The online version of this article (doi:10.1007/s13244-011-0101-8) contains supplementary material, which is available to authorized users.
The term “cardiomyopathy” identifies a heterogeneous group of cardiac diseases characterised by direct myocardial involvement leading to impaired cardiac function. Since the term was introduced by Harvey and Brigden in the 1960s, substantial progress has been made, in terms of understanding the pathophysiological substrate, underlying causes and peculiarities, and most importantly, in defining a classification system for cardiomyopathies. Primary cardiomyopathies include those with genetic, acquired or mixed causes, and refer to a disease that is predominantly limited to the myocardium, whereas secondary cardiomyopathies are characterised by myocardial involvement that is part of a generalised or diffuse systemic disorder. In addition, several cardiovascular diseases not regarded as cardiomyopathies may also affect the myocardium, causing systolic or diastolic dysfunction and hampering differentiation from heart muscle diseases . Although with the current arsenal of diagnostic imaging tools, the diagnosis of cardiomyopathies has been facilitated, in many cases the correct diagnosis remains challenging and sometimes elusive. Nevertheless, these techniques have significantly contributed towards an increased awareness of cardiomyopathies among clinicians, and they have an increasing impact on patient management and risk stratification. Transthoracic echocardiography is currently the first-line imaging technique for the diagnosis, evaluation and decision-making in cardiomyopathy patients. In the last decade, magnetic resonance imaging (MRI) and, to a lesser extent, multidetector (or multirow) computed tomography (MDCT) have become increasingly important in the diagnosis of cardiomyopathies. In particular, the comprehensive approach of MRI, including non-invasive tissue characterisation, makes it indispensable in the work-up of many cardiomyopathies.
Dilated cardiomyopathy (DCM) is the most common cardiomyopathy worldwide with a prevalence of 40–50 cases per 100,000. DCM is currently classified as primary (genetic, acquired or mixed), secondary (e.g. infiltrative or autoimmune) and idiopathic. Genetic inheritance is likely to play a role in the development of the disease in 20-35% of patients, but also acquired conditions like metabolic abnormalities, inflammatory and infectious processes, neuromuscular diseases and a large variety of cardiotoxic agents (chemotherapeutic agents, alcohol, illicit drugs) can lead to DCM [1–4]. Independently of the underlying cause, DCM is characterised by an increase in diameter and volume of the left or both ventricles, leading to progressive dilatation and impaired systolic function that is not secondary to or cannot be exclusively justified by abnormal loading conditions (e.g. valve disease, hypertension) or by the concomitant coronary artery disease (CAD) (Figs. 1 and 2) (Movie 1) [1–3]. Thus, the term DCM represents a final common pathway that is the end result of myocardial damage.
Independently of the underlying cause, DCM is characterised by an increase in ventricular chamber size. As demonstrated by the Frank-Starling mechanism, this serves as a first compensatory step aiming to maintain an appropriate stroke volume. However, above a critical sarcomere stretch, the efficiency of interaction between actin and myosine filaments decreases, resulting in impairment of stroke volume. Myocardial fibre elongation increases the ventricular radius, causing eccentric ventricular hypertrophy, with decreased wall thickness to chamber diameter ratio and increased ventricular sphericity. According to the Laplace law, these changes increase significantly myocardial wall stress with increased oxygen demand and subsequent worsening of the left ventricular (LV) systolic performance . The main histological features of DCM are myocyte elongation, myocardial apoptosis and hypertrophy of the remaining myocytes . Additionally, there is an excessive collagen deposition and decreased capillary density, with both reactive (interstitial and perivascular) and reparative (replacement) patterns of fibrosis [7, 8]. Myocardial fibrosis is considered the result of damage due to microvascular ischaemia and myocardial wall inflammation. The cellular and extracellular changes result in a normal, thinned or slightly thickened myocardial wall (Fig. 1).
The clinical presentation of DCM is variable, but the severity of symptoms is usually related to the grade of systolic impairment. Although patients can be asymptomatic, especially in the early phases of the disease, most of them have symptoms of left heart failure, such as dyspnoea and effort-related fatigue. In some cases, severe LV systolic dysfunction and advanced heart failure symptoms are present in patients with normal or mildly dilated ventricles (less than 10-15% above normal range), i.e. mildly dilated forms of DCM . Sudden cardiac death can be the first clinical evidence of DCM and it is due to sustained ventricular tachycardia and ventricular fibrillation. It is deemed that the more severe the systolic dysfunction and the degree of replacement fibrosis, the larger the arrhythmogenic substrate that can provoke malignant arrhythmias. Other potentially life-threatening manifestations of DCM are non-sustained ventricular arrhythmias, conduction abnormalities, syncope and embolic events. As the disease progresses, right heart failure may develop, and it is considered an aggravating factor (Fig. 3) [9, 10]. Thus, right ventricular (RV) dilatation and dysfunction can be present, but are not requirements for the diagnosis of DCM.
The requirements for appropriate imaging in cardiomyopathies nowadays exceed the pure diagnostic objective, whereby assessment of the more intricate aspects, such as depiction of underlying aetiology, risk assessment, therapy planning and determination of prognosis, are becoming increasingly important. MRI, because of its non-invasive nature, its excellent spatial, contrast and temporal resolution, and capability for tissue characterisation, has become a well-validated and widely accepted technique for studying DCM patients. In addition, the constant improvement in MDCT technology, especially since the introduction of the 64-row systems, offers reliable imaging of the heart and coronaries, offering new, yet incompletely explored approaches to studying DCM patients (Fig. 4). Several studies have independently shown that MDCT is highly appropriate for excluding coronary artery disease, yielding excellent negative predictive values [11–14]. Moreover this technique enables the characterisation of the coronary venous system, which may be of great help in the planning of cardiac resynchronisation therapy (CRT). In patients with contra-indications for MRI, such as those with permanent cardiac implantable devices, MDCT is an interesting diagnostic alternative.
