| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
Clinical Investigations |
1 Department of Cardiology, VU University Medical Center, Amsterdam, The Netherlands
2 Department of Nuclear Medicine and PET Research, VU University Medical Center, Amsterdam, The Netherlands
Delayed contrast enhancement (DCE) visualized by cardiac MRI (CMR) is a common feature in patients with hypertrophic cardiomyopathy (HCM), presumed to be related to myocardial fibrosis. The pathophysiologic basis of hyperenhancement in this patient group, however, remains unclear as limited histologic comparisons are available. The present study compares the perfusable tissue index (PTI), an alternative marker of myocardial fibrosis obtained by PET, with DCE-CMR in HCM. Methods: Twenty-one patients with asymmetric septal HCM, 12 chronic myocardial infarction (MI) patients, and 6 age-matched healthy control subjects were studied with DCE-CMR and PET. PET was performed using 15O-labeled water and carbon monoxide to obtain the PTI. Results: No hyperenhancement was observed in control subjects and the PTI was within normal limits (1.10 ± 0.07 [mean ± SD]). In MI patients, the extent of hyperenhancement (25% ± 16% [mean ± SD]) was inversely related to the decrease in the PTI (0.94 ± 0.12; r = –0.65, P < 0.05). Average hyperenhancement in HCM was 14% ± 12%, predominantly located in the interventricular septum. The PTI in the hypertrophied interventricular septum, however, was not reduced (1.12 ± 0.13). Furthermore, in contrast to MI patients, there was a modest positive correlation between the extent of DCE and the PTI in HCM (r = 0.45, P < 0.05). Conclusion: DCE in the hypertrophied septum of HCM patients is not accompanied by a decline in the PTI, and there is a positive correlation between the extent of DCE and the PTI. These results suggest that hyperenhancement may not be caused solely by fibrotic replacement scarring in this patient group. Other pathologic changes associated with HCM may also cause gadolinium-diethylenetriaminepentaacetic acid hyperenhancement.
Key Words: hypertrophic cardiomyopathy • MRI • delayed contrast enhancement • PET • perfusable tissue index
This article has been cited by other articles:
|
|
 |
|
  M. S. Maron, E. Appelbaum, C. J. Harrigan, J. Buros, C. M. Gibson, C. Hanna, J. R. Lesser, J. E. Udelson, W. J. Manning, and B. J. Maron Clinical Profile and Significance of Delayed Enhancement in Hypertrophic Cardiomyopathy Circ Heart Fail, September 1, 2008; 1(3): 184 - 191. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 B. Sotgia, R. Sciagra, I. Olivotto, G. Casolo, L. Rega, I. Betti, A. Pupi, P. G. Camici, and F. Cecchi Spatial Relationship Between Coronary Microvascular Dysfunction and Delayed Contrast Enhancement in Patients with Hypertrophic Cardiomyopathy J. Nucl. Med., July 1, 2008; 49(7): 1090 - 1096. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 W. G. van Dockum, M. J.W. Gotte, P. Knaapen, and A. C. van Rossum Septal alcohol ablation in hypertrophic obstructive cardiomyopathy: improving cardiac function by generating a myocardial scar Eur. Heart J., May 2, 2007; 28(10): 1271 - 1271. [Full Text] [PDF]
|
|
|
|
 |
|
 R. J. Gibbons, P. A. Araoz, and E. E. Williamson The Year in Cardiac Imaging J. Am. Coll. Cardiol., December 5, 2006; 48(11): 2324 - 2339. [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]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| JOURNAL OF NUCLEAR MEDICINE TECHNOLOGY | THE JOURNAL OF NUCLEAR MEDICINE |
