Rapid Fire Abstracts
Geoffrey W. de Mooij, MSc
PhD Candidate Cardiology
Amsterdam UMC, Netherlands
Geoffrey W. de Mooij, MSc
PhD Candidate Cardiology
Amsterdam UMC, Netherlands
Caitlin E.M. Vink, MD
MD
Amsterdam UMC, Netherlands
Sonia Borodzicz-Jazdzyk, MD, PhD
Post-doc CMR Research Fellow
Amsterdam UMC, Netherlands
Elize A M de Jong, MSc
PhD Candidate
UMC Utrecht, Netherlands
Janneke Woudstra, MD
PhD Candidate
Amsterdam UMC, Netherlands
Tim P. van de Hoef, MD, PhD
Interventional Cardiologist
UMC Utrecht, Netherlands
Steven Chamuleau, MD, PhD
Professor
Amsterdam Medical Center, Netherlands
Etto C. Eringa, PhD
Associate Professor
Physiology, Netherlands
Marco J.W. Götte, MD, PhD
MD, PhD
Amsterdam UMC, Netherlands
Yolande Appelman, MD, PhD
MD, PhD
Amsterdam UMC, Netherlands
In Angina with Non-Obstructed Coronary Arteries (ANOCA), angina-like symptoms are mainly induced by increased vasoconstriction and impaired vasodilation of the microcirculation. Cardiac Magnetic Resonance (CMR) T1 mapping is a non-invasive, contrast-free technique, which can distinguish healthy, infarcted and ischemic myocardium by detecting free water content in the myocardial tissue. When the T1 relaxation time is prolonged, there is an increase in myocardial water content, indicating for an increased myocardial blood volume (MBV). Recent studies identified reduced MBV in ANOCA patients as an added cause of angina, suggesting that the reactivity of T1 mapping on stress induced vasodilation might be reduced in ANOCA patients. This study aims to assess differences in T1 mapping reactivity between symptoms-based ANOCA patients and healthy controls.
Methods: This is a sub-analysis of the MICORDIS study. All subjects underwent adenosine stress perfusion CMR, after abstaining from caffeine and xanthine for 24 hours. T1-mapping was performed using an modified Look-Locker inversion recovery (MOLLI) sequence. T1 (ms) was measured during native rest and stress. All CMR images were post-processed using cvi42 software.
Results: Twenty-four ANOCA patients and twenty-five sex- and age matched healthy controls were included for analysis. Global T1 mapping values in patients and controls between rest and stress showed a significant increase (1219.31 ms ± 36.1 versus 1274.86 ms ± 47.18; p< 0.001 and 1197.1 ms ± 47.41 versus 1257.46 ms ± 46.87; p< 0.001). Compared to controls, global native T1 (ms) at rest showed a significant increase in ANOCA patients (1221.87 ms ± 35.77 versus 1197.01 ms ± 47.41; p=0.044). Stress global T1 mapping and ΔT1 reactivity values did not differ between ANOCA patients and control (1273.76 ms ± 48.67 versus 1257.46 ms ± 46.87; p=0.243 and 4.37% ± 2.8 versus 5.09% ± 2.83; p=0.382). In the per-segment analysis, patients with ANOCA did show a significant reduced ΔT1 compared to controls (4.06% ± 3.01 versus 5.19% ± 4.1; p= 0.028).
Conclusion: Patients with ANOCA have a significant increase of T1 (ms) between rest and stress. Additionally, their native T1 value at rest is significantly increased compared to those of healthy controls, indicating an increased state of vasodilation at rest. The response to a vasodilator agent is diminished in ANOCA patients compared to healthy controls, indicated by lower ΔT1 in the per-segment analysis. These findings could be explained by the capped maximal vasodilation, where increased T1 values at rest result in decreased ΔT1. Increased T1 values at rest and decreased Δ T1 could confirm the reduced MBV in ANOCA patients, caused by the impaired vasodilatory function.