The use of Cardiovascular Magnetic Resonance Imaging in Acute Coronary Syndromes

Introduction

The clinical role of Cardiovascular Magnetic Resonance (CMR) continues to expand¹, supported by ongoing technological advances that have shortened acquisition times while maintaining and often improving image quality. New applications of CMR in cardiovascular imaging continue to emerge and results from larger clinical trials are beginning to define the role of CMR in a range of clinical scenarios. Current accepted indications for CMR include the assessment of congenital heart disease, the great vessels, acquired myocardial and pericardial disease and chronic coronary artery disease (CAD)¹. The role of CMR in the assessment of acute coronary syndromes (ACS) is less well established. However, evidence is accumulating that CMR provides often unique information in chest pain syndromes that can aid the detection and differential diagnosis of ACS, guide clinical decision-making and improve risk-stratification after an event.

Following a review of the relevant CMR methodology, this article presents the current evidence for CMR in ACS and gives an outlook of future developments.

CMR methods

The following CMR methods are most commonly used for the assessment of ACS (see Figure 1) and can be incorporated into a clinical protocol that can be performed within an hour.

Figure 1.

Figure 1a. CMR methods for assessment of ACS. The figure shows short axis views (of different patients) illustrating the different imaging techniques used, their morphological correlates main clinical application.

Figure 1b. These methods can be integrated into a suggested CMR protocol that provides a comprehensive assessment of ACS patients and can be performed in less than 1 hour. Gd = gadolinium.

Cine Imaging

The assessment of global and regional left ventricular (LV) and right ventricular (RV) function by CMR is typically based on a cine data set aligned in the true LV short axis that covers the heart in 10-12 consecutive two-dimensional slices². Alternatively, three-dimensional cine data sets covering the entire heart in a single breath-hold can be acquired^{3, 4}. In addition to its high tissue contrast, the main advantage of CMR over other imaging modalities is that imaging planes can be freely and reproducibly defined. Consequently, CMR is the most accurate and reproducible imaging modality for the assessment of global ventricular volumes and function ^{5, 6}. In addition, regional contractile function can be assessed either by visual interpretation of cine loops^{7, 8} or by measuring wall motion, thickening and strain using myocardial tagging methods^{9, 10}. Myocardial tagging during low dose dobutamine stress has been used to measure parameters of diastolic dysfunction such as the time to peak untwist which may identify coronary stenosis^11,12. Following AMI, low dose dobutamine cine CMR can be used to predict viability and functional recovery^13-16. High dose dobutamine stress CMR has high diagnostic accuracy to identify inducible LV wall motion abnormalities indicative of flow-limiting coronary stenosis^17-19.

First Pass Myocardial perfusion

Current first pass myocardial perfusion CMR methods track the passage of a bolus of a T1-shortening contrast agent injected into a peripheral vein^{20, 21}. Data acquired during intravenous vasodilator-stress (most commonly with adenosine) delineate relatively underperfused regions associated with myocardial ischemia. The spatial resolution of CMR myocardial perfusion imaging of 2 to 3 mm is vastly superior to other imaging modalities, so that subendocardial ischemia can be more reliably identified. Recent developments have seen further improvements in spatial resolution to around 1 mm in the imaging plane²² and acquisition at 3-Tesla promises improved signal to noise ratio and diagnostic yield^{23, 24}. Both of these developments should continue to enhance the value of CMR perfusion assessment. The interpretation of CMR myocardial perfusion studies in clinical practice is most commonly visual, but quantitative approaches that measure characteristics of myocardial signal intensity profiles are available^{21, 25-28} and have been validated against x-ray angiography, SPECT and PET^29-31. The recent MR-IMPACT study in 234 patients reported improved detection of coronary stenosis by CMR compared with SPECT in the first multi-centre, multi-vendor comparison³². In the context of ACS, myocardial perfusion CMR imaging can be used to delineate microvascular obstruction and ischaemia, as described in subsequent sections.

