Published online before print June 23, 2003, doi: 10.1161/01.CIR.0000078641.19365.4C
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
(Circulation. 2003;108:54.)
© 2003 American Heart Association, Inc.
Clinical Investigation and Reports |
Differentiation of Heart Failure Related to Dilated Cardiomyopathy and Coronary Artery Disease Using Gadolinium-Enhanced Cardiovascular Magnetic Resonance
From the Center for Advanced MR in Cardiology (CAMRIC) (J.A.M., J.C.C.M., S.K.P., C.H.L., A.J.S.C., D.J.P.) and Department of Cardiology (S.K.P., A.J.S.C., D.J.P.), Royal Brompton Hospital, London, UK; St George’s Hospital London (W.J.M.); and Siemens Medical Solutions (C.H.L.), Erlangen, Germany.
Correspondence to Dr D.J. Pennell, CMR Unit, Royal Brompton Hospital, Sydney St, London, SW3 6NP UK. E-mail d.pennell{at}ic.ac.uk
 |
Abstract |
|---|
 Top Abstract IntroductionMethodsResultsDiscussionConclusionsReferences |
|---|
Background— Heart failure treatment depends partly on the underlying cause of the disease. We evaluated cardiovascular magnetic resonance (CMR) for the problem of differentiating dilated cardiomyopathy (DCM) from left ventricular (LV) dysfunction caused by coronary artery disease (CAD).
Methods and Results— Late gadolinium enhancement with CMR was performed in 90 patients with heart failure and LV systolic dysfunction (63 patients with DCM and unobstructed coronary arteries and 27 with significant CAD at angiography). We also studied 15 control subjects with no coronary risk factors and/or unobstructed coronary arteries. None (0%) of the control subjects had myocardial gadolinium enhancement; however, all patients (100%) with LV dysfunction and CAD had enhancement, which was subendocardial or transmural. In patients with DCM, there were 3 findings: no enhancement (59%); myocardial enhancement indistinguishable from the patients with CAD (13%); and patchy or longitudinal striae of midwall enhancement clearly different from the distribution in patients with CAD (28%).
Conclusions— Gadolinium CMR is a powerful technique to distinguish DCM from LV dysfunction related to CAD and yields new insights in DCM. These data suggest that using the coronary angiogram as the arbiter for the presence of LV dysfunction caused by CAD could have lead to an incorrect assignment of DCM cause in 13% of patients, possibly because of coronary recanalization after infarction. The midwall myocardial enhancement in patients with DCM is similar to the fibrosis found at autopsy; it has not previously been visualized in vivo and warrants further investigation. CMR may become a useful alternative to routine coronary angiography in the diagnostic workup of DCM.
Key Words: magnetic resonance imaging • cardiomyopathy • heart failure
|
Introduction |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionConclusionsReferences |
|---|
The treatment of patients with left ventricular (LV) systolic dysfunction is determined in part by the identification of the underlying disease process. The primary diagnostic issue centers on differentiating an underlying cause for the LV dysfunction that is related to dilated cardiomyopathy (DCM) or coronary artery disease (CAD). In many centers, coronary angiography is routinely performed for this task. In those patients with unobstructed coronary arteries and no other etiological factor, the diagnosis of DCM is usually made. This differentiation is important clinically for several reasons in patients with CAD: They have a worse prognosis,1,2 they may benefit from revascularization and/or aneurysmectomy, and secondary preventive pharmacotherapy with statins and aspirin are typically used. Conversely, in patients with DCM, secondary causes such as excess ethanol ingestion or myocardial iron overload3 need to be excluded, and as genetic studies of DCM begin to identify inherited abnormalities,4,5 accurate phenotyping and family screening will become more important for early diagnosis.
The value of cardiovascular magnetic resonance (CMR) in the treatment of heart failure is becoming established in initial functional assessment6,7 and in the determination of secondary causes.3 In serial follow-up of ventricular function, CMR offers excellent interstudy reproducibility8 that allows the technique to be used to determine treatment responses.9 Gadolinium-enhanced CMR can also characterize areas of myocardial infarction,10,11 and limited results suggest that gadolinium enhancement is absent in nonischemic LV dysfunction.10 We therefore evaluated whether gadolinium enhancement might be a useful clinical tool in distinguishing LV dysfunction related to DCM or CAD and whether it may also offer new insights in DCM.
|
Methods |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionConclusionsReferences |
|---|
Patient Population
We prospectively acquired 105 gadolinium-enhanced CMR studies in 90 patients with chronic stable heart failure with dilated heart and LV systolic dysfunction and 15 control subjects (normal ventricular function and ECG and no cardiac risk factors). All patients were recruited from a specialist heart failure clinic. The patients with idiopathic DCM were a consecutive series who consented to participate during their routine outpatient appointment from
300 potentially suitable patients with this diagnosis. The study patients had a clinical diagnosis of heart failure made on the basis of compatible clinical presentation and history combined with documented systolic LV dysfunction and dilation by echocardiography or radionuclide imaging. All 90 patients had undergone coronary angiography and 63 had unobstructed coronary arteries and no identifiable secondary cause (including no documented infarction by history or the presence of Q waves satisfying standard ECG criteria of infarction12) and were being treated with a clinical diagnosis of DCM; 27 subjects had angiographically documented CAD (>50% stenosis in ≥1 coronary arteries) and had a history of myocardial infarction. All 15 control subjects had normal systolic function and a low (<10%) 10-year risk for coronary events13; 9 had unobstructed coronary arteries, with angiography having been performed for atypical chest pain. The patient characteristics are detailed in Table 1. Exclusion criteria were the presence of contraindications to CMR, suspected infiltrative heart disease (no evidence of hilar lymphadenopathy or suggestive skin, eye, joint, neurological, or gastrointestinal disorder in the included patients in 1.5 to 11 years of follow-up), hypertrophic cardiomyopathy, previous revascularization, significant valve disease, or a history of myocarditis. All participants gave written informed consent. The project was approved by the institutional ethics committee.
|
Cardiovascular Magnetic Resonance
A Siemens Sonata 1.5-T scanner was used (Erlangen, Germany). Steady-state, free precession cines were acquired during 8-second breath-holds (TE/TR 1.6/3.2 ms, flip angle 60°) in long-axis planes and sequential 8-mm short-axis slices (2-mm gap between slices) from the atrioventricular ring to the apex. Intravenous gadolinium-DTPA was given (0.1 mmol/kg) and contrast-enhanced images were acquired after 10 to 15 minutes in 6 identical short-axis planes by using an inversion-recovery segmented gradient echo sequence, starting with a basal slice 1 cm below the aortic outflow tract and stopping before the apical slices, which can be affected by partial volume effects.10 Inversion times were adjusted to null normal myocardium (260 to 400 ms) with voxel sizes of 1.7x1.4x8.0 mm.
