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Cardiovascular magnetic resonance: applications and practical considerations for the general cardiologist
  1. Jayanth Ranjit Arnold,
  2. Gerry P McCann
  1. Department of Cardiovascular Sciences, University of Leicester, Leicester, UK
  1. Correspondence to Dr Jayanth Ranjit Arnold, Cardiovascular Sciences, University of Leicester, Leicester LE3 9QP, UK; jra14{at}


Cardiovascular magnetic resonance (CMR) is a rapidly evolving non-invasive imaging modality offering comprehensive, multiparametric assessment of cardiac structure and function in a variety of clinical situations. Cine imaging with CMR is the gold standard non-invasive imaging technique for the quantification of ventricular volumes and systolic function. It also affords superior visualisation of apical and right ventricular morphological abnormalities. In coronary artery disease, CMR stress perfusion imaging identifies functionally significant coronary artery disease with high sensitivity and specificity, and international guidelines recommend CMR perfusion imaging in patients with chest pain at intermediate-high risk of coronary disease. Late gadolinium enhancement (LGE) imaging is the most sensitive imaging technique for identifying infarction/viability. In non-ischaemic cardiomyopathy, LGE imaging plays vital diagnostic and prognostic roles in a number of cardiomyopathies (eg, hypertrophic and dilated cardiomyopathies, and amyloidosis). In vivo tissue characterisation with CMR enables the identification of oedema/inflammation in acute coronary syndromes/myocarditis and the diagnosis of chronic fibrotic conditions (eg, in hypertrophic and dilated cardiomyopathy, aortic stenosis and amyloidosis). CMR T2* imaging uniquely offers non-invasive assessment of iron overload states, facilitating diagnosis and management. A multiparametric CMR approach also enables differentiation of cardiac masses/tumours and is a useful adjunct to echocardiography in the assessment of valve disease. The emergence of automated, inline, quantitative methodologies will expand the scope of CMR and reduce its cost in forthcoming years.

  • cardiac magnetic resonance (CMR) imaging
  • myocardial disease
  • pericardial disease
  • valvular heart disease
  • heart failure

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During the past two decades, cardiovascular magnetic resonance (CMR) has transitioned from research tool to mainstream clinical modality. Its multimodality capability affords a comprehensive cardiovascular assessment with advanced diagnostic and prognostic information. Given the aptitude of CMR in multiple clinical scenarios, informing diagnosis, guiding therapy and predicting outcome (figure 1/online supplementary table 1), it is important that general cardiologists understand its principal applications and practical clinical considerations. This review covers the common clinical indications for CMR; complex congenital heart disease is beyond the scope of this review.

Supplemental material

Figure 1

Clinical applications of CMR modalities summary of the role of CMR modalities in diagnosis and directing therapy. ACS, acute coronary syndrome; ARVC, arrhythmogenic right ventricular cardiomyopathy; CAD, coronary artery disease; CMR, cardiovascular magnetic resonance; HCM, hypertrophic cardiomyopathy; LGE, late gadolinium enhancement.

Figure 2

Overview of CMR imaging elements. A core CMR scan (upper panel) comprises localisers, anatomical imaging, followed by long-axis and short-axis cine imaging and scar/fibrosis assessment. Additional optional elements (lower panel), depending on the clinical indication, may include ischaemia imaging, tissue characterisation, flow assessment and vascular assessment. CMR, cardiovascular magnetic resonance.

Basic MR principles

Conventionally, CMR is performed at magnetic field strengths of 1.5–3.0 Tesla—30–60 000 times stronger than Earth’s magnetic field. When placed within the scanner, hydrogen nuclei (protons) within the body align with the magnet’s main field. This is temporarily realigned by applying a radiofrequency pulse. On its removal, the protons return to equilibrium, releasing energy as radiofrequency signal, which is measured by receiver coils in order to generate images. Emitted signals reflect the density of protons and two relaxation parameters (‘longitudinal’ relaxation time, T1, and ‘transverse’ relaxation time, T2) intrinsically dependent on tissue composition (short T1/T2: fat; long T1/T2: water; long T1/short T2: myocardium). Depending on the clinical question, pulse sequences (comprising precisely timed radiofrequency pulses) are weighted accordingly. A detailed discussion of MR physics and pulse sequences is found elsewhere.1 2