Early and late gadolinium enhancement

Following acute ischemic injury, the myocardial distribution volume of extra-cellular gadolinium-based contrast agents is increased because of the presence of sarcrolemmal disintegration and abnormal wash-out kinetics. In chronic myocardial infarction, the presence of fibrotic tissue increases the distribution volume of the contrast agents. The resulting differences in contrast distribution between normal and injured myocardium can be delineated with T1-sensitive inversion-recovery CMR methods. Imaging within the first few minutes after contrast administration is the method of choice to delineate microvascular obstruction (MVO), which prevents contrast delivery to the infarct core and thus results in low signal on T1-weighted imaging³³. Acutely injured and chronically infarcted tissue without MVO on the other hand retains contrast agent and therefore appears bright^34-37. The preferred imaging time for scar is between 10 and 20 minutes after contrast agent administration, when the differences between scar, normal myocardium and blood pool are maximal. This method is referred to in the literature variably as late gadolinium enhanced CMR (the currently preferred term), late-contrast enhanced, delayed contrast-enhanced or hyperenhancement CMR. It has become the reference standard for the in vivo assessment of myocardial viability because of its very high spatial definition and high contrast to normal myocardium, which allows a detailed assessment of the spatial distribution of scar. Because of its high spatial resolution late gadolinium enhanced CMR can detect infarction in as little as 1ml of tissue, substantially less than other in vivo methods. The technique has been extensively validated in animal models showing excellent agreement with histology and has been applied in numerous recent human studies^33-38. Most notably, it was shown that CMR is more sensitive in detecting subendocardial MI than SPECT or PET and in chronic CAD that the extent of scar on CMR predicts the potential for functional recovery after revascularisation ^39-41. Figure 2 shows a case example of early and late gadolinium enhancement following acute MI.

Figure 2.

Diastolic (A) and systolic (B) frame from a cine CMR study acquired at the mid-ventricular level in short axis orientation in a patient with a recent anterior wall acute STEMI. The arrows in B demonstrate the akinetic anterior wall with no systolic thickening compared to the other myocardial segments. Panel 1C is an early gadolinium enhancement image taken 2 minutes after injection of a gadolinium-containing contrast agent and shows a large region of MVO (dark areas) in the anterior wall. The late gadolinium enhancement image acquired 15 minutes after contrast application in panel 1D shows an extensive region of infarction as demarked by the bright white regions of hyperenhancement with a core of MVO still visible. Such extensive transmural infarction with a high burden of MVO suggests that functional recovery in this region is unlikely.

T2-weighted imaging

Myocardial edema is a feature of many forms of acute myocardial injury that are associated with inflammation. Edema alters myocardial T2-relaxation and can therefore be detected with T2-weighted CMR imaging⁴². Following acute myocardial infarction, T2-weighted CMR can be used to delineate the ischemic risk region, which typically extends beyond the scar (see Figure 3). This is discussed in greater detail later. However, both the relatively small contrast-to-noise ratio between edematous and normal myocardium (around 2 to 3) and artefacts from slow flowing blood at the subendocardial border can make interpretation of T2-weighted images more challenging than other CMR methods, although recent methodological developments promise to improve these limitations⁴³.

Figure 3.

CMR images taken 24 hours after primary percutaneous intervention in a patient with a lateral STEMI. Panel A shows the T2 weighted images revealing a large area of edema that represents the region of “threatened myocardium” and is clearly larger that the area of late gadolinium enhancement shown in panel D. Resting first pass perfusion in Panel B shows a region of microvascular obstruction in the subendocardial region at the infarct core that closely correlates with the early gadolinium enhanced images (panel C).

Coronary MR angiography

CMR imaging can be used to delineate coronary morphology and detect at least proximal coronary stenosis⁴⁴. Coronary MR angiography, however, is rarely used in ACS, where invasive angiography is a routine test and non-invasive coronary imaging has little to add to the diagnostic process.

In summary, CMR offers a wide range of tools that can be utilized for the detection, differential diagnosis and management of patients with acute and chronic manifestations of CAD. Data acquisition times for most CMR methods continue to be reduced, allowing multi-parametric assessment in a single imaging session. In the following sections the established and evolving clinical applications of CMR in ACS will be discussed.

