This new approach improved the overall accuracy of CMR with improvement in the specificity and positive predictive value.

In another study evaluating patients presenting to the ED with acute chest pain, Ingkanisorn et al²⁴ evaluated the diagnostic value of adenosine CMR in 135 patients who presented to the ED with chest pain and a negative initial troponin. The main study outcome was detecting any evidence of significant CAD. Patients were contacted at 1 year to determine the incidence of significant CAD, defined as significant coronary artery stenosis (>50%) on invasive coronary angiography, abnormal correlative stress test, new MI, or death. Adenosine CMR perfusion abnormalities had 100% sensitivity and 93% specificity for the detection of significant CAD, and an abnormal CMR added significant prognostic value in predicting a future diagnosis of CAD, MI, or death over clinical risk factors. Furthermore, no patient with a normal adenosine CMR study had a subsequent diagnosis of CAD or an adverse outcome.

The use of CMR in the ED setting may allow for a more rapid and effective triage of patients presenting with acute chest pain, particularly because of its ability to discriminate patients with ACS from patients without ACS. Current CMR technology allows for the performance of a comprehensive cardiac examination in approximately 30 minutes. Cardiac magnetic resonance imaging provides information on right and left ventricular systolic function (ventricular volumes, ejection fraction, and wall motion abnormalities), allows for the identification of myocardial edema to suggest acute injury, evaluation of myocardial perfusion both at rest and with pharmacological stress, and detection of MI size and transmurality with delayed enhancement imaging. Currently, there is no other noninvasive test that provides all of this information at one time. Other noninvasive diagnostic imaging modalities that are useful in the evaluation of patients presenting to the ED with acute chest pain include contrast echocardiography,²⁵ SPECT-myocardial perfusion imaging,²⁶ and most recently, coronary computed tomography angiography.²⁷ Although these imaging modalities are useful in excluding ACS (high negative predictive value), they are not entirely helpful in identifying patients with true ACS and thereby in refining patient management in those who need more aggressive treatment given their lower positive predictive values. Newer CMR approaches that include T2-weighted imaging allow for the detection of myocardial edema, which may differentiate patients with and without ACS. It may also provide further insights as to the specific subset of ACS (unstable angina or non-ST elevation MI [NSTEMI]). Specifically, CMR imaging in patients with unstable angina manifests as an area of signal hyperintensity on the T2-weighted images (myocardial injury/edema) without evidence of delayed hyperenhancement (MI). Detecting patients with unstable angina is of particular interest, because this subset of patients is the most challenging to identify.

Cardiac magnetic resonance imaging in the ED setting can also evaluate other etiologies of chest pain besides CAD such as pericardial disease, pulmonary embolism,^28-30 acute myocarditis,^31,32 aortic dissection,³³ and nonischemic cardiomyopathies.^34,35 However, a dedicated study with appropriate pulse sequences for a target disease/organ would be necessary.

CMR IN PATIENTS AFTER ACUTE MI

Cardiac magnetic resonance imaging also has a major role in evaluating patients after sustaining an acute MI. Specifically, information regarding right and left ventricular size and systolic function, ventricular volumes and ejection fraction, presence and/or absence of MVO, and evaluation of infarct size and transmurality provides powerful prognostic information.