Cine MRI is nowadays considered the reference technique for accurately measuring cardiac chamber size, ventricular function and myocardial mass (Figs. 1 and 3) [10, 15–18]. Moreover, derived parameters, such as myocardial wall thickness, wall thickness to chamber radius ratio and regional functional parameters (e.g. systolic wall thickening and wall motion), can be reliably assessed. DCM-related pathological conditions such as thrombus formation or valve dysfunction can be depicted by cine MRI as well. Techniques such as myocardial tagging have been shown to be very helpful in understanding the altered myocardial deformation patterns in DCM patients [19, 20]. MRI can be used for myocardial tissue characterisation, using T2-/T2*-weighted sequences and/or contrast-enhanced MRI. These sequences may even replace endomyocardial biopsy in some diseases (e.g. iron deposition cardiomyopathy). T2-weighted sequences allow increased myocardial free water content to be depicted, which occurs in the setting of acute myocardial infarction or in other diseases characterised by inflammation, such as acute myocarditis. Affected regions will appear bright compared with the normal myocardium. In the case of diffuse myocardial oedema, some authors recommend to measure the difference in signal intensity between myocardium and skeletal muscle (Fig. 5) . T2*-weighted sequences are of great value for the diagnosis of myocardial iron deposition diseases, leading to a shortening of T2* relaxation time (Fig. 6). This parameter can be used to predict complications such as heart failure and arrhythmias and can be used to initiate and monitor chelation therapy [22, 23]. Compared with normal myocardium, in pathological myocardium the gadolinium contrast kinetics are altered, secondary to changes in distribution volume and/or wash-out of gadolinium. For the diagnosis of focal myocardial disease, such as necrosis/fibrosis, contrast-enhanced imaging using fast gradient-echo sequences with a preparatory inversion pulse [the so-called “late gadolinium enhancement” (LGE) or “delayed enhancement” technique] have been shown to be of great value . Although initially applied to depict myocardial necrosis/fibrosis in the setting of acute or chronic myocardial infarction, the LGE MRI technique allows several non-ischaemic patterns of myocardial enhancement to be described in a wide range of myocardial diseases . A weakness of the LGE MRI technique, however, is that it is optimised for depicting focal myocardial pathological conditions, and therefore it may fail to show diffusely spread disease, such as diffuse myocardial fibrosis, found in patients with DCM . Comparing global myocardial enhancement with skeletal muscle enhancement early after gadolinium administration is of use to depict generalised myocardial hyperaemia, which can be found in patients with myocardial inflammation not only in the acute phase but also in chronic forms of myocarditis (Fig. 5) [27, 28]. Besides, myocardial T1 mapping techniques are appealing for the depiction of diffuse myocardial fibrosis, and represent a valuable addition to the LGE MRI technique. Shortening of the myocardial T1 relaxation time is related to the amount of myocardial collagen deposition [26, 29, 30]. Performing fast gradient-echo sequences using multiple increasing inversion times (e.g. 50–1,000 ms) before and after contrast-medium administration at the blood/myocardium equilibrium phase, allows the decay in myocardial signal intensity to be measured, and T1 maps to be generated with the use of curve fitting techniques (Movie 2). Although this technique is promising, further investigation is needed to test its robustness in assessing patients in mainstream clinical practice. Finally, a free bonus of the LGE MRI technique is that concomitant cardiac disease, such as pericardial inflammation or thrombus formation, can be accurately depicted as well [31–33].
Even if MDCT is not yet considered as a first-line imaging technique for the evaluation of LV performance and volumes, it is important to mention that in patients undergoing an MDCT examination for coronary artery evaluation, reliable information about cardiac morphology and function can be obtained without any additional radiation exposure [34–37]. Although nowadays the prospective trigger mode is preferable because of the significant reduction in irradiation dose, reliable data regarding ventricular volumes and function can be obtained using retrospective electrocardiogram (ECG) gating. Several papers reported good agreement among MDCT and echocardiography, and MRI and invasive catheter ventriculography, with good interobserver agreement [38–41].
As the LV ejection fraction is the strongest prognostic determinant in heart failure patients, while LV volume and mass are independent predictors of mortality and morbidity, a first primordial step in assessing DCM patients is the reliable quantification of the severity of chamber dilatation and dysfunction. Often stroke volumes are within normal limits or only modestly decreased despite the severely impaired ejection fraction. The LV enlargement may furthermore dilate the mitral valve ring, dislocate the papillary muscles, and impair leaflet coaption, thereby causing mitral valve regurgitation and putting additional load on the already diseased ventricle (Fig. 1). Except for mildly dilated forms of DCM, the LV and/or RV show a moderate to severe degree of dilatation with a severely impaired ejection fraction (e.g. lower than 20%) (Figs. 1 and 3). The volumetric measurement of the ventricles is usually performed in the cardiac short-axis plane (MRI) or using reconstructed images in the cardiac short-axis plane (MDCT). For MDCT evaluation of LV function, end-diastole is usually identified as the image with the maximum diameter (approximately at 85% of RR diameter), while the minimum diameter (about 25% of RR) corresponds to end-systole. Software has been developed to semi-automatically determine ventricular volumes and function, and myocardial mass.
In DCM patients, the atria may be enlarged as well, but this is usually less pronounced than the ventricular dilatation. Left atrial dilatation can be related to mitral valve regurgitation and/or to increased LV filling pressure, emphasising the need for assessment of diastolic (dys)function in DCM patients. Phase-contrast (or velocity-encoded) cine MRI is an accurate technique for quantifying the severity of valve regurgitation and for providing information on diastolic function. Although MDCT can provide MR-equivalent high-quality morphological views of the mitral valve, and even show valve motion, it provides no or at most limited information regarding the severity of regurgitation. However, the superb morphological visualisation of the mitral valve and subvalvular apparatus provide a means of better characterising the mechanism(s) of mitral valve regurgitation. Moreover, slow or turbulent flow in dilated cavities facilitates thrombus formation. Both MRI and MDCT can be regarded as excellent tools for depicting this potentially harmful complication (Fig. 7).
Myocardial contraction abnormalities are invariably present in DCM patients, visible as hypokinetic to dyskinetic wall motion, diminished to absent systolic wall thickening, and a variable degree of ventricular dyssynchrony often with abnormal systolic motion of the interventricular septum and apical rocking (Movie 3). Cine MRI is without any doubt the reference tool for assessing myocardial wall motion and thickening patterns, and has potential in the assessment of ventricular dyssynchrony. Regional abnormalities are usually described using the 17-segment AHA approach.