Safety and patient selection

The confined scanner bore (60–70 cm diameter) and scan duration (30–60 min) may pose difficulty for some patients. With careful explanation and preparation (and sometime sedation), most will complete the examination, but approximately 5% will be unable to proceed (claustrophobia). A strong magnetic field is always present within the scanning room, making any ferromagnetic object a potential projectile hazard. Hence, access must be restricted and patients screened for implanted devices, aneurysm clips and foreign bodies (including drug/ECG patches/stickers). All valve prostheses and most coronary stents are safe but should be verified by trained staff (an extensive list is available at MR-conditional pacemakers/defibrillators are increasingly implanted (safe up to 1.5-Tesla) but should be scanned in liaison with the electrophysiology department (devices placed in MR safe mode and rechecked following the scan). There is mounting evidence that ‘legacy’ devices can be scanned safely, with appropriate precautions (box 1, online supplementary figure 1).3

Supplemental material

Box 1

Choice of imaging technique in cardiovascular assessment

Situations where cardiovascular magnetic resonance (CMR) may be suitable

  • When avoidance of radiation exposure is desirable.

  • Body habitus affecting echocardiographic or single-photon emission computed tomography (SPECT) assessment (raised body mass index (BMI)/soft tissue attenuation).

  • Serial assessment of volumetry, mass and function (good reproducibility and accuracy).

  • For tissue characterisation.

Coronary artery disease (CAD) assessment

  • Suspected angina (intermediate-risk and high-risk of CAD).

  • Known CAD for ischaemia assessment.

  • Significant coronary calcification precluding assessment by CT coronary angiography (CTCA).

  • CTCA confirms CAD, but the cause of symptoms remains unclear.

  • Viability assessment required to guide management (revascularisation).

  • Previous myocardial infarction.

  • Left bundle branch block.

Situations where CMR may be unsuitable

  • Severe renal impairment (gadolinium-based contrast agents contraindicated).

  • Claustrophobia.

  • Metal implants and devices which are not MRI safe/conditional.

  • Issues with ECG gating.

  • Inability to breath hold or lie flat for the scan duration.

  • Diagnosis of non-flow-limiting CAD (CT is preferable).

‘Vectorcardiogram’ triggering and gating are conventionally used to ‘time’ acquisitions and minimise motion artefact.4 Vectorcardiography distinguishes the predictable nature of cardiac electrical activity from artefacts generated by the magnetic effects of moving blood. With regular R–R intervals, ‘retrospective’ triggering is used (capturing the entire cardiac cycle), and with irregular cycles, ‘prospective’ triggering is used (capturing a continuous initial portion of the cycle). Unlike two-dimensional (2D) echocardiography, which acquires actual cardiac cycles, most CMR sequences ‘fuse’ multiple cycles to generate images. Despite superior spatial resolution, temporal resolution is lower than with echocardiography, which remains preferable for fast-moving structures. ‘Real-time’ CMR imaging provides faster acquisition but compromises image resolution and contrast.

Breath-hold acquisition is conventionally employed (usually 5–10 s) to minimise respiratory motion (‘ghosting artefact’). Non-breath-hold acquisition is also possible, though lengthens the scan. Hence, when planning CMR, important considerations impacting image quality and diagnostic confidence include breath-holding ability, heart rate/rhythm and ability to lie flat.

CMR examinations typically use gadolinium-based contrast agents (GBCAs) - paramagnetic, T1-shortening agents that distribute within intravascular and extracellular compartments. GBCAs are renally excreted and, in severe renal insufficiency, have been associated with nephrogenic systemic fibrosis, a very rare, irreversible and potentially life-threatening condition.5 Although less likely with newer macrocyclic agents, avoidance in severe renal insufficiency (estimated glomerular filtration rate <30 mL/min/g) is recommended. Serious allergic reactions following GBCA administration are rare (~1:20 000) and should be managed according to standard protocols.6 In pregnancy, although there is no evidence of harm, avoidance is recommended. Minute quantities of GBCAs are excreted in breast milk, and even less absorbed, meriting no restriction; nonetheless, many centres restrict breast feeding for 24 hours.7 There are recent reports of GBCA retention within the brain (dentate nuclei/globus pallidus), though clinical significance remains uncertain.8 However, no long-term sequelae are reported following 30 years’ use (approximately 300 million doses administered worldwide).

