Submitted Successfully!
To reward your contribution, here is a gift for you: A free trial for our video production service.
Thank you for your contribution! You can also upload a video entry or images related to this topic.
Version Summary Created by Modification Content Size Created at Operation
1
Lorenzo Monti
 -- 2919 2024-01-17 17:39:39 |
2 format correct
Mona Zou
 Meta information modification 2919 2024-01-18 08:37:24 |

Video Upload Options

Do you have a full video?
Send video materials Upload full video

Confirm

Are you sure to Delete?
Yes No
Cite
If you have any further questions, please contact Encyclopedia Editorial Office.
Carrabba, N.; Amico, M.A.; Guaricci, A.I.; Carella, M.C.; Maestrini, V.; Monosilio, S.; Pedrotti, P.; Ricci, F.; Monti, L.; Figliozzi, S.; et al. Cardiac Magnetic Resonance (CMR) Mapping. Encyclopedia. Available online: https://encyclopedia.pub/entry/53984 (accessed on 03 May 2024).
Carrabba N, Amico MA, Guaricci AI, Carella MC, Maestrini V, Monosilio S, et al. Cardiac Magnetic Resonance (CMR) Mapping. Encyclopedia. Available at: https://encyclopedia.pub/entry/53984. Accessed May 03, 2024.
Carrabba, Nazario, Mattia Alexis Amico, Andrea Igoren Guaricci, Maria Cristina Carella, Viviana Maestrini, Sara Monosilio, Patrizia Pedrotti, Fabrizio Ricci, Lorenzo Monti, Stefano Figliozzi, et al. "Cardiac Magnetic Resonance (CMR) Mapping" Encyclopedia, https://encyclopedia.pub/entry/53984 (accessed May 03, 2024).
Carrabba, N., Amico, M.A., Guaricci, A.I., Carella, M.C., Maestrini, V., Monosilio, S., Pedrotti, P., Ricci, F., Monti, L., Figliozzi, S., Torlasco, C., Barison, A., Baggiano, A., Scatteia, A., Pontone, G., & Dellegrottaglie, S. (2024, January 17). Cardiac Magnetic Resonance (CMR) Mapping. In Encyclopedia. https://encyclopedia.pub/entry/53984
Carrabba, Nazario, et al. "Cardiac Magnetic Resonance (CMR) Mapping." Encyclopedia. Web. 17 January, 2024.
Cardiac Magnetic Resonance (CMR) Mapping
Edit
This entry is adapted from the peer-reviewed paper 10.3390/jcm13020337

Cardiac magnetic resonance (CMR) imaging has witnessed substantial progress with the advent of parametric mapping techniques, most notably T1 and T2 mapping. These advanced techniques provide valuable insights into a wide range of cardiac conditions, including ischemic heart disease, cardiomyopathies, inflammatory cardiomyopathies, heart valve disease, and athlete’s heart. Mapping could be the first sign of myocardial injury and oftentimes precedes symptoms, changes in ejection fraction, and irreversible myocardial remodeling. The ability of parametric mapping to offer a quantitative assessment of myocardial tissue properties addresses the limitations of conventional CMR methods, which often rely on qualitative or semiquantitative data. However, challenges persist, especially in terms of standardization and reference value establishment, hindering the wider clinical adoption of parametric mapping. Future developments should prioritize the standardization of techniques to enhance their clinical applicability, ultimately optimizing patient care pathways and outcomes.

cardiac magnetic resonance parametric mapping T1 mapping T2 mapping ischemic heart disease hypertrophic cardiomyopathy dilated cardiomyopathy inflammatory cardiomyopathies aortic valve stenosis athlete’s heart