Accurate myocardial tissue characterisation is pivotal in DCM patients. For example, as reported by Bello et al. , the response to b-blockade therapy was significantly better with functional improvement and reversed ventricular remodelling in heart failure patients without evidence of myocardial scarring by LGE MRI than those with myocardial scarring. A first aim is to exclude myocardial damage due to CAD as the underlying cause of ventricular dilatation and dysfunction [43–45]. The presence and pattern of myocardial LGE provides crucial information regarding the ischaemic or non-ischaemic origin. Ischaemic LGE involves the subendocardium with a variable transmural extension in a coronary artery perfusion territory (Fig. 8). In non-CAD-related DCM, myocardial LGE presents most commonly as a linear or patchy midwall enhancement. It may involve the subepicardial part of the myocardium and the right ventricle as well, and importantly it does not respect a perfusion territory (Fig. 3) [44–46]. It should be emphasised, however, that most DCM patients present no myocardial LGE . Finally, a small percentage of DCM patients show a CAD-like pattern of enhancement, despite a lack of obstructive CAD on coronary angiography. A likely hypothesis is that these patients had concomitant CAD with recanalisation of the occlusive coronary artery or had an embolic event. Ventricular remodelling and dysfunction will be influenced significantly by the extent of CAD-related myocardial scarring. Although use of MDCT has been reported to depict CAD-related myocardial scarring in chronic infarct patients, currently this application is not routinely used .
Although LGE MRI is able to depict subtle forms of myocardial scarring (<1 g) , this sequence is of limited value in depicting diffuse myocardial fibrosis, probably explaining why most DCM patients in the study by McCrohon et al.  showed normal LGE MRI. Recently, substantial progress has been made with the development of myocardial T1 mapping techniques. Diffuse collagen deposition increases the extracellular space, causing an increased interstitial accumulation of gadolinium at steady state, thus reducing the myocardial T1 relaxation time [26, 29, 30, 49, 50]. Several groups have reported in DCM patients a tight relation between the expansion in extracellular space (reflecting myocardial fibrosis) and the impairment in myocardial blood flow, ventricular dilatation and ventricular dysfunction [29, 50–52].
It is believed that approximately 5-10% of patients with acute myocarditis progress towards DCM and ultimately will need cardiac transplantation [1, 53]. While the role of MRI in the diagnosis of acute myocarditis is well established, with recently published recommendations by an expert committee (“Lake Louise Criteria”) , the role of MRI in chronic myocarditis is less well defined, but is probably important because patients with DCM secondary to chronic myocarditis may show a favourable response to immunomodulatory therapy. De Cobelli et al.  reported in patients with biopsy-proven chronic myocarditis a similar focal pattern of enhancement as in patients with acute myocarditis in up to 70% of a group of patients with chronic inflammation at endomyocardial biopsy. Moreover, patients with persistent chronic myocarditis frequently showed generalised myocardial oedema and increase in global myocardial enhancement. On the other hand, focal myocardial LGE, probably reflecting myocardial scarring, had low sensitivity and specificity in depicting chronic myocarditis [28, 55]. Finally, Mahrholdt et al.  evaluated patients with acute myocarditis at the 3-month follow-up and reported a significant reduction in the extent of midwall/subepicardial focal myocardial enhancement representing residual inflammation or fibrotic scarring.
In DCM patients, myocardial trabeculations, along the LV free wall, often appear more prominent than in healthy subjects . The exact mechanism is unclear but may represent a compensatory phenomenon. Differentiation between DCM and left ventricular non-compaction cardiomyopathy (LVNC) may be challenging, especially in mild forms of LVNC (Fig. 9) [57, 58]. Nowadays recognised as a distinct cardiomyopathy, LVNC is thought to be caused by intrauterine arrest of the process of compaction of the loosely interwoven meshwork of myocardial fibres [59, 60]. As a result, LVNC patients present with prominent trabeculations, deep intertrabecular recesses and a thin epicardial compacta. An alternative hypothesis suggests that the prominent trabeculations represent an adaptive mechanism to compensate for abnormally contracting myocardium . Most commonly, the apical and midventricular part of the inferior and lateral LV wall are affected (Fig. 10) . Attempts to define diagnostic morphological criteria for LVNC have been shown to be challenging, mainly due to the lack of an easy-to-use parameter enabling the differentiation of LVNC patients from normal subjects or other disease entities [61–63]. In brief, criteria have been defined taking into account the two-layered appearance of the myocardial wall, the ratio of non-compacted to compacted myocardium, the number of visible trabeculations apically to the papillary muscles, and the presence of deep intertrabecular spaces visualised on colour Doppler imaging. In a recent study by Kohli and co-workers, it was shown that these diagnostic criteria are likely too sensitive with up to a quarter of heart failure patients and 8% of control subjects fulfilling one or more criteria for LVNC [64, 65]. On the other hand, other papers, including MRI findings, suggest that the echocardiographic criteria might be too strict, and that techniques such as MRI may enhance detection of more subtle forms of LVNC [60, 66, 67]. The superior spatial and contrast resolution of MRI makes this technique appealing for the detection of LVNC. The location and extent of the trabecular network, and the thickness of the trabeculations and compacta can be well visualised using a combination of cine MRI in different cardiac imaging planes. In addition, these sequences allow the impact of morphological abnormalities on regional and global function to be assessed. LGE MRI may reveal underlying myocardial disease such as replacement fibrosis [68, 69]. In 2005, Petersen et al.  established MRI criteria for the diagnosis of LVNC, similar to the above-mentioned echocardiographic criteria. An NC/C ratio >2.3 in diastole distinguished LVNC from normals, athletes and a series of cardiac diseases with a sensitivity and specificity of 86 and 99% respectively. Jacquier et al.  proposed to quantify the percentage of trabeculated LV myocardium, and reported in normals 12 ± 5% trabeculated myocardium vs 32 ± 10% in LVNC patients. Although promising, the applicability of the above MRI criteria in daily clinical practice needs further confirmation.