Clinical indications

Common CMR indications include the assessment of coronary artery disease (CAD), heart failure and cardiomyopathy (figure 1). Other indications include valvular and pericardial assessment, cardiac masses and angiography/aortography. A ‘standard’ CMR usually evaluates cardiac anatomy/function (10–15 min) and scar/fibrosis (10 min); the operator may then choose from a ‘menu’ of additional options according to the clinical question (figure 2).

Cardiac anatomy/function

Conventionally, following localiser images, T1-weighted imaging is undertaken in axial and/or coronal planes to delineate cardiac situs and vascular connections. If acquired, these images must be examined for incidental non-cardiac abnormalities (eg, lung, mediastinum, bone and upper abdominal lesions), with review by radiology colleagues if required.

Volumetric ventricular assessment by CMR (figure 3A–D) is regarded as the non-invasive reference standard, providing reproducible, accurate assessment of left/right ventricular (LV/RV) volumes, systolic function and mass.9 This is routinely performed using steady-state free precession (SSFP) cine imaging (10–15 breath-hold acquisitions, 5–10 s each, total time ~5–8 min).

Figure 3

Cine/functional imaging. Standard cine imaging comprises long-axis images acquired in four-chamber, two-chamber and three-chamber views (A–C, respectively) followed by a short-axis stack of images parallel to the mitral valve annulus, covering the entire ventricle (D), from which volumetric assessment is performed. Myocardial tagging (E) involves the tracking of deformation using selective RF saturation prepulses applied in a grid pattern. Myocardial regional function may be evaluated by tissue tracking (F), a postprocessing technique applied on routinely acquired cine images tracking individual pixels throughout the cardiac cycle. Examples of myocardial pathology evident on cine imaging: (G) two-chamber cine image showing an anterior aneurysm (white arrowheads); (H) three-chamber cine image showing severe asymmetric septal hypertrophy (asterisk) in a patient with hypertrophic cardiomyopathy; (I) four-chamber cine image showing apical hypertrophic cardiomyopathy (hypertrophied regions asterisked); (J) two-chamber cine image showing Takotsubo cardiomyopathy, preserved contractile function basally (white arrowheads) with severe hypokinesis distally (red arrowheads); (K) three-chamber cine image showing left ventricular non-compaction (red arrows); (L) short-axis image showing severe right ventricular enlargement with aneurysm formation (white arrows) in a patient with arrhythmogenic right ventricular cardiomyopathy (ARVC).

In CAD assessment, cine imaging identifies regional wall motion abnormalities and accurately quantifies LV systolic function, a powerful predictor of outcome and key determinant in the choice of drug and/or device therapy.10 Additionally acquired tagged images (figure 3E) enable evaluation of myocardial strain/torsion and hindrance by pericardial adhesions of normal pericardial/epicardial layer slippage.11 Recent software developments allow strain quantification from routinely acquired cine images (figure 3F) but presently this remains a research tool: echocardiography remains the clinical standard for diastolic assessment.12

In hypertrophic states (figure 3H-I), the location/extent of LV hypertrophy is more accurately defined with CMR than with echocardiography (where oblique/foreshortened views may be unavoidable).13 Importantly, CMR affords superior visualisation of apical structures (aneurysms, LV non-compaction and apical hypertrophic cardiomyopathy (HCM), figure 3G-K). RV morphological changes are also more readily apparent (figure 3L): in arrhythmogenic right ventricular cardiomyopathy (ARVC), CMR provides accurate assessment of RV regional abnormalities, volumes and function (integral to the 2010 ARVC modified task-force criteria (online supplementary table 2)).14

Scar and fibrosis assessment

‘Late’ gadolinium enhancement (LGE) imaging is conventionally performed with gradient-echo inversion-recovery sequences (5–15 min following GBCA administration, dose 0.1–0.2 mmol/kg, figure 4). GBCAs rapidly wash out of normal, viable tissue; slower washout in scarred/fibrosed regions, due to decreased capillary density and expanded interstitial space, manifests as hyperenhancement. To accentuate signal differences, the radiographer adjusts the ‘inversion time’ parameter to ‘null’ signal from normal tissue.

