CLINICAL RESEARCH: CARDIAC IMAGING
Noninvasive diagnosis of coronary artery disease in patients with heart failure and systolic dysfunction of uncertain etiology, using late gadolinium-enhanced cardiovascular magnetic resonance
Carlos J. Soriano, MD*,
Francisco Ridocci, MD, PhD, FESC*,*,
Jordi Estornell, MD ,
Javier Jimenez, MD*,
Vicente Martinez, MD, PhD and
José A. De Velasco, MD, PhD*
* Servicio de Cardiología, Consorcio Hospital General Universitario de Valencia
Unidad de TC y RM, ERESA, Valencia, Spain
Manuscript received July 13, 2004;
revised manuscript received October 24, 2004,
accepted November 1, 2004.
* Reprint requests and correspondence: Dr. Francisco Ridocci, Servicio de Cardiología, Hospital General Universitario, Avda. Tres Cruces 2a, 46014 Valencia, Spain
(Email: ridocci_fra{at}gva.es).
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Abstract
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OBJECTIVES: We evaluated the feasibility of using late gadolinium-enhanced (LGE) cardiovascular magnetic resonance (CMR) to distinguish left ventricular (LV) systolic dysfunction related or not to coronary artery disease (CAD) in patients with heart failure (HF) but without clinical suspicion of CAD as the underlying cause.
BACKGROUND: In patients with known CAD, LGE-CMR is capable of distinguishing LV systolic dysfunction related to CAD from dilated cardiomyopathy.
METHODS: Seventy-one patients with HF and LV systolic dysfunction, without a previous history of myocardial infarction, with neither Q waves nor clinical data suggesting CAD, underwent both LGE-CMR and coronary angiography.
RESULTS: Twenty-six patients (37%) had angiographically proven CAD ( 70% stenosis of a major epicardial vessel) (angio [+] group), and 45 (63%) had unobstructed coronary arteries (angio [–] group). Twenty-one patients in the angio (+) group (21 of 26, 81%) showed subendocardial and/or transmural enhancement, whereas only 4 (9%) of 45 in the angio (–) group showed it (p < 0.001). In 7 patients (7 of 71, 10%), we found a different pattern of mid-wall enhancement—namely, 3 of 26 patients in the angio (+) group and 4 of 45 in the angio (–) group (11% vs. 9%, p = 0.7). Mid-wall enhancement in the angio (+) group was distributed in segments other than those which had subendocardial enhancement.
CONCLUSIONS: In patients with HF and LV systolic dysfunction without clinical suspicion of CAD, LGE-CMR is an excellent tool for classifying patients in relation to the presence or absence of underlying CAD. Thus, CMR might offer a valid alternative to coronary angiography for the detection of CAD in these patients.
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Abbreviations and Acronyms
| | CAD = coronary artery disease | | CMR = cardiovascular magnetic resonance | | ECG = electrocardiographic | | HF = heart failure | | LGE = late gadolinium enhancement/enhanced | | LV = left ventricle/ventricular | | MI = myocardial infarction |
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Coronary artery disease (CAD) constitutes the main cause of heart failure (HF) with left ventricular (LV) systolic dysfunction, both in the U.S. (1,2) and Europe (3,4). In clinical practice, patients are classified as having HF of ischemic or nonischemic etiology based on a history of myocardial infarction (MI) or angiographic evidence of CAD. This differentiation is important because ischemic etiology has been shown to be independently associated with a worse long-term outcome (5–7). In addition, patients with ischemic cardiomyopathy may benefit from coronary revascularization (8) and adequate secondary preventive measures. According to current practice guidelines, coronary angiography should be performed in HF patients with LV systolic dysfunction and previous CAD, whether with current angina or without it, but having areas of myocardial viability on noninvasive testing. However, it is unclear how to evaluate HF patients without a history of CAD who do not produce any findings suggesting an underlying ischemic cause (2,9).
