17:I[462708,["/_next/static/chunks/3yo3kiro3bmlp.js","/_next/static/chunks/3vr2wvd8f2efb.js","/_next/static/chunks/2vtmb68_vu-9t.js","/_next/static/chunks/2s8mt6_8wrpfo.js","/_next/static/chunks/3vkulz2i3l61y.js","/_next/static/chunks/1cqw2i1silz0i.js","/_next/static/chunks/14dbm3lm_t629.js","/_next/static/chunks/335_v2mb569ld.js","/_next/static/chunks/3ykn5ops9bft5.js","/_next/static/chunks/3cmavum774kjt.js","/_next/static/chunks/3th-0-a2xf9qs.js","/_next/static/chunks/0p0xpwde6kzmv.js","/_next/static/chunks/401-sxxnzbtf_.js","/_next/static/chunks/0wywtv698a1v0.js","/_next/static/chunks/2botzqwpnrzyj.js"],"ArticleReader"] 18:T602f,## Summary Chronic coronary disease (CCD) encompasses stable obstructive and nonobstructive coronary atherosclerosis, prior myocardial infarction (MI) or revascularization, chronic angina syndromes, and ischemia or angina without obstructive epicardial coronary disease. Management has two parallel goals: **prevent cardiovascular death/MI/stroke** and **reduce angina while preserving function and quality of life**.[1] The first bedside decision is whether the patient is truly stable. New rest pain, rapidly increasing angina, prolonged chest discomfort, dynamic ECG changes, acute heart failure, syncope, shock, or a rise/fall in cardiac troponin belongs on an acute coronary syndrome (ACS) pathway rather than a chronic outpatient pathway. See [Acute Coronary Syndrome](acute-coronary-syndrome.md). For stable symptoms, define pretest clinical likelihood and choose testing to answer a specific question. Coronary CT angiography (CCTA) is useful when anatomic definition is needed; stress imaging is useful when the key question is inducible ischemia and functional risk. Routine repeated anatomic or ischemic testing is not recommended in an asymptomatic patient whose clinical or functional status has not changed.[1] Disease-modifying therapy includes tobacco cessation, regular physical activity, a cardioprotective dietary pattern, cardiac rehabilitation when eligible, blood-pressure control, intensive lipid lowering, appropriate antithrombotic therapy, and treatment of diabetes, CKD, obesity, and heart failure.[1] The 2026 U.S. dyslipidemia guideline restored explicit LDL-C treatment goals: patients with established atherosclerotic cardiovascular disease (ASCVD) at very high risk generally have an LDL-C goal **<55 mg/dL (1.4 mmol/L)**; other patients with clinical ASCVD generally have a goal **<70 mg/dL (1.8 mmol/L)**.[2] For angina, either a beta-blocker or calcium-channel blocker (CCB) is a reasonable first-line agent, selected according to heart rate, blood pressure, LV function, conduction disease, and comorbidity.[1] Sublingual nitroglycerin treats acute episodes and can be used before predictable exertion. Ranolazine is useful when symptoms persist or when heart rate/blood pressure limit other drugs. Long-term beta-blocker therapy should not be continued solely to improve outcomes in every stable CCD patient; an outcome-driven indication is strongest when MI occurred within the previous year, LVEF is ≤50%, or another primary reason for beta-blockade is present.[1] Revascularization is indicated for important prognostic anatomy in selected patients and for lifestyle-limiting angina despite appropriate medical therapy when anatomy is suitable. ISCHEMIA showed that a routine initial invasive strategy did not reduce the major ischemic composite in stable patients with moderate/severe ischemia compared with an initial conservative strategy, while invasive care provided greater symptom benefit in patients with frequent angina.[3,4] ORBITA-2 confirmed that PCI can reduce angina beyond placebo in selected patients with objective ischemia.[5] ## Clinical spectrum CCD includes:[1] - prior MI, now outside the acute phase; - prior PCI or CABG; - obstructive coronary artery disease (CAD) with or without angina; - nonobstructive coronary atherosclerosis identified by CCTA or angiography; - ischemia documented by noninvasive testing; - chronic stable angina; - vasospastic angina; - coronary microvascular dysfunction and angina/ischemia with no obstructive coronary arteries (ANOCA/INOCA). The term “stable CAD” should not imply biologic inactivity. Plaques evolve, thrombosis risk persists, and symptoms can arise from epicardial stenosis, diffuse atherosclerosis, spasm, microvascular dysfunction, or combinations of these mechanisms. ## Pathophysiology ApoB-containing lipoproteins enter and are retained in the arterial intima. Inflammatory signaling, macrophage foam-cell formation, smooth-muscle migration, extracellular-matrix deposition, calcification, and fibrous-cap remodeling create atherosclerotic plaque. Clinical risk depends on total plaque burden, plaque biology, thrombogenicity, anatomy, and systemic risk rather than stenosis percentage alone. Myocardial ischemia occurs when oxygen supply cannot meet demand. Demand rises with heart rate, contractility, and wall stress. Supply depends on coronary perfusion pressure, diastolic time, oxygen content, epicardial conductance, and microvascular resistance. Consequently: - a fixed stenosis may cause exertional ischemia but not rest symptoms; - tachycardia, anemia, hypotension, or severe hypertension can provoke supply-demand mismatch; - coronary spasm can produce rest ischemia; - microvascular dysfunction can produce angina despite no flow-limiting epicardial stenosis. ## Recognize instability first | Finding | Concern | Immediate next step | |---|---|---| | New or accelerating rest pain | Unstable angina/NSTEMI | ECG, high-sensitivity troponin, acute-risk pathway | | Persistent chest pressure with diaphoresis, nausea, dyspnea | Acute MI | Emergency evaluation | | Syncope, hypotension, shock | Arrhythmia, mechanical disease, acute ischemia, aortic disease | Monitored emergency care | | Acute pulmonary edema | MI, acute heart failure, mechanical complication | Emergency stabilization | | Tearing chest/back pain, pulse or neurologic deficit | Acute aortic syndrome | Emergency aortic imaging pathway | | Pleuritic pain with hypoxemia and VTE risk | Pulmonary embolism | PE risk assessment and imaging pathway | A patient with known CCD can still develop ACS. Do not attribute a changed symptom pattern to “usual angina” without reassessment. ## Clinical assessment ### Symptoms Typical chronic angina is pressure, heaviness, squeezing, burning, or tightness in the retrosternal chest, often provoked by exertion or emotional stress and relieved by rest or nitroglycerin. Radiation may involve an arm, jaw, shoulder, epigastrium, or back. Dyspnea, fatigue, or reduced exercise tolerance may be the