Chest ACCP Education Calendar
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Guest Access | Sign In via User Name/Password
This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF) Free
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Article Archive
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Smedema, J.-P.
Right arrow Articles by Crijns, H. J. G. M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Smedema, J.-P.
Right arrow Articles by Crijns, H. J. G. M.
(Chest. 2005;128:30-35.)
© 2005 American College of Chest Physicians

Cardiac Involvement in Patients With Pulmonary Sarcoidosis Assessed at Two University Medical Centers in the Netherlands*

Jan-Peter Smedema, MD, MMed(Int); Gabriel Snoep, MD; Marinus P. G. van Kroonenburgh, MD, PhD; Robert-Jan van Geuns, MD, PhD; Willem R. M. Dassen, PhD; Anton P. Gorgels, MD, PhD and Harry J. G. M. Crijns, MD, PhD

* From the Departments of Cardiology (Drs. Smedema, Dassen, Crijns, and Gorgels), Radiology (Dr. Snoep), and Nuclear Medicine (Dr. van Kroonenburgh), University Hospital Maastricht, Maastricht; and Department of Cardiology and Radiology (Dr. van Geuns), Erasmus Medical Centre, Rotterdam, the Netherlands.

Correspondence to: J. P. Smedema, MD, MMed(Int), Department of Cardiology, University Hospital Maastricht, Dr Debyelaan 25, 6202 AZ Maastricht, the Netherlands; e-mail: j.smedema{at}cardio.azm.nl


   Abstract
TOP
 Abstract
Introduction
 Materials and Methods
 Results
 Discussion
 Conclusion
 References
 
Study objectives: We aimed to determine cardiac involvement in patients with pulmonary sarcoidosis (PS) followed up at two university medical centers in the Netherlands.

Design: We reviewed the findings in consecutive patients assessed by our departments during 1998 to 2004, and classified them as patients who had presented with symptoms of cardiac sarcoidosis (CS) [group A], and those who had been screened for this condition (group B).

Setting: Two university medical centers in the Netherlands.

Patients: One hundred one patients (69 men [mean age, 47.6 years] and 32 women [mean age, 47.3 years]) with biopsy-proven PS.

Interventions: Twelve-lead ECG (n = 101), ambulatory ECG (n = 74), echocardiography (n = 80), 201Tl single-photon emission CT (n = 61), cardiac MRI (n = 87), coronary angiography to exclude coronary artery disease (n = 17), and endomyocardial biopsy (n = 9).

Measurements: ECG, structural, and functional cardiac abnormalities according to the modified guidelines of the Japanese Ministry of Health and Welfare (1993).

Results: Sixteen of 19 patients in group A and 3 of 82 patients in group B received a diagnosis of CS. During a mean follow-up of 1.7 years (range, 3 months to 4 years), four patients in group A died (20%) and nine patients received a pacemaker and/or an implantable cardioverter-defibrillator (47%), while the patients in group B had an uncomplicated course.

Conclusions: Once symptomatic CS develops in PS patients, the prognosis becomes very grim. In contrast, the prognosis in asymptomatic cardiac involvement in PS patients is good. Considering the poor prognosis of symptomatic CS, pulmonologists should consider regular screening of their PS patients for cardiac involvement with straightforward detection methods.

Key Words: cardiac sarcoidosis • heart failure • MRI • myocardial fibrosis • sudden death • ventricular tachycardia


   Introduction
TOP
 Abstract
 Introduction
Materials and Methods
 Results
 Discussion
 Conclusion
 References
 
Sarcoidosis is a multisystem granulomatous disorder of unknown etiology with symptomatic cardiac involvement in approximately 5% of patients.12 The clinical features of cardiac sarcoidosis (CS) include congestive heart failure, cor pulmonale, supraventricular and ventricular arrhythmias, conduction disturbances, ventricular aneurysms, pericardial effusion, and sudden death.3

The diagnosis of CS is made in the coexistence of noncaseating granulomas on myocardial biopsy or biopsies of any extracardiac tissue (with the exclusion of other causes for granulomatous inflammation such as mycobacterial or fungal infection) and cardiovascular abnormalities for which other possible causes have been excluded. The guidelines from the Japanese Ministry of Health and Welfare provides an excellent diagnostic framework (Table 1 ).4 The prevalence of sarcoidosis in the Netherlands is estimated to be 20 to 30 per 100,000, while the prevalence of cardiac involvement is unknown.


