Relation of Myocardial Perfusion Reserve and Left Ventricular Ejection Fraction in Ischemic and Nonischemic Cardiomyopathy

https://doi.org/10.1016/j.amjcard.2022.02.022Get rights and content

Quantification of myocardial perfusion reserve (MPR) using vasodilator stress cardiac magnetic resonance is increasingly used to detect coronary artery disease. However, MPR can also be altered because of changes in microvascular function. We aimed to determine whether MPR can distinguish between ischemic cardiomyopathy (IC) secondary to coronary artery disease and non-IC (NIC) with microvascular dysfunction and no underlying epicardial coronary disease. A total of 60 patients (mean age 65 ± 14 years, 30% women), including 31 with IC and 29 with NIC, were identified from a pre-existing vasodilator stress cardiac magnetic resonance registry. Short-axis cine slices were used to measure left ventricular ejection fraction (LVEF) using the Simpson method of disks. MPR index (MPRi) was determined from first-pass myocardial perfusion images during stress and rest using the upslope ratio, normalized for the arterial input and corrected for rate pressure product. Patients in both groups were divided into subgroups of LVEF ≤35% and LVEF >35%. Differences in MPRi between the subgroups were examined. MPRi was moderately correlated with LVEF in patients with NIC (r = 0.53, p = 0.03), whereas the correlation in patients with IC was lower (r = 0.32, p = 0.22). Average LVEF in NIC and IC was 34% ± 8% and 35% ± 8%, respectively (p = 0.63). MPRi was not significantly different in IC compared with NIC (1.17 [0.88 to 1.61] vs 1.23 [1.07 to 1.66], p = 0.41), including the subgroups of LVEF (IC: 1.20 ± 0.56 vs NIC: 1.15 ± 0.24, p = 0.75 for LVEF ≤35% and IC: 1.35 ± 0.44 vs NIC: 1.58 ± 0.50, p = 0.19 for LVEF >35%). However, MPRi was significantly lower in patients with LVEF ≤35% compared with those with LVEF>35% (1.17 ± 0.40 vs 1.47 ± 0.47, p = 0.01). Similar difference between LVEF groups was noted in the patients with NIC (1.15 ± 0.24 vs 1.58 ± 0.50, p = 0.006) but not in the patients with IC (1.20 ± 0.56 vs 1.35 ± 0.44, p = 0.42). MPRi can be abnormal in the presence of left ventricular dysfunction with nonischemic etiology. This is a potential pitfall to consider when using this approach to detect ischemia because of epicardial coronary disease using myocardial perfusion imaging.

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.

References (32)

Cited by (1)

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).

View full text