dominant ischemic symptom, particularly in older adults and people with diabetes. Document: - onset, duration, frequency, triggers, and recovery time; - exertional threshold and whether it is changing; - rest/nocturnal symptoms; - nitroglycerin use and response; - dyspnea, palpitations, presyncope/syncope; - prior MI, PCI, CABG, stroke, PAD, heart failure, CKD, and diabetes; - bleeding history and current antithrombotic therapy; - tobacco/nicotine and stimulant exposure; - adherence and adverse effects from cardiovascular medications; - functional limitation and the activities the patient wants to regain. ### Physical findings Look for: - blood pressure and pulse rate/rhythm; - congestion or low-output signs; - murmurs, particularly aortic stenosis or mitral regurgitation; - diminished peripheral pulses or other evidence of polyvascular disease; - findings suggesting anemia, thyroid disease, familial hypercholesterolemia, or another contributor. A normal bedside assessment does not exclude coronary disease. ## Baseline investigations Common initial tests include: - 12-lead ECG; - fasting or nonfasting lipid profile; - creatinine/eGFR and electrolytes; - HbA1c or glucose; - CBC when anemia is plausible; - liver enzymes when relevant to lipid-lowering therapy; - echocardiography when LV function, prior MI, heart failure, murmur, or structural disease needs characterization. High-sensitivity troponin is appropriate when acute myocardial injury is suspected; it is not a routine screening biomarker for every stable patient. ## Diagnostic testing ### CCTA CCTA is particularly useful when the aim is to determine whether obstructive or nonobstructive coronary atherosclerosis is present. It can identify plaque that would be missed by a normal stress study and can clarify left-main or multivessel anatomy in selected patients. Limitations include iodinated contrast, calcification artifact, high/irregular heart rates, and reduced image quality in some patients. ### Functional ischemia testing Stress echocardiography, nuclear perfusion imaging, and stress cardiac magnetic resonance assess inducible ischemia. Test choice depends on resting ECG, ability to exercise, body habitus, kidney function, prior revascularization, local expertise, radiation considerations, and the clinical question. Exercise capacity itself is valuable prognostic information when safe exercise testing is feasible. ### Invasive coronary angiography Consider invasive angiography when: - symptoms are severe or refractory despite appropriate therapy; - noninvasive testing suggests high-risk anatomy or a large ischemic burden in a patient for whom revascularization would be reasonable; - left-main or complex multivessel disease is suspected; - noninvasive studies are inconclusive but clinically important symptoms persist; - coronary physiology or invasive functional testing is needed to clarify epicardial versus microvascular/spasm mechanisms. Intermediate stenoses should be assessed physiologically when appropriate rather than revascularized on visual severity alone. > **Current practice:** In a clinically stable patient with known CCD and no meaningful change in symptoms or function, routine periodic stress imaging or repeat coronary anatomy solely because time has passed is not recommended.[1] ## ANOCA and INOCA Persistent angina with no obstructive epicardial disease is not synonymous with noncardiac pain. Potential mechanisms include: - coronary microvascular dysfunction; - epicardial vasospasm; - microvascular spasm; - endothelial dysfunction; - mixed functional disease. Clues include reproducible angina, ischemic ECG or perfusion findings, reduced coronary flow reserve, or symptoms with rest/circadian patterns. Selected patients benefit from specialized testing such as PET or CMR flow assessment, or invasive coronary functional testing. Mechanism-directed treatment may include CCBs and nitrates for vasospasm, risk-factor reduction, and tailored antianginal therapy for microvascular dysfunction. Avoid repeated PCI when no flow-limiting epicardial target exists. ## Secondary prevention ### Lifestyle and rehabilitation Every patient with CCD should receive an individualized plan for:[1] - smoking and nicotine cessation; - regular aerobic and resistance activity within clinical limits; - reduction of prolonged sedentary time; - a dietary pattern emphasizing vegetables, fruits, whole grains, legumes, nuts, fish, and unsaturated fats while limiting trans fat and highly processed foods; - weight management when relevant; - cardiac rehabilitation after qualifying MI, PCI, CABG, or other indications. ### Lipid lowering Maximally tolerated statin therapy remains the foundation for most patients with CCD. The 2026 ACC/AHA dyslipidemia guideline uses explicit secondary-prevention goals:[2] | Clinical risk | LDL-C goal | Practical response if above goal | |---|---:|---| | ASCVD at very high risk | <55 mg/dL (<1.4 mmol/L) | Intensify statin and add evidence-based nonstatin therapy as needed | | Clinical ASCVD not at very high risk | <70 mg/dL (<1.8 mmol/L) | Intensify therapy according to absolute risk, tolerability, and shared decision-making | The same guideline recommends at least one adult lifetime measurement of lipoprotein(a) and supports apoB measurement in selected treated patients, especially those with ASCVD, type 2 diabetes, cardiometabolic disease, or elevated triglycerides, to clarify residual atherogenic-particle risk.[2] See [Dyslipidemia in Adults](dyslipidemia-in-adults.md). ### Antiplatelet and antithrombotic therapy For CCD patients without another indication for oral anticoagulation, low-dose aspirin is standard secondary-prevention therapy unless bleeding risk or intolerance changes the balance.[1] A practical dose is **75-100 mg once daily**. Clopidogrel is an alternative when aspirin cannot be used. After PCI, antiplatelet duration depends on whether PCI followed an acute event, bleeding risk, ischemic risk, stent/lesion factors, and need for oral anticoagulation. Shorter dual-antiplatelet strategies are appropriate for many high-bleeding-risk patients; do not continue dual therapy indefinitely without a current indication.[1] For selected patients with CCD who do not need therapeutic oral anticoagulation and have **high recurrent ischemic risk with low-to-moderate bleeding risk**, the 2023 guideline supports consideration of **rivaroxaban 2.5 mg twice daily plus low-dose aspirin**. This strategy reduces ischemic events but increases major bleeding and is not appropriate for routine use in low-risk or high-bleeding-risk patients.