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CLINICAL STATEMENTS AND GUIDELINES

Circulation. 2023;148:e9–e119. DOI: 10.1161/CIR.0000000000001168 August 29, 2023

Virani et al 2023 AHA/ACC/ACCP/ASPC/NLA/PCNA Chronic Coronary Disease Guideline

Synopsis Nonobstructive CAD is present in >50% of patients undergoing elective coronary angiography and is associated with an increased risk of all-cause death and MI.3–5 INOCA refers to myocardial ischemia caused by coronary vasomotor dysfunction without obstructive CAD.6 In INOCA, the myocardial oxygen supply-demand mismatch may be caused by coronary microvascular dysfunction, coronary vasospasm, or both. Microvascular angina is the clinical manifestation of coronary microvascular dysfunction, and vasospastic angina is the clinical manifestation of myocardial ischemia caused by dynamic epicardial coronary obstruction caused by a vasomotor disorder. Table 15 outlines the diagnostic criteria for microvascular angina proposed by COVADIS (Coronary Vasomotion Disorders International Study Group).7 The criteria used to diagnose vasospastic angina are outlined in Table 16.8 For nonobstructive CAD imaging recommendations, see Section 3.1. (“Diagnostic Evaluation”) of this guideline and the 2021 AHA/ ACC chest pain guideline.9 The CorMicA (Coronary Microvascular Angina) trial showed that in patients with persistent stable chest pain and nonobstructive CAD, invasive coronary physiology testing is feasible and safe, with clear diagnostic use in identifying specific INOCA endotypes.1

Recommendation-Specific Supportive Text

1 In the CorMicA trial, a stratified medical therapy

approach guided by invasive coronary physiology testing (guidewire-based assessment of coronary flow reserve index of microvascular resistance [IMR], and FFR), followed by vasoreactivity testing with acetylcholine improved angina severity and QOL in patients with INOCA (<50% diameter reduction or FFR >0.80).1,2 Based on the results of testing in the intervention arm (vasospastic angina versus microvascular angina), patients were stratified to medical therapy, as shown in Table 17.1 Patients with noncardiac chest pain were discharged from the cardiology clinic and antianginal medications were discontinued. At 6 months, the intervention resulted in improvement of 11.7 units in the Seattle Angina Questionnaire summary score, as well as improvement in QOL, as assessed by the EuroQoL (EQ-5D-5L).1 No differences were observed in MACE between the intervention and control arms at 6-month follow-up. The improvements in angina severity and QOL were sustained at 1-year follow-up.2

Table 15.  Clinical Criteria for Suspecting Microvascular Angina* Criteria Evidence Diagnostic Parameters

1 Symptoms of myocardial ischemia Effort or rest angina; exertional dyspnea

2 Absence of obstructive CAD (<50% diameter reduction or FFR >0.80) Coronary CTA; invasive coronary angiography

3 Objective evidence of myocardial ischemia Ischemic changes on ECG during an episode of chest pain; stress-induced chest pain and/or ischemic changes on ECG in the presence or absence of transient/reversible abnormal myocardial perfusion and/ or wall motion abnormality

4 Evidence of impaired coronary microvascular function Impaired coronary flow reserve (cut-off value depending on methodology between ≤0.20 and ≤0.25); coronary microvascular spasm, defined as reproduction of symptoms, ischemic shifts on ECG but no epicardial spasm during acetylcholine testing; abnormal coronary microvascular resistance indices (eg, IMR >25); coronary slow flow phenomenon, defined as TIMI frame count >25

Suspected microvascular angina is diagnosed if symptoms of ischemia are present (criteria 1) with no obstructive CAD (criteria 2) but only (a) objective evidence of myocardial ischemia (criteria 3) or (b) evidence of impaired coronary microvascular function (criteria 4) alone. *Definitive microvascular angina is only diagnosed if all 4 criteria are present for a diagnosis of microvascular angina. CAD indicates coronary artery disease; CFR, coronary flow reserve; CTA, computed tomographic angiography; ECG, electrocardiogram; FFR, fractional flow reserve; and IMR, index of microcirculatory resistance.

Adapted with permission from Ong P, et al.7 Copyright 2018, with permission from Elsevier.

Table 16.  Diagnostic Criteria for Vasospastic Angina Nitrate-responsive angina: during spontaneous episode, with at least 1 of the following: Rest angina, especially between night and early morning Marked diurnal variation in exercise tolerance, reduced in morning Hyperventilation can precipitate an episode Calcium channel blockers (not beta blockers) suppress episodes Transient ischemic electrocardiographic changes: during spontaneous episode, including any of the following in at least 2 contiguous leads: ST segment elevation ≥0.1 mV ST segment depression ≥0.1 mV New negative U waves Coronary artery spasm: defined as transient total or subtotal coronary artery occlusion (>90% constriction) with angina and ischemic electrocardiographic changes either spontaneously or in response to a provocative stimulus (typically acetylcholine, ergot, or hyperventilation) “Definitive” vasospastic angina is diagnosed if nitrate-responsive angina is evident during spontaneous episodes and either the transient ischemic ECG changed during the spontaneous episodes or coronary artery spasm criteria are fulfilled. “Suspected” vasospastic angina is diagnosed if nitrate-responsive angina is evident during spontaneous episodes but transient ischemic electrocardiographic changes are equivocal or unavailable and coronary artery spasm criteria are equivocal. ECG indicates electrocardiogram. Modified from Beltrame JF, et al.8 by permission of Oxford University Press, copyright 2017; and by permission of The Author, copyright 2015.

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