JNM
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

This Article
Right arrow Figures Only
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Sipola, P.
Right arrow Articles by Kuikka, J. T.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Sipola, P.
Right arrow Articles by Kuikka, J. T.
Journal of Nuclear Medicine Vol. 44 No. 4 487-493
© 2003 by Society of Nuclear Medicine

Clinical Investigations

Cardiac Adrenergic Activity Is Associated with Left Ventricular Hypertrophy in Genetically Homogeneous Subjects with Hypertrophic Cardiomyopathy

Petri Sipola, MD1, Esko Vanninen, MD, PhD2, Hannu J. Aronen, MD, PhD1,3, Kirsi Lauerma, MD, PhD3, Sakari Simula, MD, PhD2,4, Pertti Jääskeläinen, MD, PhD4, Markku Laakso, MD, PhD4, Keijo Peuhkurinen, MD, PhD4, Johanna Kuusisto, MD, PhD4 and Jyrki T. Kuikka, PhD2,5

1 Department of Clinical Radiology, University of Kuopio and Kuopio University Hospital, Kuopio, Finland
2 Department of Clinical Physiology and Nuclear Medicine, University of Kuopio and Kuopio University Hospital, Kuopio, Finland
3 Department of Radiology, Helsinki University Central Hospital, Helsinki, Finland
4 Department of Medicine, University of Kuopio and Kuopio University Hospital, Kuopio, Finland
5 Niuvanniemi Hospital, Kuopio, Finland

Hypertrophic cardiomyopathy (HCM) is a genetic disease caused by mutations in genes encoding sarcomeric proteins. However, other genetic and possibly also environmental factors modify the phenotypic expression of left ventricular (LV) hypertrophy. The present study investigated whether cardiac adrenergic activity affects the severity of LV hypertrophy in genetically identical patients with HCM. Methods: The study population consisted of 21 patients with HCM caused by the Asp175Asn substitution of the {alpha}-tropomyosin gene (TPM1-Asp175Asn) and 9 healthy volunteers. LV mass and segmental wall thickness were measured with MRI. Presynaptic cardiac adrenergic activity was measured with 123I-metaiodobenzylguanidine (MIBG) SPECT. Global and segmental washouts of 123I-MIBG were calculated. Results: Global myocardial 123I-MIBG washout was faster in patients with TPM1-Asp175Asn than in healthy volunteers (50% ± 9% vs. 37% ± 8%, P = 0.001). In linear regression analysis, global 123I-MIBG washout was associated with the LV mass index and LV maximal wall thickness index in HCM patients (r = 0.512, P = 0.018, and r = 0.478, P = 0.028, respectively). The mean 123I-MIBG washout was higher in LV segments >= 15 mm thick than in LV segments < 15 mm thick (56 ± 10 vs. 49% ± 10%, P = 0.002). Conclusion: In patients with HCM sharing the same causal gene defect, the degree of LV hypertrophy is related to 123I-MIBG washout, suggesting that cardiac adrenergic activity modifies phenotypic expression in HCM.

Key Words: cardiomyopathy • genetics • hypertrophy • MRI • norepinephrine • scintigraphy






HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
JOURNAL OF NUCLEAR MEDICINE TECHNOLOGY THE JOURNAL OF NUCLEAR MEDICINE
Copyright © 2003 by the Society of Nuclear Medicine.