[1] > **Caution:** The vascular-protection dose of rivaroxaban is not the therapeutic dose used for atrial fibrillation or acute venous thromboembolism. Never substitute one regimen for another indication. ### Blood pressure and diabetes Treat hypertension using contemporary BP guidance and comorbidity-specific drug selection. ACE inhibitors or ARBs are particularly useful when hypertension coexists with diabetes, CKD, or LV systolic dysfunction. For type 2 diabetes, select glucose-lowering therapy with cardiovascular outcome benefit when indicated, including SGLT2 inhibitors and/or GLP-1 receptor agonists according to the patient's ASCVD, heart-failure, kidney, weight, and glycemic phenotype. See [Type 2 Diabetes Mellitus](../endocrinology/type-2-diabetes-mellitus.md). ## Antianginal therapy The target is acceptable symptom control without symptomatic hypotension, bradycardia, conduction disease, or intolerable adverse effects. Treatment does not need to follow one rigid sequence.[1] | Therapy | Typical adult use | Best fit | Major cautions | |---|---|---|---| | Beta-blocker | Agent/dose titrated to symptoms, HR, BP, LV function | Prior MI within 1 year, reduced LVEF, tachycardia, hypertension, angina | Bradycardia, AV block, bronchospasm with nonselective drugs, fatigue | | Dihydropyridine CCB | Amlodipine 5 mg daily, increase to 10 mg daily as needed/tolerated | Angina with hypertension or when bradycardia limits other agents | Edema, hypotension | | Non-dihydropyridine CCB | Diltiazem/verapamil regimens vary by formulation | Angina with tachycardia when LV systolic function is preserved | Avoid or use great caution in HFrEF, bradycardia, AV block; interactions | | Sublingual nitroglycerin | 0.3-0.4 mg at onset; repeat every 5 min as needed, up to 3 total doses in 15 min | Acute angina; can use 5-10 min before predictable exertion | Hypotension; never combine with PDE-5 inhibitors or soluble guanylate-cyclase stimulators[8] | | Ranolazine ER | 500 mg twice daily; may increase to 1000 mg twice daily | Persistent angina when HR/BP limit other drugs | QT prolongation, CYP3A interactions, cirrhosis; max 500 mg twice daily with moderate CYP3A inhibitors[7] | If chest pain is new, occurs at rest, is more severe than usual, or does not respond as expected to the patient's established rescue plan, treat it as possible ACS rather than repeatedly self-dosing at home. ### Beta-blocker duration Beta-blockers are valuable antianginal and rate-control drugs and are indicated for HFrEF and other conditions. However, the 2023 CCD guideline states that **long-term beta-blocker therapy is not recommended solely to improve cardiovascular outcomes** when the patient has no MI within the past year, LVEF is >50%, and no other primary indication exists.[1] ### Persistent symptoms When one agent is insufficient: 1. verify that symptoms are ischemic and stable; 2. confirm adherence and dose tolerance; 3. combine mechanistically complementary agents when BP/HR permit; 4. add ranolazine when useful; 5. reassess anatomy/ischemia when symptoms remain lifestyle limiting; 6. discuss revascularization when a suitable flow-limiting lesion is present. ## Revascularization ### Symptom-driven revascularization PCI or CABG is reasonable when angina remains lifestyle limiting despite medical therapy and the lesion is anatomically and physiologically appropriate for intervention.[1] ORBITA-2 randomized patients with stable angina and objective ischemia who were receiving little or no antianginal medication. PCI reduced angina symptom burden compared with a placebo procedure, supporting a genuine symptom benefit from PCI in appropriately selected patients.[5] ### Prognostic revascularization CABG has an important survival role in selected patients with significant left-main disease, complex multivessel disease, or ischemic LV dysfunction when anatomy and surgical risk are appropriate. Diabetes, anatomic complexity, LV function, frailty, kidney disease, and patient preferences influence PCI-versus-CABG decisions.[1] ### What ISCHEMIA changed ISCHEMIA enrolled stable patients with at least moderate ischemia. A routine initial invasive strategy did not reduce the primary composite ischemic outcome compared with an initial conservative strategy over the initial follow-up period, though invasive care improved health status most clearly in patients who had frequent angina.[3,4] This means: - a positive stress study alone is not an automatic indication for PCI; - symptom burden and high-risk coronary anatomy matter; - guideline-directed prevention remains essential whether or not revascularization is performed; - revascularization can be very valuable for symptoms even when a survival advantage is not expected. > **Clinical pearl:** Revascularization treats a lesion; secondary prevention treats the patient's atherosclerotic disease. Successful PCI does not replace lipid lowering, antithrombotic therapy, smoking cessation, BP control, or rehabilitation. ## Follow-up and monitoring At follow-up, review: - interval ACS, stroke, TIA, heart-failure admission, or revascularization; - angina frequency, triggers, rescue-nitrate use, and functional capacity; - blood pressure and heart rate; - tobacco use and physical activity; - adherence and adverse effects; - lipid response and whether the current LDL-C goal is achieved; - kidney function and potassium when RAAS-active therapy or diuretics require it; - HbA1c and kidney/cardiometabolic status in diabetes; - bleeding on antithrombotic therapy. A change in symptom pattern should trigger diagnostic reassessment. Stable patients do not need repetitive imaging merely on a calendar.[1] ## Special populations ### Heart failure or reduced LVEF Use full guideline-directed heart-failure therapy and reassess whether coronary anatomy is contributing to LV dysfunction. Beta-blocker therapy has a clear primary indication when LVEF is reduced. See [Heart Failure With Reduced Ejection Fraction](heart-failure-with-reduced-ejection-fraction.md). ### Chronic kidney disease CKD increases both ischemic and bleeding risk. Contrast exposure, medication dosing, potassium, and renal progression require attention. ISCHEMIA-CKD found no benefit from a routine initial invasive strategy in advanced CKD with stable moderate/severe ischemia and showed important procedural tradeoffs, reinforcing selective rather than automatic angiography.