Obstructive CAD may cause myocardial ischaemia and dysfunction, and initiate compensatory ventricular remodelling with progressive dilatation, which ultimately may lead to ischaemic heart failure (Fig. 8). The crucial question to solve in these patients is whether percutaneous or surgical coronary revascularisation will improve function in the dysfunctional regions and ultimately improve patient outcome . As the myocardial substrate underlying the dysfunction in the setting of CAD is heterogeneous, including stunned, ischaemic, hibernating, necrotic and scarred myocardium, the goal of myocardial viability assessment is to determine the ischaemic substrate. It is important to emphasise that different ischaemic substrates can be present within the same coronary perfusion territory [73, 74]. Only the viable substrates may recover function following reperfusion. Even if there are not yet any prospectively controlled studies on the effects of revascularisation, there is a substantial amount of clinical evidence that patients with reversible LV dysfunction may benefit from a revascularisation procedure [75, 76].
The role of MDCT in these patients is mainly focused on visualisation of coronary artery plaques, but no information is provided regarding the viability of the myocardium downstream of the coronary atherosclerotic plaque. MRI is nowadays emerging as one of the preferential techniques for characterising the ischaemic substrate and determining myocardial viability. Three different approaches, or a combination of approaches, can be used for MRI myocardial viability assessment, i.e. end-diastolic wall thickness, contractility reserve and scar imaging (Fig. 11). First, measurement of end-diastolic wall thickness relies on the premise that infarction with subsequent scarring leads to wall thinning, and the magnitude of wall thinning is related to the degree of infarct transmurality [77, 78]. A wall thickness of 6 mm has been proposed as a cut-off to differentiate between non-viable and viable segments. This approach has excellent sensitivity (95%, range 94-100%), but poor specificity (41%, range 19-53%) for predicting functional recovery [76–79]. Patients may present “preserved” segmental wall thickness but not recover function following revascularisation, which is probably caused by the presence of subendocardial scarring in this segment. For this reason, the use of the thickness of the non-enhanced rim on LGE MRI may be superior to end-diastolic wall thickness in predicting recovery . Contractile reserve assessment, using low-dose dobutamine stress MRI is the second approach to assessing myocardial viability. Whereas the contractility of normal viable myocardium increases during dobutamine stress, the response of ischaemic, dysfunctional myocardial segments depends on the myocardial substrate (Fig. 12) [78, 81–83]. This approach has good specificity (83%, range 70-95%) but moderate sensitivity (74%, range 50-89%) [68–71]. The third approach relies on the use of LGE MRI to depict the presence and transmural extent of myocardial scarring. Lack of myocardial LGE in dysfunctional myocardium is indicative of viability, and these segments have a high probability of functional recovery post-revascularisation. On the other hand, the probability of functional recovery is inversely related to the transmural extent of myocardial LGE [84, 85]. Despite excellent sensitivity (95%, range 91–99%), LGE MRI has low specificity (45%, range 37–54%). In particular, for subendocardial infarcts, LGE MRI does not provide information on whether the non-enhanced epicardial rim contains normal, viable or jeopardised myocardium . In order to increase diagnostic accuracy, an integrated MRI approach can be used. For instance, adding low-dose dobutamine stress MRI in a second step after LGE MRI may be helpful in determining the myocardial substrate of the non-enhanced epicardial rim. As mentioned above, determining the thickness of the non-enhanced epicardial rim may provide additional value regarding viability  with a cut-off value of 3 mm yielding good diagnostic accuracy for the differentiation between viable and non-viable segments.
As sudden cardiac death due to ventricular arrhythmias may be the first clinical manifestation of DCM, identification of patients at risk who may benefit from implantable cardioverter defibrillator (ICD) implantation or from an ablation procedure is of primordial importance. Several papers have shown that non-ischaemic cardiomyopathy patients with midwall myocardial LGE involving more than 25% of wall thickness are at high risk at inducible ventricular tachycardia and should be referred for definitive anti-arrhythmic device therapy [86–89]. LGE MRI adds predictive value especially in the DCM patients with a mildly to moderately decreased ejection fraction, those with abnormal myocardial enhancement having potential benefit from prophylactic ICD placement . In a recent study by Hombach et al.  that included 141 DCM patients, midwall myocardial LGE was not an independent prognostic factor, stressing the need for large prospective studies on this topic . Bogun et al. used LGE MRI to plan an appropriate mapping and ablation strategy in a small group of DCM patients . The location of the scar (endocardial versus epicardial) was an important factor in determining the optimal approach to ablation. However, the success of catheter ablation was low in patients with a scar located in the midwall.
In patients with DCM, ventricular dilatation and replacement fibrosis lead to a heterogeneous excitation spread across the LV wall with a delay in intraventricular conduction and a left bundle branch block morphology on the ECG. Segmental wall motion analysis shows hypokinesis to dyskinesis with a variable degree of dyssynchrony [92, 93]. Ventricular dyssynchrony worsens systolic performance, impedes ventricular filling, and causes paradoxical septal motion during early systole. Cardiac resynchronisation therapy (CRT) consists of the implantation of a biventricular pacemaker in order to improve synchronicity of myocardial contraction leading to improved ventricular performance. In properly selected patients, CRT implantation is associated with improvement of symptoms and a decrease in mortality and hospitalisation for heart failure. However, up to 40% of CRT-treated patients show no benefit from CRT, urging the need for better identification of responders to CRT treatment.
MRI is a promising tool for identifying and selecting patients eligible for CRT [93, 94]. MRI has the advantage of integrating functional/dyssynchrony imaging with morphological and tissue characterisation imaging. Novel MRI techniques such as DENSE (displacement encoding with stimulated echoes) and TVM (tissue velocity mapping) are appealing for the quantification of the degree of dyssynchrony throughout the LV. In addition, LGE MRI enables the depiction of myocardial scar presence and extent. The higher the scar burden, the lower the chance of CRT response [95–97]. Moreover, as reported by Chalil et al.  correct placement of CRT leads is crucial. Positioning of the pacing lead in the scarred myocardium is followed by a lack of CRT response. MRI is currently the best technique for guiding the interventional cardiologist to correctly position CRT leads. The lead should be placed in the myocardium displaying the latest activation. On the other hand, scar stimulation by pacing prevents correct impulse transmission, and consequent inhibition of myocardial contractility.
