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Oral Abstract

Oral Abstract Clinical #1- Advancing Patient Care

Incremental Yield of Stress Perfusion Cardiac Magnetic Resonance over Exercise Stress Echocardiography for Detection of Myocardial Injury in Hodgkin Lymphoma Survivors - A Prospective Multimodality Imaging Study

Thursday, January 30, 2025
11:20 AM – 11:30 AM East Coast USA Time
Location: Diplomat Ballroom
Background: Hodgkin lymphoma (HL) survivors are at increased for coronary artery disease and left ventricular (LV) systolic dysfunction due to damaging effects of radiation and chemotherapy on the heart. Stress perfusion CMR (s-CMR) and exercise stress echo (s-Echo) have been used to screen HL patients, but their performance is uncertain. This study prospectively compared s-CMR to s-Echo to determine relative yield for detection of myocardial injury in HL survivors. 

Methods: The population comprised HL survivors (disease free ≥5 years) without known cardiovascular disease (CVD). s-CMR and s-Echo were acquired via standardized protocols: CMR (1.5T) included cine (SSFP), perfusion (GRE), and late gadolinium enhancement (LGE). Cine- and LGE- were attained in co-registered LV short and (2/3/4) long axis orientations; perfusion-CMR (~4 equidistant short axis) was attained during adenosine (140ug/kg/min) pharmacologic stress. CMR was analyzed for global LV volumes/EF, regional wall motion score, LGE pattern/transmurality, and perfusion deficits (present/absent). S-Echo was performed via symptom-limited treadmill stress (Bruce) protocol. An established cutoff for impaired LVEF (< 53%) was used for s-CMR and s-echo; sub-clinical CVD was defined using a composite of impaired LVEF (< 53%) or inducible ischemia on s-CMR (abnormal perfusion) or s-Echo: (exercise wall motion abnormality). Fisher’s Exact test was used to test associations for categorical variables. Logistic regression was used to estimate odds ratios (ORs) and test associations. 

Results:

133 HL survivors were studied (50% male, median age at diagnosis: 29yo [IQR 23-37], median age at enrollment: 46yo [IQR 37-53]) (Table 1); s-CMR and s-Echo were attained within a narrow interval (mean 2.7±9.8days). LVEF was similar on s-CMR (60.6% [57-66]) and s-Echo (61.0% [59.3-63.7]), although LV end-diastolic (70ml/m2 [63-78] vs. 53.2ml/m2 [46-60]) and LV end-systolic (28ml/m2 [22-33] vs. 21ml/m2 [17-24]) volumes were higher on s-CMR. LV mass was lower on s-CMR compared to s-echo (56gm/m2 [49-67-] vs. 65gm/m2 [58-78]). Presence of LV dysfunction was 2-fold higher on s-CMR vs. s-Echo (10.2% [n=13] vs. 5.3% [n=7], p:< 0.0001. Stress perfusion abnormalities were observed in 7.5% (n=10) of patients by s-CMR, while exercise-induced wall motion abnormalities were present in 1.5% (n=2 [n=1 with s-CMR/echo concordance]) by s-Echo, p:< 0.0001 (Fig1). LGE was present in 6.4% of pts (n=8; 3 ischemic, 5 non-ischemic pattern). s-CMR yielded >2-fold increase in identifying aggregate subclinical CVD (LVEF < 53% or inducible ischemia) compared to s-Echo (18% vs. 7%; p< 0.0001). Factors associated with sub-clinical CVD on CMR included age at enrollment (OR 1.06 [95%CI: 1.02-1.12]; p=0.009), and high-dose chest RT (OR 8.14 [95%CI: 1.51-50.21]; p=0.023) (Table 2).

Conclusion: Among HL survivors, stress perfusion CMR provides incremental yield to stress echo for detection of global LV dysfunction and subclinical CVD.

Figure 1: Markers of subclinical cardiovascular disease (a) LV dysfunction (EF <53%) and (b) Aggregate markers of subclinical CVD including LV dysfunction and ischemia.
Tsay_Figure 1.pdf