The Role of Cardiovascular Magnetic Resonance in the Evaluation of Patients with Ischaemic Heart Disease

Theodoros D. Karamitsos, MD, PhD and Stefan Neubauer, MD, FRCP, FACC, FMedSci
University of Oxford Centre for Clinical Magnetic Resonance Research
Department of Cardiovascular Medicine, John Radcliffe Hospital, Oxford, UK

Address for correspondence:
Theodoros D. Karamitsos, MD PhD
Department of Cardiovascular Medicine
John Radcliffe Hospital
OX3 9DU Oxford, UK
Tel: +44 1865 221867
Fax: +44 1865 221111
Email: theo.karamitsos@cardiov.ox.ac.uk


Abstract
Cardiovascular magnetic resonance (CMR) imaging is playing an increasing role in the diagnosis of ischaemic heart disease, the assessment of prognosis and monitoring of therapy. It is considered the current gold standard technique for the evaluation of global and regional left ventricular function and the assessment of myocardial viability. Cardiovascular magnetic resonance under inotropic or vasodilator stress is rapidly gaining acceptance in clinical practice for the identification of inducible ischaemia. Magnetic resonance coronary angiography needs further improvement in spatial and temporal resolution to allow reliable detection of coronary stenoses. Newer techniques such as oedema imaging with T2-weighted methods extend the frontiers of CMR to the investigation of acute coronary syndromes. This review presents the relevant CMR techniques and discusses the role of CMR in the diagnostic and prognostic evaluation of patients with ischaemic heart disease.


Introduction
Ischaemic heart disease (IHD) is a common disorder that is associated with significant morbidity, mortality and financial burden to healthcare services. It is a major cause of death in the United States, accounting for 1 of every 2.8 deaths in 2005[1] Moreover, IHD accounts for the majority (about 70%) of heart failure cases.

Non-invasive imaging plays a central role in the diagnosis of IHD, the assessment of prognosis and monitoring of therapy. 2-D echocardiography and single-photon emission computed tomography (SPECT) are mainly used to detect myocardial ischaemia and assess viability in such patients. Echocardiography also provides a good general assessment of left ventricular (LV) systolic and diastolic function but may be constrained by limited imaging windows, requires geometric assumptions in quantifying global LV systolic function and has limited ability to provide specific tissue characterisation. Nuclear imaging techniques involve ionizing radiation and have limited spatial resolution.

Cardiovascular magnetic resonance (CMR) is a rapidly emerging non-invasive imaging technique which provides high resolution images of the heart in any desired plane with a nearly unrestricted field of view and without the use of ionizing radiation. A CMR study in patients with IHD provides information on myocardial anatomy, function (regional and global), ischaemia, viability and, with some limitations, coronary artery anatomy.

This article will present the relevant CMR techniques and discuss the role of CMR in the diagnostic and prognostic evaluation of patients with IHD.


CMR techniques

A brief description of the basic CMR techniques used in the evaluation of patients with IHD is given here. Magnetic resonance imaging uses hydrogen atoms (protons), which are abundant in the human body, to generate images capitalising on the nuclear property of spin. When protons are placed in a strong magnetic field, they act like tiny bar magnets and align themselves parallel and antiparallel to the direction of the primary field, with a small excess of parallel protons that gives rise to a net magnetization vector. These hydrogen nuclei are then excited intermittently by pulses of radio-frequency waves and as a consequence the magnetisation vector rotates by an amount termed the flip angle. Once this pulse is discontinued, the magnetisation vector starts to recover to its former position, releasing signals in the form of radio waves. This relaxation of net vector is attributable to two distinct but simultaneous processes, referred to as the longitudinal (T1) and the transverse (T2) relaxations. Proton density, longitudinal relaxation time (T1) and transverse relaxation time (T2) vary substantially for different tissues. These differences are highlighted with specific MR sequences (combination of radio-frequency pulses and magnetic gradient field switches) to generate contrast in MR images. Another way to modify contrast is by changing specific parameters of the MR sequences. The basic pulse CMR sequences are called spin-echo, gradient-echo and steady-state free precession (SSFP) sequences. A detailed description of CMR pulse sequences is beyond the scope of this review. To prevent artifacts from cardiac motion, most of the CMR images are generated with sequences gated to the R wave of the electrocardiogram. Respiratory motion, which is another source of artifacts in the CMR images, is eliminated by acquiring most CMR images in end-expiratory breath-hold. Most of the CMR images are acquired without the use of exogenous contrast. However, some CMR applications, for example, perfusion or infarct imaging, require the use of gadolinium-based contrast agents, which are distributed within the extracellular interstitial space. Free gadolinium is highly toxic, and to eliminate heavy metal toxicity all gadolinium-based contrast agents are chelated by appropriate ligands. Extra caution should be taken with patients with severe renal impairment (eGFR <30 ml/min). It is recommended that operators strictly adhere to indications and contra-indications of the gadolinium chelate intended to be used in these patients who are at risk of nephrogenic systemic fibrosis (NSF).