Another clinically relevant application for MRI and MDCT is the identification of coronary venous anatomy (Fig. 13). In particular, MDCT is a fast and very useful technique in CRT therapy planning. As mentioned above, CRT leads should be placed in the area of latest activation. Once this has been identified, visualisation of the vein tributary to that segment is mandatory. If there is no evidence of a coronary vein on MDCT/MRI in these segments, the transvenous approach is not recommended because it would result in an erroneous lead placement. In these cases, a surgical approach with epicardial lead positioning is preferable. The efficacy of MDCT in depicting coronary venous anatomy, including anatomical variants, is excellent, showing good agreement with anatomical studies and invasive venography [99, 100].
As previously mentioned, the ventricular dilatation associated with systolic dysfunction can be due to DCM or secondary to coronary artery disease. In the last two decades, coronary artery imaging by MRI and MDCT has been extensively studied as an alternative to invasive catheter angiography. Despite high initial expectations, it has nowadays become evident that MRI has a limited role in depicting coronary artery plaques . Supported by encouraging results of several single-centre and multicentre trials, MDCT is now considered a reliable method for the detection and, in particular, for the exclusion of CAD [12, 102]. However, it should be emphasised that MDCT still faces many challenges, in particular imaging of heavily calcified plaques and stent imaging, although further improvement can be expected with newer generation equipment .
In the end, the role of an imaging method is to provide accurate information for the clinician, to minimise the degree of uncertainty in the diagnosis and patient management, and to improve patient outcome. MRI is becoming generally accepted as an important imaging technique in patients with DCM offering the clinician not only accurate information regarding the severity of ventricular dilatation and dysfunction but also regarding myocardial tissue composition, which is important in establishing the underlying cause, in predicting the risk of future events, and in selecting eligible candidates for CRT. The fast and continuous progress in MDCT technology has enabled accurate information regarding coronary artery and venous anatomy to be provided, but this technique has the potential to offer a broader cardiac assessment, including tissue characterisation and functional assessment.
Movie 1 Extreme form of DCM in a 63-year-old man (WMV 168 kb)13244_2011_101_MOESM1_ESM.wmv
Movie 2 Example of the Lock-Looker sequence obtained in the midventricular short-axis plane to derive a myocardial T1 map in a patient with DCM (courtesy of P.G. Masci, Pisa, Italy) (AVI 16612 kb)13244_2011_101_MOESM2_ESM.avi
Movie 3 Severe DCM in a 63-year-old man. SSFP cine MRI in the horizontal long-axis plane shows severe LV dilatation (end-diastolic volume: 549 ml) with moderately severe global dysfunction (ejection fraction: 28%). Right-sided systolic shift of the interventricular septum with an apical rocking motion reflecting LV dyssynchrony (WMV 223 kb)13244_2011_101_MOESM3_ESM.wmv
Elliott P, Andersson B, Arbustini E et al (2008) Classification of the cardiomyopathies: a position statement from the European Society of Cardiology working group on myocardial and pericardial diseases. Eur Heart J 29:270–276 PubMed
Jefferies JL, Towbin JA (2010) Dilated cardiomyopathy. Lancet 375:752–762 PubMed
Charron P, Arad M, Arbustini E et al (2010) Genetic counseling and testing in cardiomyopathies: a position statement of the European Society of Cardiology Working Group on Myocardial and Pericardial Diseases. Eur Heart J 31:2715–2726 PubMed
Dec GW, Fuster V (1994) Idiopathic dilated cardiomyopathy. N Engl J Med 331:1564–1574 PubMed
Fujita N, Duerinckx AJ, Higgins CB (1993) Variation in left ventricular regional wall stress with cine magnetic resonance imaging: normal subjects versus dilated cardiomyopathy. Am Heart J 125:1337–1345 PubMed
Beltrami CA, Finato N, Rocco M et al (1995) The cellular basis of dilated cardiomyopathy in humans. J Mol Cell Cardiol 27:291–305 PubMed
de Leeuw N, Ruiter DJ, Balk AH (2001) Histopathologic findings in explanted heart tissue from patients with end-stage idiopathic dilated cardiomyopathy. Transpl Int 14:299–306 PubMed
Sun JP, James KB, Yang XS et al (1997) Comparison of mortality rates and progression of left ventricular dysfunction in patients with idiopathic dilated cardiomyopathy and dilated versus nondilated right ventricular cavities. Am J Cardiol 80:1583–1587 PubMed
Leschka S, Alkadhi H, Plass A et al (2005) Accuracy of MSCT coronary angiography with 64-slice technology: first experience. Eur Heart J 26:1482–1487 PubMed
Budoff MJ, Dowe D, Jollis JG et al (2008) Diagnostic performance of 64-multidetector row coronary computed tomographic angiography for evaluation of coronary artery stenosis in individuals without known coronary artery disease: results from the prospective multicenter ACCURACY (Assessment by Coronary Computed Tomographic Angiography of Individuals Undergoing Invasive Coronary Angiography) trial. J Am Coll Cardiol 52:1724–1732 PubMed
Dewey M, Zimmermann E, Deissenrieder F et al (2009) Noninvasive coronary angiography by 320-row computed tomography with lower radiation exposure and maintained diagnostic accuracy: comparison of results with cardiac catheterization in a head-to-head pilot investigation. Circulation 120:867–875 PubMed