The importance of identifying and sizing myocardial necrosis is crucial when assessing myocardial viability. Studies have shown that the degree of transmurality of scar on DE-MRI has important prognostic implications. Kim et al³⁶ studied DE-MRI in animal models and found that it occurs only in regions of nonviable tissue, with excellent histological correlations. In a landmark study, they went on to study a cohort with chronic coronary disease awaiting coronary artery bypass surgery and performed cardiac MRI both before and several months after revascularization. They found that most patients with less than 50% infarct transmurality had viable myocardium and experienced improvement in regional LV function after revascularization. Patients with greater than 50% transmurality are far less likely to experience improvement in regional LV function after revascularization and are deemed to have nonviable myocardium. Not surprisingly, patients without viable myocardium do not benefit from revascularization. In fact, if taken for revascularization, they have increased perioperative mortalities and lower event-free survival times when compared to medical management.³⁷ After recognition that DE-MRI was an accurate method to assess myocardial viability in patients with chronic MI, investigators tested whether CMR could predict LV recovery after acute MI. Gerber et al⁸ studied 20 patients with CMR at 4 days and again at 7 months after acute MI. Compared with the lack of early hypoenhancement, lack of delayed hyperenhancement had better diagnostic accuracy in predicting functional improvement in dysfunctional segments. The early hypoenhanced regions, which represent only the fraction of infarcted tissue with concomitant MVO, greatly underestimate the amount of irreversibly injured myocardium present after acute MI. They also found that the threshold for myocardial viability after acute MI corresponded to a delayed hyperenhancement transmurality of less than 75%, as opposed to less than 50% in the chronic MI model. That is, one can predict segmental LV recovery if the infarct as determined by DE-MRI is less than 75% of LVWT. The difference in these thresholds between acute and chronic MI is likely related to the associated myocardial edema in acute MI, which increases the volume of distribution of gadolinium, causing the infarct to appear larger.

Another study reported the diagnostic performance of a comprehensive CMR protocol including LV function, myocardial perfusion during rest and adenosine stress, viability (DE-MRI), and coronary magnetic resonance angiography to detect significant stenosis in a higher-risk population of patients with a clinical diagnosis of NSTEMI.³⁸ The comprehensive CMR analysis revealed a sensitivity of 96% and a specificity of 83% to detect a significant stenosis, compared to invasive coronary angiography. Moreover, CMR was considerably more sensitive and accurate than the Thrombolysis in Myocardial Infarction risk score. Cardiac magnetic resonance imaging accurately predicted the presence of significant CAD in patients with NSTEMI.

Baks et al⁹ evaluated early and late infarct size and LV wall function in 22 patients with cine, first-pass perfusion, and DE-MRI was performed at 5 days and 5 months after primary PCI. Total infarct size decreased by 31% over time. Segments without MVO had early increased wall thickness and late partial functional recovery but the segments with MVO demonstrated late wall thinning and no functional recovery after 5 months. Shapiro et al³⁹ studied 17 patients presenting with first acute ST-segment elevation MI treated with primary PCI who underwent CMR within 6 days after presentation and again at 6 months. Using the DE-MRI technique for the assessment of delayed hyperenhancement and MVO, they showed that the degree of infarct transmurality seems to be a more powerful predictor of LV recovery than MVO.

In addition to assessing infarct size, degree of MVO, and potential LV recovery, CMR has recently been evaluated experimentally to measure an area at risk during acute infarction (Fig. 4).⁴⁰ Hypoperfused segments during an ischemic period, when subtracted from the actual infarct size, are defined as "the area at risk" or the "area at jeopardy." Minimizing the size of infarction is the goal of current medical and interventional therapies and having a tool to quantify the degree of myocardial salvage would greatly enhance our ability to define whether new therapies are beneficial.⁴¹ Aletras et al⁴⁰ used T2-weighted CMR to experimentally determine the jeopardized myocardium 2 days after a 90-minute coronary artery occlusion in dogs. By subtracting the final infarct size as determined by DE-MRI from the area of signal hyperintensity seen on the T2-weighted images, an area at risk was determined and shown to correlate well with radioactive microsphere data (Fig. 5). On the basis of this original animal data, there is hope that imaging the area at risk in patients after acute MI will further refine diagnosis, treatment, and prognosis. Studies are currently ongoing to address this question in the clinical setting.