[9] ### Older adults and frailty Treatment should account for competing mortality, bleeding, orthostasis, cognitive burden, polypharmacy, and whether an intervention will improve the patient's own functional goals. Avoid undertreatment based on age alone, but avoid procedural escalation when frailty and competing disease make meaningful benefit unlikely. ### Women and ANOCA/INOCA Women are disproportionately represented among patients with angina and nonobstructive epicardial arteries. Repeated reassurance without mechanism-focused evaluation can miss coronary microvascular dysfunction or vasospasm. Persistent symptoms warrant targeted assessment when results would change management. ## Disposition and referral ### Emergency referral Use emergency pathways for: - new/prolonged rest pain; - dynamic ischemic ECG changes; - troponin-defined acute myocardial injury with ischemic symptoms; - syncope with suspected cardiac cause; - acute heart failure or shock; - malignant arrhythmia. ### Cardiology referral or re-referral Appropriate when: - symptoms persist despite reasonable antianginal therapy; - diagnosis remains uncertain; - high-risk anatomy is suspected; - LV systolic dysfunction is newly recognized; - recurrent angina occurs after PCI/CABG; - ANOCA/INOCA requires advanced functional testing; - antithrombotic decisions are complex because ischemic and bleeding risks are both high. ## Prognosis Risk is heterogeneous. Major adverse prognostic features include: - prior MI or recurrent ASCVD events; - multivessel or left-main disease; - reduced LVEF or heart failure; - diabetes; - CKD; - PAD or polyvascular disease; - continued smoking; - uncontrolled blood pressure; - persistently elevated LDL-C/apoB burden; - inability to sustain preventive therapy. Modern prevention substantially lowers risk, but CCD remains a lifelong systemic atherosclerotic condition. ## Current practice changes Two recent shifts are particularly relevant. The 2023 CCD guideline moved away from routine indefinite beta-blocker therapy after remote MI when LVEF is preserved and no other indication remains, while reinforcing symptom-driven selection of beta-blockers or CCBs.[1] The 2026 dyslipidemia guideline reintroduced explicit LDL-C targets for secondary prevention and sets **<55 mg/dL** for very-high-risk ASCVD, intensifying the expectation that residual lipid risk be treated rather than accepted.[2] At the same time, randomized evidence has clarified the role of revascularization: routine invasive treatment does not improve major outcomes for every stable patient with ischemia, but PCI can provide meaningful angina relief in carefully selected symptomatic patients.[3-5] ## Related library topics - [Acute Coronary Syndrome](acute-coronary-syndrome.md) - [Dyslipidemia in Adults](dyslipidemia-in-adults.md) - [Primary Hypertension in Adults](primary-hypertension-in-adults.md) - [Heart Failure With Reduced Ejection Fraction](heart-failure-with-reduced-ejection-fraction.md) - [Type 2 Diabetes Mellitus](../endocrinology/type-2-diabetes-mellitus.md) - [Peripheral Artery Disease](../vascular-medicine/peripheral-artery-disease.md) ## References 1. Virani SS, Newby LK, Arnold SV, et al. **2023 AHA/ACC/ACCP/ASPC/NLA/PCNA Guideline for the Management of Patients With Chronic Coronary Disease.** *Circulation*. 2023;148:e9-e119. DOI: 10.1161/CIR.0000000000001168. PMID: 37471501. https://doi.org/10.1161/CIR.0000000000001168 2. Blumenthal RS, Morris PB, Gaudino M, et al. **2026 ACC/AHA/AACVPR/ABC/ACPM/ADA/AGS/APhA/ASPC/NLA/PCNA Guideline on the Management of Dyslipidemia.** *Circulation*. 2026. DOI: 10.1161/CIR.0000000000001423. https://doi.org/10.1161/CIR.0000000000001423 3. Maron DJ, Hochman JS, Reynolds HR, et al; ISCHEMIA Research Group. **Initial Invasive or Conservative Strategy for Stable Coronary Disease.** *N Engl J Med*. 2020;382:1395-1407. DOI: 10.1056/NEJMoa1915922. PMID: 32227755. https://doi.org/10.1056/NEJMoa1915922 4. Spertus JA, Jones PG, Maron DJ, et al; ISCHEMIA Research Group. **Health-Status Outcomes with Invasive or Conservative Care in Coronary Disease.** *N Engl J Med*. 2020;382:1408-1419. DOI: 10.1056/NEJMoa1916370. PMID: 32227753. https://doi.org/10.1056/NEJMoa1916370 5. Rajkumar CA, Foley MJ, Ahmed-Jushuf F, et al. **A Placebo-Controlled Trial of Percutaneous Coronary Intervention for Stable Angina.** *N Engl J Med*. 2023;389:2319-2330. DOI: 10.1056/NEJMoa2310610. PMID: 38015442. https://doi.org/10.1056/NEJMoa2310610 6. Eikelboom JW, Connolly SJ, Bosch J, et al. **Rivaroxaban with or without Aspirin in Stable Cardiovascular Disease.** *N Engl J Med*. 2017;377:1319-1330. DOI: 10.1056/NEJMoa1709118. PMID: 28844192. https://doi.org/10.1056/NEJMoa1709118 7. U.S. National Library of Medicine. **Ranolazine extended-release tablets: current prescribing information.** DailyMed. Updated 2026. https://dailymed.nlm.nih.gov/dailymed/lookup.cfm?setid=5f4fc8a4-2bd5-4378-8882-e739c951390e 8. U.S. National Library of Medicine. **Nitroglycerin sublingual tablets: prescribing information.** DailyMed. https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=15b04ca8-9338-4500-9cb2-7448833b4e49 9. Bangalore S, Maron DJ, O'Brien SM, et al; ISCHEMIA-CKD Research Group. **Management of Coronary Disease in Patients with Advanced Kidney Disease.** *N Engl J Med*. 2020;382:1608-1618. DOI: 10.1056/NEJMoa1915925. PMID: 32227756. https://doi.org/10.1056/NEJMoa191592519:T6073,## Summary Chronic coronary disease (CCD) encompasses stable obstructive and nonobstructive coronary atherosclerosis, prior myocardial infarction (MI) or revascularization, chronic angina syndromes, and ischemia or angina without obstructive epicardial coronary disease. Management has two parallel goals: **prevent cardiovascular death/MI/stroke** and **reduce angina while preserving function and quality of life**.[1] The first bedside decision is whether the patient is truly stable. New rest pain, rapidly increasing angina, prolonged chest discomfort, dynamic ECG changes, acute heart failure, syncope, shock, or a rise/fall in cardiac troponin belongs on an [acute coronary syndrome](/library/acute-coronary-syndrome) (ACS) pathway rather than a chronic outpatient pathway. See [Acute Coronary Syndrome](acute-coronary-syndrome.md). For stable symptoms, define pretest clinical likelihood and choose testing to answer a specific question. Coronary CT angiography (CCTA) is useful when anatomic definition is needed; stress imaging is useful when the key question is inducible ischemia and functional risk. Routine repeated anatomic or ischemic testing is not recommended in an asymptomatic patient whose clinical or functional status has not changed.[1] Disease-modifying therapy includes tobacco cessation, regular physical activity, a cardioprotective dietary pattern, cardiac rehabilitation when eligible, blood-pressure control, intensive lipid lowering, appropriate antithrombotic therapy, and treatment of diabetes, CKD, obesity, and heart failure.