Mark DB, Berman DS, Budoff MJ et al (2010) ACCF/ACR/AHA/NASCI/SAIP/ SCAI/SCCT 2010 expert consensus document on coronary computed tomographic angiography: a report of the American College of Cardiology Foundation Task Force on Expert Consensus Documents. Circulation 121:2509–2543 PubMed
Semelka RC, Tomei E, Wagner S et al (1990) Interstudy reproducibility of dimensional and functional measurements between cine magnetic resonance studies in the morphologically abnormal left ventricle. Am Heart J 119:1367–1373 PubMed
Buser PT, Wagner S, Auffermann W et al (1990) Three-dimensional analysis of the regional contractility of the normal and the cardiomyopathic left ventricle using cine-magnetic resonance imaging. Z Kardiol 79:573–579 PubMed
Gaudio C, Tanzilli G, Mazzarotto P et al (1991) Comparison of left ventricular ejection fraction by magnetic resonance imaging and radionuclide ventriculography in idiopathic dilated cardiomyopathy. Am J Cardiol 67:411–415 PubMed
Strohm O, Schulz-Menger J, Pilz B et al (2001) Measurement of left ventricular dimensions and function in patients with dilated cardiomyopathy. J Magn Reson Imaging 13:367–371 PubMed
MacGowan GA, Shapiro EP, Azhari H et al (1997) Shortening in the fiber and cross-fiber directions in the normal human left ventricle and in idiopathic dilated cardiomyopathy. Circulation 96:535–541 PubMed
Abdel-Aty H, Boyé P, Zagrosek A et al (2005) Diagnostic performance of cardiovascular magnetic resonance in patients with suspected acute myocarditis. Comparison of different approaches. J Am Coll Cardiol 45:1815–1822 PubMed
Tanner MA, Galanello R, Dessi C et al (2007) A randomized, placebo-controlled, double-blind trial of the effect of combined therapy with deferoxamine and deferiprone on myocardial iron in thalassemia major using cardiovascular magnetic resonance. Circulation 115:1876–1884 PubMed
Simonetti OP, Kim RJ, Fieno DS et al (2001) An improved MR imaging technique for the visualization of myocardial infarction. Radiology 218:215–223 PubMed
Mahrholdt H, Wagner A, Judd RM et al (2005) Delayed enhancement cardiovascular magnetic resonance assessment of non-ischaemic cardiomyopathies. Eur Heart J 26:1461–1474 PubMed
Iles L, Pfluger H, Phrommintikul A et al (2008) Evaluation of diffuse myocardial fibrosis in heart failure with cardiac magnetic resonance contrast-enhanced T1 mapping. J Am Coll Cardiol 52:1574–1580 PubMed
Gutberlet M, Spors B, Thoma T et al (2008) Suspected chronic myocarditis at cardiac MR: diagnostic accuracy and association with immunohistologically detected inflammation and viral persistence. Radiology 246:401–409 PubMed
Flett AS, Hayward MP, Ashworth MT et al (2010) Equilibrium contrast cardiovascular magnetic resonance for the measurement of diffuse myocardial fibrosis: preliminary validation in humans. Circulation 122:138–144 PubMed
Mollet NR, Dymarkowski S, Volders W et al (2002) Visualization of ventricular thrombi with contrast-enhanced MRI in patients with ischemic heart disease. Circulation 106:2873–2876 PubMed
Bogaert J, Taylor AM, Van Kerckhove F et al (2004) Use of inversion-recovery contrast-enhanced MRI technique for cardiac imaging: spectrum of diseases. AJR Am J Roentgenol 182:609–615 PubMed
de Roos A, Kroft LJ, Bax JJ et al (2006) Cardiac applications of multislice computed tomography. Br J Radiol 79:9–16 PubMed
Juergens KU, Fischbach R (2006) Left ventricular function studied with MDCT. Eur Radiol 16:342–357 PubMed
Schroeder S, Achenbach S, Bengel F et al (2008) Cardiac computed tomography: indications, applications, limitations, and training requirements: report of a Writing Group deployed by the Working Group Nuclear Cardiology and Cardiac CT of the European Society of Cardiology and the European Council of Nuclear Cardiology. Eur Heart J 29:531–556 PubMed
Abadi S, Roguin A, Engel A et al (2010) Feasibility of automatic assessment of four-chamber cardiac function with MDCT: initial clinical application and validation. Eur J Radiol 74:175–181 PubMed
Taylor AJ, Cerqueira M, Hodgson JM et al (2010) ACCF/ SCCT/ ACR/ AHA/ ASE/ ASNC/ NASCI/ SCAI/ SCMR 2010 appropriate use criteria for cardiac computed tomography: a report of the American College of Cardiology Foundation Appropriate Use Criteria Task Force, the Society of Cardiovascular Computed Tomography, the American College of Radiology, the American Heart Association, the American Society of Echocardiography, the American Society of Nuclear Cardiology, the North American Society for Cardiovascular Imaging, the Society for Cardiovascular Angiography and Interventions, and the Society for Cardiovascular Magnetic Resonance. J Am Coll Cardiol 56:1864–1894 PubMed
Wu YW, Tadamura E, Yamamuro M et al (2008) Estimation of global and regional cardiac function using 64-slice computed tomography: a comparison study with echocardiography, gated-SPECT and cardiovascular magnetic resonance. Int J Cardiol 128:69–76 PubMed
Thilo C, Hanley M, Bastarrika G et al (2010) Integrative computed tomographic imaging of cardiac structure, function, perfusion, and viability. Cardiol Rev 18:219–229 PubMed
Vural M, Uçar O, Selvi NA et al (2010) Assessment of global left ventricular systolic function with multidetector CT and 2D echocardiography: a comparison between reconstructions of 1-mm and 2-mm slice thickness at multidetector CT. Diagn Interv Radiol 16:236–240 PubMed
Bello D, Shah DJ, Farah GM (2003) Gadolinium cardiovascular magnetic resonance predicts reversible myocardial dysfunction and remodeling in patients with heart failure undergoing β-blocker therapy. Circulation 108:1945–1953 PubMed
Koito H, Suzuki J, Ohkubo N et al (1996) Gadolinium-diethylenetriamine pentaacetic acid enhanced magnetic resonance imaging of dilated cardiomyopathy: clinical significance of abnormally high signal intensity of left ventricular myocardium. J Cardiol 28:41–49 PubMed