Cine imaging

Figure 1. End-diastolic still images from multiple contiguous short-axis SSFP cines that encompass the left ventricle, from base to apex. Note the position of the short-axis (SA) slices marked on the still frames of end-diastolic horizontal (HLA) and vertical long-axis (VLA) cine images.
Figure 1. End-diastolic still images from multiple contiguous short-axis SSFP cines that encompass the left ventricle, from base to apex. Note the position of the short-axis (SA) slices marked on the still frames of end-diastolic horizontal (HLA) and vertical long-axis (VLA) cine images.

Steady-state free precession sequences, which allow excellent delineation of the blood–myocardium interface, are the current standard to evaluate global and regional ventricular contractile function, including the more difficult to assess right ventricle[2]. In contrast to 2-D echocardiography, CMR does not have the weakness of geometric assumptions in the calculation of ventricular volumes. Multiple short-axis slices parallel to the atrioventricular ring image both ventricles from base to apex (Figure 1), and after drawing endocardial and epicardial contours[3], left and right ventricular (RV) volumes are calculated by summing the endocardial areas multiplied by the interslice distance. Stroke volume, cardiac output and ejection fraction are calculated using standard equations. Assessment of LV volumes, function and mass has been extensively validated in autopsy studies in humans and has excellent intra-observer and inter-observer variability[4]. This allows for smaller sample size in studies requiring serial follow-up scans. Cardiovascular magnetic resonance is also an excellent technique for assessing regional contractile function. It allows the identification of even subtle wall motion abnormalities at rest and during dobutamine stress. Assessment of regional wall motion is usually performed qualitatively by visual interpretation of cine images. Quantification of wall thickening and regional myocardial velocities and strain is possible with techniques like MR tagging, but this is usually reserved for research studies.

Infarct imaging
Figure 2. Late gadolinium enhancement images in the horizontal long-axis (left panel), vertical long-axis (middle panel) and the short-axis (right panel) views showing an infarct (50-75% transmural extent) involving the interventricular septum and anterior wall (white arrows).
Figure 2. Late gadolinium enhancement images in the horizontal long-axis (left panel), vertical long-axis (middle panel) and the short-axis (right panel) views showing an infarct (50-75% transmural extent) involving the interventricular septum and anterior wall (white arrows).

The presence and extent of a myocardial infarction can be assessed with late gadolinium enhancement (LGE) imaging. The physiologic basis of LGE is an increase in its volume of distribution within areas of scarring or fibrosis and an abnormally prolonged wash-out related to decreased functional capillary density in the irreversibly injured myocardium[5-7]. Therefore, infarcted myocardium retains contrast agent which is demonstrated as enhancement (high signal) on T1-weighted images acquired with inversion recovery gradient echo sequences. In normal myocardium, contrast media quickly washes in and out of the myocardial interstitium. By nulling the normal myocardial signal, the area of myocardial injury appears with relatively high contrast compared to the black normal myocardium (Figure 2). Numerous studies in animal models of ischaemic injury that directly compared LGE-CMR to histopathology showed that CMR is effective in identifying the presence, location and extent of myocardial infarction in both the acute and chronic settings[8, 9] Late gadolinium enhancement-CMR has high spatial resolution, more than 40-fold greater than SPECT, allowing visualisation of even microinfarcts that cannot be detected by other imaging techniques[10].

First-pass myocardial perfusion imaging

Figure 3. Stress perfusion still frame (panel A) showing a near transmural defect in the lateral wall (black arrows) which corresponds to a 75-100% transmural extent infarct (black arrows) on the late gadolinium enhancement image (panel B) indicating the absence of peri-infarct ischaemia.
Figure 3. Stress perfusion still frame (panel A) showing a near transmural defect in the lateral wall (black arrows) which corresponds to a 75-100% transmural extent infarct (black arrows) on the late gadolinium enhancement image (panel B) indicating the absence of peri-infarct ischaemia.

