Lower stress perfusion in patients with myocardial infarction with non-obstructive coronary arteries compared to controls in long-term follow-up with quantitative perfusion mapping

Abstract

Introduction Myocardial infarction with non-obstructive coronary arteries (MINOCA) constitutes a heterogenous condition with different coronary, cardiac and non-cardiac etiologies. Cardiovascular magnetic resonance imaging (CMR) has emerged as an important diagnostic tool in recent years and is now recommended in patients with MINOCA as a working diagnosis. However, despite early CMR following admission for MINOCA, no cause can be found in around 25% of all patients. A pathophysiological mechanism may be diffuse global coronary microvascular dysfunction (CMD) which has emerged as an important cause of myocardial ischemia. Quantitative adenosine stress CMR perfusion mapping allows for absolute quantification of myocardial perfusion, reflecting CMD in the absence of obstructive coronary disease in MINOCA patients. Purpose To study the presence of CMD in MINOCA patients with an initial normal CMR scan compared to healthy controls. Methods Patients from the multicenter myocardial infarction in our city with normal Coronaries 2 (SMINC-2) study, with a normal CMR scan 2–4 days after hospitalization, and healthy age- and sex-matched controls underwent stress perfusion at 1.5T (MAGNETOM Aera). Native rest T1 and T2 short-axis maps were acquired. Quantitative perfusion maps were acquired during adenosine stress (140 micrograms/kg/min) and at rest following an intravenous contrast bolus (0.05 mmol/kg of gadoteric acid, Gd-DOTA). Post contrast T1 maps were acquired after intravenous contrast (total dose 0.2 mmol/kg) rendering extracellular volume (ECV) maps. Global native T1, T2, ECV and rest and stress perfusion values were acquired by averaging segmental values per patient. Myocardial perfusion reserve (MPR) was calculated as perfusion in stress divided by rest. Values were presented as mean±standard deviation and compared with the independent t-test in normally distributed data, and with the Mann-Whitney U test in non-normally distributed data. Clinical data regarding cardiovascular risk factors, smoking and medications were presented as numbers (percentages) and compared with Fisher's exact test. Rate pressure product (RPP) was calculated as systolic blood pressure multiplied by heart rate in rest and stress. Results In total, 15 patients (59±16 years old, 60% female), and 15 healthy age- and sex-matched controls, were included. There was a trend towards higher incidence of hypertension in patients compared to controls, however no difference in other risk factors (Table 1). Compared to controls, MINOCA patients had lower perfusion in stress (Figure 1). There was no difference in global native T1, T2, ECV, rest perfusion, MPR or hemodynamic parameters between the MINOCA patients and the controls (p>0.05 for all, Table 1). Conclusions Myocardial stress perfusion is lower in MINOCA patients with a normal initial CMR scan compared to age- and sex-matched controls suggesting CMD as a possible pathophysiological mechanism in MINOCA. Funding Acknowledgement Type of funding sources: Foundation. Main funding source(s): Swedish Heart and Lung Foundation