Wu E, Judd RM, Vargas JD et al (2001) Visualization of the presence, location and transmural extent of healed Q-wave and non-Q-wave myocardial infarction. Lancet 357:21–28 PubMed
McCrohon JA, Moon JCC, Prasad SK et al (2003) Differentiation of heart failure related to dilated cardiomyopathy and coronary artery disease using gadolinium-enhanced cardiovascular magnetic resonance. Circulation 108:54–59 PubMed
Soriano CJ, Ridocci F, Estornell J et al (2005) Noninvasive diagnosis of coronary artery disease in patients with heart failure and systolic dysfunction of uncertain etiology, using late gadolinium-enhanced cardiovascular magnetic resonance. J Am Coll Cardiol 45:743–748 PubMed
Nikolaou K, Knez A, Sagmeister S et al (2004) Assessment of myocardial infarctions using multidetector-row computed tomography. J Comput Assist Tomogr 28:286–292 PubMed
Wagner A, Schulz-Menger J, Dietz R et al (2003) Long-term follow-up of patients with acute myocarditis by magnetic resonance imaging. Magma 16:17–20 PubMed
Sueyoshi E, Sakamoto I, Uetani M (2010) Contrast-enhanced myocardial inversion time at the null point for detection of left ventricular myocardial fibrosis in patients with dilated and hypertrophic cardiomyopathy: a pilot study. AJR Am J Roentgenol 194:293–298
Knaapen P, Götte MJW, Paulus WJ et al (2006) Does myocardial fibrosis hinder contractile function and perfusion in idiopathic dilated cardiomyopathy? PET and MR imaging study. Radiology 240:380–388 PubMed
Mahrholdt H, Goedecke C, Wagner A et al (2004) Cardiovascular magnetic resonance assessment of human myocarditis. A comparison to histology and molecular biology. Circulation 109:1250–1258 PubMed
De Cobelli F, Pieroni M, Esposito A et al (2006) Delayed gadolinium-enhanced cardiac magnetic resonance in patients with chronic myocarditis presenting with heart failure or recurrent arrhythmias. J Am Coll Cardiol 47:1649–1654 PubMed
Voigt A, Elgeti T, Durmus T et al (2011) Cardiac magnetic resonance imaging in dilated cardiomyopathy in adults—towards identification of myocardial inflammation. Eur Radiol 21:925–935 PubMed
Imai H, Kumai T, Sekiya M et al (1992) Left ventricular trabeculae evaluated with MRI in dilated cardiomyopathy and old myocardial infarction. J Cardiol 22:83–90 PubMed
Richardson P, McKenna W, Bristow M et al (1996) Report of the 1995 World Health Organization/International Society and Federation of Cardiology Task Force on the Definition and Classification of Cardiomyopathies. Circulation 93:841–842 PubMed
Maron BJ, Towbin JA, Thiene G et al (2006) Contemporary definitions and classification of the cardiomyopathies: an American Heart Association Scientific Statement from the Council on Clinical Cardiology, Heart Failure and Transplantation Committee; Quality of Care and Outcomes Research and Functional Genomics and Translational Biology Interdisciplinary Working Groups; and Council on Epidemiology and Prevention. Circulation 113:1807–1816 PubMed
Elshershari H, Okutan V, Celiker A (2001) Isolated noncompaction of the ventricular myocardium. Cardiol Young 11:472–475 PubMed
Pignatelli RH, McMahon CJ, Dreyer WJ et al (2003) Clinical characterization of left ventricular noncompaction in children. A relatively common form of cardiomyopathy. Circulation 108:2672–2678 PubMed
Captur G, Nihoyannopoulos P (2010) Left ventricular non-compaction: genetic heterogeneity, diagnosis and clinical course. Int J Cardiol 140:145–153 PubMed
Oechslin EN, Attenhofer Jost CH, Rojas JR et al (2000) Long-term follow-up of 34 adults with isolated left ventricular noncompaction: a distinct cardiomyopathy with poor prognosis. J Am Coll Cardiol 36:493–500 PubMed
Belanger AR, Miller MA, Donthireddi UR et al (2008) New classification scheme of left ventricular noncompaction and correlation with ventricular performance. Am J Cardiol 102:92–96 PubMed
Kohli SK, Pantazis AA, Shah JS et al (2008) Diagnosis of left-ventricular non-compaction in patients with left-ventricular systolic dysfunction: time for a reappraisal of diagnostic criteria? Eur Heart J 29:89–95 PubMed
Anderson RH (2008) Ventricular non-compaction—a frequently ignored finding? Eur Heart J 29:10–11 PubMed
McCrohon JA, Richmond DR, Pennell DJ et al (2002) Isolated noncompaction of the myocardium. A rarity or missed diagnosis? Circulation 106:e22–e23 PubMed
Borreguero LJJ, Corti R, de Soria RF et al (2002) Diagnosis of isolated noncompaction of the myocardium by magnetic resonance imaging. Circulation 105:e177–e178 PubMed
Dodd JD, Holmvang G, Hoffmann U et al (2007) Quantification of left ventricular noncompaction and trabecular delayed hyperenhancement with cardiac MRI: correlation with clinical severity. AJR Am J Roentgenol 189:974–980 PubMed
Alsaileek AA, Syed I, Seward JB et al (2008) Myocardial fibrosis of left ventricle: magnetic resonance imaging in noncompaction. J Magn Reson Imaging 27:621–624 PubMed
Petersen SE, Selvanayagam JB, Francis JM et al (2005) Differentiation of athlete’s heart from pathological forms of cardiac hypertrophy by means of geometric indices derived from cardiovascular magnetic resonance. J Cardiovasc Magn Reson 7:551–558 PubMed
Jacquier A, Thuny F, Jop B et al (2010) Measurement of trabeculated left ventricular mass using cardiac magnetic resonance imaging in the diagnosis of left ventricular non-compaction. Eur Heart J 31:1098–1104 PubMed
Underwood SR, Bax JJ, vom Dahl J et al (2004) Imaging techniques for the assessment of myocardial hibernation. Report of a Study Group of the European Society of Cardiology. Eur Heart J 25:815–836 PubMed
Wu M, Bogaert J, D’hooge J et al (2010) Closed-chest animal model of chronic coronary artery stenosis. Assessment with magnetic resonance imaging. Int J Cardiovasc Imaging 26:299–308 PubMed