[1] The 2026 U.S. dyslipidemia guideline restored explicit LDL-C treatment goals: patients with established atherosclerotic cardiovascular disease (ASCVD) at very high risk generally have an LDL-C goal **<55 mg/dL (1.4 mmol/L)**; other patients with clinical ASCVD generally have a goal **<70 mg/dL (1.8 mmol/L)**.[2] For angina, either a beta-blocker or calcium-channel blocker (CCB) is a reasonable first-line agent, selected according to heart rate, blood pressure, LV function, conduction disease, and comorbidity.[1] Sublingual nitroglycerin treats acute episodes and can be used before predictable exertion. Ranolazine is useful when symptoms persist or when heart rate/blood pressure limit other drugs. Long-term beta-blocker therapy should not be continued solely to improve outcomes in every stable CCD patient; an outcome-driven indication is strongest when MI occurred within the previous year, LVEF is ≤50%, or another primary reason for beta-blockade is present.[1] Revascularization is indicated for important prognostic anatomy in selected patients and for lifestyle-limiting angina despite appropriate medical therapy when anatomy is suitable. ISCHEMIA showed that a routine initial invasive strategy did not reduce the major ischemic composite in stable patients with moderate/severe ischemia compared with an initial conservative strategy, while invasive care provided greater symptom benefit in patients with frequent angina.[3,4] ORBITA-2 confirmed that PCI can reduce angina beyond placebo in selected patients with objective ischemia.[5] ## Clinical spectrum CCD includes:[1] - prior MI, now outside the acute phase; - prior PCI or CABG; - obstructive coronary artery disease (CAD) with or without angina; - nonobstructive coronary atherosclerosis identified by CCTA or angiography; - ischemia documented by noninvasive testing; - chronic stable angina; - vasospastic angina; - coronary microvascular dysfunction and angina/ischemia with no obstructive coronary arteries (ANOCA/INOCA). The term “stable CAD” should not imply biologic inactivity. Plaques evolve, thrombosis risk persists, and symptoms can arise from epicardial stenosis, diffuse atherosclerosis, spasm, microvascular dysfunction, or combinations of these mechanisms. ## Pathophysiology ApoB-containing lipoproteins enter and are retained in the arterial intima. Inflammatory signaling, macrophage foam-cell formation, smooth-muscle migration, extracellular-matrix deposition, calcification, and fibrous-cap remodeling create atherosclerotic plaque. Clinical risk depends on total plaque burden, plaque biology, thrombogenicity, anatomy, and systemic risk rather than stenosis percentage alone. Myocardial ischemia occurs when oxygen supply cannot meet demand. Demand rises with heart rate, contractility, and wall stress. Supply depends on coronary perfusion pressure, diastolic time, oxygen content, epicardial conductance, and microvascular resistance. Consequently: - a fixed stenosis may cause exertional ischemia but not rest symptoms; - tachycardia, anemia, hypotension, or severe hypertension can provoke supply-demand mismatch; - coronary spasm can produce rest ischemia; - microvascular dysfunction can produce angina despite no flow-limiting epicardial stenosis. ## Recognize instability first | Finding | Concern | Immediate next step | |---|---|---| | New or accelerating rest pain | Unstable angina/NSTEMI | ECG, high-sensitivity troponin, acute-risk pathway | | Persistent chest pressure with diaphoresis, nausea, dyspnea | Acute MI | Emergency evaluation | | Syncope, hypotension, shock | Arrhythmia, mechanical disease, acute ischemia, aortic disease | Monitored emergency care | | Acute pulmonary edema | MI, acute heart failure, mechanical complication | Emergency stabilization | | Tearing chest/back pain, pulse or neurologic deficit | Acute aortic syndrome | Emergency aortic imaging pathway | | Pleuritic pain with hypoxemia and VTE risk | Pulmonary embolism | PE risk assessment and imaging pathway | A patient with known CCD can still develop ACS. Do not attribute a changed symptom pattern to “usual angina” without reassessment. ## Clinical assessment ### Symptoms Typical chronic angina is pressure, heaviness, squeezing, burning, or tightness in the retrosternal chest, often provoked by exertion or emotional stress and relieved by rest or nitroglycerin. Radiation may involve an arm, jaw, shoulder, epigastrium, or back. Dyspnea, fatigue, or reduced exercise tolerance may be the dominant ischemic symptom, particularly in older adults and people with diabetes. Document: - onset, duration, frequency, triggers, and recovery time; - exertional threshold and whether it is changing; - rest/nocturnal symptoms; - nitroglycerin use and response; - dyspnea, palpitations, presyncope/syncope; - prior MI, PCI, CABG, stroke, PAD, heart failure, CKD, and diabetes; - bleeding history and current antithrombotic therapy; - tobacco/nicotine and stimulant exposure; - adherence and adverse effects from cardiovascular medications; - functional limitation and the activities the patient wants to regain. ### Physical findings Look for: - blood pressure and pulse rate/rhythm; - congestion or low-output signs; - murmurs, particularly aortic stenosis or mitral regurgitation; - diminished peripheral pulses or other evidence of polyvascular disease; - findings suggesting anemia, thyroid disease, familial hypercholesterolemia, or another contributor. A normal bedside assessment does not exclude coronary disease. ## Baseline investigations Common initial tests include: - 12-lead ECG; - fasting or nonfasting lipid profile; - creatinine/eGFR and electrolytes; - HbA1c or glucose; - CBC when anemia is plausible; - liver enzymes when relevant to lipid-lowering therapy; - echocardiography when LV function, prior MI, heart failure, murmur, or structural disease needs characterization. High-sensitivity troponin is appropriate when acute myocardial injury is suspected; it is not a routine screening biomarker for every stable patient. ## Diagnostic testing ### CCTA CCTA is particularly useful when the aim is to determine whether obstructive or nonobstructive coronary atherosclerosis is present. It can identify plaque that would be missed by a normal stress study and can clarify left-main or multivessel anatomy in selected patients. Limitations include iodinated contrast, calcification artifact, high/irregular heart rates, and reduced image quality in some patients. ### Functional ischemia testing Stress echocardiography, nuclear perfusion imaging, and stress cardiac magnetic resonance assess inducible