1. CMR Mapping and Ischemic Heart Disease

The utility of CMR in ischemic heart disease (IHD) is emphasized in the most recent European and US guidelines due to its capacity to assess the entire pathophysiological pathway of the ischemic cascade [1]. It allows for both functional and morphological characterization of the ischemic heart. On one hand, CMR has rapidly become the gold standard for the functional assessment of the heart, providing an optimal evaluation of myocardial kinesis and wall thickening/thinning, and enabling accurate assessments of ventricular volumes and systolic function. On the other hand, the morphological characterization of the heart is crucial in IHD, relying on diagnostic CMR’s capability to detect myocardial edema and ischemic scarring. In addition, the prognostic role of detecting ischemic scarring via CMR is growing, and it may help us to reclassify patients who really need prophylactic implantable-cardioverter defibrillator therapy [2].
T1w and T2w sequences are routinely used for evaluating cardiac morphology/structure and myocardial edema, respectively. Despite their widespread use and widely accepted diagnostic and prognostic value, in both T1w and T2w sequences the signal intensity is represented on an arbitrary scale and cannot be compared among subjects or across serial testing in a single subject. Thus, these sequences allow only for a semiquantitative approach, requiring a normal tissue as a reference (the “remote myocardium”) for the signal quantification of a region of interest, limiting their importance in cases of diffuse disease.
Recognition of edema in myocardial diffuse diseases with CMR remains a major challenge. The quantification of global edema can be evaluated through normalizing the signal to skeletal muscle [3][4]. This approach, optimally obtained using a body coil, provides a signal intensity ratio (T2 SI ratio) and may overcome an important limitation of T2w imaging, i.e., artifacts leading to an artificially low signal intensity of the tissue. The T2 SI ratio does not use low-signal-intensity areas as reference regions and thus is not sensitive to such artifacts. On the other hand, the selection of the skeletal muscle is under the discretion of the reader and thus is often a source of observer bias. Furthermore, different skeletal muscles may be more or less suitable as a reference [5]. In addition, artifacts due to the long acquisition times required can also be limiting. Overall, these challenges can result in insufficient diagnostic value in over 20% of cases [6].
The characterization of necrotic tissue and scars is entrusted to LGE acquisition protocols. The LGE phenomenon is caused by delayed gadolinium washout from the diseased versus healthy myocardium, leading to shortening of the T1 times. As a result, areas with focal fibrosis are notably enhanced, appearing brighter on T1w images. LGE imaging also offers insights into the irreversible damage of the microvascular circulation through visualizing microvascular obstruction (MVO) and intramyocardial hemorrhage (IMH). MVO and IMH can be identified as low or absent signal areas in LGE images, typically located within the central portions of the infarcted tissue. However, even for LGE techniques, there are multiple limitations in the current application: small subendocardial enhancements can sometimes be missed, and quantifying diffuse myocardial involvement (e.g., microscopic fibrosis) is challenging. Furthermore, LGE is sensitive to both motion artifacts and incomplete nulling of the myocardium, and it does not differentiate well between acute and chronic myocardial infarction. Moreover, exact quantification of MVO and IMH is challenging due to the spatial definition of these areas and the need for manual planimetry quantification.
To overcome the limitations of traditional qualitative or semiquantitative measurements in evaluating IHD based on T1w and T2w images, parametric mapping has emerged as a promising tool for myocardial characterization. It can provide additional information through advanced quantification of imaging biomarkers [7]. Firstly, through measuring intrinsic tissue properties, mapping allows for a pixel-wise fitting of each decay curve, enabling direct visualization of tissue MR properties, such as T1, T2, and T2*. Characterizing the myocardium using absolute values (e.g., in milliseconds) eliminates the need for a reference to normal remote tissue. This is a significant advantage in cases of diffuse disease presentation, such as diffuse fibrosis, and in scenarios with large infarcts, where the necrotic area might occasionally be underestimated. The direct quantitative comparison of maps within individuals over time can also aid in differentiating between acute and chronic myocardial infarctions and ischemia-reperfusion injuries [8].
T2 mapping quantitatively evaluates tissue water content, and its sensitivity and specificity for myocardial edema have been well-documented [9]. In fact, both in ST-segment elevation myocardial infarction (STEMI) and non-ST-segment elevation myocardial infarction (NSTEMI), baseline T2 myocardial time is significantly elevated in the infarct zone, decreasing to near-normal values six months after reperfusion. This differentiation of the timing of infarction is achieved with higher diagnostic accuracy than semiquantitative T2w methods [10]. T2 mapping also outperforms T2w imaging in identifying infarct-related arteries and estimating the area of myocardial injury in NSTEMI [11]. Furthermore, both T2 and T1 mapping correlate well with the area at risk (AAR), which is the surrounding zone of a necrotic area where cells can still recover if coronary reperfusion is rapidly established [12]. T2 mapping is also valuable for detecting MVO and IMH, underscoring its role in prognostication after reperfusion therapy [13], even though T2* mapping remains the standard for this quantification. T1 mapping can assess the transmural extent of myocardial infarction thereby differentiating viable from non-viable myocardium without the use of LGE in both acute and chronic myocardial infarction. Moreover, T1 mapping performed better in chronic compared to acute myocardial infarction due to the absence of myocardial edema [14].
Another significant implication is the ability of T1 mapping techniques to visualize permanent myocardial injury [15]. The advantage of performing mapping without the need for contrast agents makes the exam accessible and safe for individuals with chronic kidney disease and allows for multiple acquisitions over time, facilitating patient follow-up. Furthermore, it offers a quantitative method independent of the need for a reference myocardium for comparison, eliminating the manual contouring and semi-automated approaches often used for LGE evaluation. T1 mapping also enables the assessment of forms of diffuse fibrosis that may be missed by conventional approaches [16]. Additionally, T1-mapping protocols allow for the calculation of ECV and the generation of ECV maps, estimated through measuring pre- and post-contrast relaxivity changes adjusted via hematocrit, serving as a surrogate for diffuse myocardial fibrosis.