Detecting and differentiating ACS

Detection of ACS

Patients with suspected ACS are increasingly managed with early interventional strategies⁴⁵. However, in low-risk patients or in the presence of concomitant medical problems that increase the risk of complications from cardiac catheterization, an initial non-invasive functional test may be preferred⁴⁵. In this context, CMR presents an attractive alternative to established diagnostic methods. A study by Kwong and colleagues suggested that CMR imaging may more accurately identify ACS than conventional markers⁴⁶. In 161 consecutive patients presenting to the emergency room with cardiac chest pain but no evidence for MI, CMR was performed within 12 hours of presentation. The CMR protocol comprised myocardial perfusion at rest, cine imaging and late gadolinium enhancement. The study reports a sensitivity and specificity of 84% and 85%, respectively, of CMR for detecting subsequent ACS defined as 70% coronary stenosis or positive stress test within 8 weeks of the index event. Detection of regional wall motion abnormalities was the most powerful part of the CMR study in this setting where perfusion abnormalities may be normal in between episodes of pain and infarction may not yet be established. CMR was more sensitive than ECG, troponin and the Thrombolysis in Myocardial Infarction (TIMI) risk score and was the strongest predictor of ACS on multivariate logistic regression analysis.

CMR is also helpful in differentiating acute from chronic MI by combining late gadolinium enhancement with T2-weighted imaging, which will delineate the edema associated with acute infarction. In a study of 73 patients with acute and chronic MI by Abdel Aty and colleagues, CMR was 96% sensitive in differentiating acute from chronic MI⁴². The incremental value of T2-weighted imaging for the detection of ACS was the subject of a recent study of 64 consecutive patients⁴⁷ presenting with chest pain to the emergency room with negative cardiac enzymes and no ECG changes suggestive of coronary ischemia. Adding T2-weighted imaging and left ventricular wall thickness measurements to a core CMR protocol of cine and late gadolinium enhancement imaging increased the specificity, positive predictive value, and overall accuracy in detecting ACS from 84% to 96%, 55% to 85%, and 84% to 93%, respectively. CMR provided incremental value in the detection of ACS over and above traditional risk stratification with the changes detected by CMR occurring before the rise in cardiac enzymes (6±12 hours).

As well as detecting early changes following ACS, CMR is useful in the setting of delayed presentations where cardiac markers may have returned to normal, while abnormalities on T2-weighted CMR can persist for several weeks⁴⁸.

Differential diagnosis of ACS

CMR can facilitate the differential diagnosis of ACS, in particular in the context of a normal coronary angiogram. In a study of 27 patients with troponin-positive chest pain and normal x-ray coronary angiogram, half showed subepicardial or mid-wall late gadolinium enhancement, suggesting myocarditis, while the other half demonstrated subendocardial or transmural enhancement typical of myocardial infarction⁴⁹. Another study of 61 patients presenting with troponin positive chest pain and normal coronary angiography showed that contrast enhanced CMR was able to identify a cause in 65% of cases with the commonest being myocarditis (50%), followed by myocardial infarction and cardiomyopathy⁵⁰. Laissy and colleagues came to similar results in a study of 55 patients, which included 24 patients with clinically suspected myocarditis and normal coronary angiography and 31 with a history of atypical myocardial infarction and coronary stenosis⁵¹. In all but one patient with myocarditis, CMR perfusion was normal and late gadolinium enhanced CMR showed either epicardial or diffuse non-segmental enhancement, while MI patients showed typical endocardial enhancement. The pattern of CMR abnormalities in myocarditis may even predict long-term outcome⁵². Figure 4 shows an example of enhancement in a patient with myocarditis.

Figure 4.

CMR images from a 49 year-old female presenting with chest pain and breathlessness. Cardiac serum biomarkers were raised and an ECG showed widespread T wave inversion. Coronary angiography showed normal coronary arteries with no evidence for coronary atheroma. CMR shows a regional wall motion abnormality predominantly in the inferior segments (panel A diastole, panel B systole). Late gadolinium enhancement images (panel C) show extensive epicardial hyperenhacement in the inferior and near transmural enhancement in the lateral segments. Based on all available results, a clinical diagnosis of myocarditis was made. The patient declined cardiac biopsy.

Tako Tsubo cardiomyopathy, or apical ballooning syndrome, is a syndrome with distinctive features such as acute chest pain and shortness of breath, ST-segment elevation on electrocardiogram and release of cardiac enzymes. Consequently it can mimic acute myocardial infarction (AMI) at clinical presentation. The diagnosis is usually suspected during invasive coronary angiography, which typically reveals non-obstructed coronary arteries and an apical wall motion abnormality crossing coronary supply territories. CMR can reliably make the diagnosis of abnormal apical contraction that characterizes the syndrome and late gadolinium enhanced CMR shows absence of myocardial necrosis in this syndrome and reliably predicts recovery (Figure 5) ^{53, 54}. A study by Eitel et al demonstrated the ability of CMR to distinguish acute apical myocardial infarction from apical ballooning syndrome without infarction and myocarditis in patients with angiographically normal coronary arteries and characteristic wall motion abnormalities⁵⁵.