ischemia. Test choice depends on resting ECG, ability to exercise, body habitus, kidney function, prior revascularization, local expertise, radiation considerations, and the clinical question. Exercise capacity itself is valuable prognostic information when safe exercise testing is feasible. ### Invasive coronary angiography Consider invasive angiography when: - symptoms are severe or refractory despite appropriate therapy; - noninvasive testing suggests high-risk anatomy or a large ischemic burden in a patient for whom revascularization would be reasonable; - left-main or complex multivessel disease is suspected; - noninvasive studies are inconclusive but clinically important symptoms persist; - coronary physiology or invasive functional testing is needed to clarify epicardial versus microvascular/spasm mechanisms. Intermediate stenoses should be assessed physiologically when appropriate rather than revascularized on visual severity alone. > **Current practice:** In a clinically stable patient with known CCD and no meaningful change in symptoms or function, routine periodic stress imaging or repeat coronary anatomy solely because time has passed is not recommended.[1] ## ANOCA and INOCA Persistent angina with no obstructive epicardial disease is not synonymous with noncardiac pain. Potential mechanisms include: - coronary microvascular dysfunction; - epicardial vasospasm; - microvascular spasm; - endothelial dysfunction; - mixed functional disease. Clues include reproducible angina, ischemic ECG or perfusion findings, reduced coronary flow reserve, or symptoms with rest/circadian patterns. Selected patients benefit from specialized testing such as PET or CMR flow assessment, or invasive coronary functional testing. Mechanism-directed treatment may include CCBs and nitrates for vasospasm, risk-factor reduction, and tailored antianginal therapy for microvascular dysfunction. Avoid repeated PCI when no flow-limiting epicardial target exists. ## Secondary prevention ### Lifestyle and rehabilitation Every patient with CCD should receive an individualized plan for:[1] - smoking and nicotine cessation; - regular aerobic and resistance activity within clinical limits; - reduction of prolonged sedentary time; - a dietary pattern emphasizing vegetables, fruits, whole grains, legumes, nuts, fish, and unsaturated fats while limiting trans fat and highly processed foods; - weight management when relevant; - cardiac rehabilitation after qualifying MI, PCI, CABG, or other indications. ### Lipid lowering Maximally tolerated statin therapy remains the foundation for most patients with CCD. The 2026 ACC/AHA dyslipidemia guideline uses explicit secondary-prevention goals:[2] | Clinical risk | LDL-C goal | Practical response if above goal | |---|---:|---| | ASCVD at very high risk | <55 mg/dL (<1.4 mmol/L) | Intensify statin and add evidence-based nonstatin therapy as needed | | Clinical ASCVD not at very high risk | <70 mg/dL (<1.8 mmol/L) | Intensify therapy according to absolute risk, tolerability, and shared decision-making | The same guideline recommends at least one adult lifetime measurement of lipoprotein(a) and supports apoB measurement in selected treated patients, especially those with ASCVD, type 2 diabetes, cardiometabolic disease, or elevated triglycerides, to clarify residual atherogenic-particle risk.[2] See [Dyslipidemia in Adults](dyslipidemia-in-adults.md). ### Antiplatelet and antithrombotic therapy For CCD patients without another indication for oral anticoagulation, low-dose aspirin is standard secondary-prevention therapy unless bleeding risk or intolerance changes the balance.[1] A practical dose is **75-100 mg once daily**. Clopidogrel is an alternative when aspirin cannot be used. After PCI, antiplatelet duration depends on whether PCI followed an acute event, bleeding risk, ischemic risk, stent/lesion factors, and need for oral anticoagulation. Shorter dual-antiplatelet strategies are appropriate for many high-bleeding-risk patients; do not continue dual therapy indefinitely without a current indication.[1] For selected patients with CCD who do not need therapeutic oral anticoagulation and have **high recurrent ischemic risk with low-to-moderate bleeding risk**, the 2023 guideline supports consideration of **rivaroxaban 2.5 mg twice daily plus low-dose aspirin**. This strategy reduces ischemic events but increases major bleeding and is not appropriate for routine use in low-risk or high-bleeding-risk patients.[1] > **Caution:** The vascular-protection dose of rivaroxaban is not the therapeutic dose used for [atrial fibrillation](/library/atrial-fibrillation) or acute venous thromboembolism. Never substitute one regimen for another indication. ### Blood pressure and diabetes Treat hypertension using contemporary BP guidance and comorbidity-specific drug selection. ACE inhibitors or ARBs are particularly useful when hypertension coexists with diabetes, CKD, or LV systolic dysfunction. For type 2 diabetes, select glucose-lowering therapy with cardiovascular outcome benefit when indicated, including SGLT2 inhibitors and/or GLP-1 receptor agonists according to the patient's ASCVD, heart-failure, kidney, weight, and glycemic phenotype. See [Type 2 Diabetes Mellitus](../endocrinology/type-2-diabetes-mellitus.md). ## Antianginal therapy The target is acceptable symptom control without symptomatic hypotension, bradycardia, conduction disease, or intolerable adverse effects. Treatment does not need to follow one rigid sequence.[1] | Therapy | Typical adult use | Best fit | Major cautions | |---|---|---|---| | Beta-blocker | Agent/dose titrated to symptoms, HR, BP, LV function | Prior MI within 1 year, reduced LVEF, tachycardia, hypertension, angina | Bradycardia, AV block, bronchospasm with nonselective drugs, fatigue | | Dihydropyridine CCB | Amlodipine 5 mg daily, increase to 10 mg daily as needed/tolerated | Angina with hypertension or when bradycardia limits other agents | Edema, hypotension | | Non-dihydropyridine CCB | Diltiazem/verapamil regimens vary by formulation | Angina with tachycardia when LV systolic function is preserved | Avoid or use great caution in HFrEF, bradycardia, AV block; interactions | | Sublingual nitroglycerin | 0.3-0.4 mg at onset; repeat every 5 min as needed, up to 3 total doses in 15 min | Acute angina; can use 5-10 min before predictable exertion | Hypotension; never combine with PDE-5 inhibitors or soluble guanylate-cyclase stimulators[8] | | Ranolazine ER | 500 mg twice daily; may increase to 1000 mg twice daily | Persistent angina when HR/BP limit other drugs | QT prolongation, CYP3A interactions, cirrhosis; max 500 mg twice daily with moderate CYP3A inhibitors[7] | If chest pain is new, occurs at rest, is more severe than usual, or does not respond as expected to the patient's established rescue plan, treat it as possible ACS rather than repeatedly self-dosing at home. ### Beta-blocker duration Beta-blockers are valuable antianginal and rate-control drugs and are indicated for HFrEF and other conditions. However, the 2023 CCD guideline states that **long-term beta-blocker therapy is not recommended solely to improve cardiovascular outcomes** when the patient has no MI within the past year, LVEF is >50%, and no other primary indication exists.