Myocardial perfusion imaging by CMR involves the administration of a bolus of gadolinium and the acquisition of multiple images to follow the transit (first-pass) of contrast through the cardiac chambers and myocardium. Suspected coronary artery disease can be effectively demonstrated during stress-induced ischaemia under pharmacological vasodilation with adenosine or dipyridamole. Most CMR centres prefer adenosine as the stressor agent because it is generally well tolerated, easily controlled and safe[11]. Adenosine is injected for 3 to 6 minutes at a rate of 140 µg/kg/min, whereas dipyridamole is infused for 4 minutes (total dose 0.56 mg/kg). After induction of vasodilation by either stressor agent, first-pass perfusion imaging is performed during intravenous bolus injection of a gadolinium-based contrast agent using ultra-fast saturation recovery sequences. These sequences typically allow three to four short- and/or long-axis slices to be acquired every heartbeat. Coronary vasodilators increase myocardial blood flow three to five times the resting level in regions subtended by normal coronary arteries. In contrast, the hyperaemic response to myocardial regions downstream of significantly diseased coronary arteries is attenuated because the arteriolar beds are already maximally vasodilated. Such areas therefore show lower peak enhancement with delayed uptake of the contrast and, hence, appear hypointense (dark) compared to adjacent normal myocardium (Figure 3). Although absolute quantification of regional myocardial blood flow (in mL/min/g) is possible, analysis of perfusion images in clinical practice is most commonly qualitative (visual). .

T2-weighted oedema imaging

T2-weighted CMR images can detect increases in myocardial water content (oedema) associated with acute ischaemic syndromes even in the absence of irreversible myocardial injury[12]. Typically, in acute myocardial infarction, T2-weighted images reveal an area of high signal which exceeds that of irreversible injury (as defined by the LGE technique)[13]. Therefore, it is possible to image a patient 2 to 3 days after an acute myocardial infarction treated with primary percutaneous intervention and determine the amount of ischaemic myocardium (high signal 'area at risk' on T2-weighted images), the amount of necrosis (area of hyper-enhancement on LGE images) and the amount of myocardial salvage (the difference between area at risk and area of necrosis). Moreover, because oedema resolves about 1 month following myocardial infarction, a combined T2-weighted and LGE imaging protocol can differentiate acute from chronic myocardial infarction[14]. Cardiovascular magnetic resonance edema imaging is a promising technique which is expected to be of significant value in testing therapies that alter infarct size.

Dobutamine stress CMR
In an analogous manner to dobutamine stress echo, CMR cine imaging can be performed under dobutamine stress to detect ischaemia[15] Dobutamine is infused intravenously during 3-minute stages at doses of 10, 20, 30 and 40 µg/kg/min. Atropine in small incremental doses is added, up to the maximal dose of 1.0 mg intravenously, if the target heart rate [(220-age) x 0.85] is not reached. At each stress level, three short-axis (basal, mid-equatorial and apical) and three long-axis (2-, 3-, 4-chamber view) cines are acquired. These are compared to the rest cine images (which were acquired before dobutamine) for evidence of new or worsened wall motion abnormalities. A pathologic response is characterised by stress-induced wall motion abnormalities (hypokinesis, akinesis or dyskinesis) in at least one segment that was graded normal at rest. For standardised assessment and reporting, the use of the LV 17-segment model of the American Heart Association is recommended. Termination criteria are identical to those of dobutamine stress echocardiography. Due to the risk of severe side effects, patients have to be closely monitored (continuous monitoring of heart rhythm, blood pressure and symptoms). A low-dose dobutamine protocol, defined as an infusion of up to 10µg/kg/min, can be used to identify viable myocardium and predict recovery of function following revascularisation[16].

