Relation of Myocardial Perfusion Reserve and Left Ventricular Ejection Fraction in Ischemic and Nonischemic Cardiomyopathy
Introduction
Abnormalities in myocardial perfusion reserve (MPR) are known to be associated with coronary artery disease (CAD). In the ISCHEMIA study, patients with stable ischemic heart disease and left ventricular (LV) dysfunction (LVD) had worse outcomes than patients without LVD. Moreover, patients with LVD assigned to an initial invasive treatment strategy aimed at coronary revascularization had better clinical outcomes compared with a conservative strategy without initial coronary revascularization; whereas no such difference was present in patients without LVD.1 In patients with depressed LV ejection fraction (LVEF), assessment of myocardial perfusion can potentially be used to differentiate ischemic from nonischemic heart disease as the etiology of the LVD and thus guide treatment decisions. However, abnormal MPR may be present not only in LVD because of obstructive CAD, but also in the setting of nonischemic cardiomyopathy (NIC) because of underlying microvascular dysfunction.2,3 Indeed, previous studies have demonstrated an impairment of myocardial perfusion in patients with dilated cardiomyopathy4,5 and that the reduction of MPR is correlated with LVEF.3 Cardiac magnetic resonance (CMR) is commonly used to evaluate patients with LVD. It is considered the reference standard for quantifying LVEF, and the burden and pattern of myocardial fibrosis. When combined with vasodilator stress perfusion imaging, CMR can also be used to quantify MPR.6,7 Semiquantitative approaches, such as the upslope ratio, for determining MPR from stress CMR images have been validated against invasive fractional flow reserve8,9 and shown to be independently associated with the occurrence of major adverse cardiac events.10,11 In this study, we aimed to determine whether MPR measured using stress perfusion CMR can distinguish between ischemic cardiomyopathy (IC) and NIC, and how this ability is influenced by the underlying LVEF.
Section snippets
Methods
We identified 60 patients, including 31 with IC and 29 with NIC, from a pre-existing registry of patients who underwent vasodilator stress CMR at the University of Chicago. All patients provided written informed consent before their imaging to be included in this registry, which was approved by the institutional review board. The definition of IC was based on the following criteria: (1) history of obstructive epicardial coronary disease, including previous myocardial infarction or coronary
Results
Patient characteristics are shown in Table 1, along with the key imaging findings. Thirty-one patients with IC had a definite evidence of obstructive coronary disease based on invasive coronary angiography or coronary computed tomography. In the NIC group, 29 patients were diagnosed with dilated cardiomyopathy, 15 patients (52%) did not have a specifically identified underlying etiology (i.e., idiopathic), 2 patients (7%) had alcohol-associated cardiomyopathy, 1 patient (3%) had LV
Discussion
Stress myocardial perfusion imaging is commonly performed in clinical practice to differentiate ischemic from NIC. In this study, we quantified MPRi using stress perfusion CMR to evaluate the relation between MPRi and LVEF in IC and NIC. There was no difference in MPRi between IC and NIC. However, in patients with NIC, MPRi was correlated with LVEF, although this relation was not seen in patients with IC. The reason for this finding is that IC is associated with significant regional reductions
Disclosures
Dr. A. Patel has received research support from Philips, Arterys, CircleCVI, and Neosoft. The remaining authors have no conflicts of interest to declare.
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This project was supported by the National Center for Advancing Translational Sciences (NCATS) of the National Institutes of Health (NIH) (Bethesda, Maryland) through grant number 5UL1TR002389-02 that funds the Institute for Translational Medicine (ITM) (Chicago, Illinois). Dr. H. Patel was funded by a T32 Cardiovascular Sciences Training (Chicago, Illinois) Grant (5T32HL7381). Dr. Kawaji, was funded by a K25 Grant (HL141634) (Bethesda, Maryland).