Rapid Fire Session

Session: Rapid Fire Session 2: Multiparametric Mapping, Cardiomyopathy (Monitor 3)

Differentiating Ischemic From Healthy Myocardium Using Cardiovascular Magnetic Resonance Dipyridamole Rest and Stress T1 Mapping

Thursday, February 5, 2026

3:52 PM - 3:59 PM

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

Presenting Author(s)

Stefan K. Piechnik, PhD, FSCMR

Professor of Biomedical Imaging
University of Oxford
Oxford, England, United Kingdom

Primary Author(s)

YC

YUAN TING CHANG

Resident of Department of Radiology
Taipei Veterans General Hospital, Taiwan (Republic of China)

Co-Author(s)

CY

Chun-Ho Yun, MD

Director
Mackay Memorial Hospital
Taipei, Taipei, Taiwan (Republic of China)
CC

Chen-Yen Chien

Attending physician
MacKay Memorial Hospital, Taiwan (Republic of China)
WH

Wei-Ming Huang, MD

Assistant Professor
Mackay Memorial Hospital
Taipei, Taipei, Taiwan (Republic of China)
CH

Chung-Lieh Hung

Attending physician
Mackay Memorial Hospital, Taiwan (Republic of China)
Qiang Zhang, PhD, FSCMR

Associate Professor of AI in Cardiovascular Imaging
University of Oxford
Oxford, England, United Kingdom
Ricardo A. Gonzales, PhD, FSCMR

Postdoctoral Research Fellow
Harvard Medical School
Charlestown, Massachusetts, United States
MB

Matthew K. Burrage, MD, PhD

Research Fellow
University of Oxford, United Kingdom
Vanessa M. Ferreira, MD, PhD, FSCMR

Professor of Cardiovascular Medicine
University of Oxford
Oxford, England, United Kingdom

Background: Cardiovascular magnetic resonance (CMR) stress T1 mapping using adenosine and regadenoson can differentiate ischemic, infarcted, and healthy myocardium. However, the effect of dipyridamole remains unclear. This study evaluates whether dipyridamole-induced stress T1-mapping can distinguish myocardial tissue types.

Methods: Twenty-five healthy controls and 20 patients with coronary artery disease (CAD) underwent rest and dipyridamole stress T1-mapping (ShMOLLI), followed by gadolinium-based quantitative perfusion imaging at 1.5T. Native T1 values and stress T1 reactivity (dT1) were assessed across different myocardial tissues. Correlations between dT1 and myocardial blood flow (MBF) were examined.

Results: In healthy controls, global rest T1 was 934 ± 26 ms, with a stress-induced increase of 6.5 ± 0.6% (p < 0.0001). Infarcted myocardium showed elevated resting T1 (1146 ± 71 ms) with an absent stress response (dT1 = -0.9% ± 1.8%). Ischemic myocardium had mildly elevated rest T1 (965 ± 26 ms; p < 0.001) and blunted reactivity (dT1 = 1.3 ± 0.6%) compared to healthy myocardium. Remote myocardium had rest T1 similar to normal tissue (936 ± 19 ms; p > 0.05) but reduced stress reactivity (dT1 = 4.5 ± 1.1%; p < 0.0001) compared to norm. dT1 strongly correlated with stress MBF (r = 0.80) and myocardial perfusion reserve (r = 0.70) (both p < 0.0001).

Conclusion: Dipyridamole-induced stress T1-mapping can differentiate infarcted, ischemic, and healthy myocardium, supporting its use in non-contrast CMR for myocardial tissue characterization.

Characteristics of the study population

	Healthy subjects (n=25)	CAD patients (n=20)	p value
Age (yrs)	44.5±16.3	62.5±10.3	< .0001
BMI (kg/m²)	22.4±4.6	26.5±4.4	0.831
Male (%)	11 (44)	13 (65)	0.161
Risk factors (%)
Hypertension	0	10 (50)
Diabetes mellitus	0	9 (45)
Hypercholesterolemia	0	2 (10)
Family history of CAD	0	3 (15)
History of CAD	0	11 (55)
smoking	0	1 (5)
Medication (%)
Aspirin	0	13 (65)
Beta-blocker	0	8 (40)
Statin	0	14 (70)
CMR clinical indices
LVEF (%)	59.2±4.4	62.1±7.6	0.147
LVEDVI (ml/m2)	61.0±13.4	65.5±17.0	0.266
Number of remote myocardial segments^&		57
Number of ischemic myocardial segments^#		55
Number of infarcted myocardial segments^#		14
Invasive coronary angiography
1-vessel CAD^$		7
2-vessel CAD		4
3-vessel CAD		9

^& no ischemia or infarction

^# Based on results of first-pass perfusion and late gadolinium enhancement imaging

^$ ≥70% stenosis in a major coronary vessel

Abbreviations: CAD: coronary artery disease; CMR: cardiovascular magnetic resonance; LVEF: left ventricular ejection fraction; LVEDVI: indexed left ventricular end‐diastolic volumeMyocardial T1 values and quantitative myocardial perfusion results in healthy subjects and CAD patients

	Healthy Subjects (n=25)	CAD patients (n=20)
	Normal	Remote	Ischemic	Infarct	LV blood pool
Rest T1 (ms)	934 ± 26	936 ± 19	965 ± 26	1146 ± 71		1486 ± 79
Stress T1 (ms)	994 ± 28	979 ± 22	978 ± 27	1135 ± 71		1489 ± 83
dT1 (%)	6.5 ± 0.6	4.5 ± 1.1	1.3 ± 0.6	-0.9 ± 1.8		0.2 ± 2.8
Resting MBF	0.9 ± 0.2	0.9 ± 0.3	0.9 ± 0.4	0.6 ± 0.2
Stress MBF	3.1 ± 0.7	2.1 ± 0.7	1.5 ± 0.5	0.7 ± 0.4
MPR	3.8 ± 0.8	2.6 ± 1.0	2.0 ± 0.8	1.1 ± 0.3

Abbreviations: CAD: coronary artery disease; dT1:delta T1; MBF: myocardial blood flow; MPR: myocardial perfusion reserveCorrelation between T1 reactivity and MPR, sMBF and rMBF. T1 reactivity is expressed as percentage change in T1 (dT1). Abbreviations: rMBF: myocardial blood flow at rest; sMBF=myocardial blood flow at stress; MPR=myocardial perfusion reserve