Magnetic resonance coronary angiography

Magnetic resonance coronary angiography (MRCA) is a challenging and demanding technique. This is because of the small size and tortuous course of the coronary arteries which move rapidly due to cardiac contraction and respiratory motion. Diagnostic images showing the origins and proximal course of coronary arteries can, however, be obtained. The left and right coronary systems can be imaged separately, or newer ‘whole heart’ sequences can image both coronary systems in one large image volume covering the entire heart. Both methods use either multiple breath-holds or free-breathing navigator respiratory gating which tracks the position of the diaphragm to ensure that images are acquired only when the diaphragm is within 3 to 5 mm of its end-expiratory position. Free-breathing navigator MRCA offers improved patient comfort as compared with breath-holding techniques and does not require significant patient effort[17]. The spatial resolution of 3-D MRCA imaging (0.7 to 0.8 mm in-plane resolution and 1 to 3 mm through-plane resolution) is still greatly inferior compared to that of X-ray coronary angiography (<0.3 mm) or multidetector computed tomography (~0.4mm)[17]. Magnetic resonance coronary angiography is typically performed without the need for exogenous contrast agents, as special prepulses (e.g. fat-saturation prepulses, magnetisation transfer contrast prepulses or T2 preparatory pulses) make the coronary lumen appear bright whereas the signal from surrounding myocardium is suppressed[18]. The use of SSFP sequences and parallel imaging techniques have substantially improved image quality of 3-D MRCA, encompassing the entire coronary arteries within a reasonably short imaging time[18].

CMR in patients with chronic ischaemic heart disease
Figure 4. Timeline for a multi-parametric CMR study in patients with ischaemic heart disease involving cine imaging, first-pass perfusion at stress and rest and LGE. The full short-axis cine stack is acquired during the break between stress and rest perfusion. During this break, flow imaging can also be performed (e.g. if the patient has concomitant valvular disease). The second short break after rest perfusion can be used for early post-contrast images (thrombus imaging). If needed, T2-weighted oedema imaging can be added to this protocol (before contrast administration for stress perfusion), extending its duration by 5-10 minutes.
Figure 4. Timeline for a multi-parametric CMR study in patients with ischaemic heart disease involving cine imaging, first-pass perfusion at stress and rest and LGE. The full short-axis cine stack is acquired during the break between stress and rest perfusion. During this break, flow imaging can also be performed (e.g. if the patient has concomitant valvular disease). The second short break after rest perfusion can be used for early post-contrast images (thrombus imaging). If needed, T2-weighted oedema imaging can be added to this protocol (before contrast administration for stress perfusion), extending its duration by 5-10 minutes.

In clinical practice, a comprehensive CMR study including cine imaging, first-pass (stress and rest) perfusion and LGE is sufficient to give reliable answers to important clinical questions (Figure 4). The first and most common question is related to global and regional LV function assessment given that the degree of LV dysfunction is an important prognostic indicator and a significant determinant of outcome in patients with IHD. Cardiovascular magnetic resonance provides accurate and reproducible assessment of global and regional cardiac function and can be used to guide important and expensive therapeutic procedures, such as the implantation of defibrillators or biventricular pacemakers in such patients. Another important query has to do with the presence of viable myocardial tissue prior to revascularisation procedures. The transmural extent of infarction on LGE-CMR predicts the likelihood of contractile recovery after revascularisation following revascularisation with either percutaneous coronary intervention or coronary artery bypass graft[19, 20]. In practical terms, the important question is whether the transmural extent of late enhancement is greater than 50%, which indicates an overall low chance of recovery, or less than 50%, which suggests intermediate or good chance of recovery post-revascularisation. In myocardial segments with intermediate (25–75%) hyper-enhancement, some evidence suggests that low-dose dobutamine CMR adds diagnostic information, however this is rarely needed[16]. The simplicity of the LGE technique which does not involve any form of stress or monitoring has resulted in its widespread adoption in clinical practice. Even segments with significant wall thinning (<6 mm), which were considered non-viable previously, may show no significant scarring on LGE and, hence, these patients may benefit from revascularisation.

Another important aspect of IHD which can be assessed by CMR is the presence of inducible ischaemia. Dobutamine stress or first pass perfusion under vasodilator stress CMR can be used for this purpose. Several studies have shown that both these stress techniques have good sensitivity, specificity and diagnostic accuracy to detect significant coronary artery disease[21]. The application of dobutamine stress CMR is particularly advantageous in patients with poor acoustic windows. Otherwise, the diagnostic accuracy of this technique is similar to dobutamine stress echocardiography[15]. First-pass perfusion imaging under vasodilator stress seems to gain wider application because of the practical difficulties with dobutamine stress in the MR environment. A multicentre-multivendor trial compared CMR perfusion with SPECT in 234 patients and showed at least equivalent diagnostic performance of CMR (area under the receiver operator characteristic curve 0.86 for CMR vs 0.75 for SPECT, P=0.12)[22]. Recently, a multicomponent CMR approach incorporating elements of cine function, LGE and stress perfusion imaging has been proposed to increase the accuracy of coronary artery disease detection[23]. Areas of hypo-enhancement present at both stress and rest ('fixed defects') without exhibiting LGE are considered to be artifacts, thereby improving the specificity of the test.

