Tissue Characterization Through Multiparametric Cardiac Magnetic Resonance Imaging Allows for the Distinction Between Pathological and Physiological Left Ventricular Hypertrophy (RF_FR_370)

Friday, January 31, 2025

2:10 PM – 2:20 PM East Coast USA Time

Location: Blue Room PreFunction

Presenting Author(s)

Otavio Coelho-Filho, MD, PhD, MPH

Associate Professor
University of Campinas - UNICAMP, Brazil

Co-Author(s)

AC

Andréa Coy-Canguçu

Medical Student
Catholic Pontifical University of Campinas, Brazil
LD

Luis Miguel Da Silva

Researcher
State University of Campinas, Brazil
LP

Layde Rosane Paim, N/A

Student
University of Campinas, Brazil
AA

Adriana Aparecida Bau

Researcher
State University of Campinas, Brazil
CN

Camila Nicolela G. Martins, MD

Student
University of Campinas, Brazil
JM

Jose Roberto Matos-Souza, MD, PhD

Professor
University of Campinas, Brazil
WN

Wilson Nadruz, Jr., MD, PhD

Associate Professor
State University of Campinas, Brazil
MJ

Michael Jerosch-Herold, PhD

Associate Professor
Harvard Medical School

Primary Author(s)

Otavio Coelho-Filho, MD, PhD, MPH

Associate Professor
University of Campinas - UNICAMP
State University of Campinas, Brazil

Co-Author(s)

Otavio Coelho-Filho, MD, PhD, MPH

Associate Professor
University of Campinas - UNICAMP
State University of Campinas, Brazil

Background: Physiological and pathological left ventricular (LV) hypertrophy exhibit distinct molecular mechanisms and are related to different clinical outcomes. However, there are no clearcut imaging methods to distinguish their phenotypes.

Methods: In this prospective single-centered cohort adult patients (age > 18 years), underwent deep phenotyping through clinical assessment, blood sampling, 12-lead electrocardiography, transthoracic echocardiography, cardiopulmonary exercise testing, and cardiac magnetic resonance (CMR). The primary measures of interest were native T1, extracellular volume fraction (ECV) and intracellular water lifetime (tau)—an indirect measure of cardiomyocyte diameter.

Results: A total of 171 participants were included in the study and divided in four groups: heart failure with reduced ejection fraction (HFrEF, N = 43), heart failure with preserved ejection fraction (HFpEF, N = 45), athletes (N = 43), and controls (N = 40). The median age varied among the groups [HFrEF (age, y): 53 (47.0-62.0); HFpEF: 63 (58.0-68.5); athletes: 30 (23.0-42.0); controls: 38 (30.25-49.25); p< 0.001] as well as sex [HFrEF (male, %): 20 (46.5%); HFpEF: 23 (51.1%); athletes: 37 (86.0%); controls: 15 (38.5%); p< 0.001]. Native T1 was highest in HFrEF patients and lowest in athletes with no significant difference between HFpEF patients and controls [HFrEF (ms): 1279.5 (1236.5 - 1309.3); HFpEF: 1250.0 (1224.5 - 1296.0); athletes: 1170.4 (1151.3 - 1202.3); controls: 1249.0 (1183.3-1276.0); p< 0.001]. ECV showed a similar pattern, it was highest in HFrEF patients, lowest in athletes and intermediate in HFpEF patients and controls [HFrEF (%): 31.0 (27.9 – 34.2); HFpEF: 30.5 (26.1 - 34.7); athletes: 25.9 (24.9 – 29.7); controls: 27.2 (24.6 – 31.2); p</span>= 0.001]. HFrEF patients had the greatest LV cardiomyocyte mass, but the lowest tau (increased length and reduced diameter), HFpEF patients and athletes had both increased cardiomyocyte mass and tau (increased length and diameter), whereas controls had normal cardiomyocyte mass and intermediate tau (normal length and diameter) [LV cardiomyocyte mass: HFrEF (g/m2): 99.5 (73.6-131.7); HFpEF: 80.8 (64.6-101.7); athletes: 82.0 (71.8-92.7); controls: 52.3 (42.1-63.5); p</span>< 0.001] [tau: HFrEF (s): 0.113 (0.081-0.162); HFpEF: 0.146 (0.126-0.173); athletes: 0.157 (0.114-0.211); controls: 0.137 (0.097-0.185; p</span>< 0.001].

Conclusion: Multiparametric CMR tissue characterization allows for the differentiation of physiological and pathological LV hypertrophy phenotypes among HF spectrum patients, athletes and normal subjects.