Rapid Fire Session

Session: Rapid Fire Session 2: CMR – Analysis (including machine learning) ( Monitor 5)

4D phenomics characterization of left ventricular function in obstructive hypertrophic cardiomyopathy patients on mavacamten

Thursday, February 5, 2026

3:45 PM - 3:52 PM

Location: Galapagos / Aruba / Ilhabela (2nd Lower Level)

Presenting Author(s)

Justin J. Tse, PhD, MSc, BSc

Research Associate
University of Calgary
Calgary, Alberta, Canada

Primary Author(s)

Justin J. Tse, PhD, MSc, BSc

Research Associate
University of Calgary
Calgary, Alberta, Canada

Co-Author(s)

RM

Rylan Marianchuk, BSc

Masters Student
University of Calgary
Calgary, Alberta, Canada
Sahar Sajjad, BSc

Graduate Student
Libin Cardiovascular Institute, Cumming School of Medicine, University of Calgary
Calgary, Alberta, Canada
KA

Kate Aspinall, BSc

Undergraduate student
Libin Cardiovascular Institute, Cumming School of Medicine, University of Calgary
Calgary, Alberta, Canada
TB

Talia A. Beckie, BEng

Cardiac Imaging Systems Engineer
Libin cardiovascular Institute, University of Calgary
Calgary, Alberta, Canada
CJ

Cory R. Jensen, BSc

Cardiac Machine Learning Developer
Libin Cardiovascular Institute, University of Calgary, Canada
SD

Steven Dykstra, MSc, BEng

PhD Candidate
University of Calgary
Calgary, Alberta, Canada
FH

Fereshteh Hasanzadeh, MSc

Masters Student
University of Calgary
calgary, Alberta, Canada
JF

Jacqueline Flewitt, MSc

Manager of Strategic Partnerships
Libin Cardiovascular Institute; University of Calgary
Calgary, Alberta, Canada
JN

Julian B. Neves, MSc

Junior Data Engineer
Libin Cardiovascular Institute, University of Calgary, Canada
SC

Stephanie Corriveau, PhD

Ad Clinical trial lead & Senior Scientific Advisor - CV
Bristol Myers Squibb
Montreal, Quebec, Canada
OK

Omid Kiamanesh, MD

Cardiologst
Libin Cardiovascular Institute, University of Calgary, Canada
GP

Grant Peters, MD

Clinical Assistant Professor
Libin Cardiovascular Institute, University of Calgary
Calgary, Alberta, Canada
CL

Carmen P. P. Lydell, MD

Clinical Assistant Professor
Libin Cardiovascular Institute of Alberta, University of Calgary
Calgary, Alberta, Canada
MB

Michael Bristow, MD

Clinical Associate Professor
University of Calgary, Alberta, Canada
MG

Marco J.W Götte, MD, PhD

MD, PhD
Stephenson Cardiac Imaging Centre
Calgary, Alberta, Canada
RM

Robert JH Miller, MD

Cardiologist
Libin Cardiovascular Institute, University of Calgary, Canada
LK

Louis Kolman, MD

Clinical Assistant Professor
Libin Cardiovascular Institute; University of Calgary
Calgary, Alberta, Canada
Dina Labib, MD, PhD, FSCMR

Associate Scientific Director, Personalized Diagnostics Program; Adjunct Assistant Professor
University of Calgary
Calgary, Alberta, Canada
James A. White, MD

Professor
Libin Cardiovascular Institute; University of Calgary
Calgary, Alberta, Canada

Background: Cardiac myosin inhibition therapy delivers symptomatic relief in patients with obstructive hypertrophic cardiomyopathy (oHCM). While studies have supported favourable global measures of cardiac remodelling following introduction of myosin inhibitors, the structural and functional influences experienced by hypertrophied versus non-hypertrophied tissues in oHCM have not been investigated. To assess this, we performed 4D modelling using automated 4Deep phenomics to objectively characterize serial changes in regional structural and deformation features in patients completing 1-year of mavacamten therapy.