Another important question in clinical practice is the detection of significant coronary artery stenoses. This is still a challenge for CMR as reliable detection of coronary artery stenoses beyond the proximal coronary arteries is not a robust technique. The only multicentre but single-vendor study of 3-D MRCA involved 109 patients and demonstrated 93% sensitivity, 58% specificity and 81% negative predictive value for the identification of ≥50% diameter stenosis by invasive quantitative coronary angiography[24]. The sensitivity and negative predictive values for the identification of left-main or three-vessel disease were 100%, thereby demonstrating a role for MRCA for this subset. However, 16% of proximal and middle segments of coronary arteries were non-interpretable and were excluded from final analysis. Therefore, current guidelines consider MRCA a first-line investigation technique only for patients in whom an anomalous artery origin is suspected or when a known anomalous coronary artery origin needs to be further characterised[17]. The utility of coronary MRCA in general practice has not been established, and multivendor trials have not been conducted yet.


CMR in acute coronary syndromes
Figure 5. Recent anterior myocardial infarction and microvascular obstruction. A large area of microvascular obstruction (black, white arrows) within a large full thickness anteroseptal infarct.
Figure 5. Recent anterior myocardial infarction and microvascular obstruction. A large area of microvascular obstruction (black, white arrows) within a large full thickness anteroseptal infarct.

Evidence is rapidly accumulating that CMR can provide unique information in acute coronary syndromes. A combination of cine, rest perfusion and LGE imaging showed a sensitivity and specificity of ~85% for detecting acute coronary syndromes[25]. The addition of T2-weighted imaging to cine and late enhancement CMR allows the differentiation between acute and chronic myocardial infarction[14]. This new approach improved the overall accuracy of CMR to identify patients with acute coronary syndromes from 84% to 96%[26]. The safety and diagnostic accuracy of adenosine stress CMR imaging early after ST-segment elevation myocardial infarction has also been demonstrated[27]. Cardiovascular magnetic resonance has excellent sensitivity and specificity for LV thrombus detection post-infarction and is superior to both transthoracic and transoesophageal echocardiography[28]. Intracavitary thrombi can be usually seen on cine CMR, although further confirmation on early post-contrast images (1-3 minutes following gadolinium administration) may be needed. Cardiovascular magnetic resonance can also demonstrate areas with poor tissue perfusion despite restoration of epicardial coronary blood flow, the so-called no-reflow phenomenon. This is the consequence of multiple processes that result in severe microcirculatory damage, including tissue oedema, platelet plugging, neutrophil adhesion, myocyte necrosis and intracapillary red blood cell stasis. Using a late gadolinium technique, due to delayed contrast penetration the area of microvascular damage appears as a hypo-enhanced (black) region within a larger area of hyper-enhancement (Figure 5). Cardiovascular magnetic resonance can also aid in the differential diagnosis of acute coronary syndromes from other entities such as myocarditis and acute aortic syndromes. Patients with myocarditis may show areas of subepicardial/mid-wall hyper-enhancement in the septal and inferolateral walls which are most frequently affected[29]. T2-weighted images early after symptom onset may show regions of increased signal, defining focal areas of myocardial oedema. Cardiovascular magnetic resonance also has excellent diagnostic accuracy, combining high sensitivity and specificity, for the detection of nearly all forms of aortic dissection[30]. Other less common clinical entities which may mimic acute coronary syndromes, such as Tako-tsubo cardiomyopathy (apical ballooning syndrome), can be readily identified and characterised by CMR[31].