View this table:
[in this window]
[in a new window]

  		Table 1. Criteria for the Diagnosis of CS in this Study*

 
Postmortem studies56 revealed cardiac involvement in 20 to 30% of patients with sarcoidosis in the United States. In Japan, cardiac involvement is reported to be present in as many as 58% of patients, and is responsible for as many as 85% of deaths from sarcoidosis.78 We aimed to determine cardiac involvement in sarcoidosis patients followed up at two university medical centers in the Netherlands, and reviewed the findings in consecutive patients who had presented with symptoms of CS, and in those who had been screened for this condition.


   Materials and Methods
TOP
 Abstract
 Introduction
 Materials and Methods
Results
 Discussion
 Conclusion
 References
 
Study Population
Between July 2000 and May 2004, 101 patients (69 men [age range, 33 to 71 years; mean age, 47.6 years] and 32 women [age range, 29 to 72 years; mean age, 47.3 years]; white race [n = 87; 85%]; African [n = 4]; Asian [n = 9]; and Middle Eastern [n = 1]) with histologically proven pulmonary sarcoidosis (PS) underwent cardiac assessment in the cardiology departments of, the Erasmus Medical Centre (n = 16) and University Hospital Maastricht (n = 85). The diagnosis of sarcoidosis was confirmed if the clinical presentation and chest radiogragraphic finding were supported by histologic evidence of noncaseating granulomas by transbronchial biopsy, and the possibility of infection, environmental factors, or hypersensitivity reaction to medication causing granulomatous inflammation had been eliminated. Patients presented with symptoms suggestive of CS (n = 19) or had been screened for cardiac involvement (n = 82). Patients underwent clinical assessment, including determination of highest serum levels of angiotensin-converting enzyme (n = 64), 12-lead ECGs (n = 101), ambulatory ECG monitoring (n = 74), radiologic chest stage by radiography and/or high-resolution CT (n = 101), transthoracic echocardiograms (n = 80), 201Tl single-photon emission CT (SPECT) [n = 61], and gadolinium-diethylenetriamine pentaacetic acid (DTPA) cardiac MRI (CMR) [n = 87]. Of the 88 CMR studies, 5 were discarded because of insufficient image quality. Seventeen patients underwent diagnostic coronary angiography to exclude coronary artery disease (CAD), endomyocardial biopsies were performed in 6 patients, and 3 patients underwent postmortem examinations. Because of the limited diagnostic yield of endomyocardial biopsies, and the invasive nature with an associated risk of morbidity, we were not justified in systematically subjecting patients who were screened for CS to this procedure. For the purpose of the present study, the Japanese guidelines were modified by excluding endomyocardial biopsy as a diagnostic parameter. Since the guidelines were compiled before CMR had become integral part of cardiac assessment, we further modified our diagnostic scheme by incorporating CMR assessment of wall thickness and motion. The diagnosis of CS, according to the modified guidelines (Table 1), was made in 19 of 101 patients included in the study.

ECG and Ambulatory ECG
A 12-lead surface ECG was performed (MAC; Marquette; Milwaukee, WI; paper speed 25 mm/s), and the findings were classified as abnormal, ie, in keeping with the ECG criteria of the guidelines (Table 1). Ambulatory ECGs (n = 74) were performed for 24 to 72 h, and results were considered abnormal when evidence of intermittent atrioventricular conduction delay or block; intermittent bundle-branch blocks or ventricular arrhythmias, such as frequent monomorphic and/or polymorphic premature ventricular complexes (PVCs) > 100 per 24 h; nonsustained ventricular tachycardias (VTs); and/or sustained VTs were found.

Echocardiography
Studies were performed with a phased-array imaging system (Sonos 5500; Hewlett Packard; Andover, MA) and considered abnormal when regional or global systolic dysfunction, wall thickening, or thinning was found.