FIGURE 4: Myocardial edema imaging is a powerful technique for determining the acuity of myocardial injury and the area at risk (see text). The patient in (A) had an acute occlusion of the left anterior descending coronary artery, as manifested by T2-weighted signal hyperintensity. This finding is consistent with acute injury of the anterior and anteroseptal walls (asterisks) of the left ventricle. The patient in (B) presented with ischemic electrocardiographic changes but normal cardiac enzymes. Although the CMR demonstrated T2-weighted signal hyperintensity in the inferior wall (asterisk) of the left ventricle, indicative of acute myocardial injury, his delayed enhancement images did not reveal an MI. This constellation of findings is consistent with unstable angina.

FIGURE 5: Microvascular obstruction as assessed by the delayed enhancement technique is also useful for prognosis. Using the delayed enhancement technique, the area of MI appears as a signal hyperintensity. If MVO is present, gadolinium cannot penetrate into the core of the infarct, and this manifests as a signal void within the area of delayed hyperenhancement. This patient presented with a large anterior wall MI with significant MVO. Delayed enhancement images in the short- (A) and long-axis (B) views demonstrate both the hyperenhanced infarct and a subendocardial signal void indicative of MVO (arrows). This large area of MVO suggests that the patient will not recover regional LV function.

CMR FOR STEM CELL RESEARCH

Preclinical studies assessing the role of stem cells to reverse myocardial damage have been promising. In humans, the results have been mixed at best. The Transplantation of Progenitor Cells and Regeneration Enhancement in Acute Myocardial Infarction trial, which enrolled 20 patients, found improvement in regional wall motion and LVEF in the infarct zone in patients with acute MI at 4 months after infusion of bone marrow or blood-derived progenitors.^37,42 However, other attempts to "regrow" damaged myocardium in humans in double-blind randomized and placebo-controlled trials (Autologous Stem Cell Transplantation in Acute Myocardial Infarction, Bone Marrow Transfer to Enhance ST-Elevation Infarct Regeneration, Transcatheter Endovascular Implantation of Valves, and Remodeling in Acute Myocardial Infarction) by delivering autologous bone marrow cells have yielded little or no benefit.^43-46 These negative results are largely believed to be due to the elimination of infused cells from the heart (<3% of stem cells are retained in the myocardium). Investigators also speculate that MVO in many patients and the route of delivery of infused stem cells may hinder successful cell engraftment. To overcome these limitations, several groups are using CMR in an attempt to track in vivo delivery of stem cells. Iron oxide labels, which generate magnetic resonance contrast, are either attached or incorporated into the stem cell and act as an in vivo tagging system.⁴⁷ Additionally, CMR also provides MVO and functional data important for determining the success of cellular engraftment. Ultimately, the role of stem cell therapy for the regeneration of myocardial tissue is in its infancy, but its success, in part, may be shouldered by the use of CMR technology.

LIMITATIONS

Undoubtedly, CMR is a powerful noninvasive imaging tool for the evaluation of patients with acute chest pain and acute MI. However, the technique poses certain limitations. First, with regard to evaluating patients with acute chest pain, MRI scanners are not widely available in the emergency setting, and expertise in the performance and interpretation of CMR is limited (trained technicians and qualified radiologists/cardiologists). Additionally, CMR does not allow for the reliable direct visualization of the entire coronary tree, and other tests, such as coronary computed tomography angiography, are superior in this regard. Finally, from a clinical standpoint, at times it may be undesirable to have patients presenting with acute chest pain in the MRI scanner without access to hemodynamic or ST segment monitoring for the scan duration.

CONCLUSIONS

Cardiac magnetic resonance imaging offers an impressive range of information (function, anatomy, viability, perfusion, and advanced research applications) that is pertinent to the clinical evaluation and subsequent management of patients presenting with acute chest pain. The technique does not suffer the same pitfalls of other noninvasive imaging modalities with regard to radiation exposure or spatial resolution. Initial studies have shown its usefulness in the setting of acute chest pain. In addition, it has become the criterion standard for imaging in the setting of myocardial injury and MI. In the future, CMR has the potential to be the imaging study of choice in the evaluation of patients with acute chest pain and/or MI.