Abstract 12669: If there is LV Myocardial Fibrosis Should We Expect to Find RV Myocardial Fibrosis? A Cardiovascular MRI Study
Introduction: CMR has become the leading technique to detect hypertrophic cardiomyopathy (HCM) providing complete coverage of both ventricles with high spatial resolution. Late gadolinium enhancement (LGE) accurately identifies regions of myocardial fibrosis. Via CMR, innumerable studies have established that LVH is the predominant phenotypic expression of HCM. It is well known that myocardial fibrosis can occur in patients with HCM and is independently linked to a poorer prognosis than those without fibrosis by CMR. The genotypic expressions would appear to affect the entire heart yet, classically, investigations have been limited to the LV, in some part due to the inability to image the smaller, thinner RV. Thus, little information is available about the RV in HCM.
Hypothesis: We hypothesize that there is significant RV involvement in HCM when incorporating a CMR analysis for RV hypertrophy and fibrosis.
Methods: Review of all patients referred for HCM was performed. SSFP/LGEE was used to diagnose patients with HCM, using gadolinium administration (0.15mmol/kg, MultiHance, Bracco Diagnostics, Princeton, NJ). Post-injection (2/10 minutes) LGE images were obtained via T1-weighted, IR preps. Regions of myocardium with abnormally high signals (>2SD) were designated as fibrotic. LV/RVMass Index was calculated.
Results: Via 73 patients referred for HCM from 2006–2010, 19 (26%;) were CMR confirmed. Image quality was judged excellent in18/19 (95%). The mean LVMI was 94±37gm2 (> 2SD > normal) while the mean RVMI was 21±6 gm2 (1SD > normal). All pts met formal LVH criteria while 10/19 (53%) met RVH criteria. 16/19 (84%) had evidence of LV fibrosis while 13/19 (68%) had evidence for RV fibrosis. No patient with RV fibrosis had absent LV fibrosis. In neither the LV nor the RV was there a difference in the degree of hypertrophy as to prediction of likelihood for fibrosis (99±40 vs.83±27g/m2 and 21±25 vs.21±26g/m2, respectively).
Conclusion: The high frequency of RV fibrosis in the setting of HCM is surprising in that this phenomenon is rarely described. However, given the genetic abnormalities, there is no reason to expect the phenotypic expression should be limited to just the LV. Interestingly, as for the LV, the degree of RVH had little predictive power to define RV fibrosis.
- © 2010 by American Heart Association, Inc.