Figure 4

Gadolinium imaging. Standard gadolinium imaging comprises four-chamber, two-chamber and three-chamber views (A–C, respectively) followed by a short-axis stack of images (D). Examples of myocardial pathology evident on gadolinium imaging: (E) left anterior descending (LAD) coronary artery territory acute coronary syndrome with gadolinium uptake reflecting combined oedema/irreversible injury (white arrow); (F) microvascular obstruction in an acute LAD territory infarct, due to delayed penetration of gadolinium contrast into the infarct core, evident as a central black zone (white arrowheads) surrounded by hyperenhanced infarct areas; (G) apical thrombus evident as a dark filling defect (white arrow) on ‘early’ gadolinium imaging; (H) typical midwall fibrosis in a case of idiopathic dilated cardiomyopathy (white arrows); (I) patchy septal fibrosis in hypertrophic cardiomyopathy (red arrow); (J) cardiac amyloidosis with characteristic difficulty in “nulling” the myocardium; (K) subendocardial enhancement in eosinophilic myocarditis with small, apical thrombus (red arrow); (L) multi-focal patchy enhancement in cardiac sarcoidosis (red arrowheads).

Ischaemic cardiomyopathy

LGE imaging provides high spatial resolution, high contrast images, making CMR the non-invasive gold standard for identifying infarction/replacement fibrosis. In CAD, CMR identifies smaller infarcts routinely missed by lower resolution modalities (eg, SPECT).15 Lower resolution, ‘single-shot’ CMR images may be acquired in seconds, detecting most areas of scarring/infarction.16 Infarct assessment (figures 4A-D) is pivotal in guiding patient selection for revascularisation (those with viable myocardium) and predicting adverse outcome.10 17 The transmural extent of LGE predicts functional improvement following revascularisation: recovery is more likely in segments with ≤50% transmural infarction than those with ≥75%.17 Viability assessment with CMR has the advantage of obviating pharmacological stress. However, an important caveat is that it may overestimate infarct size in the acute phase (2–3 weeks) of acute coronary syndromes (ACSs), as reversible oedema increases gadolinium uptake (figure 4E).18

In ACS, LGE imaging also detects microvascular obstruction, a strong predictor of adverse remodelling and unfavourable prognosis.19 Extensive microcirculatory damage, thrombosis and oedema-related vessel compression delay GBCA penetration into the infarct core, manifesting as a characteristic central black zone surrounded by hyperenhancement (figure 4F).20

‘Early’ gadolinium imaging is useful for identifying thrombus (ventricular/atrial): early after contrast administration, when the blood pool remains bright, avascular thrombus appears as a dark filling defect (figure 4G). CMR is superior to echocardiography for detecting ventricular thrombi.21

Non-ischaemic cardiomyopathy

In non-ischaemic disease, the pattern/distribution of LGE may offer clues regarding aetiology and prognostic significance (figures 4H-L). Myocarditis typically causes subepicardial/midmyocardial scarring, usually (though not always) in a non-coronary distribution with subendocardial sparing. A diagnosis of non-ischaemic dilated cardiomyopathy (DCM) may be confirmed by midwall fibrosis (figure 4H), a recognised risk factor for cardiac death, ventricular arrhythmia and heart failure hospitalisation .22

LGE imaging may also prove instructive in hypertrophic states. In HCM, collagen deposition and fibre disarray may cause patchy, midwall (sometime diffuse) LGE, even when overt hypertrophy is absent (figure 4I).23 In HCM, LGE is a risk factor for ventricular arrhythmia and sudden cardiac death (SCD).24 Diffuse fibrosis is also found in hypertensive heart disease and aortic stenosis (though usually less pronounced).23 In Anderson-Fabry disease (an X-linked lysosomal storage disorder), LGE has an inferolateral midmyocardial predilection.25

In cardiac amyloidosis, global diffuse enhancement is characteristically seen with a dark blood pool: amyloid fibrils avidly bind GBCA, with consequent difficulty nulling the myocardium (figure 4J). The presence of LGE is correlated with adverse prognosis.26 Global subendocardial enhancement is also seen in small-vessel vasculitides and endomyocardial fibrosis (eg, hypereosinophilic disease), with the pathognomonic ‘apical V sign’ (figure 4K). Cardiac sarcoidosis is associated with multiple foci of patchy enhancement (figure 4L), which are predictive of mortality and ventricular arrhythmia.27 The presence of mediastinal lymphadenopathy should be sought, as its absence makes this diagnosis unlikely.

