Left Atrial Delayed Enhancement Burden in Cardiac Amyloidosis: An Underappreciated Predictor of Atrial Fibrillation? (RF_TH_263)

Thursday, January 30, 2025

6:10 PM – 6:20 PM East Coast USA Time

Location: Blue Room PreFunction

Presenting Author(s)

MT

Maxine Tang, MD, MSc

Advanced Cardiac Imaging Fellow
Northwestern Medicine

Primary Author(s)

MT

Maxine Tang, MD, MSc

Advanced Cardiac Imaging Fellow
Northwestern Medicine

Co-Author(s)

IM

Iva Minga, MD

Advanced Cardiac Imaging Fellow
University of Chicago Medicine
SS

Seyed Ehsan Saffari, PhD

Professor
Duke-National University of Singapore, Singapore
JG

Jia Guo, MD

Fellow
University of Chicago
HP

Hena Patel, MD

Assistant Professor
University of Chicago Medicine
CD

Cristiane C. De Carvalho Singulane, MD

Postdoctoral Researcher
University of Virginia Health System
Amit R. Patel, MD

Professor of Medicine
Division of Cardiology, University of Virginia Health System, Charlottesville, Virginia, USA.
RL

Roberto M. Lang, MD

Professor of Medicine, Division of Cardiology
University of Chicago Medicine
KA

Karima Addetia, MD

Associate Professor
University of Chicago
U Chicago

Background: Transthyretin (TTR) and light chain (AL) cardiac amyloidosis (CA) are characterized by deposition of amyloid fibrils in atrial and ventricular myocardium. Left atrial (LA) delayed enhancement (LADE) on cardiovascular magnetic resonance (CMR) is an emerging marker of atrial myopathy and has been linked to atrial fibrillation (AF) but is difficult to quantify due to thin LA walls. Little is known about the association between LADE and AF in CA. We hypothesized that LADE can be quantified in CA due to the presence of LA wall thickening in this population. We aimed to quantify LADE in a CA population using custom software and assess its association with AF.

Methods: 141 patients with a new diagnosis of CA (72 TTR, 69 AL) who underwent DE CMR at the time of diagnosis were enrolled. Patients with distant onset of AF ( >2 years prior to CMR) and those with suboptimal visualization of the LA were excluded. Clinical parameters included gender, age, obesity, hypertension (HTN), obstructive sleep apnea, coronary artery disease, smoking, and diabetes. CMR parameters included biventricular and LA volumes and function, and extracellular volume (ECV). Two experienced CMR readers provided visual assessment of LADE. Using custom software (MATLAB, Fig 1) %LADE was quantified by semi-automated segmentation of the LA wall on 4-chamber PSIR DE images and determined using image intensity ratio, a published method, (LA wall signal intensity/mean LA blood pool signal intensity) threshold of 0.97. 50 patients were randomly selected to assess interobserver reliability.

Results: TTR patients were older, with higher rates of HTN and diabetes. TTR patients had significantly higher biventricular volumes, lower biventricular function, greater wall thickness, higher LA volume, lower LA ejection fraction. ECV was similar between AL/TTR. Visual presence/absence of LADE correlated with %LADE (92±25% vs. 59±34%, p< 0.001). Intraclass correlation coefficient of 0.954 (p< 0.001) showed high inter-observer reproducibility. On univariate cox regression, age, HTN, indexed right ventricular end systolic and LA volumes, LA ejection fraction, and ECV correlated with AF in TTR, but LADE did not. In AL, only LA volume index, LA ejection fraction, and LADE were associated with AF. %LADE had the strongest association with AF, (HR 6.61). On multivariate cox regression analysis adjusted for age and HTN, LA volume (HR 1.05) and LADE (HR 6.78) were associated with AF in AL (p< 0.05). On Kaplan-Meier analysis, the lowest tertile of %LADE in all patients and AL patients had a significantly lower rate of AF over the follow-up period compared to tertiles 2 and 3 (Fig 2).

Conclusion: LADE was reproducibly quantified in CA patients on standard CMR PSIR DE images using a custom software. Of all clinical and CMR parameters, %LADE was most strongly associated with new AF in AL-CA but not in TTR-CA. These results were likely influenced by the high prevalence of AF in the TTR population.