2. CMR Mapping and Cardiomyopathies

Cardiomyopathies constitute a heterogeneous group of myocardial disorders, demanding a comprehensive approach to their diagnosis. As emphasized by the latest ESC guidelines [17], CMR plays a pivotal role in the non-invasive assessment of cardiomyopathies, offering unparalleled insights into their pathophysiology and facilitating early diagnoses and personalized treatment strategies. In particular, CMR parametric mapping can visualize any change in myocardial composition spacing, from evaluation of cardiomyocyte intracellular deposits (e.g., iron overload in hemochromatosis, or glycosphingolipid in Anderson–Fabry disease) to extracellular modifications of the interstitium (e.g., myocardial fibrosis or accumulation of collagen or amyloid proteins) [18]. This multifaceted approach provides invaluable insights into the pathological processes at play, offering a level of detail that was previously attainable only through invasive histological examinations.
In the realm of hypertrophic cardiomyopathy (HCM) research, cardiac MRI stands as a valuable tool for comprehensively characterizing the heart. It’s widely acknowledged for its ability to assess critical parameters, such as myocardial thickness, extracellular volume (ECV), and regional strain, all of which play pivotal roles in understanding this condition. Notably, T2 mapping has emerged as an essential component in assessing the severity of hypertrophy. In fact, T2 time variations are more pronounced in relation to hypertrophy severity compared to T1 time prolongation. The utilization of LGE to pinpoint areas of myocardial fibrosis is not only diagnostically valuable but also holds significant prognostic implications. However, the introduction of T1 mapping technology has helped mitigate some of the traditional challenges associated with LGE quantification. Elevated native T1 values now allow us to identify diffuse fibrosis or areas of interest even when LGE findings are absent [7][8]. Understanding myocardial edema, represented by T2 prolongation, is a complex task influenced by factors like collagen accumulation, ischemia, and microvascular dysfunction [19]. T2 mapping, therefore, emerges as a valuable tool, particularly in distinguishing HCM from physiological left ventricular hypertrophy (LVH) in athletes. Elevated T1 and ECV measurements show strong associations with the left ventricular mass index across the entire spectrum of HCM patients, aiding in distinguishing various phenocopies. For example, consider Anderson–Fabry disease (FD) where a notably reduced native T1 value serves as a red flag, raising suspicions of FD. This reduction is particularly prominent at the basal septum and often precedes ventricular hypertrophy. However, it’s crucial to acknowledge that at more advanced stages, inflammation and lymphocyte recall can lead to a pseudo-normalization of T1 time, potentially misleading clinicians. Experts have proposed a three-phase model for FD, encompassing accumulation, inflammatory, and terminal phases [20]. On the other hand, in the evaluation of cardiac amyloidosis (CA), the accumulation of amyloid fibrils triggers an expansion in ECV, resulting in myocardial damage and edema. The LGE patterns in CA patients exhibit a characteristic evolution, transitioning from a fuzzy and focal appearance in earlier stages to diffuse, subendocardial, transmural, or binary patterns in advanced cases. Native T1 mapping has now emerged as a sensitive and specific diagnostic tool for identifying light-chain (AL) and ATTR CA without necessitating contrast agents. In light-chain amyloid cardiomyopathy, the combined influence of amyloid accumulation (ECV) and myocardial edema (T2) is reflected in native T1 values [21]. In addition, serial ECV mapping may lead us to evaluate the treatment efficacy for amyloid cardiomyopathy (Figure 1).
