12 Chapter 1 to the pathophysiology of ANOCA are thought to be oxidative stress, which induces inflammation through reactive oxygen species (ROS) causing vascular remodeling, or an increased autonomic nerve system, leading to elevated catecholamine levels.17 However, the pathogenesis of ANOCA remains multifactorial and largely unknown. Diagnostic modalities in ANOCA Current diagnostic methods for ANOCA are integrated into the guidelines for evaluating chronic chest pain, primarily focusing on obstructed CAD.2, 18, 19 However, these guidelines often provide limited consideration for further diagnostic testing post-exclusion of obstructed CAD, frequently resulting in a diagnosis of non-cardiac chest pain without completing an invasive evaluation for ANOCA.20 Coronary CTA, a recommended and widely used diagnostic imaging test for obstructed CAD, typically reveals no severe coronary abnormalities in ANOCA. Recent recommendations in current guidelines suggest the use of additional modalities if non-obstructive CAD is diagnosed in symptomatic patients, though these have only been recently incorporated and are not yet widely implemented in clinical practice. Invasive coronary function testing (CFT) evaluated CMD by assessing coronary flow reserve (CFR) and minimal microvascular resistance (MR) using adenosine, as well as vasospasm provocation testing typically using acetylcholine, an endothelium dependent vasodilator, as the provocative agent (Figure 2). In most protocols, acetylcholine is administered manually through intracoronary bolus injections in incremental doses (2, 20, 100, and 200 μg) in the LAD. If no vasospasm occurs in the LAD during assessment, a single dose of 80 μg acetylcholine is administered in the RCA. Vasospasm has been defined as recognizable chest pain and ischemic changes on electrocardiography (ECG), with or without >90% epicardial vasoconstriction on CAG distinguishing epicardial and microvascular spasm. Following occurrence of vasospasm, a re-challenge is performed using the dose that induced vasospasm after intracoronary nitrite administration. This approach allows for assessment of the coexistence of epicardial vasospasm and microvascular vasospasm since microvascular vasospasm is less likely to resolve after nitrate administration. Additionally, it provides insights into the effectiveness on symptoms of nitrate treatment.21, 22. Coronary pressure and flow measurements are taken under resting conditions and during hyperemia induced by 150 μg adenosine, an endotheliumindependent vasodilator.23 CFR is calculated as the ratio of hyperemic average peak flow velocity to basal averaged peak flow velocity. MR, on the other hand, is determined as the ratio of distal coronary pressure to distal coronary flow and during maximal coronary vasodilatation, reflecting structural microvascular alterations. CMD is defined as CFR ≤2,5 and/or a hyperemic microvascular resistance (HMR) >2.5 mmHg/cm/s.11
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