Cardiovascular magnetic resonance (CMR) is emerging as a useful technique for evaluating HF patients, as it allows a precise and noninvasive measurement of LV function and good correlation with other cardiac imaging techniques (10–12). Moreover, it may be an aid in diagnosing secondary causes of heart failure (13–16). Late gadolinium-enhanced (LGE)-CMR is a technique that visualizes both transmural and subendocardial scarring caused by a previous MI (17–20), and a previous study suggests that enhancement does not appear in nonischemic cardiomyopathy (18). In a recent study, LGE has been shown to be a powerful technique to distinguish LV systolic dysfunction related to CAD from dilated cardiomyopathy (19). In the present study, we evaluated whether LGE can distinguish LV systolic dysfunction related or not to CAD in HF patients without a history of previous MI or clinical data suggesting CAD.
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Methods
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Study population.
The study was approved by our Institutional Medical Ethics Committee, and written, informed consent was obtained from all subjects. The study population was prospectively enrolled from our cardiology department either at hospital admission or during scheduled visits to our HF clinic. We thus enrolled 71 consecutive patients with HF and LV systolic dysfunction but without a previous history of MI, Q waves satisfying standard electrocardiographic (ECG) criteria of infarction (21), or clinical data suggesting CAD (angina or enzymatic criteria of MI [21] or previous revascularization). All patients had symptoms of HF and had echocardiographically documented LV systolic dysfunction with enlarged end-diastolic LV dimension (>95% percentile, corrected by height) (22). Patients were excluded if they had contraindications to CMR, primary valvular disease, constrictive, hypertrophic, or infiltrative cardiomyopathy, or a history of myocarditis. All patients underwent coronary angiography to determine the presence of obstructive CAD (70% stenosis of a major epicardial vessel). They also underwent LGE-CMR. No patient was excluded because of technical limitations or poor image quality on CMR. Patients were classified in two groups based on results from coronary angiography: LV systolic dysfunction with obstructive CAD (angio [+] group) and LV systolic dysfunction without obstructive CAD (angio [–] group).
CMR.
The CMR images were obtained with a 1.5-T system (Magnetom Sonata; Siemens Medical Solutions, Erlangen, Germany). First, long-axis and short-axis cine images of the whole LV myocardium were obtained using ECG-gated, steady-state, free-precession pulse sequence (8-mm slice thickness with a 3-mm gap between short-axis slices). The LGE images were acquired 10 min after intravenous injection (0.1 mmol/kg gadolinium DTPA; Schering AG, Berlin, Germany) with a segmented inversion-recovery, three-dimensional, turbo-fast, gradient-echo pulse sequence (repetition time/echo time 500/1.43 ms, flip angle 10°, field of view 360 to 400 mm) along 12 short-axis and long-axis planes (23). The resulting voxel size was 1.9 x 1.4 x 4 mm. The inversion time was adjusted iteratively with different values ranging from 240 to 340 ms in order to null normal myocardium.
Data analysis.
Short-axis cine images were used to calculate LV volumes and LV ejection fractions by dedicated analysis software (Argus; Siemens Medical Solutions). Previously reported normal CMR ventricular function parameters were used as a reference (24,25). A standard 17-segment cardiac model (26) was used for short-axis slice segmentation and assessing the extent of LGE. The complete set of short-axis, delayed-enhancement images from the atrioventricular ring to the apex were divided into three groups for assessing the extent of LGE in basal, mid-cavity, and apical segments, respectively. The short-axis slices of each group were segmented following the model (26), and the extent of LGE in each segment was assessed blindly to the coronary angiographic results on the following semiquantitative rating scale: 0 = no enhancement; 1 = <50% or subendocardial; 2 = 50% or transmural. If late enhancement of mid-wall distribution was found, it was classified in each segment as present or absent. The final enhancement score assigned to each segment of the 17-segment model was simplified by taking into account only the maximum score obtained from all the corresponding segments of the basal, mid-cavity, and apical short-axis slices groups (usually four for each). The coronary angiogram was read by a single cardiologist who was blinded to the CMR results.
Statistical analysis.
The distribution of continuous variables was characterized by reporting the mean value ± SD, whereas the distribution of categorical variables was expressed as frequencies. Comparisons between groups were made, where appropriate, with the two-sample t test for continuous data and chi-square or Fisher exact test for discrete data. A level of two-tailed p < 0.05 was used to indicate statistical significance.
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Results
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Baseline characteristics.