Data Analysis
Ventricular function parameters were assessed in a standard way, 14 using in-house software (CMRtools, Imperial College). CMR has excellent reproducibility,8 and normal ranges are published.15 Wall motion and gadolinium enhancement were assessed blindly by using 12 segments in each of 6 short-axis slices.11 Segmental wall motion was visually assessed as 0=normal, 1=moderate hypokinesis, 2=severe hypokinesis, 3=akinesis, and 4=dyskinesis. The average segmental transmural extent of enhancement in each segment was assessed visually by using the following scale: 0=none, 1=1% to 25%, 2=26% to 50%, 3=51% to 75%, and 4=76% to 100% enhancement. The segments scores were summed, yielding a range per patient of 0 (no enhancement in any slice) to 288. Coronary angiography was read blindly by a single cardiologist.
Statistical Analysis
All continuous variables are expressed as mean±SD; comparison between groups were made by means of unpaired t tests. ANOVA was used to assess differences between more than 2 groups. 
2 testing or Fisher’s exact test were performed for noncontinuous variables where appropriate. A 2-tailed probability value of <0.05 was considered statistically significant.
|
Results |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionConclusionsReferences |
|---|
The DCM group was younger, with fewer men and fewer risk factors than in the ischemic group (Table 1). Q waves on the ECG were more common in the ischemic group, with poor R-wave progression being the most common ECG finding in the DCM group. The LV parameters were similar between groups, but the ischemic group had a higher New York Heart Association grade and lower right ventricular (RV) volumes (Table 2). None (0%) of the control subjects had late enhancement. All patients (100%) in the ischemic group had subendocardial or transmural enhancement (Figure 1 and Table 3). The proportion of subjects with enhancement was higher in the ischemic group (100% versus 41%, P<0.001), as was the gadolinium score (66 versus 15, P<0.001).
|
|
|
In the DCM group, 37 (59%) had no gadolinium enhancement (subgroup 1, Figure 2). In the remaining 26 (41%), however, gadolinium enhancement occurred in 2 distinct patterns: subendocardial enhancement, which was indistinguishable (subendocardial extending toward the epicardium) from the ischemic group (subgroup 2, 13%, Figure 3), or midwall striae or patches of enhancement (subgroup 3, 28%, Figures 4 and 5
). In DCM subgroup 2, there was marked wall thinning in the enhanced regions with more pronounced wall motion abnormalities in the enhancing versus the nonenhancing segments (6.3±2.3 mm versus 10.7±1.9 mm, P<0.0001). In 50% of these 8 patients, the enhancement was extensive (Figure 3A). The remaining 4 patients had more limited subendocardial infarction and wall thinning (Figure 3B). In all cases, there was no event suggestive of infarction and no Q waves were present, but all had undergone hospitalization for heart failure decompensation of unknown cause.
|
|
|
|
In DCM subgroup 3, the enhancement was in the midwall of the myocardium, clearly distinct from the subendocardium and subepicardium. There were 2 distributions of enhancement: longitudinal striae, following the fiber orientation of the ventricular muscle bundles (Figure 4), and basal to midventricular patchy foci (Figure 5). Finally, 1 patient was diagnosed with arrhythmogenic RV dysplasia.16
|
Discussion |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionConclusionsReferences |
|---|
We investigated CMR for differentiating between DCM and CAD as the underlying cause of LV systolic dysfunction in patients with chronic stable heart failure. The differentiation between control subjects and patients with dysfunction caused by CAD was complete (0% versus 100% enhancement). The patients with DCM could be divided into 3 types: subgroup 1 (59%) showed no enhancement; subgroup 2 (13%) had subendocardial or transmural enhancement that was indistinguishable from the ischemic patients; and subgroup 3 (28%) had longitudinal or patchy midwall enhancement not in the territory of a coronary artery and not subendocardial or otherwise similar to the enhancement in the patients with CAD. The findings in DCM subgroups 1 and 3 are consistent with the clinical diagnosis of dilated cardiomyopathy. The most common pattern of no gadolinium enhancement (subgroup 1) clearly distinguishes these patients from those with CAD. The finding of no gadolinium enhancement in 20 patients with DCM has also been reported by Wu et al10; however, our report differs in that in a minority we have also found enhancement of the midwall or subendocardium. This may have resulted from our larger sample size of 63. The midwall enhancement seen in DCM subgroup 3 probably reflects the focal segmental fibrosis at autopsy.17,18 Myocardial fibrosis in DCM can be divided into 3 groups: mild diffuse fibrosis, severe diffuse fibrosis, and segmental fibrosis. Current CMR techniques are unlikely to detect diffuse microscopic fibrosis and hence most patients with DCM will have absent enhancement. However, our data suggest that CMR does have sufficient resolution to image foci of fibrosis for the first time in vivo. The overall extent of fibrosis in DCM is lower than that seen in CAD,19 and our results are consistent with this.