Thallium Myocardial Scintigraphy
After treadmill peak exercise, or during IV infusion of dipyridamol, 201Tl was administered and SPECT was performed on a triple-detector gamma camera (MultiSPECT-3; Siemens; Erlangen, Germany) equipped with low-energy, high-resolution collimators. The images were made in a 64 x 64 matrix (60 frames per 45 s). The thallium scan was considered suggestive of CS when areas with reversed uptake and/or irreversible perfusion defects were present, and/or reversible perfusion defects were found in patients with normal coronary arteries at angiography. Regional defects were localized according to the 17-segment model.9

CMR
Studies were performed using a 1.5-T MRI scanner (Philips; Best, the Netherlands; and General Electric; Milwaukee, WI) with a cardiac-dedicated, phased-array coil. The CMR studies were ECG triggered by standard software, and obtained in diastole to minimize artifact due to cardiac motion. Studies consisted of multislice/multiphase steady-state-free precession, spin echo, and fat-saturated, T2-weighted, breath-hold sequences of the short axis, vertical long axis, and four-chamber views. Steady-state-free precession sequences were performed to assess regional wall-motion abnormalities. T2-weighted studies were performed to assess the presence of myocardial inflammation. Ten minutes after the additional administration of 0.1 to 0.2 mmol/kg gadolinium-DTPA (Schering; Berlin, Germany), a spin echo (slice thickness, 8 mm; gap, 0.8 mm; matrix, 512 x 512; field of view, 360 mm) and/or three-dimensional inversion recovery-gradient echo breath-hold sequence (short axis, vertical long axis, and four-chamber views) [slice thickness, 10 mm; no gap; matrix, 256 x 256; field of view, 400 mm] were used to assess for the presence of contrast-enhancing lesions. The inversion time (250 to 400 ms) was determined on an individual basis to obtain optimal nulling of the unenhanced myocardial signal. Regional differences in left ventricular (LV) wall enhancement were measured and localized according to the 17-segment model9 (MASS Suite Postprocessing Software; MEDIS; Leiden, the Netherlands). The total time required for the investigation was 30 to 45 min. The study findings were independently evaluated by four blinded observers, three cardiologists, and one radiologist, with experience in CMR. The study findings were considered to be abnormal when at least two observers described identical abnormalities.

Coronary Angiography
Diagnostic coronary angiography was performed when considered indicated by the managing physician, and was generally done in patients with symptoms and findings suggestive of significant CAD. One patient underwent diagnostic coronary angiography as part of the diagnostic workup before cardiac transplantation.

Statistical Analysis
All statistical analyses were performed using statistical software (Version 11.5; SPSS; Chicago, IL). Group data are expressed as mean ± SD. Continuous variables were assessed using the parametric t test for independent samples or Mann-Whitney test when appropriate, and all categorical variables were assessed using the {chi}2 test. Statistical significance was defined at p < 0.05.


   Results
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
Discussion
 Conclusion
 References
 
Patient Characteristics
The demographic and clinical characteristics of group A and group B are presented in Table 2 . Significantly more patients in group A had CS compared to group B. Pulmonary involvement based on radiologic chest stage was significantly more extensive in group B, while the degree of functional impairment was significantly higher in group A.


View this table:
[in this window]
[in a new window]

  		Table 2. Summary of Demographic and Background Medical Data*

 
Findings at Cardiac Assessment
The findings at cardiac assessment are presented in Table 2, with Tables 3, 4 presenting more detailed information on the findings in all patients with CS. The ECG, ambulatory ECG, echocardiogram, and CMR studies revealed significantly more conduction abnormalities, ventricular arrhythmias, and regional loss of LV wall thickness and function in group A. Of the diagnostic techniques, ECG and CMR showed the most abnormalities.


View this table:
[in this window]
[in a new window]

  		Table 3. Findings in 19 Patients Presenting With Symptoms of Cardiac Involvement*

 

View this table:
[in this window]
[in a new window]

  		Table 4. Findings in Three Asymptomatic PS Patients With Cardiac Involvement Diagnosed by Screening*

 
The ECG demonstrated conduction abnormalities in 10 of the 16 patients (63%) with CS. In four patients in group B, ECG signs of right ventricular hypertrophy were present.

