Abstract 3774: Reduced Hyperemic Myocardial Blood Flow in Hypertrophic Cardiomyopathy: New Insights from Multi-Parametric Magnetic Resonance Imaging
Background: While microvascular dysfunction has been noted in hypertrophic cardiomyopathy (HCM) it remains unknown whether the impairment of the hyperemic response correlates with left ventricular wall thickness. Extreme hypertrophy is an independent risk factor for sudden death in HCM but the underlying mechanism is unclear and current risk factor stratification does not reliably assess myocardial perfusion.
Methods and Results: Multi-parametric magnetic resonance imaging (MRI) was performed in 33 HCM patients (38% men) and 15 healthy controls (36% men), aged 18–78 years (mean±SD: 42±14 years) with steady state free precession cine, first-pass perfusion measurement at rest and during adenosine stress, and late enhancement (fibrosis) imaging. Segmental end-diastolic wall thickness (ED WT in mm), absolute rest and stress myocardial blood flow (MBF; ml/min/g), and extent of fibrosis (% of segmental myocardial mass) were analyzed with a mixed effects statistical model, and using the AHA LV segmentation model. Resting MBF, adjusted for age and gender, was not significantly different between HCM patients and controls. Hyperemic MBF (hMBF) was significantly lower in HCM (by −1.83±0.34 (SE) ml/min/g; p<0.001) compared to normal volunteers (mean hMBF±SE: 3.02±0.31 ml/min/g), with adjustment for age (ns), gender (ns), fibrosis (ns), wall thickness (p<0.005) and resting MBF (p<0.001). Within the group of HCM patients, hMBF decreased with ED wall thickness (p<0.005). The incidence of fibrosis (p<0.001) increased significantly over quartiles of ED WT. The ratio of endocardial to epicardial (endo/epi) hMBF, adjusted for wall thickness, was significantly lower in HCM vs. healthy controls. Within the HCM patients the incidence of hyperemic endo/epi MBF<1:1 increased over quartiles of ED WT (p=0.03), suggesting a preferential reduction of hyperemic MBF in the endocardium, and predominantly in the most hypertrophied segments.
Conclusions: In HCM, perfusion reserve as measured by hyperemic MBF is reduced, particularly in the endocardium, and in proportion to the magnitude of hypertrophy. Myocardial ischemia may be an important component of the risk attributable to major hypertrophy in HCM.