DCM subgroup 2 patients have normal luminal appearances by coronary angiography, but the pattern of subendocardial to transmural enhancement strongly suggests the presence of prior infarction. The occurrence of recanalization after an occlusive coronary event or embolization from minimally stenotic but unstable plaque is well documented.20,21 Autopsy studies in DCM have also described patients with endocardial and transmural fibrosis indistinguishable from myocardial infarction,22 which have been grouped as DCM variants or excluded as myocardial infarction.22 Half of the subgroup 2 patients had extensive gadolinium enhancement, and all had significant risk factors for CAD. This would be most consistent with the assertion that the correct clinical diagnosis should be LV dysfunction related to CAD. The more limited endocardial enhancement in the remaining subjects suggests infarction of lesser degree. However, LV remodeling occurs with nonextensive infarctions,23 especially in the absence of suitable modern therapy,24 and it is noteworthy that none of these patients had a history of acute infarction, having presented directly with heart failure as their first cardiovascular symptom. This is consistent with untreated LV remodeling after ischemic damage as the cause, although the coexistence of LV dysfunction from DCM combined with CAD cannot be excluded. There was no clinical evidence for other potential pathologies such as viral myocarditis25 or sarcoidosis.26
These data suggest therefore that the clinical diagnosis in 13% of our DCM population was either partly or wholly incorrect, which has important therapeutic implications. In addition, as genotyping of DCM matures,4,5 accurate phenotyping is important to prevent the unnecessary adverse psychological effects of investigating relatives. Accurate phenotyping also improves the power of gene studies, allowing smaller sample sizes in the investigation of genotypes and gene environment interactions.27,28
Clinical Implications
Noninvasive tests are not reliable in distinguishing dysfunction related to DCM or CAD because segmental wall motion abnormalities are common in DCM,29 and scintigraphic perfusion techniques are complicated by attenuation artifacts and denervation in large DCM hearts, leading to false-positive results.30 Our data show that the coronary disease risk score and RV volumes are different between the DCM and ischemic groups, but substantial overlap occurs. Thus, coronary angiography is usually performed in all cases so that LV dysfunction will not be missed. However, coronary angiography is flawed in identifying the myocardial substrate for heart failure because significant CAD may exist without infarction, and "normal" coronaries may exist in the presence of myocardial damage. This was graphically illustrated in the Assessment of Treatment with Lisinopril And Survival (ATLAS) study, which identified the incorrect assignment at autopsy of an ischemic/nonischemic cause in 17% of patients with an established clinical label of LV dysfunction caused by CAD and 28% of patients with an established clinical label of DCM.31 It is also implicit in reports attempting to deal with the contingent relation of coronary artery appearance and myocardial damage, which classify patients with heart failure as nonischemic who have single-vessel disease without prior history of infarction or revascularization.32 Our study suggests that CMR distinguishes LV dysfunction related to DCM or CAD on the basis of identifying gadolinium enhancement and patterns within the myocardium, which is the target tissue in question. This also suggests the potential to reduce the costs and inherent risks associated with invasive cardiac catheterization on which the diagnosis of DCM has until now depended. Although the newer noninvasive techniques of coronary angiography by magnetic resonance and computed tomography are likely to be cheaper and lower risk, the same limitations would apply.
Limitations
We used a dose of gadolinium of 0.1 mmol/kg, but higher doses up to 0.2 mmol/kg have been used for late gadolinium enhancement.10,11 An optimal dose has not been defined, although doses in the range of 0.1 to 0.2 mmol/kg are suitable, but higher dosing is more expensive and usually requires a longer delay after injection before imaging to allow blood pool signal to fall. A confounding possibility of the use of late gadolinium enhancement to identify DCM would be balanced severe ostial stenoses of left and right coronary arteries in the absence of any infarction potentially leading to a clinical picture of DCM with global dysfunction on the basis of pan-myocardial hibernation. This is very rare, and it is likely that such a patient would have severe unresponsive symptoms. Further studies will clarify this issue. Other conditions cause gadolinium uptake in the myocardium, and this must be considered in interpretation of results in patients with DCM.33,34
|
Conclusions |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionConclusionsReferences |
|---|
Our data suggest that gadolinium CMR can exclude the presence of LV dysfunction related to CAD in heart failure. Furthermore, CMR can identify 2 substantial subgroups of patients with DCM who have either midwall fibrosis or who have an infarction pattern of enhancement and require further evaluation for CAD. Further studies are needed to establish the relation of these new findings to prognosis in heart failure and to confirm whether gadolinium CMR could be used to avoid invasive coronary angiography in patients with DCM.
|
Acknowledgments |
|---|
Dr McCrohon was supported by CORDA (The Marian Silcock Fellowship). Drs Moon and McKenna were supported by the British Heart Foundation. CAMRIC was founded by the British Heart Foundation. Research support was received from Siemens. We thank Ross Murphy for help in patient recruitment, Mary Sheppard for discussions on the histopathology of fibrosis in DCM, and Raymond Kim and Robert Judd, who provided training in gadolinium CMR techniques for Dr Moon.
|
Footnotes |
|---|
Dr Lorenz is an employee of Siemens Medical Systems, manufacturer of the magnetic resonance scanner used in this study.
Received January 24, 2003; revision received April 1, 2003; accepted April 4, 2003.
|
References |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionConclusionsReferences |
|---|
1. Adams KF, Dunlap SH, Sueta CA, et al. Relation between gender, etiology and survival in patients with symptomatic heart failure. J Am Coll Cardiol. 1996; 28: 1781–1788.[Abstract]
2. Bart BA, Shaw LK, McCants CB, et al. Clinical determinants of mortality in patients with angiographically diagnosed ischemic or non-ischemic cardiomyopathy. J Am Coll Cardiol. 1997; 30: 1002–1008.[Abstract]
3. Anderson LJ, Holden S, Davies B, et al. Cardiovascular T2* (T2 star) magnetic resonance for the early diagnosis of myocardial iron overload. Eur Heart J. 2001; 22: 2171–2179.
4. Itoh-Satoh M, Hayashi T, Nishi H, et al. Titin mutations as the molecular basis for dilated cardiomyopathy. Biochem Biophys Res Commun. 2002; 291: 385–393.[CrossRef][Medline] [Order article via Infotrieve]
5. Olson TM, Illenberger S, Kishimoto NY, et al. Metavinculin mutations alter actin interaction in dilated cardiomyopathy. Circulation. 2002; 105: 431–437.
6. Bellenger NG, Francis JM, Davies CL, et al. Establishment and performance of a magnetic resonance cardiac function clinic. J Cardiovasc Magn Reson. 2000; 2: 15–22.[Medline] [Order article via Infotrieve]
7. Rajappan K, Bellenger NG, Anderson L, et al. The role of cardiovascular magnetic resonance in heart failure. Eur J Heart Failure. 2000; 2: 241–252.
8. Bellenger NG, Davies LC, Francis JM, et al. Reduction in sample size for studies of remodeling in heart failure by the use of cardiovascular magnetic resonance. J Cardiovasc Magn Reson. 2000; 2: 271–278.[Medline] [Order article via Infotrieve]
9. Doherty NE, Seelos KC, Suzuki JI, et al. Application of cine NMR imaging for sequential evaluation of response to angiotensin-converting enzyme inhibitor therapy in dilated cardiomyopathy. J Am Coll Cardiol. 1992; 19: 1294–1302.[Abstract]
10. Wu E, Judd RM, Vargas JD, et al. Visualisation of the presence, location and transmural extent of healed Q-wave and non-Q-wave myocardial infarction. Lancet. 2001; 357: 21–28.[CrossRef][Medline] [Order article via Infotrieve]
11. Kim RJ, Wu E, Rafael A, et al. The use of contrast-enhanced magnetic resonance imaging to identify reversible myocardial dysfunction. N Engl J Med. 2000; 343: 1445–1453.
12. Alpert JS, Thygesen K, Antman E, et al. Myocardial infarction redefined-a consensus document of the Joint European Society of Cardiology/American College of Cardiology Committee for the redefinition of myocardial infarction. J Am Coll Cardiol. 2000; 36: 959–969.