[1] ### Persistent symptoms When one agent is insufficient: 1. verify that symptoms are ischemic and stable; 2. confirm adherence and dose tolerance; 3. combine mechanistically complementary agents when BP/HR permit; 4. add ranolazine when useful; 5. reassess anatomy/ischemia when symptoms remain lifestyle limiting; 6. discuss revascularization when a suitable flow-limiting lesion is present. ## Revascularization ### Symptom-driven revascularization PCI or CABG is reasonable when angina remains lifestyle limiting despite medical therapy and the lesion is anatomically and physiologically appropriate for intervention.[1] ORBITA-2 randomized patients with stable angina and objective ischemia who were receiving little or no antianginal medication. PCI reduced angina symptom burden compared with a placebo procedure, supporting a genuine symptom benefit from PCI in appropriately selected patients.[5] ### Prognostic revascularization CABG has an important survival role in selected patients with significant left-main disease, complex multivessel disease, or ischemic LV dysfunction when anatomy and surgical risk are appropriate. Diabetes, anatomic complexity, LV function, frailty, kidney disease, and patient preferences influence PCI-versus-CABG decisions.[1] ### What ISCHEMIA changed ISCHEMIA enrolled stable patients with at least moderate ischemia. A routine initial invasive strategy did not reduce the primary composite ischemic outcome compared with an initial conservative strategy over the initial follow-up period, though invasive care improved health status most clearly in patients who had frequent angina.[3,4] This means: - a positive stress study alone is not an automatic indication for PCI; - symptom burden and high-risk coronary anatomy matter; - guideline-directed prevention remains essential whether or not revascularization is performed; - revascularization can be very valuable for symptoms even when a survival advantage is not expected. > **Clinical pearl:** Revascularization treats a lesion; secondary prevention treats the patient's atherosclerotic disease. Successful PCI does not replace lipid lowering, antithrombotic therapy, smoking cessation, BP control, or rehabilitation. ## Follow-up and monitoring At follow-up, review: - interval ACS, stroke, TIA, heart-failure admission, or revascularization; - angina frequency, triggers, rescue-nitrate use, and functional capacity; - blood pressure and heart rate; - tobacco use and physical activity; - adherence and adverse effects; - lipid response and whether the current LDL-C goal is achieved; - kidney function and potassium when RAAS-active therapy or diuretics require it; - HbA1c and kidney/cardiometabolic status in diabetes; - bleeding on antithrombotic therapy. A change in symptom pattern should trigger diagnostic reassessment. Stable patients do not need repetitive imaging merely on a calendar.[1] ## Special populations ### Heart failure or reduced LVEF Use full guideline-directed heart-failure therapy and reassess whether coronary anatomy is contributing to LV dysfunction. Beta-blocker therapy has a clear primary indication when LVEF is reduced. See [Heart Failure With Reduced Ejection Fraction](heart-failure-with-reduced-ejection-fraction.md). ### Chronic kidney disease CKD increases both ischemic and bleeding risk. Contrast exposure, medication dosing, potassium, and renal progression require attention. ISCHEMIA-CKD found no benefit from a routine initial invasive strategy in advanced CKD with stable moderate/severe ischemia and showed important procedural tradeoffs, reinforcing selective rather than automatic angiography.[9] ### Older adults and frailty Treatment should account for competing mortality, bleeding, orthostasis, cognitive burden, polypharmacy, and whether an intervention will improve the patient's own functional goals. Avoid undertreatment based on age alone, but avoid procedural escalation when frailty and competing disease make meaningful benefit unlikely. ### Women and ANOCA/INOCA Women are disproportionately represented among patients with angina and nonobstructive epicardial arteries. Repeated reassurance without mechanism-focused evaluation can miss coronary microvascular dysfunction or vasospasm. Persistent symptoms warrant targeted assessment when results would change management. ## Disposition and referral ### Emergency referral Use emergency pathways for: - new/prolonged rest pain; - dynamic ischemic ECG changes; - troponin-defined acute myocardial injury with ischemic symptoms; - syncope with suspected cardiac cause; - acute heart failure or shock; - malignant arrhythmia. ### Cardiology referral or re-referral Appropriate when: - symptoms persist despite reasonable antianginal therapy; - diagnosis remains uncertain; - high-risk anatomy is suspected; - LV systolic dysfunction is newly recognized; - recurrent angina occurs after PCI/CABG; - ANOCA/INOCA requires advanced functional testing; - antithrombotic decisions are complex because ischemic and bleeding risks are both high. ## Prognosis Risk is heterogeneous. Major adverse prognostic features include: - prior MI or recurrent ASCVD events; - multivessel or left-main disease; - reduced LVEF or heart failure; - diabetes; - CKD; - PAD or polyvascular disease; - continued smoking; - uncontrolled blood pressure; - persistently elevated LDL-C/apoB burden; - inability to sustain preventive therapy. Modern prevention substantially lowers risk, but CCD remains a lifelong systemic atherosclerotic condition. ## Current practice changes Two recent shifts are particularly relevant. The 2023 CCD guideline moved away from routine indefinite beta-blocker therapy after remote MI when LVEF is preserved and no other indication remains, while reinforcing symptom-driven selection of beta-blockers or CCBs.[1] The 2026 dyslipidemia guideline reintroduced explicit LDL-C targets for secondary prevention and sets **<55 mg/dL** for very-high-risk ASCVD, intensifying the expectation that residual lipid risk be treated rather than accepted.