CMR and/or echocardiography diagnosed decreased systolic left ventricular function (mean, 35%; range, 20 to 56%) with global or regional wall motion abnormalities in 12 CS patients (75%). In 10 of the 16 CS patients, CMR and SPECT were available. In four patients, CMR and SPECT diagnosed defects, while CMR revealed small defects in four patients with normal SPECT study findings. The findings with SPECT were not significantly different between groups A and B. In eight patients in group B, small, irreversible perfusion defects were detected that were mainly located in the inferior LV wall. SPECT demonstrated reversible perfusion defects in the anterior wall in two patients with CAD in group B and an irreversible perfusion defect in this region in one patient with CAD in group A. Coronary angiography was performed in 17 patients, and revealed significant CAD in 2 patients in group A. Hypertrophic cardiomyopathy was diagnosed in two patients, one of whom also had CS.

Clinical Data at Follow-up
The management, duration of follow-up, and outcome during follow-up are presented in Tables 3, 4. Of the 16 patients with CS in group A, 9 patients received a pacemaker and/or implantable cardioverter/defibrillator (ICD). Three patients died of ventricular arrhythmias, one of treatment-resistant VTs after implantation of an ICD, and one patient died of complications after cardiac transplantation. Nine patients were treated with immune-suppressive drugs, corticosteroids, with methotrexate or azathioprine. None of the patients in group B had significant cardiovascular complications or died during follow-up.


   Discussion
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
Conclusion
 References
 
Our study is the first to systematically evaluate cardiac involvement in patients with sarcoidosis in the Netherlands, and the largest to employ CMR. Earlier studies in the Sweden (86 patients), Ireland (50 patients), Israel (42 patients), the United States (88 patients), Japan (41 patients), and France (50 patients) used ECG, echocardiography, 201Tl SPECT, and CMR in prospective studies101112131415161718 evaluating the prevalence of cardiac involvement in referred patients with sarcoidosis.

Abnormalities were found in up to 23% of European and 63.4% of Japanese patients. In our study, depending on the technique used, abnormalities were found in 10 to 26% of patients without cardiac symptoms. SPECT detected small, irreversible perfusion defects in 13 patients, while gadolinium-enhancing lesions were present in 12 patients. Both SPECT and CMR demonstrated lesions in four patients. Wagner et al19 previously demonstrated the ability of gadolinium-enhanced CMR to diagnose even small amounts of myocardial scar tissue not detected by SPECT in patients with CAD.

Histologic assessment of gadolinium-DTPA–enhanced myocardium has been correlated with fibrosis and active myocarditis.202122 Since T2-weighted studies revealed increased signal, signifying inflammation in only one patient, delayed enhancement in our patients suggest the presence of myocardial scar tissue. The favorable prognosis of abnormal SPECT findings in asymptomatic sarcoidosis patients was demonstrated by Kinney and Caldwell23 in 52 similar patients in whom the presence of perfusion defects diagnosed with SPECT did not predict survival during a mean follow-up of 89 months. Since CMR is a relatively new diagnostic technique, and experience in evaluating patients with sarcoidosis is limited, long-term follow-up will have to determine the significance of small gadolinium-enhancing lesions in asymptomatic patients.

The significantly poorer New York Heart Association (NYHA) functional class in patients in group A, despite less radiologic pulmonary involvement, is explained by more extensive LV involvement, resulting in a lower LV ejection fraction (LVEF), heart failure, and ventricular arrhythmias. When considering the study of Yazaki et al,24 who determined with multivariate analysis that the presence of higher NYHA functional class increased LV end-diastolic diameter and sustained VTs were independent predictors of death, we anticipated poorer outcome in group A. Although the introduction of the ICD is expected to improve outcome in patients with CS, during a mean follow-up of 15 months (3 to 54 months) in our population it delivered therapy in only one of six patients who received the device.25

Study Limitations
Theoretically, bias was introduced by evaluating a preselected patient population that had been referred to tertiary centers. This, however, seems unlikely when considering the fact that only a few of the patients who were screened for CS actually had this condition. It seems more likely that cardiac involvement may have been underestimated, since the diagnosis was based on the modified guideline of the Japanese Ministry of Health and Welfare. In the absence of diagnostic cardiac histology, CS could only be diagnosed in the presence of ECG abnormalities. As previously published by Silverman et al,5 and demonstrated by patients 1 and 3 (Table 3), cardiac involvement may well be present in the absence of diagnostic ECG abnormalities.