13. Anderson KM, Odell PM, Wilson PWF, et al. Cardiovascular disease risk profiles. Am Heart J. 1990; 121: 293–298.[CrossRef]
14. Bellenger NG, Pennell DJ. Ventricular function. In: Manning WJ, Pennell DJ, eds. Cardiovascular Magnetic Resonance. New York, NY: Churchill Livingstone; 2002.
15. Lorenz CH, Walker ES, Morgan VL, et al. Normal human right and left ventricular mass, systolic function and gender differences by cine magnetic resonance imaging. J Cardiovasc Magn Reson. 1999; 1: 7–21.[Medline] [Order article via Infotrieve]
16. McCrohon JA, John AS, Lorenz CH, et al. Left ventricular involvement in arrhythmogenic right ventricular cardiomyopathy. Circulation. 2002; 105: 1394.
17. Maehashi N, Yokota Y, Takarada A, et al. The role of myocarditis and myocardial fibrosis in dilated cardiomyopathy: analysis of 28 necropsy cases. Jpn Heart J. 1991; 32: 1–15.[Medline] [Order article via Infotrieve]
18. Roberts WC, Siegel RJ, McManus BM. Idiopathic dilated cardiomyopathy: analysis of 152 necropsy patients. Am J Cardiol. 1987; 60: 1340–1355.[CrossRef][Medline] [Order article via Infotrieve]
19. Parodi O, De Maria M, Oltrona L, et al. Myocardial blood flow distribution in patients with ischaemic heart disease or dilated cardiomyopathy undergoing heart transplantation. Circulation. 1993; 88: 509–522.
20. Topol EJ, Yadav JS. Recognition of the importance of embolization in atherosclerotic vascular disease. Circulation. 2000; 101: 570–580.
21. Arroyo LH, Lee RT. Mechanisms of plaque rupture: mechanical and biologic interactions. JAMA. 1999; 281: 921–926.
22. Isner JM, Virmani R, Itscoitz SB, et al. Left and right ventricular myocardial infarction in idiopathic dilated cardiomyopathy. Am Heart J. 1980; 99: 235–242.[CrossRef][Medline] [Order article via Infotrieve]
23. Willenheimer R. Left ventricular remodelling and dysfunction: can the process be prevented? Int J Cardiol. 2000; 72: 143–150.[CrossRef][Medline] [Order article via Infotrieve]
24. Bellenger NG, Swinburn JM, Rajappan K, et al. Cardiac remodelling in the era of aggressive medical therapy: does it still exist? Int J Cardiol. 2002; 83: 217–225.[CrossRef][Medline] [Order article via Infotrieve]
25. Saffitz JE, Schwartz DJ, Southworth W, et al. Coxsackie viral myocarditis causing transmural right and left ventricular infarction without coronary narrowing. Am J Cardiol. 1983; 52: 644–647.
26. Roberts WC, McAllister HA, Ferrans VJ. Sarcoidosis of the heart: a clinicopathologic study of 35 necropsy patients (group 1) and review of 78 previously described necropsy patients Am J Med. 1977; 63: 86–108.[CrossRef][Medline] [Order article via Infotrieve]
27. Myerson SG, Montgomery HE, Whittingham M, et al. Left ventricular hypertrophy with exercise and the angiotensin converting enzyme gene I/D polymorphism: a randomized controlled trial with losartan. Circulation. 2001; 103: 226–230.
28. Brull D, Dhamrait S, Myerson SG, et al. Bradykinin B2KBR receptor polymorphism and left ventricular growth response. Lancet. 2001; 358: 1155–1156.[CrossRef][Medline] [Order article via Infotrieve]
29. Wallis DE, O’Connell JB, Henkin RE, et al. Segmental wall motion abnormalities in dilated cardiomyopathy: a common finding and good prognostic sign. J Am Coll Cardiol. 1984; 4: 674–679.[Abstract]
30. Bulkley BH, Hutchins GM, Bailey I, et al. Thallium 201 imaging and gated cardiac blood pool scans in patients with ischemic and idiopathic congestive cardiomyopathy: a clinical and pathologic study. Circulation. 1977; 55: 753–760.
31. Uretsky BF, Thygesen K, Armstrong PW, et al. Acute coronary findings at autopsy in heart failure patients with sudden death: results from the Assessment of Treatment with Lisinopril And Survival (ATLAS) trial. Circulation. 2000; 102: 611–616.
32. Felker GM, Shaw LK, O’Connor CM. A standardized definition of ischemic cardiomyopathy for use in clinical research. J Am Coll Cardiol. 2002; 39: 210–218.
33. Moon JCC, Mundy HR, Lee PJ, et al. Myocardial fibrosis in glycogen storage disease type 3. Circulation. 2003; 107: e47.[CrossRef][Medline] [Order article via Infotrieve]
34. Moon JCC, McKenna WJ, McCrohon JA, et al. Toward clinical risk assessment in hypertrophic cardiomyopathy with gadolinium cardiovascular magnetic resonance. J Am Coll Cardiol. 2003; 41: 1561–1567.