Wu M, D’hooge J, Ganame J et al (2010) Non-invasive characterization of the area-at-risk using magnetic resonance imaging in chronic ischemia. Cardiovasc Res 89:166–174 PubMed
Bax JJ, Visser FC, Poldermans D et al (2001) Time course of functional recovery of stunned and hibernating segments after surgical revascularization. Circulation 104:I314–I318 PubMed
Schinkel AF, Bax JJ, Poldermans D et al (2007) Hibernating myocardium: diagnosis and patient outcomes. Curr Probl Cardiol 32:375–410 PubMed
Baer FM, Smolarz K, Jungehulsing M et al (1992) Chronic myocardial infarction: assessment of morphology, function, and perfusion by gradient echo magnetic resonance imaging and 99mTc-methoxyisobutyl-isonitrile SPECT. Am Heart J 123:636–645 PubMed
Baer FM, Voth E, Schneider C et al (1995) Comparison of low-dose dobutamine-gradient-echo magnetic resonance imaging and positron emission tomography with [18F]fluorodeoxyglucose in patients with chronic coronary artery disease. A functional and morphological approach to the detection of residual myocardial viability. Circulation 91:1006–1015 PubMed
Kühl HP, van der Weerdt A, Beek A et al (2006) Relation of end-diastolic wall thickness and the residual rim of viable myocardium by magnetic resonance imaging to myocardial viability assessed by fluorine-18 deoxyglucose positron emission tomography. Am J Cardiol 97:452–457 PubMed
Dendale PAC, Franken RP, Waldmann GJ et al (1995) Low-dosage dobutamine magnetic resonance imaging as an alternative to echocardiography in the detection of viable myocardium after acute infarction. Am Heart J 130:134–140 PubMed
Dendale P, Franken PR, van der Wall EE et al (1997) Wall thickening at rest and contractile reserve early after myocardial infarction: correlation with myocardial perfusion and metabolism. Coron Artery Dis 8:259–264 PubMed
Senior R, Lahiri A (1995) Enhanced detection of myocardial ischemia by stress dobutamine echocardiography utilizing the “biphasic” response of wall thickening during low and high dose dobutamine infusion. J Am Coll Cardiol 26:26–32 PubMed
Kim RJ, Wu E, Rafael A et al (2000) The use of contrast-enhanced magnetic resonance imaging to identify reversible myocardial dysfunction. N Engl J Med 343:1445–1453 PubMed
Ramani K, Judd RM, Holly TA (1998) Contrast magnetic resonance imaging in the assessment of myocardial viability in patients with stable coronary artery disease and left ventricular dysfunction. Circulation 98:2687–2694 PubMed
Assomull RG, Prasad SK, Lyne J et al (2006) Cardiovascular magnetic resonance, fibrosis, and prognosis in dilated cardiomyopathy. J Am Coll Cardiol 48:1977–1985 PubMed
Shimizu I, Iguchi N, Watanabe H et al (2010) Delayed cardiovascular magnetic resonance as a novel technique to predict cardiac events in dilated cardiomyopathy patients. Int J Cardiol 142:224–229 PubMed
Masci PG, Marinelli M, Piacenti M et al (2010) Myocardial structural, perfusion, and metabolic correlates of left bundle branch block mechanical derangement in patients with dilated cardiomyopathy. A tagged cardiac magnetic resonance and positron emission tomography study. Circ Cardiovasc Imaging 3:482–490 PubMed
Tigen K, Karaahmet T, Kirma C et al (2010) Diffuse late gadolinium enhancement by cardiovascular magnetic resonance predicts significant intraventricular systolic dyssynchrony in patients with non-ischemic dilated cardiomyopathy. J Am Soc Echocardiogr 23:416–422 PubMed
Bleeker GB, Kaandorp TA, Lamb HJ et al (2006) Effect of posterolateral scar tissue on clinical and echocardiographic improvement after cardiac resynchronization therapy. Circulation 113:969–976 PubMed
Marsan NA, Westenberg JJ, Ypenburg C et al (2009) Magnetic resonance imaging and response to cardiac resynchronization therapy: relative merits of left ventricular dyssynchrony and scar tissue. Eur Heart J 30:2360–2367 PubMed
Aggarwal NR, Martinez MW, Gersh BJ et al (2009) Role of cardiac MRI and nuclear imaging in cardiac resynchronization therapy. Nat Rev Cardiol 6:759–770 PubMed
Leyva F (2010) Cardiac resynchronization therapy guided by cardiovascular magnetic resonance. J Cardiovasc Magn Reson 9:12–64
Chalil S, Foley PW, Muyhaldeen SA et al (2007) Late gadolinium enhancement-cardiovascular magnetic resonance as a predictor of response to cardiac resynchronization therapy in patients with ischaemic cardiomyopathy. Europace 9:1031–1037 PubMed
Van de Veire NR, Marsan NA, Schuijf JD et al (2008) Noninvasive imaging of cardiac venous anatomy with 64-slice multi-slice computed tomography and noninvasive assessment of left ventricular dyssynchrony by 3-dimensional tissue synchronization imaging in patients with heart failure scheduled for cardiac resynchronization therapy. Am J Cardiol 101:1023–1029 PubMed
Hundley WG, Bluemke DA, Finn JP et al (2010) ACCF/ACR/AHA/NASCI/SCMR 2010 expert consensus document on cardiovascular magnetic resonance: a report of the American College of Cardiology Foundation Task Force on Expert Consensus Documents. Circulation 121:2462–2508 PubMed
Miller JM, Rochitte CE, Dewey M et al (2008) Diagnostic performance of coronary angiography by 64-row CT. N Engl J Med 359:2324–2336 PubMed
Ehara M, Kawai M, Surmely JF et al (2007) Diagnostic accuracy of coronary in-stent restenosis using 64-slice computed tomography: comparison with invasive coronary angiography. J Am Coll Cardiol 49:951–959 PubMed
- The emerging role of magnetic resonance imaging and multidetector computed tomography in the diagnosis of dilated cardiomyopathy
- Springer Berlin Heidelberg
Neu im Fachgebiet Radiologie
Meistgelesene Bücher aus der Radiologie
e.Med Kampagnen-Visual, Mail Icon II