Jcm 13 00337 g002
Figure 1. ECV mapping in amyloidosis. CMR-derived ECV map at baseline and after 12 months of Tafamidis treatment in a patient with amyloidosis (52.1 ± 8.2 vs. 49 ± 8.5, %). Tafamidis stabilized cardiac amyloidosis deposition in hereditary transthyretin cardiomiopathy. LV: left ventricular.
The role of cardiac mapping in arrhythmogenic right ventricular cardiomyopathy (ARVC) is a subject of ongoing debate. Cardiac MRI plays a crucial role in assessing structural abnormalities of the right ventricle, which is essential for diagnosing ARVC. This is particularly important as the accuracy of transthoracic echocardiography in defining right ventricular (RV) structure and function is often inadequate. Cardiac MRI mapping is not only useful for diagnosis and risk stratification of ARVC, identifying regions of fibrofatty replacement in the right or left ventricle, but it also helps detect early-stage disease and guide patient management. In this context, T1 mapping becomes an essential tool for clinicians. Native T1 values are notably elevated in early-stage patients and individuals at risk within affected families. There are even anecdotal cases demonstrating how parametric CMR mapping assists in the non-invasive diagnosis of arrhythmogenic cardiomyopathy, even when it involves the left ventricle [22].
Dilated cardiomyopathy (DCM) necessitates the use of cardiac MRI mapping for a comprehensive assessment of myocardial viability, fibrosis distribution, and contractility. Anomalies in native myocardial T1 relaxation times emerged as potential indicators of an unfavorable prognosis among individuals with DCM. Additionally, extracellular volume fraction (ECV) exhibited a robust correlation with major adverse cardiac events (MACE) across all anatomical regions, with the strongest association identified in the anteroseptal region. Quantitative CMR features for MACEs in DCM patients showed potential predictive value. In the context of a chronic presentation of DCM, myocardial T2 relaxation time is notably prolonged, regardless of the extent of left ventricular dysfunction [23]. T2 mapping enhances the identification of early-stage DCM, especially when myocardial morphology is challenging to differentiate from athletic myocardial adaptation. Although the burden of non-ischemic scarring detected via LGE is a useful tool for indication of implantable cardioverter defibrillators (ICDs) [24], the incorporation of quantitative CMR markers allows for a tailored approach to therapeutic strategies, including the placement of implantable cardioverter defibrillators (ICDs) and cardiac resynchronization therapy.
MRI is used to evaluate restrictive cardiomyopathy (RCM), but the use of tissue characterization parameters is not widely documented. These parameters could help distinguish RCM from constrictive pericarditis (CP) and other forms of cardiomyopathy. T1w sequences and cine-SSFP imaging can reveal widespread thickening of pericardial layers accompanied by hypointense calcifications in CP patients, despite nearly 20% exhibiting normal pericardial thickness. T1 and T2 mapping techniques can identify conditions of accumulation or infiltration associated with altered myocardial relaxation properties or other restrictive conditions causing diffuse inflammation or fibrosis [25]. One of the most important uses of MRI mapping in RCM is to identify conditions leading to iron overload in the myocardium. T2* mapping is a highly specific method that allows quantitative assessment of iron levels in the heart and liver. However, native T1 mapping has the potential to improve the detection of mild iron burden, but this superior reproducibility is lost in the presence of significant iron accumulation. ECV does not currently play a role in the management of patients with cardiac siderosis.

3. CMR Mapping and Myocarditis

The Lake Louise Criteria (LLC) have been widely utilized for the diagnosis of myocarditis through CMR [26]. They establish a diagnosis of myocardial inflammation when a minimum of two out of the following three tissue-based CMR markers are observed:
(a)
Edema: this is detected as high signal intensity in the myocardium on STIR T2w images.
(b)
Hyperemia: This is characterized by increased regional gadolinium contrast agent uptake in the abnormal myocardium during the initial minutes following the injection, commonly referred to as early gadolinium enhancement (EGE). While EGE was initially part of the LLC criteria, later studies demonstrated that its exclusion from the original criteria does not seem to significantly affect their diagnostic accuracy [27]. Alternatively, hyperemia can be assessed using traditional cine steady-state free precession images acquired shortly after contrast administration.
(c)
Fibrosis/Necrosis: this is depicted as myocardial contrast deposition with subepicardial/intramyocardial distribution on LGE images.
The introduction of parametric mapping images has addressed the traditional limitations of T1w or T2w images and has gained significant recognition in the updated 2018 LLC [28]. In this revised version of the criteria, the confirmation of acute myocardial inflammation involves the presence of at least one CMR marker for edema, observed on either T2w images or T2 mapping, in conjunction with the presence of at least one T1-based marker indicative of associated myocardial injury. These markers for myocardial injury can be assessed on LGE images, T1 mapping, or through extracellular volume fraction measurements. The incorporation of mapping techniques has demonstrated a substantial improvement in the diagnostic accuracy of CMR for myocarditis [29]. Furthermore, parametric mapping techniques offer a valuable alternative for detecting myocardial inflammation using CMR in situations where the administration of contrast agents must be avoided.
Elevated native T1 values are indicative of myocardial inflammation, likely arising from a complex interplay of factors including intracellular and extracellular myocardial edema, hyperemia, capillary leakage, and myocyte necrosis. In the context of conditions like viral myocarditis, rheumatoid arthritis, and systemic lupus erythematosus, native T1 values have been found to increase. However, it’s important to note that T1 values can also rise in regions with myocardial fibrosis, attributed to the expansion of the extracellular space or myocardial damage. Consequently, interpreting these findings becomes challenging, as it may be unclear whether they reflect active inflammation, chronic fibrosis, or a combination of both. Furthermore, T2 mapping offers distinct advantages over conventional T2w imaging in the detection of acute myocardial inflammation and edema. It excels in differentiating both focal and global myocardial edema. Additionally, T2 mapping effectively addresses many common limitations associated with T2-STIR, such as incomplete blood suppression, signal dropouts in the lateral wall, and lower signal-to-noise ratios. Finally, in patients with chronic myocarditis, only T2 mapping has acceptable diagnostic performance [30], and is useful for risk stratification [31]. The degree of T2 relaxation time prolongation, and to a lesser extent the percentage of myocardium with prolonged T2 time, are reliable predictors of MACE and heart failure (HF) hospitalization in patients with myocarditis. T2 time tends to shorten after resolution of the inflammation, whereas LGE may persist. Persistent time prolongation after the acute phase correlates with MACE, HF hospitalization, and LV dysfunction, making T2 mapping a useful monitoring tool in patients with myocarditis [31].

4. CMR Mapping and Inflammatory Cardiomyopathies

Inflammatory cardiomyopathies represent a heterogeneous group of heart muscle disorders characterized by non-ischemic inflammation of the myocardium that can involve the myocardium as a response to a wide range of etiologies, such as infectious agents, drugs, and toxins, or systemic immune-mediated diseases [32]. These conditions can be challenging to diagnose and manage due to their varied etiologies and, more importantly, their different clinical presentations. CMR represents the gold-standard imaging test in cases of suspected inflammatory cardiomyopathy in both acute and chronic settings [33]. Furthermore, CMR shows remarkable diagnostic inter-observer agreement as well as an optimal safety profile, and holds potential to facilitate patient monitoring, assess therapeutic efficacy, and provide prognostic information [34].