This article has been cited by other articles:
 |
|
 |
|
  A. Valle-Munoz, J. Estornell-Erill, C. J. Soriano-Navarro, M. Nadal-Barange, N. Martinez-Alzamora, F. Pomar-Domingo, M. Corbi-Pascual, R. Paya-Serrano, and F. Ridocci-Soriano Late gadolinium enhancement-cardiovascular magnetic resonance identifies coronary artery disease as the aetiology of left ventricular dysfunction in acute new-onset congestive heart failure Eur J Echocardiogr, December 1, 2009; 10(8): 968 - 974. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 B. Y.C. Cheong, R. Muthupillai, J. M. Wilson, A. Sung, S. Huber, S. Amin, M. A. Elayda, V.-V. Lee, and S. D. Flamm Prognostic Significance of Delayed-Enhancement Magnetic Resonance Imaging: Survival of 857 Patients With and Without Left Ventricular Dysfunction Circulation, November 24, 2009; 120(21): 2069 - 2076. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. R. Patel, P. J. Cawley, J. F. Heitner, I. Klem, M. A. Parker, W. A. Jaroudi, T. J. Meine, J. B. White, M. D. Elliott, H. W. Kim, et al. Detection of Myocardial Damage in Patients With Sarcoidosis Circulation, November 17, 2009; 120(20): 1969 - 1977. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. Moreo, G. Ambrosio, B. De Chiara, M. Pu, T. Tran, F. Mauri, and S. V. Raman Influence of Myocardial Fibrosis on Left Ventricular Diastolic Function: Noninvasive Assessment by Cardiac Magnetic Resonance and Echo Circ Cardiovasc Imaging, November 1, 2009; 2(6): 437 - 443. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A Pepe, V Positano, M Capra, A Maggio, C L Pinto, A Spasiano, G Forni, G Derchi, B Favilli, G Rossi, et al. Myocardial scarring by delayed enhancement cardiovascular magnetic resonance in thalassaemia major Heart, October 15, 2009; 95(20): 1688 - 1693. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 T. D. Karamitsos, J. M. Francis, S. Myerson, J. B. Selvanayagam, and S. Neubauer The Role of Cardiovascular Magnetic Resonance Imaging in Heart Failure J. Am. Coll. Cardiol., October 6, 2009; 54(15): 1407 - 1424. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
O. Bruder, S. Schneider, D. Nothnagel, T. Dill, V. Hombach, J. Schulz-Menger, E. Nagel, M. Lombardi, A. C. van Rossum, A. Wagner, et al. EuroCMR (European Cardiovascular Magnetic Resonance) Registry: Results of the German Pilot Phase J. Am. Coll. Cardiol., October 6, 2009; 54(15): 1457 - 1466. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 F P JUNQUEIRA, R MACEDO, A C COUTINHO, R LOUREIRO, P V DE PONTES, R C DOMINGUES, and E L GASPARETTO Myocardial delayed enhancement in patients with pulmonary hypertension and right ventricular failure: evaluation by cardiac MRI Br. J. Radiol., October 1, 2009; 82(982): 821 - 826. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
F Leyva, P W X Foley, B Stegemann, J A Ward, L L Ng, M P Frenneaux, F Regoli, R E A Smith, and A Auricchio Development and validation of a clinical index to predict survival after cardiac resynchronisation therapy Heart, October 1, 2009; 95(19): 1619 - 1625. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 N H Prakken, B K Velthuis, M J Cramer, and A Mosterd Advances in cardiac imaging: the role of magnetic resonance imaging and computed tomography in identifying athletes at risk Br. J. Sports Med., September 1, 2009; 43(9): 677 - 684. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
K. Shivkumar and R. Tung Improving our understanding of epicardial ventricular tachycardia in nonischemic cardiomyopathy. J. Am. Coll. Cardiol., August 25, 2009; 54(9): 809 - 811. [Full Text] [PDF]
|
|
|
|
 |
|
 M. Wilson, R. O'Hanlon, S. Prasad, S. Basavarajaiah, N. Stephens, R. Senior, A. Shaw, S. Sharma, and G. Whyte Myocardial fibrosis in an veteran endurance athlete BMJ Case Reports, August 17, 2009; 2009(aug17_1): bcr1220081345 - bcr1220081345. [Abstract] [Full Text]
|
|
|
|
|
|
G.-Y. Cho, T. H. Marwick, H.-S. Kim, M.-K. Kim, K.-S. Hong, and D.-J. Oh Global 2-dimensional strain as a new prognosticator in patients with heart failure. J. Am. Coll. Cardiol., August 11, 2009; 54(7): 618 - 624. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
E SUEYOSHI, I SAKAMOTO, and M UETANI Myocardial delayed contrast-enhanced MRI: relationships between various enhancing patterns and myocardial diseases Br. J. Radiol., August 1, 2009; 82(980): 691 - 697. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 E.-Y. Choi, B. W. Choi, S.-A. Kim, S. J. Rhee, C. Y. Shim, Y. J. Kim, S.-M. Kang, J.-W. Ha, and N. Chung Patterns of late gadolinium enhancement are associated with ventricular stiffness in patients with advanced non-ischaemic dilated cardiomyopathy Eur J Heart Fail, June 1, 2009; 11(6): 573 - 580. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. V. Raman Coronary Artery or Myocyte: Wherein Lies the Diagnosis? Circ Cardiovasc Imaging, May 1, 2009; 2(3): 166 - 168. [Full Text] [PDF]
|
|
|
|
|
|
A. S. Flett, M. A. Westwood, L. C. Davies, A. Mathur, and J. C. Moon The Prognostic Implications of Cardiovascular Magnetic Resonance Circ Cardiovasc Imaging, May 1, 2009; 2(3): 243 - 250. [Full Text] [PDF]
|
|
|
|
 |
|
 P. J. Sparrow, N. Merchant, Y. L. Provost, D. J. Doyle, E. T. Nguyen, and N. S. Paul CT and MR Imaging Findings in Patients with Acquired Heart Disease at Risk for Sudden Cardiac Death1 RadioGraphics, May 1, 2009; 29(3): 805 - 823. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
I. Nakamura, N. Kotooka, Y. Komori, and K. Node Ebstein anomaly by cardiac magnetic resonance imaging. J. Am. Coll. Cardiol., April 28, 2009; 53(17): 1568 - 1568. [Full Text] [PDF]
|
|
|
|
|
|
K. N. Hor, J. Wansapura, L. W. Markham, W. Mazur, L. H. Cripe, R. Fleck, D. W. Benson, and W. M. Gottliebson Circumferential strain analysis identifies strata of cardiomyopathy in duchenne muscular dystrophy a cardiac magnetic resonance tagging study. J. Am. Coll. Cardiol., April 7, 2009; 53(14): 1204 - 1210. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
F. M. Bogun, B. Desjardins, E. Good, S. Gupta, T. Crawford, H. Oral, M. Ebinger, F. Pelosi, A. Chugh, K. Jongnarangsin, et al. Delayed-enhanced magnetic resonance imaging in nonischemic cardiomyopathy utility for identifying the ventricular arrhythmia substrate. J. Am. Coll. Cardiol., March 31, 2009; 53(13): 1138 - 1145. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. H. Kadish and J. C. Rubenstein Connecting the dots the relevance of scar in nonischemic cardiomyopathy. J. Am. Coll. Cardiol., March 31, 2009; 53(13): 1146 - 1147. [Full Text] [PDF]
|
|
|
|
 |
|
 F Alpendurada, J Wong, and D J Pennell Practical applications of cardiovascular magnetic resonance Heart Asia, March 31, 2009; 2009(3): 16 - 22. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. Nazarian, D. A. Bluemke, and H. R. Halperin Applications of Cardiac Magnetic Resonance in Electrophysiology Circ Arrhythm Electrophysiol, February 1, 2009; 2(1): 63 - 71. [Full Text] [PDF]
|
|
|
|
|
|
K. W. Cummings, S. Bhalla, C. Javidan-Nejad, A. J. Bierhals, F. R. Gutierrez, and P. K. Woodard A Pattern-based Approach to Assessment of Delayed Enhancement in Nonischemic Cardiomyopathy at MR Imaging1 RadioGraphics, January 1, 2009; 29(1): 89 - 103. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. Sen-Chowdhry, P. Syrris, S. K. Prasad, S. E. Hughes, R. Merrifield, D. Ward, D. J. Pennell, and W. J. McKenna Left-dominant arrhythmogenic cardiomyopathy: an under-recognized clinical entity. J. Am. Coll. Cardiol., December 16, 2008; 52(25): 2175 - 2187. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. G. Strauss, R. H. Selvester, J. A.C. Lima, H. Arheden, J. M. Miller, G. Gerstenblith, E. Marban, R. G. Weiss, G. F. Tomaselli, G. S. Wagner, et al. ECG Quantification of Myocardial Scar in Cardiomyopathy Patients With or Without Conduction Defects: Correlation With Cardiac Magnetic Resonance and Arrhythmogenesis Circ Arrhythm Electrophysiol, December 1, 2008; 1(5): 327 - 336. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 E. Belloni, F. De Cobelli, A. Esposito, R. Mellone, G. Perseghin, T. Canu, and A. Del Maschio MRI of Cardiomyopathy Am. J. Roentgenol., December 1, 2008; 191(6): 1702 - 1710. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. G. Friedrich There Is More Than Shape and Function J. Am. Coll. Cardiol., November 4, 2008; 52(19): 1581 - 1583. [Full Text] [PDF]
|
|
|
|
 |
|
 J.-B. le Polain de Waroux, A.-C. Pouleur, C. Goffinet, A. Pasquet, J.-L. Vanoverschelde, and B. L. Gerber Combined coronary and late-enhanced multidetector-computed tomography for delineation of the etiology of left ventricular dysfunction: comparison with coronary angiography and contrast-enhanced cardiac magnetic resonance imaging Eur. Heart J., October 2, 2008; 29(20): 2544 - 2551. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. R. Koikkalainen, M. Antila, J. M. P. Lotjonen, T. Helio, K. Lauerma, S. M. Kivisto, P. Sipola, M. A. Kaartinen, S. T. J. Karkkainen, E. Reissell, et al. Early Familial Dilated Cardiomyopathy: Identification with Determination of Disease State Parameter from Cine MR Image Data Radiology, October 1, 2008; 249(1): 88 - 96. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. H. Marwick and M. Schwaiger The Future of Cardiovascular Imaging in the Diagnosis and Management of Heart Failure, Part 2: Clinical Applications Circ Cardiovasc Imaging, September 1, 2008; 1(2): 162 - 170. [Full Text] [PDF]
|
|
|
|
|
|
S. Ghostine, C. Caussin, M. Habis, Y. Habib, C. Clement, A. Sigal-Cinqualbre, C.-Y. Angel, B. Lancelin, A. Capderou, and J.-F. Paul Non-invasive diagnosis of ischaemic heart failure using 64-slice computed tomography Eur. Heart J., September 1, 2008; 29(17): 2133 - 2140. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. Dennert, H. J. Crijns, and S. Heymans Acute viral myocarditis Eur. Heart J., September 1, 2008; 29(17): 2073 - 2082. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. Jerosch-Herold, D. C. Sheridan, J. D. Kushner, D. Nauman, D. Burgess, D. Dutton, R. Alharethi, D. Li, and R. E. Hershberger Cardiac magnetic resonance imaging of myocardial contrast uptake and blood flow in patients affected with idiopathic or familial dilated cardiomyopathy Am J Physiol Heart Circ Physiol, September 1, 2008; 295(3): H1234 - H1242. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. D. Henry, J. R. Lesser, and D. Satran Myocardial Fibrosis From Severe Carbon Monoxide Poisoning Detected by Cardiac Magnetic Resonance Imaging Circulation, August 12, 2008; 118(7): 792 - 792. [Full Text] [PDF]
|
|
|
|
 |
|
 B. J. Schietinger, G. M. Brammer, H. Wang, J. M. Christopher, K. W. Kwon, A. J. Mangrum, J. M. Mangrum, and C. M. Kramer Patterns of late gadolinium enhancement in chronic hemodialysis patients. J. Am. Coll. Cardiol. Img., July 1, 2008; 1(4): 450 - 456. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
K. C. Wu, R. G. Weiss, D. R. Thiemann, K. Kitagawa, A. Schmidt, D. Dalal, S. Lai, D. A. Bluemke, G. Gerstenblith, E. Marban, et al. Late gadolinium enhancement by cardiovascular magnetic resonance heralds an adverse prognosis in nonischemic cardiomyopathy. J. Am. Coll. Cardiol., June 24, 2008; 51(25): 2414 - 2421. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. Kuner, A. S. Barth, M. Ruschhaupt, A. Buness, L. Zwermann, E. Kreuzer, G. Steinbeck, A. Poustka, H. Sultmann, and M. Nabauer Genomic analysis reveals poor separation of human cardiomyopathies of ischemic and nonischemic etiologies Physiol Genomics, June 1, 2008; 34(1): 88 - 94. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Beer, D. Wagner, J. Myers, J. Sandstede, H. Kostler, D. Hahn, S. Neubauer, and P. Dubach Effects of Exercise Training on Myocardial Energy Metabolism and Ventricular Function Assessed by Quantitative Phosphorus-31 Magnetic Resonance Spectroscopy and Magnetic Resonance Imaging in Dilated Cardiomyopathy J. Am. Coll. Cardiol., May 13, 2008; 51(19): 1883 - 1891. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 K. Aghasadeghi and A. Aslani Differentiation of Ischemic and Dilated Cardiomyopathy on Electrocardiograms Asian Cardiovasc Thorac Ann, April 1, 2008; 16(2): 103 - 106. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. Germans and A. C van Rossum The use of cardiac magnetic resonance imaging to determine the aetiology of left ventricular disease and cardiomyopathy Heart, April 1, 2008; 94(4): 510 - 518. [Full Text] [PDF]
|
|
|
|
|
|
R. J. Kim, T. S.E. Albert, J. H. Wible, M. D. Elliott, J. C. Allen, J. C. Lee, M. Parker, A. Napoli, R. M. Judd, and for the Gadoversetamide Myocardial Infarction Imag Performance of Delayed-Enhancement Magnetic Resonance Imaging With Gadoversetamide Contrast for the Detection and Assessment of Myocardial Infarction: An International, Multicenter, Double-Blinded, Randomized Trial Circulation, February 5, 2008; 117(5): 629 - 637. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
U Sechtem, H Mahrholdt, and H Vogelsberg Cardiac magnetic resonance in myocardial disease Heart, December 1, 2007; 93(12): 1520 - 1527. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
V. Lionetti, L. Guiducci, A. Simioniuc, G. D. Aquaro, C. Simi, D. De Marchi, S. Burchielli, L. Pratali, M. Piacenti, M. Lombardi, et al. Mismatch between uniform increase in cardiac glucose uptake and regional contractile dysfunction in pacing-induced heart failure Am J Physiol Heart Circ Physiol, November 1, 2007; 293(5): H2747 - H2756. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
L. W. Jones, M. J. Haykowsky, J. J. Swartz, P. S. Douglas, and J. R. Mackey Early Breast Cancer Therapy and Cardiovascular Injury J. Am. Coll. Cardiol., October 9, 2007; 50(15): 1435 - 1441. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. G Assomull, D. J Pennell, and S. K Prasad Cardiovascular magnetic resonance in the evaluation of heart failure Heart, August 1, 2007; 93(8): 985 - 992. [Full Text] [PDF]
|
|
|
|
|
|
D. S. Owens and J. F. Plehn Recognizing Unrecognized Risk: The Evolving Role of Ventricular Functional Assessment in Population-Based Studies Circulation, July 10, 2007; 116(2): 126 - 130. [Full Text] [PDF]
|
|
|
|
|
|
R. P. Lim, M. B. Srichai, and V. S. Lee Non-Ischemic Causes of Delayed Myocardial Hyperenhancement on MRI Am. J. Roentgenol., June 1, 2007; 188(6): 1675 - 1681. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. C. Silva, Z. M. A. Meira, J. Gurgel Giannetti, M. M. da Silva, A. F. Oliveira Campos, M. de Melo Barbosa, G. M. S. Filho, R. de Aguiar Ferreira, M. Zatz, and C. E. Rochitte Myocardial Delayed Enhancement by Magnetic Resonance Imaging in Patients With Muscular Dystrophy J. Am. Coll. Cardiol., May 8, 2007; 49(18): 1874 - 1879. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. G. Assomull, J. C. Lyne, N. Keenan, A. Gulati, N. H. Bunce, S. W. Davies, D. J. Pennell, and S. K. Prasad The role of cardiovascular magnetic resonance in patients presenting with chest pain, raised troponin, and unobstructed coronary arteries Eur. Heart J., May 3, 2007; (2007) ehm113v1. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. Sen-Chowdhry, P. Syrris, D. Ward, A. Asimaki, E. Sevdalis, and W. J. McKenna Clinical and Genetic Characterization of Families With Arrhythmogenic Right Ventricular Dysplasia/Cardiomyopathy Provides Novel Insights Into Patterns of Disease Expression Circulation, April 3, 2007; 115(13): 1710 - 1720. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
G. P. McCann, C. T. Gan, A. M. Beek, H. W. M. Niessen, A. V. Noordegraaf, and A. C. van Rossum Extent of MRI Delayed Enhancement of Myocardial Mass Is Related to Right Ventricular Dysfunction in Pulmonary Artery Hypertension Am. J. Roentgenol., February 1, 2007; 188(2): 349 - 355. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. M. Kramer The Expanding Prognostic Role of Late Gadolinium Enhanced Cardiac Magnetic Resonance J. Am. Coll. Cardiol., November 21, 2006; 48(10): 1986 - 1987. [Full Text] [PDF]
|
|
|
|
|
|
R. G. Assomull, S. K. Prasad, J. Lyne, G. Smith, E. D. Burman, M. Khan, M. N. Sheppard, P. A. Poole-Wilson, and D. J. Pennell Cardiovascular Magnetic Resonance, Fibrosis, and Prognosis in Dilated Cardiomyopathy J. Am. Coll. Cardiol., November 21, 2006; 48(10): 1977 - 1985. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
H. N. Skouri, G. W. Dec, M. G. Friedrich, and L. T. Cooper Noninvasive Imaging in Myocarditis J. Am. Coll. Cardiol., November 21, 2006; 48(10): 2085 - 2093. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C. B. Marcu, A. M. Beek, and A. C. van Rossum Clinical applications of cardiovascular magnetic resonance imaging. Can. Med. Assoc. J., October 10, 2006; 175(8): 911 - 917. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
H. Mahrholdt, A. Wagner, C. C. Deluigi, E. Kispert, S. Hager, G. Meinhardt, H. Vogelsberg, P. Fritz, J. Dippon, C. -T. Bock, et al. Presentation, Patterns of Myocardial Damage, and Clinical Course of Viral Myocarditis Circulation, October 10, 2006; 114(15): 1581 - 1590. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. Ebeling Barbier, T. Bjerner, L. Johansson, L. Lind, and H. Ahlstrom Myocardial Scars More Frequent Than Expected: Magnetic Resonance Imaging Detects Potential Risk Group J. Am. Coll. Cardiol., August 15, 2006; 48(4): 765 - 771. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P. Knaapen, M. J. W. Gotte, W. J. Paulus, J. J. M. Zwanenburg, P. A. Dijkmans, R. Boellaard, J. T. Marcus, J. W. R. Twisk, C. A. Visser, A. C. van Rossum, et al. Does Myocardial Fibrosis Hinder Contractile Function and Perfusion in Idiopathic Dilated Cardiomyopathy? PET and MR Imaging Study. Radiology, August 1, 2006; 240(2): 380 - 388. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. Mandapaka, R. D'Agostino Jr, and W. G. Hundley Does Late Gadolinium Enhancement Predict Cardiac Events in Patients With Ischemic Cardiomyopathy? Circulation, June 13, 2006; 113(23): 2676 - 2678. [Full Text] [PDF]
|
|
|
|
|
|
R. Y. Kwong, A. K. Chan, K. A. Brown, C. W. Chan, H. G. Reynolds, S. Tsang, and R. B. Davis Impact of Unrecognized Myocardial Scar Detected by Cardiac Magnetic Resonance Imaging on Event-Free Survival in Patients Presenting With Signs or Symptoms of Coronary Artery Disease Circulation, June 13, 2006; 113(23): 2733 - 2743. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. I. vanden Driesen, R. E. Slaughter, and W. E. Strugnell MR findings in cardiac amyloidosis. Am. J. Roentgenol., June 1, 2006; 186(6): 1682 - 1685. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
O. Zimmermann, O. Grebe, N. Merkle, V. Hombach, and J. Torzewski Author reply to letter from J. Smedema Eur J Heart Fail, May 1, 2006; 8(3): 330 - 330. [Full Text] [PDF]
|
|
|
|
|
|
J.P. Smedema Letter to the Editor Eur J Heart Fail, May 1, 2006; 8(3): 331 - 331. [Full Text] [PDF]
|
|
|
|
|
|
J. Vogel-Claussen, C. E. Rochitte, K. C. Wu, I. R. Kamel, T. K. Foo, J. A. C. Lima, and D. A. Bluemke Delayed enhancement MR imaging: utility in myocardial assessment. RadioGraphics, May 1, 2006; 26(3): 795 - 810. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
I. Klem, J. F. Heitner, D. J. Shah, M. H. Sketch Jr, V. Behar, J. Weinsaft, P. Cawley, M. Parker, M. Elliott, R. M. Judd, et al. Improved Detection of Coronary Artery Disease by Stress Perfusion Cardiovascular Magnetic Resonance With the Use of Delayed Enhancement Infarction Imaging J. Am. Coll. Cardiol., April 18, 2006; 47(8): 1630 - 1638. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
F. De Cobelli, M. Pieroni, A. Esposito, C. Chimenti, E. Belloni, R. Mellone, T. Canu, G. Perseghin, C. Gaudio, A. Maseri, et al. Delayed Gadolinium-Enhanced Cardiac Magnetic Resonance in Patients With Chronic Myocarditis Presenting With Heart Failure or Recurrent Arrhythmias J. Am. Coll. Cardiol., April 18, 2006; 47(8): 1649 - 1654. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P A Davlouros, K Niwa, G Webb, and M A Gatzoulis The right ventricle in congenital heart disease Heart, April 1, 2006; 92(suppl_1): i27 - i38. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
O. Zimmermann, O. Grebe, N. Merkle, T. Nusser, M. Kochs, M. Bienek-Ziolkowski, V. Hombach, and J. Torzewski Myocardial biopsy findings and gadolinium enhanced cardiovascular magnetic resonance in dilated cardiomyopathy Eur J Heart Fail, March 1, 2006; 8(2): 162 - 166. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
E Perugini, C Rapezzi, T Piva, O Leone, L Bacchi-Reggiani, L Riva, F Salvi, L Lovato, A Branzi, and R Fattori Non-invasive evaluation of the myocardial substrate of cardiac amyloidosis by gadolinium cardiac magnetic resonance Heart, March 1, 2006; 92(3): 343 - 349. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. V. Babu-Narayan, P. J. Kilner, W. Li, J. C. Moon, O. Goktekin, P. A. Davlouros, M. Khan, S. Y. Ho, D. J. Pennell, and M. A. Gatzoulis Ventricular Fibrosis Suggested by Cardiovascular Magnetic Resonance in Adults With Repaired Tetralogy of Fallot and Its Relationship to Adverse Markers of Clinical Outcome Circulation, January 24, 2006; 113(3): 405 - 413. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 D. S. Berman, R. Hachamovitch, L. J. Shaw, J. D. Friedman, S. W. Hayes, L. E.J. Thomson, D. S. Fieno, G. Germano, P. Slomka, N. D. Wong, et al. Roles of Nuclear Cardiology, Cardiac Computed Tomography, and Cardiac Magnetic Resonance: Assessment of Patients with Suspected Coronary Artery Disease J. Nucl. Med., January 1, 2006; 47(1): 74 - 82. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
F. Ridocci, C. J. Soriano, and J. Estornell Imaging approach to the assessment of cardiomyopathies using delayed enhancement cardiovascular magnetic resonance Eur. Heart J., December 1, 2005; 26(23): 2601 - 2602. [Full Text] [PDF]
|
|
|
|
|
|
S. Nazarian, D. A. Bluemke, A. C. Lardo, M. M. Zviman, S. P. Watkins, T. L. Dickfeld, G. R. Meininger, A. Roguin, H. Calkins, G. F. Tomaselli, et al. Magnetic Resonance Assessment of the Substrate for Inducible Ventricular Tachycardia in Nonischemic Cardiomyopathy Circulation, November 1, 2005; 112(18): 2821 - 2825. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. E. Rochitte, P. F. Oliveira, J. M. Andrade, B. M. Ianni, J. R. Parga, L. F. Avila, R. Kalil-Filho, C. Mady, J. C. Meneghetti, J. A.C. Lima, et al. Myocardial Delayed Enhancement by Magnetic Resonance Imaging in Patients With Chagas' Disease: A Marker of Disease Severity J. Am. Coll. Cardiol., October 18, 2005; 46(8): 1553 - 1558. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Norman, M. Simpson, J. Mogensen, A. Shaw, S. Hughes, P. Syrris, S. Sen-Chowdhry, E. Rowland, A. Crosby, and W. J. McKenna Novel Mutation in Desmoplakin Causes Arrhythmogenic Left Ventricular Cardiomyopathy Circulation, August 2, 2005; 112(5): 636 - 642. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
H. Mahrholdt, A. Wagner, R. M. Judd, U. Sechtem, and R. J. Kim Delayed enhancement cardiovascular magnetic resonance assessment of non-ischaemic cardiomyopathies Eur. Heart J., August 1, 2005; 26(15): 1461 - 1474. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. Repetto, B. D. Bello, M. Pasotti, M. Agozzino, M. Vigano, C. Klersy, L. Tavazzi, and E. Arbustini Coronary atherosclerosis in end-stage idiopathic dilated cardiomyopathy: an innocent bystander? Eur. Heart J., August 1, 2005; 26(15): 1519 - 1527. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
V. Fuster and R. J. Kim Frontiers in Cardiovascular Magnetic Resonance Circulation, July 5, 2005; 112(1): 135 - 144. [Full Text] [PDF]
|
|
|
|
|
|
E. Tadamura, M. Yamamuro, S. Kubo, S. Kanao, T. Saga, M. Harada, M. Ohba, R. Hosokawa, T. Kimura, T. Kita, et al. Effectiveness of Delayed Enhanced MRI for Identification of Cardiac Sarcoidosis: Comparison with Radionuclide Imaging Am. J. Roentgenol., July 1, 2005; 185(1): 110 - 115. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
H. Abdel-Aty, P. Boye, A. Zagrosek, R. Wassmuth, A. Kumar, D. Messroghli, P. Bock, R. Dietz, M. G. Friedrich, and J. Schulz-Menger Diagnostic Performance of Cardiovascular Magnetic Resonance in Patients With Suspected Acute Myocarditis: Comparison of Different Approaches J. Am. Coll. Cardiol., June 7, 2005; 45(11): 1815 - 1822. [Abstract] [Full Text] [PDF]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||