Rapid Fire Session

Session: Rapid Fire Session 5: Quantitative MRI and Artificial Intelligence (Monitor 8)

Derivation of a Risk Score using CMR Strain Phenotypes for the Prediction of Cardiovascular Outcomes in Asymptomatic Hypertrophic Cardiomyopathy

Saturday, February 7, 2026

10:36 AM - 10:43 AM

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

Presenting Author(s)

Sahar Sajjad, BSc

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

Primary Author(s)

Sahar Sajjad, BSc

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

Co-Author(s)

Justin J. Tse, PhD, MSc, BSc

Research Associate
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
SD

Steven Dykstra, MSc, BEng

PhD Candidate
University of Calgary
Calgary, Alberta, Canada
TB

Talia A. Beckie, BEng

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

Fereshteh Hasanzadeh, MSc

Masters Student
University of Calgary
calgary, Alberta, Canada
SR

Sandra Rivest, RN

Research Coordinator
Libin Cardiovascular Institute; University of Calgary
Calgary, Alberta, Canada
JF

Jacqueline Flewitt, MSc

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

Stephanie Corriveau, PhD

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

Yuanchao Feng, PhD

Senior Analyst
University of Calgary
Calgary, Alberta, Canada
JN

Julian B. Neves, MSc

Junior Data Engineer
Libin Cardiovascular Institute, University of Calgary, 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 J.H. Miller, MD

Clinical Assistant Professor
Libin Cardiovascular Institute; University of Calgary
Calgary, Alberta, 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
AA

Augustine Amakiri, PhD

Data Analyst
University of Calgary, Canada
MK

Melanie King, PhD

Director, Program Development and Implementation
Libin Cardiovascular Institute, University of Calgary, Canada
AH

Andrew G. Howarth, MD, PhD

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

Background: Patients with symptomatic hypertrophic cardiomyopathy (HCM) have been the primary focus of conventional and emerging therapies, including cardiac myosin inhibitors. However, asymptomatic patients with HCM (New York Heart Association [NYHA] class I) remain at risk for major adverse cardiovascular events (MACE). Left ventricular (LV) and right ventricular (RV) strain have established prognostic value for many cardiac cohorts. This study aimed to develop a multivariable risk score inclusive of CMR strain markers to predict adverse outcomes in NYHA-I HCM patients.

Methods: 515 NYHA-I HCM patients were identified from the Cardiovascular Imaging Registry of Calgary. All patients underwent baseline health questionnaires and CMR imaging with a standardized protocol. LV two-dimensional global longitudinal (GLS), circumferential (GCS), and radial strain (GRS) amplitude, as well as RV GLS amplitude, were quantified from cine images using feature tracking techniques (cvi42). Patients were followed for a composite MACE outcome of all-cause mortality, heart failure hospitalization, new onset of atrial fibrillation/flutter, ventricular tachycardia, or survival of sudden cardiac arrest. Univariable and multivariable survival-based associations between strain markers and MACE were studied. A risk score was then derived from a multivariable Cox model.

Results: Baseline characteristics are shown in Table 1 (median age 58.0 (47.0, 67.0) years; 71% males). Over a median follow up of 4.8 years, 52 patients (10%) experienced the composite outcome. On univariable analysis, LV GLS, GCS, and GRS, but not RV GLS, were significantly associated with MACE. A multivariable Cox model was constructed using pre-specified clinically relevant variables (age, sex, HCM morphology, and LV mass indexed to body surface area), as well as LV GLS amplitude. In this model, LV GLS remained independently associated with MACE, with an adjusted hazard ratio of 1.15 (95% CI 1.06-1.25; p< 0.001) per 1% worsening of strain (Figure 1A). Using 500 repeats of 1000 bootstrapped samples, the multivariable model achieved a concordance-index of 0.78 (95% CI 0.70-0.84). A risk-score nomogram was subsequently derived (Figure 1B). Patients were stratified by the median risk score into low- and high-risk groups, with the latter showing a 9.1- fold increased risk of future MACE (95% CI 3.9- 21.3; p< 0.001; Figure 2).

Conclusion: To date, this is the first study aimed at developing a multivariable risk score inclusive of CMR strain for the prediction of adverse outcomes in asymptomatic NYHA-I HCM patients. This approach offers strong potential to identify a high-risk subset of asymptomatic patients who may benefit from targeted surveillance and/or therapeutics . Ongoing research is planned to validate this risk score in external cohorts.

Table 1. Baseline characteristics of the study cohort, stratified by occurrence of the primary outcome.

