Rapid Fire Abstracts
Edward Yang, MD
Resident Physician
University of Chicago Medicine
Edward Yang, MD
Resident Physician
University of Chicago Medicine
Hena Patel, MD
Assistant Professor
University of Chicago Medicine
Karima Addetia, MD
Associate Professor
University of Chicago
U Chicago
Amrit Bahga, MD
Resident Physician
University of Chicago Medicine
Cristiane C. De Carvalho Singulane, MD
Postdoctoral Researcher
University of Virginia Health System
Kwadwo A. Boateng, BSc
Medical Student
University of Virginia School of Medicine
Maxine Tang, MD, MSc
Advanced Cardiac Imaging Fellow
Northwestern Medicine
Iva Minga, MD
Advanced Cardiac Imaging Fellow
University of Chicago Medicine
Luis Landeras, MD
Section Chief Cardiothoracic Imaging
The University of Chicago
U Chicago
Amit R. Patel, MD
Professor of Medicine
Division of Cardiology, University of Virginia Health System, Charlottesville, Virginia, USA.
Jeremy A. Slivnick, MD
Assistant Professor
University of Chicago
Although cardiac amyloidosis (CA) is known to deposit in the cardiac microvasculature, little is known about its potential impact on microvascular function. Cardiac magnetic resonance (CMR) is frequently ordered in the evaluation of CA and is able to assess microvascular function via myocardial perfusion reserve index (MPRI).
Methods: CA patients (n=15) and age- and gender-matched control patients with (n=15) and without left ventricular hypertrophy (LVH) (n=15)—defined by maximal wall thickness ≥12mm—who underwent regadenoson stress CMR at 1.5T were retrospectively identified. Those with prior myocardial infarction, coronary artery disease, heart transplant, or reduced LV ejection fraction were excluded. Semiquantitative perfusion analysis with MPRI quantification was performed using endocardial and epicardial tracings at rest/stress (SuiteHeart) (Figure 1). LV mass, biventricular size, and systolic function were quantified using serial short-axis slices. MPRI and CMR parameters were compared between groups using t-tests or Wilcoxon Rank tests as appropriate.
Results: There were no significant differences with respect to biventricular volumes or function between CA patients and LVH control patients. CA and LVH control patients had significantly higher indexed LV mass when compared to healthy control patients. Meanwhile healthy control patients had significantly higher LV ejection fraction than CA patients (Figure 2). MPRI was significantly lower in CA patients as compared to both those with (1.05±0.31 vs 1.35±0.34, p=0.0279) and without (1.61±0.47, p=0.0006) LVH (Figure 3).
Conclusion: Patients with CA have greater impairment in MPRI when compared to healthy control patients with and without LVH, demonstrating the effects of amyloid on cardiac microvasculature on CMR. MPRI assessment using CMR has the potential to enhance the diagnostic value of CMR for CA assessment. Further studies are needed to better understand the potential prognostic and therapeutic implications of microvascular disease in CA.
