2023 Guidelines of the Taiwan Society of Cardiology on the Diagnosis and Management of Chronic Coronary Syndrome

Abstract

Coronary artery disease (CAD) covers a wide spectrum from persons who are asymptomatic to those presenting with acute coronary syndromes (ACS) and sudden cardiac death. Coronary atherosclerotic disease is a chronic, progressive process that leads to atherosclerotic plaque development and progression within the epicardial coronary arteries. Being a dynamic process, CAD generally presents with a prolonged stable phase, which may then suddenly become unstable and lead to an acute coronary event. Thus, the concept of "stable CAD" may be misleading, as the risk for acute events continues to exist, despite the use of pharmacological therapies and revascularization. Many advances in coronary care have been made, and guidelines from other international societies have been updated. The 2023 guidelines of the Taiwan Society of Cardiology for CAD introduce a new concept that categorizes the disease entity according to its clinical presentation into acute or chronic coronary syndromes (ACS and CCS, respectively). Previously defined as stable CAD, CCS include a heterogeneous population with or without chest pain, with or without prior ACS, and with or without previous coronary revascularization procedures. As cardiologists, we now face the complexity of CAD, which involves not only the epicardial but also the microcirculatory domains of the coronary circulation and the myocardium. New findings about the development and progression of coronary atherosclerosis have changed the clinical landscape. After a nearly 50-year ischemia-centric paradigm of coronary stenosis, growing evidence indicates that coronary atherosclerosis and its features are both diagnostic and therapeutic targets beyond obstructive CAD. Taken together, these factors have shifted the clinicians' focus from the functional evaluation of coronary ischemia to the anatomic burden of disease. Research over the past decades has strengthened the case for prevention and optimal medical therapy as central interventions in patients with CCS. Even though functional capacity has clear prognostic implications, it does not include the evaluation of non-obstructive lesions, plaque burden or additional risk-modifying factors beyond epicardial coronary stenosis-driven ischemia. The recommended first-line diagnostic tests for CCS now include coronary computed tomographic angiography, an increasingly used anatomic imaging modality capable of detecting not only obstructive but also non-obstructive coronary plaques that may be missed with stress testing. This non-invasive anatomical modality improves risk assessment and potentially allows for the appropriate allocation of preventive therapies. Initial invasive strategies cannot improve mortality or the risk of myocardial infarction. Emphasis should be placed on optimizing the control of risk factors through preventive measures, and invasive strategies should be reserved for highly selected patients with refractory symptoms, high ischemic burden, high-risk anatomies, and hemodynamically significant lesions. These guidelines provide current evidence-based diagnosis and treatment recommendations. However, the guidelines are not mandatory, and members of the Task Force fully realize that the treatment of CCS should be individualized to address each patient's circumstances. Ultimately, the decision of healthcare professionals is most important in clinical practice.

Keywords: Coronary; Diagnosis; Guidelines; Treatment.

Figure 1

Terminology and definition of chronic coronary syndrome. ACS, acute coronary syndrome; CAD, coronary artery disease; HF, heart failure; NSTEMI, non-ST-segment elevation myocardial infarction; PCI, percutaneous coronary intervention; STEMI, ST-segment elevation myocardial infarction.

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Figure 2

Schematic flow of risk/severity assessment and management in patients with suspected CCS. ACS, acute coronary syndrome; CAD, coronary artery disease; CCS, chronic coronary syndrome; CCTA, coronary computed tomography angiography; ECG, electrocardiogram; ICA, invasive coronary angiography.

Figure 3

The diagnostic work-up according to risk assessment in patients with suspected CAD. Modified from Gulati M, et al. * Also see Figure 6 for asymptomatic subjects without known CAD. ACS, acute coronary syndrome; CAC, coronary artery calcium; CAD, coronary artery disease; CCTA, coronary computed tomography angiography; ED, emergent department; TSOC, Taiwan Society of Cardiology; TwCCCC, Taiwan Chin-Shan Community Cardiovascular Cohort.

Figure 4

The 3-step approach for the diagnosis of patients with stable symptoms and suspected obstructive CAD. ACS, acute coronary syndrome; CABG, coronary artery bypass graft surgery; CAD, coronary artery disease; CCS, chronic coronary syndrome; CCTA, coronary computed tomography angiography; CMR, cardiac magnetic resonance; ECG, electrocardiography; FFR, fractional flow reserve; FFR-CT, fractional flow reserve-computed tomography; IVUS, intravascular ultrasound; iwFR, instantaneous wave-free ratio; LM, left main; LV, left ventricle; LVEF, left ventricular ejection fraction; MVD, multi-vessel disease; OCT, optical coherence tomography; p-LAD, proximal-left anterior descending artery; PTP, pretest probability; PET, positron emission tomography; SPECT, single-photon emission computed tomography.

Figure 5

The algorithm of appropriate use of cardiac catheterization for known or suspected CCS. ACS, acute coronary syndrome; CAD, coronary artery disease; CCS, chronic coronary syndrome; CCTA, coronary computed tomography angiography; ICA, invasive coronary angiography, LM, left main; MVD, multiple vessel disease; SIS, segment involvement score.

Figure 6

The screening and management of subclinical CAD in apparently healthy adults. BMI, body mass index; CAC, coronary artery calcium; CAD, coronary artery disease; HDL-C, high-density lipoprotein cholesterol; LDL-C, low-density lipoprotein cholesterol; LSM, lifestyle modification; OMT, optimal medical therapy; TwCCC, Taiwan Chin-Shan Community Cardiovascular Cohort.

Figure 7

LDL-C target and pharmacological treatment. ACS, acute coronary syndrome; LDL-C, low-density lipoprotein cholesterol; MI, myocardial infarction; MVD, multiple vessel disease; PAD, peripheral artery disease; PCSK9, proprotein convertase subtilisin-kexin type 9.

Figure 8

An “ABCDE-PS2” steps for heart and vascular wellness. BP, blood pressure; LDL-C, low-density lipoprotein cholesterol.

Figure 9

The CAD-PAD continuum of managing CCS: Choice of DPI or DAPT in patients with high ischemic risk and low bleeding risk. ALI, acute limb ischemia; CAD, coronary artery disease; DAPT, dual antiplatelet therapy; DPI, dual pathway inhibition; MACE, major adverse cardiovascular events; MI, myocardial infarction; PAD, peripheral artery disease.

Figure 10

Choice of antithrombotic regimens for CCS. ASA, aspirin; CCS, chronic coronary syndrome; DAPT: dual anti-platelet therapy; PAD, peripheral artery disease; PCI, percutaneous coronary intervention; P2Y12, purinergic receptor type Y, subtype 12; MI, myocardial infarction; NOAC, novel oral anticoagulants; Riva, rivaroxaban.

Figure 11

Tailored pharmacological approach for CCS beyond the angina paradigm. CAD, coronary artery disease; CABG, coronary artery bypass graft surgery; CCBs, calcium channel blockers; CCTA, coronary computed tomography angiography; CCS, chronic coronary syndrome; GLP-1, glucagon-like peptide-1; LDL-C, low-density lipoprotein cholesterol; OMT, optimal medical therapy; PTP, pretest probability; RAS, renin-angiotensin system; SGLT2, sodium-glucose cotransporter 2.