   Conclusion
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
 Conclusion
References
 
In our cohort of 101 PS patients, the rate of cardiac involvement in those screened for this condition was low (4%) and the prognosis was good. The CS patients who presented with cardiac failure or ventricular arrhythmias had significant morbidity and a mortality rate of 25% during a mean follow-up of 15 months. Based on the findings of our current study, we recommend regular ECG evaluation in patients with PS and early referral for additional cardiac assessment with echocardiography or CMR in patients with unexplained fatigue, dyspnea, or palpitations.


   Acknowledgements
 
The authors thank Dr. H. Kuehl, MD, PhD, Aachen University Medical Centre, and Dr. A. M. Beek, MD, Free University Medical Centre, Amsterdam, for assessing the CMR studies.


   Footnotes
 
Abbreviations: CAD = coronary artery disease; CMR = cardiac MRI; CS = cardiac sarcoidosis; DTPA = diethylenetriamine pentaacetic acid; ICD = implantable cardioverter-defibrillator; LV = left ventricular; LVEF = left ventricular ejection fraction; NYHA = New York Heart Association; PS = pulmonary sarcoidosis; PVC = premature ventricular complex; SPECT = single-photon emission CT; VT = ventricular tachycardia

Received for publication August 11, 2004. Accepted for publication January 19, 2005.


   References
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
 Conclusion
 References
 