LGE imaging may also identify atrial scarring/fibrosis (amyloid and atrial ablation). In ARVC, LGE may be present in regions of fibrofatty infiltration and is an established risk factor for SCD.

Ischaemia assessment

Ischaemia imaging (figure 5) may be performed using vasodilator (adenosine, dipyridamole and regadenoson) or inotropic (dobutamine) stress. In clinical practice, the most commonly used is adenosine (80% of studies), a safe, well-tolerated agent (half life ~12 s) with low incidence of adverse effects.28 Conventionally, perfusion is imaged over 50–60 consecutive cardiac cycles, during ‘first pass’ of a peripherally injected GBCA bolus (0.05–0.1 mmol/kg). Ideally, separate intravenous cannulae should be used for GBCA/adenosine to minimise the risk of transient heart block (resulting from a column of adenosine in the infusion line being delivered by the GBCA bolus). Images are usually acquired in three short-axis slices (approximate spatial resolution 2–3 mm, lower than for Cine/LGE imaging). Dobutamine stress may be used when adenosine is contraindicated, identifying perfusion and/or wall motion abnormalities. However, examination times are longer and adverse events are more frequent.

Figure 5

Perfusion assessment. Standard perfusion assessment (leftmost panels) typically acquired in three short-axis slices (top panel) following adenosine stress, repeated after approximately 10 min (resting scan – lowed panel). Examples of pathology: (A) anteroseptal perfusion defect (LAD territory, white arrows); (B) inferolateral perfusion defect (circumflex territory, white arrowheads); (C) inferoseptal perfusion defect (right coronary artery, red arrows); (D) circumferential perfusion defect in a patient with microvascular disease; (E) dark-rim artefact (red arrowheads); and (F) hypoperfusion in a patient with hypertrophic cardiomyopathy (white arrowheads).

The 2016 NICE stable chest pain guidelines recommend CT coronary angiography (CTCA) as the first-line investigation in patients with new onset chest pain.29 However, it acknowledges that CTCA may be unsuitable in some cases, and a role remains for techniques such as CMR. The recently updated ESC guidelines also recommend CTCA in low-risk individuals, with functional testing in higher risk/known CAD (online supplementary figure 1).30 Large-scale studies have demonstrated superior diagnostic accuracy of CMR over SPECT, currently the mainstream diagnostic modality in the UK.31 32 A meta-analysis evaluating multiple imaging modalities against invasive fractional flow (FFR) assessment confirmed high sensitivity and specificity for CMR (89%/87%).33 In the MR-INFORM trial, a CMR-informed management strategy proved non-inferior to invasive FFR-guided management.34 The CE-MARC2 trial demonstrated the capacity of CMR to improve patient management, reducing unnecessary invasive angiography in patients with suspected angina, compared with NICE clinical guidelines (CG95, published 2010).35

For interpretation of CMR perfusion, conventionally, stress and rest images are evaluated visually, to identify ‘reversible’ hypoperfusion and distinguish ischaemia from artefact. Theoretically, the latter will be evident on both scans but, in practice, is often more prominent at stress (due to higher heart rates and blood-pool/myocardial contrast gradient). These effects coupled with the limits of resolution may give rise to ‘dark-rim artefact’, a band of low-signal in the subendocardial layer during early first pass (figure 5E), characteristically shorter lived and thinner than genuine perfusion defects (figure 5A-D). However, in practice, this distinction can prove difficult, yielding diagnostic uncertainty. Infarction produces a ‘fixed’ perfusion defect, so stress perfusion must be compared with LGE images (ideally acquired in identical slice positions). Microvascular disease characteristically appears as a circumferential perfusion defect crossing coronary boundaries (figure 5D).

Tissue characterisation

A capability offered almost exclusively by CMR is in vivo tissue characterisation, comprising T1, T2 and T2*-weighted imaging (figure 6).36 37 Importantly, these sequences are mostly carried out before GBCA administration and hence, should be planned at the outset. They may also prove useful when GBCAs are contraindicated (eg, renal insufficiency – to diagnose amyloid or fibrotic states).

Figure 6

Tissue characterisation. Myocardial oedema evident on T2-mapping in inferior territory acute coronary syndrome (A-B, red arrowheads), and (C) in myocarditis, affecting the lateral wall (white arrow). Elevated T1 values in: (D) acute myocarditis affecting the basal inferolateral wall (white arrow), (E) hypertrophic cardiomyopathy, and (F) cardiac amyloidosis. Myocardial T1 values are depicted as a colour map (scale not shown). Reduced T1 times (G) in Fabry disease (T1 times approximately 890 ms). (H) T2* imaging in siderosis revealing iron overload.

In ACS, T2-weighted imaging may detect myocardial oedema (increased water content) as high signal regions (figures 6A-B), demarcating the area at risk (AAR). Oedema precedes the onset of necrosis and troponin release and persists for several days, enabling retrospective identification of culprit territories.38 The difference between AAR and irreversible scar (determined in the chronic phase using LGE imaging) denotes ‘salvaged’ myocardium, an important outcome measure in clinical trials.19

In myocarditis, T2-weighted imaging may also identify regions of inflammation, characteristically in a non-coronary distribution (figure 6C). In Takotsubo cardiomyopathy, oedema may be detectable for 1–2 weeks, even after LV recovery. A disadvantage of T2-weighted imaging is the need for a ‘normal’ reference region for comparison (remote myocardium or adjacent skeletal muscle): a false-negative assessment may result if these regions are also affected by the disease process. Newer T2-mapping techniques may overcome this limitation but remain to be clinically adopted.

By contrast, parametric T1-mapping is clinically available, providing objective, quantitative assessment of oedema/inflammation (eg, ACS/myocarditis - figure 6D). Native T1 values are also elevated in fibrotic states (eg, DCM, HCM, aortic stenosis and amyloidosis), enabling the identification of subtle, diffuse fibrosis that LGE imaging may miss (figures 6E-F).

Whereas most disease processes increase T1 values, there are two key exceptions: (1) in Anderson-Fabry disease, myocardial glycosphingolipid deposition lowers T1 values (figure 6G) and (2) in primary/secondary haemochromatosis, iron loading lowers T1.39 Myocardial iron overload is also detectable by T2*, which reflects magnetic inhomogeneity induced by iron species (figure 6H. Myocardial iron overload is indicated by T2* <20 ms: serial CMR assessment has proved useful for titrating iron chelation therapy, improving clinical outcome in these patients.40 41 T2* imaging may also identify intramyocardial haemorrhage, a severe consequence of microvascular obstruction following ACS and key predictor of adverse remodelling and future prognosis.19 Here, haemoglobin degradation products cause signal loss on T2* imaging.

Despite the wealth of information afforded by native T1 mapping, an important caveat is that T1 values are influenced by multiple variables, with significant intervendor and intersequence variation. Work is ongoing to develop greater standardisation. T1 mapping following GBCA administration may be used to calculate extracellular volume, a marker of diffuse fibrosis, elevated in a variety of disease states (eg, ACS, myocarditis, DCM, amyloidosis and diabetic cardiomyopathy).37 42 Currently, this remains primarily a research tool.

A multiparametric CMR approach is useful for assessing cardiac masses.43 The lipid content of lipomas renders them bright on T1-weighted imaging, with signal loss with fat saturation techniques. Cystic lesions appear bright on T2-weighted imaging, and LGE imaging identifies those with high fibrotic content (eg, fibromas). Cine imaging is vital for identifying tumour extent and mobility, and first-pass imaging may determine tumour vascularity (malignant lesions are usually highly vascularised; figures 7A-D).

Figure 7

Miscellaneous CMR applications Cine images (A-B) showing malignant cardiac neoplasia invading the right ventricle and atrium (white arrow) with associated pericardial effusion (asterisk); (C) first-pass perfusion imaging showing mixed vascularity (red arrow); (D) variable hyperenhancement on late gadolinium imaging (red arrowheads). (E-F) Congenital complete absence of the pericardium with gross leftward displacement of the heart, and a ‘window’ of lung tissue interposed between the heart and diaphragm (white arrow); (G-H) pericardial constriction - ‘real-time’ Cine imaging (lower resolution than standard Cine) reveals septal flattening in inspiration (white arrowheads); (I-K) extensive aortic dissection extending from the arch to the distal abdominal aorta (red arrows show dissection flap); (L) short-axis image showing trileaflet aortic valve (orifice asterisked); (M) contrast-enhanced angiography revealing pulmonary venous configuration and accessory pulmonary vein (arrowed).

