Characterization of Methamphetamine Cardiomyopathy: An MRI analysis (RF_FR_371)

Friday, January 31, 2025

2:00 PM – 2:10 PM East Coast USA Time

Location: Blue Room PreFunction

Presenting Author(s)

MM

Michael Morris, MD

Cardiac Imaging Specialist
Banner University Medical Center Phoenix

Primary Author(s)

ZW

Zachary T. Wilson, MD

Cardiology Fellow
Banner University Medical Center Phoenix (Phoenix,

Co-Author(s)

HV

Harrison VanDolah, MD

Medicine/Pediatrics Resident
Banner University Medical Center Phoenix (Phoenix,
BM

Billal Mohmand, MD

Cardiology Fellow
Banner University Medical Center Phoenix (Phoenix,
PR

Pooja Rangan, MD

Data Scientist
Banner University Medical Center Phoenix
RT

Roderick Tung, MD

Chief of Cardiology
Banner University Medical Center Phoenix
MM

Michael Morris, MD

Associate Professor
Banner University Medical Center Phoenix
BT

Balaji Tamarappoo, MD

Cardiac Imaging Specialist
Banner University Medical Center Phoenix

Background: Nonischemic cardiomyopathy is characterized by adverse myocardial remodeling detectable by multiparametric cardiac magnetic resonance imaging (CMR). Chronic methamphetamine use is associated with direct cardiotoxicity and accelerated ischemic heart disease. Our goal was to use CMR to characterize the myocardial phenotype of methamphetamine cardiomyopathy (MACM) in patients without obstructive coronary artery disease (CAD).

Methods: In a descriptive, retrospective, cross-sectional study, we analyzed multiparametric CMR data from patients with methamphetamine use (defined by a clinical diagnosis of methamphetamine abuse or a positive urine drug screen) and absence of obstructive CAD (defined as lesions with < 70% stenosis or 50—70% with iFR >0.89 by invasive angiography or CT-FFR >0.8 by coronary CT angiography) who underwent a 1.5T CMR at a single center from 2016-2023. Ventricular dimensions, ejection fraction (EF), T1, T2, extracellular volume (ECV), and delayed enhancement (DE) were assessed by level 3 trained CMR readers using commercial post processing software. Patients with elevated myocardial T1 or ECV were considered to have diffuse fibrosis if myocardial T2 values were normal or considered probable diffuse fibrosis if T2 values were not available.

Results:

98 patients with methamphetamine use completed a CMR. Of these 65 had no obstructive CAD. 41/65 patients (63.1%) were male, and average age was 46.5 ± 12.2 years. A history of myocardial infarction was reported in 21/65 (32.3%). CMR parameters demonstrated left ventricular (LV) dilatation (mean EDVI=114.4 ± 58.1 ml/m2 and mean ESVI=81.6 ± 56.6 ml/m2), decreased LVEF (mean 35.9 ± 18.6%), right ventricular (RV) dilation (mean EDVI=106 ± 42.3 ml/m2 and mean ESVI= 74.7 ± 37.1ml/m2), and decreased RVEF (mean 33.5 ± 14.6%). Native T1 (n=41) was abnormal (median 1104ms, IQR 1072-1241ms) and ECV (n=36) was increased (median 29.5%, IQR 27-32.3%) relative to local reference standards. DE was present in 29/65 (45%) with 14/29 (48.3%) mid myocardial, 2/29 (6.9%) subepicardial, 3/29 (10.3%) subendocardial, 4/29 (13.8%) transmural and 6/29 (20.7%) mixed pattern. The LV septum was the most common location for DE (15/29, 51.7%). Diffuse fibrosis, probable diffuse fibrosis, and/or DE was present in 42/65 (64%) patients.

Conclusion:

This is the largest CMR characterization study of MACM to our knowledge. Biventricular dilation and dysfunction were common, as was the presence of myocardial fibrosis. Mid myocardial DE was the most common DE pattern, usually in the LV septum. Future studies should assess the prognostic implications of these CMR findings in this cohort.