CMR and prognosis in ischaemic heart disease
Data on the prognostic role of CMR imaging in patients with IHD are rapidly becoming available. The presence of LGE in patients with suspected coronary artery disease but no known history of myocardial infarction is the most important independent predictor of major cardiac adverse events over other clinical predictors, including ejection fraction[32]. The identification of microvascular obstruction by CMR has been associated with adverse ventricular remodeling, arrhythmias and poor clinical outcome following acute myocardial infarction[33] Furthermore, the presence of extensive peri-infarct regions of intermediate hyper-enhancement (defined as hyper-enhancement with signal intensity two to three standard deviations above normal) is associated with increased mortality risk[34]. Increased infarct tissue heterogeneity identified by CMR augments the susceptibility to ventricular arrhythmias in patients with prior myocardial infarction and LV dysfunction[35]. Recently, the utility of CMR stress techniques (vasodilator perfusion and dobutamine wall motion imaging) for predicting cardiac death and non-fatal myocardial infarction in large patient populations with known or suspected coronary artery disease has been demonstrated[36] The risk of major cardiac events is increased five-fold if wall motion abnormalities are detected by dobutamine stress CMR. A patient with inducible ischaemia on adenosine stress CMR has a 12-fold increased risk for experiencing a subsequent cardiac event over 3 years. Similar data are also available for dipyridamole stress CMR[37].


CMR in non-ischaemic cardiomyopathies
Figure 6. A patient with hypertrophic cardiomyopathy. Still end-diastolic frames from SSFP cines – horizontal long-axis (A) and short-axis at the mid-ventricular level (C) showing significant asymmetric septal hypertrophy. Corresponding images using the LGE technique – (B) and (D) respectively. The pattern of mid-wall septal hyper-enhancement is mid-wall, diffuse and typically involves both LV-RV junctions (white arrows).
Figure 6. A patient with hypertrophic cardiomyopathy. Still end-diastolic frames from SSFP cines – horizontal long-axis (A) and short-axis at the mid-ventricular level (C) showing significant asymmetric septal hypertrophy. Corresponding images using the LGE technique – (B) and (D) respectively. The pattern of mid-wall septal hyper-enhancement is mid-wall, diffuse and typically involves both LV-RV junctions (white arrows).

Cardiovascular magnetic resonance is also an important technique for characterising non-ischaemic cardiomyopathies, identifying prognostically important features and highlighting pathophysiological mechanisms. A brief description of the use of CMR in non-ischaemic cardiomyopathies is included here. For readers interested in greater detail, the use of CMR in the evaluation of patients with non-ischaemic cardiomyopathies has recently been reviewed by our group[38]. In patients with hypertrophic cardiomyopathy, CMR can identify and determine the extent of hypertrophy more accurately than echocardiography. In addition, following administration of gadolinium contrast agents, CMR can detect myocardial fibrosis which has a patchy mid-wall pattern involving most commonly the hypertrophied segments and the LV-RV junctions (Figure 6). In patients with arrhythmogenic RV cardiomyopathy, CMR can detect global or regional RV contractile abnormalities, RV aneurysms, and in advanced cases, fibrofatty myocardial infiltration. Cardiovascular magnetic resonance can measure myocardial and liver iron overload as a result of thalassemia or hemochromatosis. This is useful to guide treatment and monitor response to iron chelating drug regimens. Cardiovascular magnetic resonance is also helpful in differentiating constrictive from restrictive cardiomyopathy. Systemic amyloidosis, sarcoidosis and other infiltrative diseases such as Fabry’s disease or endomyocardial fibroelastosis show characteristic abnormalities on LGE imaging. Thickened pericardium and abnormal motion of the septum due to increased interventricular dependence can be readily recognised in cases of constriction.


Conclusions
Cardiovascular magnetic resonance is a rapidly evolving field in non-invasive imaging with major applications in the evaluation of patients with ischaemic heart disease. In a single imaging session, CMR can assess cardiac anatomy and function, myocardial perfusion and viability. Detection of coronary luminal stenosis is possible in principle, but requires further improvement in resolution. In patients with acute coronary syndromes, CMR can assess both the area at risk and the area of necrosis. Because of the absence of ionizing radiation, CMR is an ideal non-invasive modality for the serial follow-up of patients with ischaemic heart disease.


Key Learning
  • Cardiovascular magnetic resonance allows a comprehensive multi-parametric assessment of patients with acute and chronic ischaemic heart disease, including global and regional biventricular function (cine imaging), myocardial ischaemia (high-dose dobutamine stress CMR or perfusion CMR with vasodilators) and viability (LGE technique or low-dose dobutamine CMR)
  • Magnetic resonance coronary angiography needs further improvement to allow reliable detection of coronary stenoses and is mainly indicated for the identification of suspected coronary anomalies
  • Cardiovascular magnetic resonance has a rapidly expanding role in the evaluation of patients with acute coronary syndromes
  • Cardiovascular magnetic resonance imaging provides several independent measures of prognosis in patients with ischaemic heart disease

