Early quantitative perfusion stress-CMR identifies microvascular dysfunction as a potential mechanism of myocardial injury in patients with working diagnosis MINOCA and otherwise normal scan.

Saturday, February 1, 2025

10:00 AM – 10:10 AM East Coast USA Time

Location: Blue Room

Presenting Author(s)

TB

Tomasz Baron, MD, PhD

Associate Professor
Uppsala University, Sweden

Primary Author(s)

TB

Tomasz Baron, MD, PhD

Associate Professor
Uppsala University, Sweden

Co-Author(s)

RS

Ramin Sahar, MD

Resident physician
Uppsala University Hospital, Sweden
JL

Joel Lenell, MD

PhD student, Resident Physician
Uppsala University, Sweden
AM

Anne-Marie Montelius, MSc

Research Nurse
Uppsala University, Sweden
JB

Johan Berglund, BMSc

Associate professor
Uppsala University, Sweden
BL

Bertil Lindahl, MD, PhD

Professor
Uppsala University, Sweden

Background: Coronary microvascular dysfunction (CMD) is considered a potential cause of myocardial infarction with nonobstructive coronary arteries (MINOCA). Quantitative perfusion stress-CMR as a part of a routine CMR early after admission may give insight into patomechanism of the myocardial injury. We aimed to evaluate presence of CMD, using quantitative perfusion stress-CMR as part of a diagnostic work-up in consecutive patients with working diagnosis MINOCA and an otherwise normal CMR scan.

Methods: Since 2021, consecutive patients with the working diagnosis MINOCA, referred for CMR, have undergone a perfusion scan after pharmacological provocation with regadenosone and at rest using dual sequence technique. The commercially available AI-based software cvi42 was used for automated quantification of myocardial blood flow at baseline (rest MBF) and during vasodilation (stress MBF) with calculation of the myocardial perfusion reserve (MPR). Adequate hemodynamic response was defined as the decrease in systolic blood pressure by > 10 mmHg and/or increase in heart rate by > 10 bpm. A normal CMR scan was defined as absence of myocardial LGE and oedema. Presence of obstructive epicardial disease was excluded in all patients by invasive coronary angiography. Microvascular dysfunction was defined as stress MBF < 2.25 ml/g/min.

Results: Twenty-five patients with working diagnosis MINOCA (63±9 years of age; 62% females; max cTnT median (IQR) 147 (80; 203) ng/L) and an otherwise normal CMR scan were included along 23 healthy controls (61±4 years of age; 52% females). Among MINOCA patients 48% had hypertension, 44% hyperlipidemia, 8% diabetes and 44% were actual or previous smokers. In the MINOCA cohort, a perfusion stress-CMR exam was performed within a median (IQR) of 14 (10; 37) days from admission. Patients with MINOCA had significantly lower global stress MBF and MPR compared to healthy volunteers (2.49±0.80 vs. 2.92±0.55 ml/g/min, p=0.034; 1.81±0.57 vs. 2.29±0.62, p=0.007, respectively), while rest MBF did not differ between the groups (1.39±0.26 vs. 1.34±0.35, p=0.548), see figures 1 and 2. Nine patients (36%) in the MINOCA-cohort and none of the healthy controls fulfilled the predefined criteria for microvascular dysfunction. There were no differences in left ventricular mass, volumes, functional parameters (LVEF, GLS) or in tissue characteristics (T1-mapping native and post-contrast, native T2) between the groups.

Conclusion: An early performed quantitative stress perfusion CMR-scan revealed significant impairment of the maximal myocardial blood flow and the perfusion reserve in patients with working diagnosis MINOCA and otherwise normal CMR scan, as compared with healthy controls. One third of MINOCA patients fulfilled criteria of microvascular dysfunction as potential patomechanism of myocardial injury.

Myocardial blood flow (MBF) at rest and stress in MINOCA patients and healthy controls.
Figure 1_abstract_SCMR2025.pdf
Myocardial perfusion reserve (MPR) in MINOCA patients and healthy controls.
Figure 2_abstract_SCMR2025.pdf