Abstract 15185: Impact of Sympathetic Activity and Fibrosis on Microvascular Function in Hypertrophic Cardiomyopathy
Purpose: In patients with hypertrophic cardiomyopathy (HCM), positron emission tomography (PET) and cardiac magnetic resonance (CMR) are potentially useful tools for risk stratification. We therefore sought to measure simultaneously abnormalities in myocardial blood flow (MBF) and cardiac sympathetic activity using PET and investigate their correlation with the patterns of left ventricular (LV) hypertrophy and myocardial fibrosis assessed with CMR.
Methods: Thirteen patients (pts) with HCM (age 53±8 years) and 12 healthy age-matched controls (52±10 years) underwent PET with 11C-hydroxyephedrine (11C-HED) and 15O-labeled water (15O-H2O), and delayed enhancement (DE) CMR on a 1.5 T scanner. Myocardial presynaptic catecholamine reuptake/turnover was assessed measuring volumes of distribution (Vd) of 11C-HED, and MBF was determined from dynamic 15O-H2O PET scans at rest and during adenosine stress (140 mcg/Kg/min). The amount of DE was quantitatively assessed on short-axis CMR images.
Results: The maximal septal thickness in HCM pts was 22±5 mm, LV mass index (LVMI) 89±19 g/m2, and ejection fraction 68±9%. None of the patients had known coronary artery disease. Resting MBF was similar in pts and controls (0.9±0.3 vs. 1.1±0.2 mL/min/g). HCM pts had lower hyperemic MBF (2.1±0.8 vs. 3.1±0.5 mL/min/g; p=0.005) and 11C-HEDVd (44±11 vs. 77±29 mL/g; p=0.002) than controls. In HCM pts septal hyperemic MBF was lower than in the lateral wall at the same level (2.0±0.9 vs. 2.4±0.9 mL/min/g, p=0.002), and was inversely correlated to maximal septal wall thickness MBF (p=0.03). 11C-HEDVd was directly correlated with hyperemic MBF (p<0.001) and inversely with the amount of myocardial fibrosis on DE-CMR (p<0.001). On the other hand, LVMI was not correlated with either 11C-HEDVd or hyperemic MBF.
Conclusions: Our preliminary findings suggest that in HCM pts the increased cardiac sympathetic activity, indicated by the reduced presynaptic nor-adrenaline reuptake, which results in increased noradrenaline concentration at the synaptic cleft, could contribute to aggravate inducible ischemia due to the anatomical abnormality of the intramural coronary arterioles.
- © 2010 by American Heart Association, Inc.