References

  1. Messroghli, D.R.; Moon, J.C.; Ferreira, V.M.; Grosse-Wortmann, L.; He, T.; Kellman, P.; Mascherbauer, J.; Nezafat, R.; Salerno, M.; Schelbert, E.B.; et al. Clinical recommendations for cardiovascular magnetic resonance mapping of T1, T2, T2 and extracellular volume: A consensus statement by the Society for Cardiovascular Magnetic Resonance (SCMR) endorsed by the European Association for Cardiovascular Imagin. J. Cardiovasc. Magn. Reson. 2017, 19, 75.
  2. Pontone, G.; Guaricci, A.I.; Fusini, L.; Baggiano, A.; Guglielmo, M.; Muscogiuri, G.; Volpe, A.; Abete, R.; Aquaro, G.; Barison, A.; et al. Cardiac Magnetic Resonance for Prophylactic Implantable-Cardioverter Defibrillator Therapy in Ischemic Cardiomyopathy: The DERIVATE–ICM International Registry. JACC Cardiovasc. Imaging 2023, 16, 1387–1400.
  3. Abdel-Aty, H.; Boyé, P.; Zagrosek, A.; Wassmuth, R.; Kumar, A.; Messroghli, D.; Bock, P.; Dietz, R.; Friedrich, M.G.; Schulz-Menger, J. Diagnostic performance of cardiovascular magnetic resonance in patients with suspected acute myocarditis: Comparison of different approaches. J. Am. Coll. Cardiol. 2005, 45, 1815–1822.
  4. Röttgen, R.; Christiani, R.; Freyhardt, P.; Gutberlet, M.; Schultheiss, H.P.; Hamm, B.; Kühl, U. Magnetic resonance imaging findings in acute myocarditis and correlation with immunohistological parameters. Eur. Radiol. 2011, 21, 1259–1266.
  5. Carbone, I.; Childs, H.; Aljizeeri, A.; Merchant, N.; Friedrich, M.G. Importance of Reference Muscle Selection in Quantitative Signal Intensity Analysis of T2-Weighted Images of Myocardial Edema Using a T2 Ratio Method. Biomed Res. Int. 2015, 2015, 232649.
  6. McCann, G.P.; Khan, J.N.; Greenwood, J.P.; Nazir, S.; Dalby, M.; Curzen, N.; Hetherington, S.; Kelly, D.J.; Blackman, D.J.; Ring, A.; et al. Complete Versus Lesion-Only Primary PCI the Randomized Cardiovascular MR CvLPRIT Substudy. J. Am. Coll. Cardiol. 2015, 66, 2713–2724.
  7. Ferreira, V.M.; Piechnik, S.K. CMR parametric mapping as a tool for myocardial tissue characterization. Korean Circ. J. 2020, 50, 658–676.
  8. Salerno, M.; Kramer, C.M. Advances in parametric mapping with CMR imaging. JACC Cardiovasc. Imaging 2013, 6, 806–822.
  9. O’Brien, A.T.; Gil, K.E.; Varghese, J.; Simonetti, O.P.; Zareba, K.M. T2 mapping in myocardial disease: A comprehensive review. J. Cardiovasc. Magn. Reson. 2022, 24, 33.
  10. Tahir, E.; Sinn, M.; Bohnen, S.; Avanesov, M.; Säring, D.; Stehning, C.; Schnackenburg, B.; Eulenburg, C.; Wien, J.; Radunski, U.K.; et al. Acute versus chronic myocardial infarction: Diagnostic accuracy of quantitative Native T1 and T2 mapping versus assessment of edema on Standard T2-weighted cardiovascular MR images for differentiation. Radiology 2017, 285, 83–91.
  11. Layland, J.; Rauhalammi, S.; Lee, M.M.Y.; Ahmed, N.; Carberry, J.; May, V.T.Y.; Watkins, S.; McComb, C.; Mangion, K.; McClure, J.D.; et al. Diagnostic accuracy of 3.0-T magnetic resonance T1 and T2 mapping and T2-weighted dark-blood imaging for the infarct-related coronary artery in Non-ST-segment elevation myocardial infarction. J. Am. Heart Assoc. 2017, 6, 210–219.
  12. Bulluck, H.; White, S.K.; Rosmini, S.; Bhuva, A.; Treibel, T.A.; Fontana, M.; Abdel-Gadir, A.; Herrey, A.; Manisty, C.; Wan, S.M.Y.; et al. T1 mapping and T2 mapping at 3T for quantifying the area-at-risk in reperfused STEMI patients. J. Cardiovasc. Magn. Reson. 2015, 17, 73.