All images courtesy of Oxford Centre for Clinical Magnetic Resonance Research


References
  1. Lloyd-Jones D, Adams R, Carnethon M, et al. Heart disease and stroke statistics -- 2009 update: a report from the American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Circulation 2009;119:480-6.
  2. Sarwar A, Shapiro MD, Abbara S, et al. Cardiac magnetic resonance imaging for the evaluation of ventricular function. Semin Roentgenol 2008;43:183-92.
  3. Karamitsos TD, Hudsmith LE, Selvanayagam JB, et al. Operator induced variability in left ventricular measurements with cardiovascular magnetic resonance is improved after training. J Cardiovasc Magn Reson 2007;9:777-83.
  4. Hudsmith LE, Petersen SE, Francis JM, et al. Normal human left and right ventricular and left atrial dimensions using steady state free precession magnetic resonance imaging. J Cardiovasc Magn Reson 2005;7:775-82.
  5. Rehwald WG, Fieno DS, Chen EL, et al. Myocardial magnetic resonance imaging contrast agent concentrations after reversible and irreversible ischemic injury. Circulation 2002;105:224-9.
  6. Mahrholdt H, Wagner A, Judd RM, et al. Delayed enhancement cardiovascular magnetic resonance assessment of non-ischaemic cardiomyopathies. Eur Heart J 2005;26:1461-74.
  7. Kim RJ, Chen EL, Lima JA, et al. Myocardial Gd-DTPA kinetics determine MRI contrast enhancement and reflect the extent and severity of myocardial injury after acute reperfused infarction. Circulation 1996;94:3318-26.
  8. Kim RJ, Fieno DS, Parrish TB, et al. Relationship of MRI delayed contrast enhancement to irreversible injury, infarct age, and contractile function. Circulation 1999;100:1992-2002.
  9. Wu E, Judd RM, Vargas JD, et al. Visualisation of presence, location, and transmural extent of healed Q-wave and non-Q-wave myocardial infarction. Lancet 2001;357:21-8.
  10. Wagner A, Mahrholdt H, Holly TA, et al. Contrast-enhanced MRI and routine single photon emission computed tomography (SPECT) perfusion imaging for detection of subendocardial myocardial infarcts: an imaging study. Lancet 2003;361:374-9.
  11. Karamitsos TD, Arnold JR, Pegg TJ, et al. Tolerance and safety of adenosine stress perfusion cardiovascular magnetic resonance imaging in patients with severe coronary artery disease. Int J Cardiovasc Imaging 2009;25:277-83.
  12. Abdel-Aty H, Cocker M, Meek C, et al. Edema as a very early marker for acute myocardial ischemia: a cardiovascular magnetic resonance study. J Am Coll Cardiol 2009;53:1194-201.
  13. Aletras AH, Tilak GS, Natanzon A, et al. Retrospective determination of the area at risk for reperfused acute myocardial infarction with T2-weighted cardiac magnetic resonance imaging: histopathological and displacement encoding with stimulated echoes (DENSE) functional validations. Circulation 2006;113:1865-70.
  14. Abdel-Aty H, Zagrosek A, Schulz-Menger J, et al. Delayed enhancement and T2-weighted cardiovascular magnetic resonance imaging differentiate acute from chronic myocardial infarction. Circulation 2004;109:2411-6.
  15. Mandapaka S, Hundley WG. Dobutamine cardiovascular magnetic resonance: a review. J Magn Reson Imaging 2006;24:499-512.
  16. Wellnhofer E, Olariu A, Klein C, et al. Magnetic resonance low-dose dobutamine test is superior to SCAR quantification for the prediction of functional recovery. Circulation 2004;109:2172-4.
  17. Bluemke DA, Achenbach S, Budoff M, et al. Noninvasive coronary artery imaging: magnetic resonance angiography and multidetector computed tomography angiography: a scientific statement from the american Heart Association Committee on Cardiovascular Imaging and Intervention of the Council on Cardiovascular Radiology and Intervention, and the Councils on Clinical Cardiology and Cardiovascular Disease in the Young. Circulation 2008;118:586-606.
  18. Stuber M, Weiss RG. Coronary magnetic resonance angiography. J Magn Reson Imaging 2007;26:219-34.
  19. Kim RJ, Wu E, Rafael A, et al. The use of contrast-enhanced magnetic resonance imaging to identify reversible myocardial dysfunction. N Engl J Med 2000;343:1445-53.