	Overall N = 515	Outcome -ve N = 463 (90%)	Outcome +ve N = 52 (10%)	p-value
Clinical characteristics
Age, yrs	58.0 (47.0, 67.0)	57.0 (45.0, 66.0)	69.0 (61.5, 77.5)	< 0.001
Male sex	368 (71%)	336 (73%)	32 (62%)	0.095
Hypertension	239 (46%)	205 (44%)	34 (65%)	0.004
Diabetes mellitus	98 (19%)	81 (17%)	17 (33%)	0.008
Atrial fibrillation / flutter	64 (12%)	48 (10%)	16 (31%)	< 0.001
CMR characteristics
HCM morphology				0.67
Septal	332 (64%)	301 (65%)	31 (60%)
Apical	132 (26%)	116 (25%)	16 (31%)
Mixed	51 (10%)	46 (10%)	5 (10%)
LV EF, %	65.5 (61.0, 70.0)	65.7 (61.3, 70.1)	62.8 (59.3, 68.8)	0.020
RV EF, %	62.1 (57.3, 68.0)	62.3 (57.3, 67.8)	61.3 (57.5, 69.5)	0.94
BSA-indexed LV mass, g/m²	74.9 (64.1, 90.3)	74.6 (63.7, 89.4)	77.7 (66.4, 93.4)	0.24
BSA-indexed LA max volume, mL/m²	44.2 (35.0, 54.2)	43.8 (34.9, 53.2)	54.1 (40.2, 65.3)	< 0.001
LGE fibrosis burden, %	5.9 (1.5, 13.2)	5.9 (1.5, 13.2)	7.4 (2.9, 13.2)	0.15
LV GLS amplitude, %	-16.1 (-18.6, -13.2)	-16.2 (-18.9, -13.3)	-14.6 (-17.2, -11.9)	0.010
LV GCS amplitude, %	-17.5 (-19.0, -15.2)	-17.6 (-19.1, -15.6)	-15.3 (-17.3, -14.3)	0.001
LV GRS amplitude, %	29.1 (24.3, 33.4)	29.5 (24.9, 33.6)	24.9 (22.0, 29.3)	0.001
RV GLS amplitude, %	-26.1 (-29.1, -22.9)	-26.1 (-29.1, -22.9)	-25.7 (-29.5, -21.8)	0.63
Follow up, y	4.8 (3.1, 7.2)	4.8 (3.2, 7.4)	4.2 (2.2, 6.5)	0.022

Values are mean ± SD, median (Q1, Q3), or counts (%)

	Overall N = 515	Outcome -ve N = 463 (90%)	Outcome +ve N = 52 (10%)	p-value
Clinical characteristics
Age, yrs	58.0 (47.0, 67.0)	57.0 (45.0, 66.0)	69.0 (61.5, 77.5)	< 0.001
Male sex	368 (71%)	336 (73%)	32 (62%)	0.095
Hypertension	239 (46%)	205 (44%)	34 (65%)	0.004
Diabetes mellitus	98 (19%)	81 (17%)	17 (33%)	0.008
Atrial fibrillation / flutter	64 (12%)	48 (10%)	16 (31%)	< 0.001
CMR characteristics
HCM morphology				0.67
Septal	332 (64%)	301 (65%)	31 (60%)
Apical	132 (26%)	116 (25%)	16 (31%)
Mixed	51 (10%)	46 (10%)	5 (10%)
LV EF, %	65.5 (61.0, 70.0)	65.7 (61.3, 70.1)	62.8 (59.3, 68.8)	0.020
RV EF, %	62.1 (57.3, 68.0)	62.3 (57.3, 67.8)	61.3 (57.5, 69.5)	0.94
BSA-indexed LV mass, g/m²	74.9 (64.1, 90.3)	74.6 (63.7, 89.4)	77.7 (66.4, 93.4)	0.24
BSA-indexed LA max volume, mL/m²	44.2 (35.0, 54.2)	43.8 (34.9, 53.2)	54.1 (40.2, 65.3)	< 0.001
LGE fibrosis burden, %	5.9 (1.5, 13.2)	5.9 (1.5, 13.2)	7.4 (2.9, 13.2)	0.15
LV GLS amplitude, %	-16.1 (-18.6, -13.2)	-16.2 (-18.9, -13.3)	-14.6 (-17.2, -11.9)	0.010
LV GCS amplitude, %	-17.5 (-19.0, -15.2)	-17.6 (-19.1, -15.6)	-15.3 (-17.3, -14.3)	0.001
LV GRS amplitude, %	29.1 (24.3, 33.4)	29.5 (24.9, 33.6)	24.9 (22.0, 29.3)	0.001
RV GLS amplitude, %	-26.1 (-29.1, -22.9)	-26.1 (-29.1, -22.9)	-25.7 (-29.5, -21.8)	0.63
Follow up, y	4.8 (3.1, 7.2)	4.8 (3.2, 7.4)	4.2 (2.2, 6.5)	0.022

Values are mean ± SD, median (Q1, Q3), or counts (%)

CMR indicates cardiac magnetic resonance; HCM, hypertrophic cardiomyopathy; LV, left ventricular; EF, ejection fraction; RV, right ventricular; BSA, body surface area; LA, left atrial; LGE, late gadolinium enhancement; GLS, global longitudinal strain; GCS, global circumferential strain; and GRS, global radial strain.Figure 1. A. Forest-plot of the results of multivariable Cox model for associations with the composite outcome. B. Nomogram derived from risk score. HCM indicates hypertrophic cardiomyopathy; BSA, body surface area; LV, left ventricular; and GLS, global longitudinal strain.
Kaplan-Meier curve for associations of low- and high-risk subgroups, stratified by the median risk score, with the composite outcome