  13. Carrabba, N.; Parodi, G.; Maehara, A.; Pradella, S.; Migliorini, A.; Valenti, R.; Colagrande, S.; Mintz, G.; Antoniucci, D. Effects of rheolytic thrombectomy and manual thrombus aspiration on infarct size and microvascular obstruction during primary angioplasty: Smart–mri substudy. J. Am. Coll. Cardiol. 2013, 61, E1849.
  14. Dastidar, A.G.; Harries, I.; Pontecorboli, G.; Bruno, V.D.; Garate, E.; De Moret, C.; Baritussio, A.; Johnson, T.W.; McAlindon, E.; Bucciarelli-Ducci, C. Native T1 mapping to detect extent of acute and chronic myocardial infarction: Comparison with late gadolinium enhancement technique. Int. J. Cardiovasc. Imaging 2019, 35, 517–527.
  15. Schwitter, J.; Arai, A.E. Assessment of cardiac ischaemia and viability: Role of cardiovascular magnetic resonance. Eur. Heart J. 2011, 32, 799–809.
  16. Weingärtner, S.; Akçakaya, M.; Basha, T.; Kissinger, K.V.; Goddu, B.; Berg, S.; Manning, W.J.; Nezafat, R. Combined saturation/inversion recovery sequences for improved evaluation of scar and diffuse fibrosis in patients with arrhythmia or heart rate variability. Magn. Reson. Med. 2013, 71, 1024–1034.
  17. Arbelo, E.; Protonotarios, A.; Gimeno, J.R.; Arbustini, E.; Barriales-Villa, R.; Basso, C.; Bezzina, C.R.; Biagini, E.; Blom, N.A.; de Boer, R.A.; et al. 2023 ESC Guidelines for the management of cardiomyopathies: Developed by the task force on the management of cardiomyopathies of the European Society of Cardiology (ESC). Eur. Heart J. 2023, 44, 3503–3626.
  18. Guglielmo, M.; Fusini, L.; Muscogiuri, G.; Baessato, F.; Loffreno, A.; Cavaliere, A.; Rizzon, G.; Baggiano, A.; Rabbat, M.G.; Muratori, M.; et al. T1 mapping and cardiac magnetic resonance feature tracking in mitral valve prolapse. Eur. Radiol. 2020, 31, 1100–1109.
  19. Huang, L.; Ran, L.; Zhao, P.; Tang, D.; Han, R.; Ai, T.; Xia, L.; Tao, Q. MRI native T1 and T2 mapping of myocardial segments in hypertrophic cardiomyopathy: Tissue remodeling manifested prior to structure changes. Br. J. Radiol. 2019, 92, 20190634.
  20. Nordin, S.; Kozor, R.; Medina-Menacho, K.; Abdel-Gadir, A.; Baig, S.; Sado, D.M.; Lobascio, I.; Murphy, E.; Lachmann, R.H.; Mehta, A.; et al. Proposed Stages of Myocardial Phenotype Development in Fabry Disease. JACC Cardiovasc. Imaging 2019, 12, 1673–1683.
  21. Fontana, M.; Pica, S.; Reant, P.; Abdel-Gadir, A.; Treibel, T.A.; Banypersad, S.M.; Maestrini, V.; Barcella, W.; Rosmini, S.; Bulluck, H.; et al. Prognostic value of late gadolinium enhancement cardiovascular magnetic resonance in cardiac amyloidosis. Circulation 2015, 132, 1570–1579.
  22. Dowd, R.; Dhanjal, T.; Schmucki, M.; Kanagala, P.; Khan, J.N. Unique role of cardiovascular magnetic resonance imaging parametric mapping in the diagnosis of arrhythmogenic left ventricular cardiomyopathy. Eur. Heart J. Cardiovasc. Imaging 2020, 22, e96.
  23. Spieker, M.; Katsianos, E.; Gastl, M.; Behm, P.; Horn, P.; Jacoby, C.; Schnackenburg, B.; Reinecke, P.; Kelm, M.; Westenfeld, R.; et al. T2 mapping cardiovascular magnetic resonance identifies the presence of myocardial inflammation in patients with dilated cardiomyopathy as compared to endomyocardial biopsy. Eur. Heart J. Cardiovasc. Imaging 2017, 19, 574–582.
  24. Guaricci, A.I.; Masci, P.G.; Muscogiuri, G.; Guglielmo, M.; Baggiano, A.; Fusini, L.; Lorenzoni, V.; Martini, C.; Andreini, D.; Pavon, A.G.; et al. CarDiac magnEtic Resonance for prophylactic Implantable-cardioVerter defibrillAtor ThErapy in Non-Ischaemic dilated CardioMyopathy: An international Registry. Europace 2021, 23, 1072–1083.