  1. Hagemann, GJ, Wurm, K (1980) The clinical, electrocardiographic and pathological features of cardiac sarcoid. Jones Williams, W Davies, BH eds. Sarcoidosis and other granulomatous disorders: proceedings of the 8th International Conference ,601-606 Alfa Omega Publishing. Cardiff, UK:
  2. Johns, CJ, Michele, TM The clinical management of sarcoidosis: a 50-year experience at the Johns Hopkins Hospital. Medicine 1999;78,65-111[CrossRef][Medline]
  3. Deng, JC, Baughman, RP, Lynch, JP Cardiac involvement in sarcoidosis. Semin Respir Crit Care Med 2002;23,513-526[CrossRef][Medline]
  4. Hiraga, H, Yuwai, K, Hiroe, M, et al Guideline for the diagnosis of cardiac sarcoidosis: study report on diffuse pulmonary diseases [in Japanese]. 1993,23-24 Japanese Ministry of Health and Welfare. Tokyo, Japan:
  5. Silverman, KJ, Hutchins, GM, Bulkley, BH Cardiac sarcoid: a clinico-pathologic study of 84 unselected patients with systemic sarcoidosis. Circulation 1979;58,1204-1211
  6. Longscope, WT, Freiman, DG A study of sarcoidosis based on a combined investigation of 160 cases, including 30 autopsies from Johns Hopkins Hospital and Massachusetts General Hospital. Medicine 1952;31,1-132[CrossRef][Medline]
  7. Matsui, Y, Iwai, K, Tachibana, T, et al Clinicopathological study on fatal myocardial sarcoidosis. Ann N Y Acad Sci 1976;278,455-469[ISI][Medline]
  8. Tachibana T, Iwai K, Takemura T. Study on the cause of death in patients with sarcoidosis in Japan [abstract]. XII World Congress on Sarcoidosis, Kyoto, Japan, September 8 to 13, 1991
  9. Cerqueira, MD, Weissman, NJ, Dilsizian, V, et al AHA writing group on myocardial segmentation and registration for cardiac imaging. Standardized myocardial segmentation and nomenclature for tomographic imaging of the heart. Circulation 2002;105,539-542[Free Full Text]
  10. Thunell, M, Bjerle, P, Sterjnberg, N ECG abnormalities in patients with sarcoidosis. Acta Med Scand 1983;213,115-118[Medline]
  11. Suzuki, T, Kanda, T, Kubota, S, et al Holter monitoring as non-invasive indicator of cardiac involvement in sarcoidosis. Chest 1994;106,1021-1024[Abstract/Free Full Text]
  12. Fahy, GJ, Marwick, T, McGreery, CJ, et al Doppler echocardiographic detection of left ventricular diastolic dysfunction in patients with pulmonary sarcoidosis. Chest 1996;109,62-66[Abstract/Free Full Text]
  13. Lewin, RF, Mor, R, Spitzer, S, et al Echocardiographic evaluation of patients with systemic sarcoidosis. Am Heart J 1985;110,116-122[CrossRef][ISI][Medline]
  14. Burstow, DJ, Tajik, J, Baily, KR, et al Two-dimensional echocardiographic findings in systemic sarcoidosis. Am J Cardiol 1989;63,478-482[CrossRef][ISI][Medline]
  15. Yamamoto, N, Gotoh, K, Yagi, Y, et al Thallium-201 myocardial SPECT findings at rest in sarcoidosis. Ann Nucl Med 1993;7,97-103[Medline]
  16. Vignaux, O, Dhôte, R, Duboc, D, et al Detection of myocardial involvement in patients with sarcoidosis applying T2-weighted, contrast-enhanced and cine magnetic resonance imaging: initial results of a prospective study. J Comput Assist Tomogr 2002;26,762-767[CrossRef][ISI][Medline]
  17. Dhôte, R, Vignaux, O, Blanche, P, et al Value of MRI for the diagnosis of cardiac involvement in sarcoidosis. Rev Med Interne 2003;24,151-157[Medline]
  18. Sköld, CM, Larsen, FF, Rasmussen, E, et al Determination of cardiac involvement in sarcoidosis by MRI and Doppler echocardiography. J Intern Med 2002;252,465-471[CrossRef][ISI][Medline]
  19. Wagner, A, Mahrholdt, H, Holly, TA, et al Contrast-enhanced MRI and single photon emission computed tomography (SPECT) perfusion imaging for the detection of subendocardial myocardial infarcts: an imaging study. Lancet 2003;361,374-379[CrossRef][ISI][Medline]
  20. Mahrholdt, H, Goedeke, C, Wagner, A, et al CMR in human myocarditis: a comparison to histology and molecular pathology. Circulation 2004;16,1250-1258
  21. Aso, H, Takeda, K, Ito, T, et al Assessment of myocardial fibrosis in cardiomyopathic hamsters with gadolinium-DTPA enhanced magnetic resonance imaging. Invest Radiol 1998;33,22-32[CrossRef][ISI][Medline]
  22. 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]
  23. Kinney, EL, Caldwell, JW Do thallium myocardial perfusion scan abnormalities predict survival in sarcoid patients without cardiac symptoms? Angiology 1990;41,573-576[Abstract/Free Full Text]
  24. Yazaki, Y, Isobe, M, Hiroe, M, et al Prognostic determinants of long-term survival in Japanese patients with cardiac sarcoidosis treated with prednisone. Am J Cardiol 2001;88,1006-1010[CrossRef][ISI][Medline]
  25. Calkins, H, Tandri, H, Daya, S Long-term outcome of patients with cardiac sarcoidosis receiving implantable cardioverter defibrillators [abstract]. J Am Coll Cardiol 2004;43(suppl),126A



This article has been cited by other articles:


Home page
 ChestHome page
D. Mehta, S. A. Lubitz, Z. Frankel, J. P. Wisnivesky, A. J. Einstein, M. Goldman, J. Machac, and A. Teirstein
Cardiac Involvement in Patients with Sarcoidosis: Diagnostic and Prognostic Value of Outpatient Testing
Chest, June 1, 2008; 133(6): 1426 - 1435.
[Abstract] [Full Text] [PDF]

Home page
 ChestHome page
A. S. Teirstein, M. Iannuzzi, and M. L. Padilla
Cardiac sarcoidosis.
Chest, April 1, 2006; 129(4): 1113 - 1113.
[Full Text] [PDF]

Home page
 Am. J. Roentgenol.Home page
J.-P. Smedema and E. Tadamura
Previous Studies on Delayed Enhanced MRI for the Detection of Cardiac Sarcoidosis
Am. J. Roentgenol., February 1, 2006; 186(2): 578 - 579.
[Full Text] [PDF]

This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF) Free
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Article Archive
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Smedema, J.-P.
Right arrow Articles by Crijns, H. J. G. M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Smedema, J.-P.
Right arrow Articles by Crijns, H. J. G. M.

HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS