Abstract 11921: Microvascular Dysfunction Exists in Dilated Cardiomyopathy and Correlates with Disease Severity
Introduction: Dilated cardiomyopathy (DCM) is traditionally regarded as a non-ischemic CM. However, PET studies have demonstrated reduced myocardial perfusion reserve (MPR) in DCM patients. CMR perfusion imaging allows calculation of MPR from quantification of myocardial blood flow (MBF) at stress and rest. We hypothesized that reduced MPR can be detected in DCM by CMR and correlates with disease severity.
Methods: Consecutive DCM patients referred for CMR and age/sex matched healthy controls were prospectively enrolled. Exclusion criteria included co-existent ischemic heart disease, diabetes and severe hypertension. Patients were classified as having severe LV systolic dysfunction (LVSD) or mild/moderate LVSD based on an LVEF cut-off value of 35%. CMR first-pass perfusion imaging (1.5T Siemens, 0.1mmol/kg Gd) was performed using a hybrid echo-planar-imaging sequence during adenosine-induced hyperemia (140µg/kg/min) and at rest. MPR was calculated from absolute stress and rest global MBF quantified by a model-constrained deconvolution algorithm.
Results: Forty two DCM patients (30 male, mean age 50 yrs, mean LVEF 37%) and 9 controls (6 male, mean age 44 yrs, mean LVEF 67%) were studied. CAD was excluded in 31 (74%) patients by coronary angiography. All other patients (n=11) were young (age<40 yrs), had no IHD risk factors and negative stress imaging tests. Severe LVSD was observed in 19 patients and mild/moderate LVSD in 23. MPR was significantly reduced in severe LVSD patients (mean MPR 1.72 ± 0.41) compared to those with mild/moderate LVSD (mean MPR 2.53 ± 0.69; p=0.001) and controls (mean MPR 2.54 ± 0.89, p=0.008) (Fig.1). MPR significantly correlated with LVEF (r=0.58, p<0.001) and log BNP (r=-0.61, p<0.001) in the DCM cohort.
Conclusions: Microvascular dysfunction, reflected by impaired MPR, is present in DCM and correlates with markers of disease severity. Further study is required to evaluate whether it is causal or secondary to adverse LV remodeling.
- © 2011 by American Heart Association, Inc.