  25. Mitropoulou, P.; Georgiopoulos, G.; Figliozzi, S.; Klettas, D.; Nicoli, F.; Masci, P.G. Multi-Modality Imaging in Dilated Cardiomyopathy: With a Focus on the Role of Cardiac Magnetic Resonance. Front. Cardiovasc. Med. 2020, 7, 97.
  26. Friedrich, M.G.; Sechtem, U.; Schulz-Menger, J.; Alakija, P.; Cooper, L.T.; White, J.A.; Gutberlet, M.; Prasad, S.; Aletras, A. Cardiovascular MRI in myocarditis. J. Am. Coll. Cardiol. 2009, 53, 1475–1487.
  27. Chu, G.C.W.; Flewitt, J.A.; Mikami, Y.; Vermes, E.; Friedrich, M.G. Assessment of acute myocarditis by cardiovascular MR: Diagnostic performance of shortened protocols. Int. J. Cardiovasc. Imaging 2013, 29, 1077–1083.
  28. Ferreira, V.M.; Schulz-Menger, J.; Holmvang, G.; Kramer, C.M.; Carbone, I.; Sechtem, U.; Kindermann, I.; Gutberlet, M.; Cooper, L.T.; Liu, P.; et al. Cardiovascular Magnetic Resonance in Nonischemic Myocardial Inflammation: Expert Recommendations. J. Am. Coll. Cardiol. 2018, 72, 3158–3176.
  29. Eichhorn, C.; Greulich, S.; Bucciarelli-Ducci, C.; Sznitman, R.; Kwong, R.Y.; Gräni, C. Multiparametric Cardiovascular Magnetic Resonance Approach in Diagnosing, Monitoring, and Prognostication of Myocarditis. JACC Cardiovasc. Imaging 2022, 15, 1325–1338.
  30. Lurz, P.; Luecke, C.; Eitel, I.; Föhrenbach, F.; Frank, C.; Grothoff, M.; Waha SDe Rommel, K.P.; Lurz, J.A.; Klingel, K.; Kandolf, R.; et al. Comprehensive Cardiac Magnetic Resonance Imaging in Patients with Suspected Myocarditis the MyoRacer-Trial. J. Am. Coll. Cardiol. 2016, 67, 1800–1811.
  31. Spieker, M.; Aberkorn, S.; Gastl, M.; Behm, P.; Katsianos, S.; Horn, P.; Jacoby, C.; Schnackenburg, B.; Reinecke, P.; Kelm, M.; et al. Abnormal T2 mapping cardiovascular magnetic resonance correlates with adverse clinical outcome in patients with suspected acute myocarditis. J. Cardiovasc. Magn. Reson. 2017, 19, 38.
  32. Thomas, K.E.; Fotaki, A.; Botnar, R.M. Europe PMC Funders Group Imaging methods: Magnetic resonance imaging. Circ. Cardiovasc. Imaging 2023, 16, e014068.
  33. Tymińska, A.; Ozierański, K.; Skwarek, A.; Kapłon-Cieślicka, A.; Baritussio, A.; Grabowski, M.; Marcolongo, R.; Caforio, A.L.P. Personalized Management of Myocarditis and Inflammatory Cardiomyopathy in Clinical Practice. J. Pers. Med. 2022, 12, 183.
  34. Barison, A.; Ricci, F.; Pavon, A.G.; Muscogiuri, G.; Bisaccia, G.; Camastra, G.; Lazzari, M.; De Lanzillo, C.; Raguso, M.; Monti, L.; et al. Cardiovascular Magnetic Resonance in Patients with Cardiac Electronic Devices: Evidence from a Multicenter Study. J. Clin. Med. 2023, 12, 6673.
More
© Text is available under the terms and conditions of the Creative Commons Attribution (CC BY) license; additional terms may apply. By using this site, you agree to the Terms and Conditions and Privacy Policy.
Upload a video for this entry
Information
Subjects: Cardiac & Cardiovascular Systems
Contributors MDPI registered users' name will be linked to their SciProfiles pages. To register with us, please refer to https://encyclopedia.pub/register :
Nazario Carrabba
,
Mattia Alexis Amico
,
Andrea Igoren Guaricci
,
Maria Cristina Carella
,
Viviana Maestrini
,
Sara Monosilio
,
Patrizia Pedrotti
,
Fabrizio Ricci
,
Lorenzo Monti
,
Stefano Figliozzi
,
Camilla Torlasco
,
Andrea Barison
,
Andrea Baggiano
,
Alessandra Scatteia
,
Gianluca Pontone
,
Santo Dellegrottaglie
View Times: 102
Entry Collection: Nuclear Magnetic Resonance
Revisions: 2 times (View History)
Update Date: 19 Jan 2024
Table of Contents
    1000/1000
    Hot Most Recent
    Feedback