摘要
Introduction: CMR has become the leading modality to define the clinical impact of hypertrophic cardiomyopathy (HCM). Late gadolinium enhancement (LGE) accurately identifies regions of myocardial fibrosis. 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. Hypothesis: We hypothesize that there is significant RV involvement in HCM when incorporates a CMR analysis for RV hypertrophy and fibrosis. Methods: A retrospective review of all patients referred for HCM was performed. SSFP/LGE techniques were used to diagnose patients with HCM, using gadolinium administration (0.15 mmol/kg). Post-injection (10 minutes) LGE images were obtained using manual T1-weighted, IR-preparations. Regions of myocardium with LGE signals were visually designated as fibrotic. LV/RV mass indices (LVMI/RVMI) and ejection fractions were calculated. Results: Via 72 patients referred for HCM, 47(65%) were CMR confirmed. The mean LVMI was 108 ± 44 g/m2 while the mean RVMI was 30 ± 21 g/m2. As well, 34/47 (72%) had evidence of LV fibrosis while 24/47 (51%) had evidence for RV fibrosis. Of the RVH positive patients, 26/34 (76%) patients were LV LGE positive and 18/34 (52%) were RV LGE positive. Conclusion: The high frequency of RVH and RV fibrosis in the setting of HCM is surprising in that this phenomenon is rarely described. However, there is no reason to expect the phenotypic expression should be limited to the LV. Interestingly, as for the LV, the presence or absence of RV fibrosis has little predictive power towards the systolic function.
Introduction: CMR has become the leading modality to define the clinical impact of hypertrophic cardiomyopathy (HCM). Late gadolinium enhancement (LGE) accurately identifies regions of myocardial fibrosis. 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. Hypothesis: We hypothesize that there is significant RV involvement in HCM when incorporates a CMR analysis for RV hypertrophy and fibrosis. Methods: A retrospective review of all patients referred for HCM was performed. SSFP/LGE techniques were used to diagnose patients with HCM, using gadolinium administration (0.15 mmol/kg). Post-injection (10 minutes) LGE images were obtained using manual T1-weighted, IR-preparations. Regions of myocardium with LGE signals were visually designated as fibrotic. LV/RV mass indices (LVMI/RVMI) and ejection fractions were calculated. Results: Via 72 patients referred for HCM, 47(65%) were CMR confirmed. The mean LVMI was 108 ± 44 g/m2 while the mean RVMI was 30 ± 21 g/m2. As well, 34/47 (72%) had evidence of LV fibrosis while 24/47 (51%) had evidence for RV fibrosis. Of the RVH positive patients, 26/34 (76%) patients were LV LGE positive and 18/34 (52%) were RV LGE positive. Conclusion: The high frequency of RVH and RV fibrosis in the setting of HCM is surprising in that this phenomenon is rarely described. However, there is no reason to expect the phenotypic expression should be limited to the LV. Interestingly, as for the LV, the presence or absence of RV fibrosis has little predictive power towards the systolic function.