Based on angiographic findings, 26 patients (26/71, 37%) showed CAD (angio [+] group) and 45 did not (45 of 71, 63%) (angio [–] group). The characteristics of the study population are summarized in Table 1. The angio [–] group was younger and with fewer risk factors than the angio (+) group. The interval between tests (angiography to CMR) was similar in both groups. Eleven patients in the angio (+) group (11 of 26, 42%) had obstructive multivessel disease. Table 2 shows the results of CMR. There were no significant differences in LV parameters between groups.
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Table 2. Cardiovascular Magnetic Resonance Findings: Left Ventricular Functional Parameters and Late Gadolinium Enhancement Distribution
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The presence of LGE was significantly higher in patients with CAD. Twenty-one patients (21 of 26, 81%) in the angio (+) group had subendocardial and/or transmural enhancement, whereas only 4 (9%) of 45 patients in the angio [–] group had subendocardial and/or transmural enhancement (p < 0.001) (Table 2, Figs. 1 and 2). The five patients in the angio (+) group who showed no subendocardial or transmural enhancement had obstructive stenosis in nonproximal segments of the right coronary artery or left circumflex coronary artery, but severe LV dysfunction. In 7 patients (7 of 71, 10%), we found a different pattern of mid-wall enhancement; 3 of 26 patients in the angio (+) group and 4 of 45 in the angio (–) group (11% vs. 9%, p = 0.7) (Table 2) had late enhancement of mid-wall distribution. All three patients in the angio (+) group who showed mid-wall enhancement had one-vessel disease. In addition, in two of three patients in the angio (+) group, both patterns coexisted, with the mid-wall distribution located in different segments than the subendocardial enhancement (Fig. 3).
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Figure 1 A patient with three-vessel coronary artery disease and severe left ventricular dysfunction (angio [+] group), with a multisegmentary pattern of subendocardial and transmural late gadolinium enhancement (LGE) suggesting previous myocardial infarction. (A) Long-axis two-chamber view showing a transmural LGE pattern in anterior and apical segments in the left anterior descending coronary artery territory (black arrows), as well as a subendocardial LGE pattern in the basal inferior segment in the right coronary artery territory (white arrow). (B) Short-axis mid-cavity view showing a transmural LGE pattern in mid-anterolateral and inferolateral segments affecting the anterolateral papillary muscle, as well as a subendocardial LGE pattern in mid-inferior segment (white arrows). (C) Short-axis apical view showing a transmural LGE pattern in apical anterior and septal segments (white arrows).
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Figure 3 Two patients with significant one-vessel disease (angio [+] group) showing coexistence of subendocardial and/or transmural with mid-wall late gadolinium enhancement (LGE) patterns. Patient #1 (A, B, and C) and Patient #2 (D). (A) Long-axis two-chamber view showing one patchy foci of mid-wall LGE distribution enhancement in the basal anterolateral segment (white arrow) coexisting with subendocardial LGE in basal inferior and apical inferior segments and with transmural LGE in the apex segment (black arrows). (B) Short-axis basal view showing patchy foci of mid-wall distribution in the basal anterolateral segment (white arrow) and subendocardial LGE in the basal inferior segment (black arrow). (C) Short-axis apical view showing subendocardial LGE in the apical inferior segment and transmural LGE in apical septal and apical lateral segments (white arrow). (D) Short-axis mid-cavity view of another patient showing longitudinal striae of mid-wall distribution LGE in mid-anteroseptal and mid-inferoseptal segments (white arrows) coexisting with transmural LGE in the mid-inferior segment (black arrow).
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Discussion
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We evaluated the capability of LGE-CMR to distinguish LV systolic dysfunction related or not to CAD in HF patients without a previous history of MI or clinical data suggesting CAD. We found an overall sensitivity of 81%, specificity of 91%, and diagnostic accuracy of 87% in determining the presence of obstructive CAD in our patients using angiography as a diagnostic standard. Our findings are consistent with previous studies that evaluated patients with known CAD (18–20), suggesting that LGE-CMR may be useful in distinguishing LV systolic dysfunction related or not to CAD. As we have shown, this differentiation is also feasible in HF patients without clinical suspicion of CAD as the underlying cause.