T1-weighted black-blood imaging is useful for identifying pleural/mediastinal involvement, and pericardial pathology (eg, thickening or congenital absence, figures 7E-F). Pericardial cysts are characterised by high signal on T2-weighted imaging. Although not definitive, the T1 characteristics of a pericardial effusion may give clues regarding its origin: on SSFP imaging, very high signal suggests a transudate, with lower signal for exudates. Furthermore, cine imaging is useful for identifying chamber collapse and paradoxical septal motion, and free-breathing, real-time imaging, for identifying ventricular interdependence (figures 7G-H).

Flow assessment

While echocardiography is the first-line investigation for valve disease, CMR may be invaluable in patients with difficult echocardiographic windows or where echocardiographic results and clinical symptoms conflict.44 45 Phase-contrast CMR imaging quantifies blood velocities in an imaging plane, based on the principle that protons moving within a magnetic field gradient acquire rotational spin phase shifts proportional to their velocity. Temporal resolution is lower with CMR (25–45 ms, cf 2 ms for Doppler echocardiography), potentially underestimating peak velocities. The presence of arrhythmia may also compromise flow quantification. Mitral and tricuspid regurgitant volumes are assessed indirectly, by comparison of LV/RV stroke volumes and aortic/pulmonary flow. CMR and echocardiographic quantitation of mitral regurgitant volumes may have poor agreement.46

Flow assessment is complemented by cine imaging for valve morphology and planimetry—the primary method for quantifying stenotic lesions (figure 7L). It is important to ensure correct plane positioning at the valve tips and to consider the use of thin, overlapping imaging slices (4–5 mm cf standard 8 mm). CMR and CT appear to give higher aortic valve areas than echocardiography.47 Although prosthetic valves may be safely imaged with CMR, the presence of metal frequently compromises image quality; spoiled gradient echo may be employed, but at the expense of lower signal-to-noise, and signal voids may still persist.

Contrast-enhanced angiography

Although CT is preferred in the acute setting for aortic dissection, CMR is useful for serial postoperative surveillance, aortic aneurysms requiring multiple follow-up imaging and following coarctation repair (figures 7I-K). Black-blood T1-weighted imaging is useful for vascular dimensions, and contrast-enhanced angiography may also be used to derive three-dimensional volume-rendered images. An intravenously injected bolus of GBCA is used, with image acquisition timed for maximal contrast enhancement in the aorta. This method can also be used for assessing pulmonary veins—for planning pulmonary vein isolation, evaluating post-isolation stenosis and anomalous vascular drainage (figure 7M). Angiography sequences avoiding GBCA use are also available.

Coronary artery imaging with CMR currently does not have a clinical role in the assessment of CAD, being restricted by limited spatial resolution and long acquisition times: CTCA remains the modality of choice. CE-MARC demonstrated that coronary imaging has no incremental diagnostic benefit above perfusion/LGE imaging.31

Future perspectives

Accelerated acquisition techniques now permit high-resolution real-time cine imaging, potentially more robust to arrhythmias. In the near future, technical innovations will enable fully automated quantitative analysis, improving accuracy and objectivity (eg, cardiac volumetry, perfusion and infarct size), with use of artificial intelligence algorithms.48 Currently, inline quantitative perfusion assessment (providing segmental blood flow within seconds) is being trialled, with the potential to improve identification of multivessel and microvascular disease.49 Time-resolved three-dimensional flow (4D) promises visualisation of flow patterns and quantification in all major vessels from a single acquisition. Finally, the clinical application of hyperpolarised CMR, which gives 10 000 times the signal-to-noise ratio of proton imaging, is currently under assessment, and is likely to allow quantification of myocardial metabolites in vivo, providing novel insight in multiple disease processes.50


The authors would like to thank Dr Aparna Deshpande and Dr Indrajeet Das for provision of images.



  • Contributors JRA conceived and drafted the manuscript, which GPM critically reviewed.

  • Funding JRA is funded through a National Institute for Health Research (NIHR) Clinician Scientist Fellowship. GPM is funded through a NIHR Research Professorship. Both authors are supported by the NIHR Leicester Biomedical Research Centre.

  • Competing interests None declared.

  • Patient consent for publication Not required.

  • Provenance and peer review Commissioned; externally peer reviewed.