  20. Selvanayagam JB, Kardos A, Francis JM, et al. Value of delayed-enhancement cardiovascular magnetic resonance imaging in predicting myocardial viability after surgical revascularization. Circulation 2004;110:1535-41.
  21. Nandalur KR, Dwamena BA, Choudhri AF, et al. Diagnostic performance of stress cardiac magnetic resonance imaging in the detection of coronary artery disease: a meta-analysis. J Am Coll Cardiol 2007;50:1343-53.
  22. Schwitter J, Wacker CM, van Rossum AC, et al. MR-IMPACT: comparison of perfusion-cardiac magnetic resonance with single-photon emission computed tomography for the detection of coronary artery disease in a multicentre, multivendor, randomized trial. Eur Heart J 2008;29:480-9.
  23. Klem I, Heitner JF, Shah DJ, et al. Improved detection of coronary artery disease by stress perfusion cardiovascular magnetic resonance with the use of delayed enhancement infarction imaging. J Am Coll Cardiol 2006;47:1630-8.
  24. Kim WY, Danias PG, Stuber M, et al. Coronary magnetic resonance angiography for the detection of coronary stenoses. N Engl J Med 2001;345:1863-9.
  25. Kwong RY, Schussheim AE, Rekhraj S, et al. Detecting acute coronary syndrome in the emergency department with cardiac magnetic resonance imaging. Circulation 2003;107:531-7.
  26. Cury RC, Shash K, Nagurney JT, et al. Cardiac magnetic resonance with T2-weighted imaging improves detection of patients with acute coronary syndrome in the emergency department. Circulation 2008;118:837-44.
  27. Greenwood JP, Younger JF, Ridgway JP, et al. Safety and diagnostic accuracy of stress cardiac magnetic resonance imaging vs exercise tolerance testing early after acute ST elevation myocardial infarction. Heart 2007;93:1363-8.
  28. Srichai MB, Junor C, Rodriguez LL, et al. Clinical, imaging, and pathological characteristics of left ventricular thrombus: a comparison of contrast-enhanced magnetic resonance imaging, transthoracic echocardiography, and transesophageal echocardiography with surgical or pathological validation. Am Heart J 2006;152:75-84.
  29. Mahrholdt H, Goedecke C, Wagner A, et al. Cardiovascular magnetic resonance assessment of human myocarditis: a comparison to histology and molecular pathology. Circulation 2004;109:1250-8.
  30. Kersting-Sommerhoff BA, Higgins CB, White RD, et al. Aortic dissection: sensitivity and specificity of MR imaging. Radiology 1988;166:651-5.
  31. Karamitsos TD, Bull S, Spyrou N, et al. Tako-tsubo cardiomyopathy presenting with features of left ventricular non-compaction. Int J Cardiol 2008;128:e34-6.
  32. Kwong RY, Chan AK, Brown KA, et al. Impact of unrecognized myocardial scar detected by cardiac magnetic resonance imaging on event-free survival in patients presenting with signs or symptoms of coronary artery disease. Circulation 2006;113:2733-43.
  33. Wu KC, Zerhouni EA, Judd RM, et al. Prognostic significance of microvascular obstruction by magnetic resonance imaging in patients with acute myocardial infarction. Circulation 1998;97:765-72.
  34. Yan AT, Shayne AJ, Brown KA, et al. Characterization of the peri-infarct zone by contrast-enhanced cardiac magnetic resonance imaging is a powerful predictor of post-myocardial infarction mortality. Circulation 2006;114:32-9.
  35. Schmidt A, Azevedo CF, Cheng A, et al. Infarct tissue heterogeneity by magnetic resonance imaging identifies enhanced cardiac arrhythmia susceptibility in patients with left ventricular dysfunction. Circulation 2007;115:2006-14.
  36. Jahnke C, Nagel E, Gebker R, et al. Prognostic value of cardiac magnetic resonance stress tests: adenosine stress perfusion and dobutamine stress wall motion imaging. Circulation 2007;115:1769-76.
  37. Bodi V, Sanchis J, Lopez-Lereu MP, et al. Prognostic value of dipyridamole stress cardiovascular magnetic resonance imaging in patients with known or suspected coronary artery disease. J Am Coll Cardiol 2007;50:1174-9.
  38. Karamitsos TD, Francis JM, Myerson S, et al. The role of cardiovascular magnetic resonance imaging in heart failure. J Am Coll Cardiol 2009 (in press).


  39. JB3749 07-2009