227 Early detection of systolic and diastolic dysfunction in asymptomatic hypertrophic cardiomyopathy mutation carriers
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Meeting abstract
227 Early detection of systolic and diastolic dysfunction in asymptomatic hypertrophic cardiomyopathy mutation carriers using cardiac magnetic resonance imaging Tjeerd Germans*1, Marco JW Gotte1, Iris K Russel1, Marieke D Spreeuwenberg1, J Tim Marcus1, Yigal M Pinto2, Pieter A Doevendans3, Arthur AM Wilde4 and Albert C van Rossum1 Address: 1VU University Medical Center, Amsterdam, The Netherlands, 2Academic Hospital Maastricht, Maastricht, The Netherlands, 3University Medical Center Utrecht, Utrecht, The Netherlands and 4Academic Medical Center, Amsterdam, The Netherlands * Corresponding author
from 11th Annual SCMR Scientific Sessions Los Angeles, CA, USA. 1–3 February 2008 Published: 22 October 2008 Journal of Cardiovascular Magnetic Resonance 2008, 10(Suppl 1):A88
doi:10.1186/1532-429X-10-S1-A88
Abstracts of the 11th Annual SCMR Scientific Sessions - 2008
Meeting abstracts – A single PDF containing all abstracts in this Supplement is available here. http://www.biomedcentral.com/content/pdf/1532-429X-10-S1-info.pdfThis abstract is available from: http://jcmr-online.com/content/10/S1/A88 © 2008 Germans et al; licensee BioMed Central Ltd.
Background Hypertrophic Cardiomyopathy (HCM) is characterized by asymmetric hypertrophy of the left ventricle (LV). While over 400 HCM mutations have been identified, increasing number of HCM mutation carriers without hypertrophy have been detected. No data on regional functional and structural abnormalities in HCM mutation carriers before the development of hypertrophy are yet available. With cardiac magnetic resonance imaging (CMR), both regional function and structure can accurately be evaluated.
Methods 28 HCM mutation carriers from 9 different families and 28 age- and gender matched controls, of whom 15 were genotype negative family members of HCM mutation carriers, underwent CMR. The imaging protocol included full coverage of the LV and left atrium with cine imaging. Subsequently, three short axis slices at basal, mid and apical level were obtained with myocardial tissue tagging (temporal resolution 14 ms, tag persistence >1000 ms). Finally, delayed contrast enhancement imaging was performed. From these datasets, global LV dimensions and left atrial volumes, end-diastolic wall thickness, septal-tolateral-wall-thickness ratio (SL-ratio), wall thickening, peak systolic circumferential strain (peak SCS), peak
systolic circumferential strain rate (peak SCSR), peak diastolic circumferential strain rate (peak DCSR) were determined.
Results Global LV dimensions were comparable between both groups. No contrast enhancement was found. Crypts were present in the inferoseptum in 23 of 28 HCM mutation carriers (82%) and in none of the controls. SL-ratio was larger in HCM mutation carriers than in controls (1.3 ± 0.21 versus 1.1 ± 0.13, p < 0.001), see Figure 1. In HCM mutation carriers, wall thickening in inferoseptal segments at basal and mid level was lower compared to controls (0.61 ± 0.31 versus 0.77 ± 0.26, p < 0.01).
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