In our study, 5 (19%) of 26 patients did not show subendocardial or transmural LGE despite the presence of obstructive coronary lesions. As patients in our angio (+) group did not have a previous history of MI, the presence of CAD might not be associated with myocardial necrosis, thus hindering the detection of scarred tissue by LGE. Regional ventricular dysfunction without late enhancement in patients with ischemic heart disease has been observed previously (17,18). On the other hand, the presence of CAD in these patients could not be the cause of LV systolic dysfunction, particularly in the absence of proximal stenosis of a major coronary artery, and therefore with little capacity to provoke large areas of myocardial hibernation (27,28). In our study, taking into account angiographic data, the sole presence of CAD would not explain the severity of LV dysfunction that showed patients in the angio (+) group without LGE.
Four (9%) of the 45 patients without coronary artery stenosis showed a pattern of subendocardial and/or transmural LGE that was indistinguishable from the patients with CAD. Similar findings have been reported previously by McCrohon et al. (19) and Bello et al. (20), with 8 (13%) of 63 patients and 2 (12%) of 17 patients, respectively. The explanation of this finding might be either a previous MI without significant CAD (29,30) or the occurrence of a silent MI between the coronary angiogram and CMR. There is little possibility of the latter in our study, considering the short time between both tests (1.7 ± 3.5 months in the angio [+] group).
In our study, late mid-wall gadolinium enhancement distribution was only found in 4 (9%) of 45 patients in the angio [–] group, and therefore it was a nonsensitive method for the diagnosis of idiopathic dilated cardiomyopathy. Moreover, the fact that mid-wall enhancement coexisted with subendocardial enhancement in 2 (9%) of 21 patients in the angio (+) group (Fig. 3) suggests that dilated cardiomyopathy and CAD can coexist. The pattern of late mid-wall gadolinium enhancement has been recently described in patients with dilated cardiomyopathy (19), as well as in other conditions, such a hypertrophic cardiomyopathy (31–34) and infiltrative disease (35,36). The clinical significance of this finding, presumably related to interstitial fibrosis, has not yet been established and warrants further investigation.
Late gadolinium enhancement may add useful information in two ways to the etiologic classification of HF with LV systolic dysfunction: 1) patients with subendocardial or transmural scarring and unobstructed coronary arteries may have LV systolic dysfunction due to a silent previous MI, as suggested by McCrohon et al. (19); and 2) patients without scarring and with one-vessel disease with no proximal stenosis of a major coronary artery should be considered as having nonischemic cardiomyopathy from a diagnostic and prognostic point of view (7).
Clinical implications.
Coronary angiography is routinely performed to exclude the presence of CAD in patients with HF and LV systolic dysfunction without a history of MI or angina, because perfusion defects and segmental wall motion abnormalities detected by noninvasive tests suggest CAD, but these signs are frequently also seen in patients with nonischemic cardiomyopathy (2). In our group of patients with LV systolic dysfunction and a low probability of CAD, the detection of LGE with CMR was a powerful diagnostic tool for classifying the underlying cause of cardiomyopathy. In our experience, it improved information obtained from angiographic data that may have important prognostic and therapeutic implications. In particular, as the absence of LGE excludes the presence of infarction or severe CAD, it may be unnecessary to perform diagnostic coronary angiography routinely in this setting.
Study limitations.
It can be argued that large areas of hibernating myocardium without necrosis can lead to severe ischemic LV systolic dysfunction without showing LGE (27,28). However, this scenario is very uncommon, particularly if there is no clinical angina. Indeed, no patient in our study presented with this condition. On the other hand, other forms of nonischemic heart disease can cause LGE (13,16,31–36). Nevertheless, the prevalence of these other disorders is rather low compared with CAD, and their clinical presentation is often different and leads to a correct diagnosis.
Conclusions.
Late gadolinium enhancement using CMR is a useful tool for classifying patients with HF and LV systolic dysfunction in relation to the presence or absence of underlying CAD. It improves on the information obtained from angiographic data. In our patients with HF and LV systolic dysfunction but without clinical suspicion of CAD, LGE-CMR allowed us to rule out the presence of significant CAD. Thus, this technique may become a valid noninvasive imaging alternative to coronary angiography.
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Figure 2 One patient with severe left ventricular dysfunction without coronary artery disease (angio [–] group) and no late gadolinium enhancement (LGE). (A) Long-axis two-chamber view. (B) Long-axis four-chamber view. (C) Short-axis mid-cavity view. Note no LGE in the suppressed myocardium.
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Acknowledgments
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The authors thank Ernesto Castillo, MD, for his help with the English translation of the manuscript.
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References
|
|---|
1. Gheorghiade M, Bonow RO. Chronic heart failure in the United States: a manifestation of coronary artery disease Circulation 1998;97:282-289.[Free Full Text]
2. Hunt SA, Baker DW, Chin MH, et al. ACC/AHA guidelines for the evaluation and management of chronic heart failure in the adult: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee to Revise the 1995 Guidelines for the Evaluation and Management of Heart Failure). 2001. American College of Cardiology Web Site. Available at: http://www.acc.org/clinical/guidelines/failure/hf_index.htm. Accessed October 2003..
3. Sutton GC. Epidemiologic aspects of heart failure Am Heart J 1990;120:1538-1540.[CrossRef][Web of Science][Medline]
4. Remme WJ, Swedberg K, Cleland J, et al. Guidelines for the diagnosis and treatment of chronic heart failureTask Force for the Diagnosis and Treatment of Chronic Heart Failure, European Society of Cardiology. Eur Heart J 2001;22:1527-1560.[Free Full Text]
5. 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]
6. 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]
7. Felker GM, Shaw LK, O'Connor CM. A standarized definition of ischemic cardiomyopathy for use in clinical research J Am Coll Cardiol 2002;39:210-218.[Abstract/Free Full Text]
8. Yusuf S, Zucker D, Peduzzi P, et al. Effect of coronary artery bypass surgery on survival: overview of 10-year results from randomized trials by the Coronary Artery Bypass Surgery Trialists Collaboration Lancet 1994;344:563-570.[CrossRef][Web of Science][Medline]
9. Eagle K, Guyton RA, Davidoff R, et al. ACC/AHA guidelines for coronary artery bypass graft surgery: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee to Revise the 1991 Guidelines for Coronary Disease Bypass Graft Surgery) J Am Coll Cardiol 1999;34:1262-1347.[Free Full Text]
10. Grothues F, Smith GC, Moon JC, et al. Comparison of interstudy reproducibility of cardiovascular magnetic resonance with two-dimensional echocardiography in normal subjects and in patients with heart failure or left ventricular hypertrophy Am J Cardiol 2002;90:29-34.[CrossRef][Web of Science][Medline]
11. Schalla S, Nagel E, Lechmkuhl H, et al. Comparison of magnetic resonance real-time imaging of left ventricular function with conventional magnetic resonance imaging and echocardiography Am J Cardiol 2001;87:95-99.[CrossRef][Web of Science][Medline]
12. Bellenger NG, Burgess MI, Ray G, et al. Comparison of left ventricular ejection fraction and volumes in heart failure by echocardiography, radionuclide ventriculography and cardiovascular magnetic resonance Eur Heart J 2000;21;:1387-1396.
13. 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.[Abstract/Free Full Text]
14. Moon JCC, Fisher NG, McKenna WJ, Pennell DJ. Detection of apical hypertrophic cardiomyopathy by cardiovascular magnetic resonance in patients with non diagnostic echocardiography Heart 2004;90:645-649.[Abstract/Free Full Text]
15. Fattori R, Rocchi G, Celletti F, Bertaccini P, Rapezzi C, Gavelli G. Contribution of magnetic resonance imaging in the differential diagnosis of cardiac amyloidosis and symmetric hypertrophic cardiomyopathy Am Heart J 1998;136:824-830.[CrossRef][Web of Science][Medline]
16. Mahrholdt H, Goedecke C, Wagner A, et al. Cardiovascular magnetic resonance assessment of human myocarditis: comparison to histology and molecular pathology Circulation 2004;109:1250-1258.[Abstract/Free Full Text]
17. 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.[Abstract/Free Full Text]
18. Wu E, Judd RM, Vargas JD, Klocke FJ, Bonow RO, Kim RJ. Visualisation of the presence, location and transmural extent of healed Q-wave and non–Q-wave myocardial infarction Lancet 2001;357:21-28.[CrossRef][Web of Science][Medline]
19. McCrohon JA, Moon JCC, Prasad SK, et al. Differentiation of heart failure related to dilated cardiomyopathy and coronary artery disease using gadolinium-enhanced cardiovascular magnetic resonance Circulation 2003;108:54-59.[Abstract/Free Full Text]
20. Bello D, Shah DJ, Farah GM, et al. Gadolinium cardiovascular magnetic resonance predicts reversible myocardial dysfunction and remodeling in patients with heart failure undergoing beta-blocker therapy Circulation 2003;108:1945-1953.[Abstract/Free Full Text]
21. Alpert JS, Thygesen K, Antman E, Bassand JP. 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.[Free Full Text]
22. Lauer MS, Larson MG, Levy D. Gender-specific reference M-mode values in adults: population-derived values with consideration of the impact of height J Am Coll Cardiol 1995;26:1039-1046.[Abstract]
23. Simonetti OP, Kim RJ, Fieno DS, et al. An improved magnetic resonance imaging technique for the visualization of myocardial infarction Radiology 2001;218:215-223.[Abstract/Free Full Text]
24. Lorenz CH, Walker ES, Morgan VL, Klein SS, Graham TP. 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.[Web of Science][Medline]
25. Penell DJ. Ventricular volume and mass by cardiovascular magnetic resonance J Cardiovasc Magn Reson 2002;4:507-513.[CrossRef][Web of Science][Medline]
26. Cerqueira MD, Weissman NJ, Dilsizian V, et al. Standardized myocardial segmentation and nomenclature for tomographic imaging of the heart: a statement for healthcare professionals from the Cardiac Imaging Committee of the Council on Clinical Cardiology of the American Heart Association Circulation 2002;105:539-542.[Free Full Text]
27. Rahimtoola SH. Concept and evaluation of hibernating myocardium Annu Rev Med 1999;50:75-86.[CrossRef][Web of Science][Medline]
28. Elsasser A, Schelepper M, Klovekorn WP, et al. Hibernating myocardium: an incomplete adaptation to ischemia Circulation 1997;96:2920-2931.[Abstract/Free Full Text]
29. Topol EJ, Yadav JS. Recognition of the importance of embolization in atherosclerotic vascular disease Circulation 2000;101:570-580.[Free Full Text]
30. Falk E, Shah PK, Fuster V. Coronary plaque disruption Circulation 1995;92:657-671.[Free Full Text]
31. Wilson JM, Villareal RP, Hariharan R, Massumi A, Muthupillai R, Flamm SD. Magnetic resonance imaging of myocardial fibrosis in hypertrophic cardiomyopathy Tex Heart Inst J 2002;29:176-180.[Web of Science][Medline]
32. Choudhury L, Mahrholdt H, Wafner A, et al. Myocardial scarring in asymptomatic or mildly symptomatic patients with hypertrophic cardiomyopathy J Am Coll Cardiol 2002;40:2156-2164.[Abstract/Free Full Text]
33. Moon JCC, Reed E, Sheppard MN, et al. The histologic basis of late gadolinium enhancement cardiovascular magnetic resonance in hypertrophic cardiomyopathy J Am Coll Cardiol 2004;43:2260-2264.[Abstract/Free Full Text]
34. Moon JCC, McKenna WJ, McCrohon JA, Elliot PM, Smith GC, Pennell DJ. Toward clinical risk assessment in hypertrophic cardiomyopathy with gadolinium cardiovascular magnetic resonance J Am Coll Cardiol 2003;41:1561-1567.[Abstract/Free Full Text]
35. Moon JCC, Sachdev B, Elkington AG, et al. Gadolinium enhanced cardiovascular magnetic resonance in Anderson-Fabry disease (1)Evidence for a disease specific abnormality of the myocardial interstitium. Eur Heart J 2003;24:2151-2155.[Abstract/Free Full Text]
36. Moon JCC, Mundy HR, Lee PJ, Mohiaddin RH, Pennell DJ. Myocardial fibrosis in glycogen storage disease type 3 Circulation 2003;107:e47.[Free Full Text]
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Abstract
Methods