Figure 5.

CMR images from a 52 year old female presenting with an episode of severe chest pain associated with marked anterior ST elevation and raised serum biomarkers. Coronary angiography revealed normal coronary arteries with no atheromatous disease. An LV angiogram showed a marked apical wall motion abnormality, raising the suspicion of Tako-Tsubo syndrome. CMR confirmed the typical diastolic apical “ballooning” on cine images (panels A and B) and absence of scar on late gadolinium enhanced images (panel C).

In summary, CMR may be a useful and accurate test to detect the presence of ACS and can be considered as an additional diagnostic tool to differentiate ACS from chronic MI and from disease entities with similar clinical presentations.

Management of ACS

Non ST elevation ACS

Current guidelines for the management of non-ST elevation ACS recommend that low risk patients with normal biomarkers should undergo a stress test (nuclear perfusion imaging or stress echocardiography) within 72 hours as an alternative to inpatient admission⁴⁵. Plein et al showed that CMR can also be used safely in the context of ACS⁵⁶. A CMR study incorporating cine imaging, rest and stress perfusion, coronary MRA and late gadolinium enhancement was performed within 2-5 days of non-ST elevation ACS in 72 patients. CMR reliably predicted the presence of coronary stenosis requiring revascularisation on subsequent X-ray coronary angiography, in particular when several of the CMR modules were interpreted in combination (sensitivity 96%, specificity 83%). Furthermore, this was superior to the prediction based on the TIMI risk score. Figure 6 gives a case example of a patient presenting with a biomarker-negative ACS, in whom CMR identified unknown previous MI and inducible ischemia in two separate coronary territories.

Figure 6.

CMR images from a patient with previous stents to the RCA and LAD 2 years earlier who presented to the emergency room with troponin-negative chest pain. CMR was performed within 24 hours of admission. Panel A shows inferior and anterior ischemia on adenosine-stress perfusion imaging. Panel B shows late gadolinium enhanced images with a region of subendocardial gadolinium enhancement in the inferior wall suggesting old myocardial infarction that was not previously known about. T2-weighted images were normal (not shown). Subsequent coronary angiography revealed tight in-stent restenosis in the RCA and significant flow-limiting disease in the LAD (panel C) as assessed by a pressure wire during hyperaemic conditions (fractional flow reserve 0.69). Both lesions were stented successfully and the patient was discharged home.

Ingkanisorn et al. showed subsequently that CMR adds significant prognostic value in predicting future diagnosis of CAD, MI, or death over clinical risk factors⁵⁷. They studied 135 troponin-negative patients presenting to the emergency room with chest pain using adenosine stress perfusion CMR. CMR had 100% sensitivity and 93% specificity to predict the development of CAD at one-year follow-up.

ST-elevation MI

Following acute ST-elevation MI (STEMI) patients may not receive definitive revascularisation at the time of initial presentation for a variety of reasons, including late presentation, concomitant medical problems that exclude reperfusion strategies or widespread or complex coronary disease that is not suitable for percutaneous revascularisation. The detection and quantification of scar by late gadolinium enhanced CMR is increasingly used to guide revascularisation decisions in these patients in particular. In a group of 50 patients with myocardial infarction, of which 6 were studied within two weeks of infarction, Kim et al. showed that late gadolinium enhanced CMR predicts reversible myocardial dysfunction. Ninety percent of the myocardial segments studied that contained hyperenhancement between 51% and 75% of tissue and virtually all of those with transmural infarction did not improve after revascularization. Conversely, 256 out of 339 (78%) of hypokinetic segments containing no hyperenhancement had improved contractility after revascularization ³⁴. A subsequent study by Nijveldt et al. in 60 patients with recent AMI confirmed that segments with >75% transmural enhancement are unlikely to function completely at follow-up, while in about half of the segments with less than 25% transmural enhancement function improved completely⁵⁸. These results were supported by Bodi et al. who showed that the amount of viable myocardium on CMR predicts functional recovery in thrombolysed STEMI patients who receive post-hoc revacularisation⁵⁹.

In patients receiving thrombolytic therapy for the treatment of acute STEMI, functional assessment with exercise testing or a pharmacological imaging study is recommended for low risk patients before discharge from hospital⁶⁰. Greenwood and colleagues showed in a small sample of 35 patients that CMR imaging with adenosine stress perfusion, viability and function assessment can be safely performed within a few days of acute STEMI and is more accurate than an exercise tolerance test for detecting residual ischemia⁶¹.

Complications of ACS

In addition to supporting management decision-making in ACS, CMR reliably detects important complications of AMI. Ventricular aneurysms and ventricular septum defects are clearly identified on cine images. With late gadolinium enhanced CMR, these pathologies can be further characterized in the context of the acute injury and may aid planning of surgical or percutaenous procedures ⁶². Early or late gadolinium enhanced imaging is also very useful to identify LV thrombus ^{63, 64} (Figure 7).

Figure 7.

CMR images in four-chamber orientation from a patient with previous antero-septal myocardial infarction. The diastolic frame from a cine CMR study (panel A) shows thinning of the interventricular septum with a mass lesion at the endocardial surface (arrow). Early gadolinium enhanced images (panel B) show that the lesion does not take up contrast. Late gadolinium enhanced images (panel C) delineate the extent of myocardial infarction (black arrow) as hyperenhancement and show that the lesion remains unenhanced (white arrow), suggesting a left ventricular thrombus.

In summary, there is early evidence that using CMR in ACS patients is safe and provides a comprehensive assessment of the sequelae of AMI that can help to guide patient management. CMR has the benefit over other imaging modalities of providing the most accurate information on cardiac morphology, function and scar. In addition, CMR can determine the presence of residual myocardial ischemia and reliably detects complications associated with ACS.

Risk-stratification after ACS

In patients with known or suspected coronary artery disease CMR has comparable predictive value for future adverse cardiac events with nuclear scintigraphy or stress echocardiography⁶⁵. Even small amounts of scar on late gadolinium enhanced CMR provide incremental prognostic value beyond the usual clinical, angiographic, and functional predictors⁶⁶. In the context of ACS, several CMR measures are associated with prognosis (see Table 1).

Table 1.

Prognostic value of CMR imaging following ACS.

Study	Year	n	Initial CMR Scan	Follow up	CMR method	Main parameter examined	Outcome	P value
Wu et al67	1998	44	10±6 days post AMI	6mth CMR; clinical 16±5mth	1st pass perfusion	MVO	Predicts poor LV recovery with ↑MACE	<0.01
Taylor et al68	2004	20	24 hrs post PPCI	3mth CMR	1st pass perfusion & LGE	MVO; infarct transmurality (>75%)	Predicts poor LV recovery	0.02; 0.048
Bodi et al59	2005	40	1 week post AMI	6mth CMR	Dobutamine stress & LGE	↓dobutamine response; infarct transmurality (>50%)	Predicts poor LV recovery	<0.0001
Hombach et al69	2005	110	6.1±2.2 days post AMI	225±92 days CMR & clinical	1st pass perfusion & LGE	MVO; infarct transmurality (>75%)	Predicts poor LV recovery with ↑MACE	0.0074
Baks et al70	2006	22	5 days post PPCI	5mth CMR	1st pass perfusion	MVO	Predicts poor LV recovery	0.006
Tarantini et al71	2006	76	6±2 days post PPCI	6±2mth transthoracic echo	LGE	In farct transmurality (>75%)	Predicts poor LV recovery	<0.001
Ingkanison  et al57	2006	135	<72 hrs post trop negative chest pain	1yr clinical	Adenosine stress prefusion	Reversible ischaemia	Highly accurate to predict CAD, MI, death	<0.0001
Larose et al72	2007	147	>30 days post AMI	Clinical median 17mth (6- 53mth)	Cine & LGE	RV function (EF<40%)	↑mortality independent of LV function	<0.003
Roes et al73	2007	231	>3mths post AMI	1.7yrs clinical	LGE	In farct size	Predicts mortality	0.005
Wu et al74	2008	122	1 week post AMI	3mth CMR; clinical 2yrs	LGE	Acute infarct size (>18% LV)	↑MACE	<0.05

AMI = acute myocardial infacrtion, PPCI = primary percutaneous coronary intervention, LGE = late gadolinium enhancement, LV = left ventricle, RV = right ventricle, CAD = coronary artery disease, MACE = major adverse cardiovascular event, trop = troponin.

Infarct size

Infarct size measured by late gadolinium enhancement is directly associated with outcome. Tarantini and colleagues⁷¹ showed in 76 patients with acute revascularized MI that the amount of transmural necrosis on late gadolinium enhanced CMR predicted adverse LV remodelling, with significant additional predictive value to infarct size and microvascular obstruction. These findings were confirmed by Roes et al who showed in 231 patients with healed myocardial infarction that infarct size on late gadolinium enhanced CMR was a stronger predictor of all-cause mortality than LVEF and LV volumes. Transmurality of infarction was also associated with worse outcome⁷³. Wu et al showed that acute infarct size as determined by CMR, which was independent of LV stunning and loading, directly relates to LV remodeling and is a stronger predictor of future events than measures of LV systolic performance⁷⁴.

Peri-infarct zone

On late gadolinium enhanced CMR images, a border zone of intermediate signal can be observed between the infarct and surrounding tissue. This peri-infarct zone may reflect partial volume or partial myocardial necrosis and edema. A study by Kwong et al. suggested that the extent of the peri-infarct zone is an independent predictor of post-MI mortality. In 144 patients with documented coronary artery disease and previous MI, they found that the amount of myocardium exhibiting an intermediate signal on late gadolinium enhanced CMR images was a strong predictor of all-cause mortality⁷⁵. A subsequent study suggested that one mechanism for this increased mortality may be that the peri-infarct zone is a substrate for arrhythmias⁷⁶. CMR data on scar and peri-infarct zone could thus prove useful in the future to identify patients for implantable cardioverter/defibrillator and cardiac resynchronisation therapy (CRT)^{77, 78}.

Microvascular obstruction

Early contrast-enhanced CMR can reliably demonstrate the presence and extent of MVO following reperfused AMI. MVO results in poor tissue perfusion despite restoration of epicardial blood flow to the infarcted region. It is the consequence of clogging of the small myocardial arterioles with embolic debris, acute inflammation, platelet aggregation and vasospasm. Studies have shown that the presence and extent of MVO following AMI as measured by early gadolinium enhancement CMR is associated with adverse ventricular remodelling^{16, 68, 79-81} and clinical outcome that is independent of the infarct size^{67, 69}. Baks et al examined patients with CMR soon after primary percutaneous revascularisation for STEMI and again at five months. They found that dysfunctional segments without MVO had early increased wall thickness and late partial functional recovery compared to segments with MVO that showed late wall thinning and no functional recovery ⁷⁰. Nijveldt et al demonstrated that MVO had incremental diagnostic value over transmurality of infarction in particular in segments with 75-100% transmural enhancement⁵⁸.

Area at risk

The area at risk (AAR) is defined as hypoperfused myocardium at the time of an ischemic episode⁸². Currently the gold-standard for determining the AAR is single photon emission tomography with injection of Technitium-99m tracer into the occluded coronary artery prior to revascularisation⁸³. In the experimental setting, myocardial contrast echo has also been used⁸⁴.

T2-weighted CMR offers a potentially attractive alternative for the non-invasive measurement of AAR. The increased water content of myocardium following acute ischemia-reperfusion injury⁸⁵ leads to high signal on T2-weighted images⁸⁶ and combined with late gadolinium enhancement allows the delineation of areas that are injured but not infarcted following reperfusion^{87, 88}. The areas of T2 enhancement are invariably transmural and subsequently larger than the regions of late gadolinium enhancement^{89 88} and the difference between the two likely represents myocardial salvage⁹⁰. The advantages of this method are that such a region can be retrospectively determined days after the acute event⁸⁷ and without the need for direct injection of agents into the coronary artery at the time of primary reperfusion. So far, no outcome studies based on a CMR assessment of AAR have been published.

Right ventricular infarction

It is well recognized that involvement of the right ventricle (RV) in acute MI is associated with adverse clinical outcome. RV function is difficult to assess reliably with most imaging modalities, while it poses no particular challenge to CMR cine imaging (Figure 8). Kaandorp et al. showed that RV infarction can be detected by late gadolinium enhancement and that the extent of scar tissue is linearly related to the severity of RV dilatation at 6 months follow-up⁹¹. Kumar et al. found in 37 patients that acute RV infarction is more frequently detected by late gadolinium enhancement than by ECG and echocardiography⁹². Finally, Larose et al. have shown that RV ejection fraction measured by CMR is an important predictor of prognosis after AMI⁷². In 147 consecutive patients studied late after MI, RVEF <40% was strongly associated with mortality (hazard ratio 4.02), independent of patient age, LV infarct size and LVEF.