[2] At the same time, randomized evidence has clarified the role of revascularization: routine invasive treatment does not improve major outcomes for every stable patient with ischemia, but PCI can provide meaningful angina relief in carefully selected symptomatic patients.[3-5] ## Related library topics - [Acute Coronary Syndrome](acute-coronary-syndrome.md) - [Dyslipidemia in Adults](dyslipidemia-in-adults.md) - [Primary Hypertension in Adults](primary-hypertension-in-adults.md) - [Heart Failure With Reduced Ejection Fraction](heart-failure-with-reduced-ejection-fraction.md) - [Type 2 Diabetes Mellitus](../endocrinology/type-2-diabetes-mellitus.md) - [Peripheral Artery Disease](../vascular-medicine/peripheral-artery-disease.md) ## References 1. Virani SS, Newby LK, Arnold SV, et al. **2023 AHA/ACC/ACCP/ASPC/NLA/PCNA Guideline for the Management of Patients With Chronic Coronary Disease.** *Circulation*. 2023;148:e9-e119. DOI: 10.1161/CIR.0000000000001168. PMID: 37471501. https://doi.org/10.1161/CIR.0000000000001168 2. Blumenthal RS, Morris PB, Gaudino M, et al. **2026 ACC/AHA/AACVPR/ABC/ACPM/ADA/AGS/APhA/ASPC/NLA/PCNA Guideline on the Management of Dyslipidemia.** *Circulation*. 2026. DOI: 10.1161/CIR.0000000000001423. https://doi.org/10.1161/CIR.0000000000001423 3. Maron DJ, Hochman JS, Reynolds HR, et al; ISCHEMIA Research Group. **Initial Invasive or Conservative Strategy for Stable Coronary Disease.** *N Engl J Med*. 2020;382:1395-1407. DOI: 10.1056/NEJMoa1915922. PMID: 32227755. https://doi.org/10.1056/NEJMoa1915922 4. Spertus JA, Jones PG, Maron DJ, et al; ISCHEMIA Research Group. **Health-Status Outcomes with Invasive or Conservative Care in Coronary Disease.** *N Engl J Med*. 2020;382:1408-1419. DOI: 10.1056/NEJMoa1916370. PMID: 32227753. https://doi.org/10.1056/NEJMoa1916370 5. Rajkumar CA, Foley MJ, Ahmed-Jushuf F, et al. **A Placebo-Controlled Trial of Percutaneous Coronary Intervention for Stable Angina.** *N Engl J Med*. 2023;389:2319-2330. DOI: 10.1056/NEJMoa2310610. PMID: 38015442. https://doi.org/10.1056/NEJMoa2310610 6. Eikelboom JW, Connolly SJ, Bosch J, et al. **Rivaroxaban with or without Aspirin in Stable Cardiovascular Disease.** *N Engl J Med*. 2017;377:1319-1330. DOI: 10.1056/NEJMoa1709118. PMID: 28844192. https://doi.org/10.1056/NEJMoa1709118 7. U.S. National Library of Medicine. **Ranolazine extended-release tablets: current prescribing information.** DailyMed. Updated 2026. https://dailymed.nlm.nih.gov/dailymed/lookup.cfm?setid=5f4fc8a4-2bd5-4378-8882-e739c951390e 8. U.S. National Library of Medicine. **Nitroglycerin sublingual tablets: prescribing information.** DailyMed. https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=15b04ca8-9338-4500-9cb2-7448833b4e49 9. Bangalore S, Maron DJ, O'Brien SM, et al; ISCHEMIA-CKD Research Group. **Management of Coronary Disease in Patients with Advanced Kidney Disease.** *N Engl J Med*. 2020;382:1608-1618. DOI: 10.1056/NEJMoa1915925. PMID: 32227756. https://doi.org/10.1056/NEJMoa19159257:["$","$L17",null,{"article":{"id":"medical-chronic-coronary-disease-in-adults","title":"Chronic Coronary Disease in Adults","slug":"chronic-coronary-disease-in-adults","description":"Chronic coronary disease (CCD) encompasses stable obstructive and nonobstructive coronary atherosclerosis, prior myocardial infarction (MI) or revascularization, chronic angina syndromes, and ischemia or angina withou…","aliases":[],"category":"Cardiology","tags":["Cardiology"],"updatedAt":"$undefined","body":"$18","headings":[{"id":"summary","text":"Summary","level":2},{"id":"clinical-spectrum","text":"Clinical spectrum","level":2},{"id":"pathophysiology","text":"Pathophysiology","level":2},{"id":"recognize-instability-first","text":"Recognize instability first","level":2},{"id":"clinical-assessment","text":"Clinical assessment","level":2},{"id":"symptoms","text":"Symptoms","level":3},{"id":"physical-findings","text":"Physical findings","level":3},{"id":"baseline-investigations","text":"Baseline investigations","level":2},{"id":"diagnostic-testing","text":"Diagnostic testing","level":2},{"id":"ccta","text":"CCTA","level":3},{"id":"functional-ischemia-testing","text":"Functional ischemia testing","level":3},{"id":"invasive-coronary-angiography","text":"Invasive coronary angiography","level":3},{"id":"anoca-and-inoca","text":"ANOCA and INOCA","level":2},{"id":"secondary-prevention","text":"Secondary prevention","level":2},{"id":"lifestyle-and-rehabilitation","text":"Lifestyle and rehabilitation","level":3},{"id":"lipid-lowering","text":"Lipid lowering","level":3},{"id":"antiplatelet-and-antithrombotic-therapy","text":"Antiplatelet and antithrombotic therapy","level":3},{"id":"blood-pressure-and-diabetes","text":"Blood pressure and diabetes","level":3},{"id":"antianginal-therapy","text":"Antianginal therapy","level":2},{"id":"beta-blocker-duration","text":"Beta-blocker duration","level":3},{"id":"persistent-symptoms","text":"Persistent symptoms","level":3},{"id":"revascularization","text":"Revascularization","level":2},{"id":"symptom-driven-revascularization","text":"Symptom-driven revascularization","level":3},{"id":"prognostic-revascularization","text":"Prognostic revascularization","level":3},{"id":"what-ischemia-changed","text":"What ISCHEMIA changed","level":3},{"id":"follow-up-and-monitoring","text":"Follow-up and monitoring","level":2},{"id":"special-populations","text":"Special populations","level":2},{"id":"heart-failure-or-reduced-lvef","text":"Heart failure or reduced LVEF","level":3},{"id":"chronic-kidney-disease","text":"Chronic kidney disease","level":3},{"id":"older-adults-and-frailty","text":"Older adults and frailty","level":3},{"id":"women-and-anocainoca","text":"Women and ANOCA/INOCA","level":3},{"id":"disposition-and-referral","text":"Disposition and referral","level":2},{"id":"emergency-referral","text":"Emergency referral","level":3},{"id":"cardiology-referral-or-re-referral","text":"Cardiology referral or re-referral","level":3},{"id":"prognosis","text":"Prognosis","level":2},{"id":"current-practice-changes","text":"Current practice changes","level":2},{"id":"related-library-topics","text":"Related library topics","level":2},{"id":"references","text":"References","level":2}],"readingMinutes":15},"linkedMarkdown":"$19","backlinks":[],"related":[],"previewBySlug":{"abcde-approach":{"title":"ABCDE Approach","description":"The ABCDE approach is a structured method for the immediate assessment and treatment of a deteriorating or critically ill patient: Airway, Breathing, Circulation, Disability, Exposure. 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