Methods: 15 patients completing baseline CMR imaging for oHCM and being initiated on mavacamten were recruited to undergo a repeat 1-year clinical and imaging-based assessment. CMR imaging was performed inclusive of routine 2D cine and late gadolinium enhancement imaging in addition to pre and post contrast T1 mapping (MOLLI). Conventional analyses were performed using commercially available software (cvi42). This was followed by automated (no user interaction) processing of cines using the 4Deep analysis package, delivering spatially-registered bi-layer 4D mesh models of the left ventricle (LV) across 480 elements. For each element, maximal wall thickness, 3D mass, and 3D principal strain were calculated, then collated for each AHA segment. LV outflow tract (LVOT) gradients were measured by 2D Doppler echocardiography and reported as maximum resting or provoked gradient.

Results: Baseline characteristics are shown in Table 1. The cohort had a median age of 65 years (7 male, 8 female). Changes in imaging markers from baseline are shown in Table 2. Conventional CMR markers revealed a significant decrease in LV mass (median absolute reduction of 13.7 g/m²; p=007), in addition to significant reductions in LV and right ventricular (RV) ejection fraction (EF), with no difference in ECV fraction. 4Deep analysis demonstrated global reductions in 3D mass with no significant reduction in global maximum and minimum principal strain amplitudes. Regional differences in remodelling were observed with percent change in 3D segmental mass (indexed to BSA) demonstrating greatest reductions in the basal anteroseptal segment (median reduction of 20%, p = 0.01), basal inferoseptum (21%, p = 0.04), basal anterolateral segment (21%, p = 0.02), mid inferoseptum (26%, p = 0.01), apical septum (23%, p = 0.01), and apical inferior wall (22%, p = 0.03; Figure 1a). End-diastolic 3D meshes for a representative patient are shown in Figure 1b.

Conclusion: This is the first study to document the regional influences of myosin inhibition therapy, being uniquely explored using 4D phenomics-based modelling. We identified heterogenous effects of Mavacamten on 3D LV mass reductions with greatest influences observed for septal segments demonstrating greatest phenotypic expression at baseline. This suggests a preferential therapeutic influence on pathologic tissue regions.

Table 1. Baseline characteristics of the study cohort

Characteristics	Baseline N = 15
Age, years	65.0 (61.0, 74.0)
Male sex	7 (47%)
BMI, kg/m²	30.1 (23.6, 42.2)
Chest pain (CCS class ≥ II)	2 (13%)
Smoking
Never Current Former	12 (80%) 1 (7%) 2 (13%)
Hypertension	9 (60%)
Diabetes mellitus	3 (20%)
Dyslipidemia	13 (87%)
Atrial fibrillation / flutter	1 (7%)
Hemoglobin, g/L	144.0 (140.0, 152.5)
CKD (eGFR < 60 mL/m²/min)	66.3 (55.7, 89.5)

Values are represented as median (Q1, Q3) or counts (%)

BMI indicates body mass index; CCS, Canadian Cardiovascular Society, CKD, chronic kidney disease. Table 1. Baseline characteristics of the study cohort

Characteristics	Baseline N = 15
Age, years	65.0 (61.0, 74.0)
Male sex	7 (47%)
BMI, kg/m²	30.1 (23.6, 42.2)
Chest pain (CCS class ≥ II)	2 (13%)
Smoking
Never Current Former	12 (80%) 1 (7%) 2 (13%)
Hypertension	9 (60%)
Diabetes mellitus	3 (20%)
Dyslipidemia	13 (87%)
Atrial fibrillation / flutter	1 (7%)
Hemoglobin, g/L	144.0 (140.0, 152.5)
CKD (eGFR < 60 mL/m²/min)	66.3 (55.7, 89.5)

Values are represented as median (Q1, Q3) or counts (%)

BMI indicates body mass index; CCS, Canadian Cardiovascular Society, CKD, chronic kidney disease. Figure 1. Panel A. Bull’s eye plots of AHA segmental distribution of median 4Deep myocardial mass indexed to body surface area at baseline and 1-year follow up and the % difference. Panel B. Baseline and 1-year follow-up end-diastolic meshes for a representative patient