Figure 8.

CMR images from a patient with acute non-ST elevation myocardial infarction, evidenced by a rise in cardiac enzymes and widespread ST segment changes on an electrocardiogram. Invasive coronary angiography revealed three vessel coronary artery disease with an occluded proximal right ventricular branch of the right coronary artery. A cine CMR image in diastole (panel A) shows a subtle wall motion abnormality in the anterior right ventricular free wall (arrow). The T2-weigthed image (panel B) shows high signal in this area with corresponding high signal on the late gadolinium enhanced image (panel C). There is no evidence for scar in the left ventricle, suggesting isolated right ventricular infarction.

In summary, CMR imaging provides several independent measures of prognosis after ACS that can all be obtained in a single imaging procedure and cannot be assessed equally with other imaging modalities. A potential role for CMR may thus be to offer an improved method for risk stratification in the early post ACS period.

Future perspectives

Owing to ongoing technological advances (faster gradients, multi-channel receiver coils, transform coding to accelerate data acquisition) scan times for many CMR methods continue to be shortened. Until now, this development has usually been invested into obtaining higher quality images (e.g. better spatial resolution, better temporal resolution, better signal to noise ratio). However, given the image quality achieved today, future improvements of imaging speed are likely to be reinvested into shortening scan time for a given CMR method. This speed up can be used to evaluate more patients per time for chronic disease, but also to answer numerous questions within a single short setting for patients with acute coronary syndromes. A likely scenario for MR imaging in these patients will resemble one of the current utilizations of CCT in patients with chest pain– the triple rule out of pulmonary embolism, aortic dissection and myocardial infarction in a single imaging session. Such an approach would look at wall motion abnormalities, edema and resting perfusion first, then use a higher bolus of contrast agent for a time resolved 3D angiography which allows assessment of the anatomy of the pulmonary arteries and the aorta within a single scan and the final assessment of late gadolinium enhancement to visualize scar tissue.

In vivo MRI of advanced plaques in human carotid arteries using contrast-enhanced techniques has identified lipid core with 85% sensitivity and 92% sensitivity⁹³. In addition, thin and ruptured plaques can be identified in vivo by MRI in a high proportion of patients in whom it was subsequently identified on examination of post-atherectomy specimens⁹⁴. Improving methods^95-97 and the introduction of 3-Tesla clinical imaging⁹⁸ raise the possibility that in the near future such techniques may be applied to the coronary arteries.

More specific techniques to visualize activation within a plaque using targeted (molecular) contrast agents could be used as a potential predictor of plaque rupture, with the potential for identification of specific disease processes in vivo. This has already been demonstrated in animal models for fibrin specific contrast agents, which allow the highlighting of ruptured plaques and thrombosis within the coronary arteries^{99, 100}. Similarly, contrast agents designed to show earlier processes of plaque vulnerability such as myeloperoxidase activity¹⁰¹ and macrophage activation^102,103 have been applied in animal models If translated into clinical application, the ability to assess non-invasively plaque activity may overcome a major limitation of the current practice of cardiology.

Which patient with ACS should undergo CMR imaging?

• In patients presenting with suspected ACS but no angiographic evidence of coronary artery stenosis, CMR can contribute to the differential diagnosis of ACS from other acute myocardial diseases such as myocarditis.

• In low risk patients presenting with suspected ACS, an early stress-perfusion CMR scan can be considered as an alternative non-invasive stress test to risk stratify and discharge patients.

• Patients with established myocardial infarction may undergo CMR following diagnostic angiography to determine of the degree of myocardial necrosis and likelihood of recovery to plan further revascularization strategies.

• Post-AMI, CMR may also be used to risk stratify patients using LV ejection fraction, infarct size and characteristics and RV involvement. Based on these data, high-risk patients, for example, with poor ventricular function and a large scar burden can be selected for ICD implantation.

• A CMR protocol for these clinical scenarios that follows the recent recommendations of the Society of Cardiovascular Magnetic Resonance¹⁰⁴ is given in Figure 1b.

Conclusions

CMR imaging is emerging as a versatile diagnostic tool for the management of the patient with suspected or established ACS. It provides additional information over other clinical tests for the detection, differential diagnosis and prognostication after ACS, owing to the high spatial definition and multi-modal data it provides. Future larger studies will determine more fully the role of CMR in the setting of ACS.