Coronary microvascular dysfunction (CMD) results from architectural abnormalities or the inability of the coronary microvasculature to vasodilate, both leading to angina, dyspnoea or reduced exercise capacity1. Understanding CMD mechanisms is crucial for developing targeted therapies and improving prognosis. Two CMD endotypes, “structural” and “functional”, were recently identified through the combined assessment of coronary flow reserve (CFR) and minimal microvascular resistance using bolus thermodilution with adenosine-induced hyperaemia2. This study aims to characterise different CMD phenotypes by assessing adaptation to incremental cycling exercise in the cath lab among participants with suspected angina with non-obstructive coronary artery disease (ANOCA).
Absolute microvascular resistance (Rμ), absolute coronary blood flow (Q), microvascular resistance reserve (MRR) and CFR were measured in the left anterior descending artery (LAD) using continuous thermodilution. Saline was infused at 10 mL/min (rest) and at 20 mL/min (hyperaemia) to assess MRRsaline. The presence of CMD was defined as an MRRsaline <2.33. Hyperaemic Rμ was classified as normal (<500 Wood units [WU]) or elevated (≥500 WU) based on saline-induced hyperaemia4. In addition, patients performed the cycling exercise using a supine cycling...
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