# Coronary Artery Disease

Manage coronary artery disease by separating acute coronary syndrome from chronic coronary disease, selecting anatomy- or ischemia-directed testing for symptomatic patients, intensifying secondary prevention, and reserving revascularization for anatomically and clinically appropriate indications.

**Clinical question:** How should physicians distinguish acute from chronic coronary disease and select testing, preventive therapy, and revascularization?

Updated: 2026-08-24T17:12:42.150370+00:00

## What matters in practice
- Treat suspected type 1 acute myocardial infarction as acute coronary syndrome; the 2025 ACS guideline specifically addresses type 1 AMI rather than type 2 MI, MINOCA, or SCAD. [7]
- In chronic coronary disease without an oral-anticoagulant indication, aspirin 81 mg daily (75-100 mg) is recommended to reduce atherosclerotic events. [9]
- After PCI for chronic coronary disease, aspirin plus clopidogrel for 6 months followed by single antiplatelet therapy is indicated; selected drug-eluting-stent recipients may transition to P2Y12 monotherapy after 1-3 months to reduce bleeding. [9]
- CCTA has high sensitivity and negative predictive value for obstructive CAD, but test selection should be individualized because comparative studies show substantial heterogeneity. [18][20]
- For chronic coronary disease with LVEF 35% or less and PCI-amenable anatomy, PCI added to medical therapy did not reduce all-cause death or heart-failure hospitalization in REVIVED-BCIS2. [12]

## First determine whether this is acute coronary syndrome

Management diverges immediately when plaque rupture–related type 1 MI is suspected.

Use an ACS pathway when the presentation is consistent with type 1 AMI, the plaque rupture, erosion, or dissection phenotype targeted by the ACS guideline. Do not extrapolate that pathway automatically to type 2 MI, myocardial infarction with nonobstructive coronary arteries (MINOCA), or spontaneous coronary artery dissection (SCAD), which are addressed separately. [7][15]

When parenteral unfractionated heparin is selected for initial ACS anticoagulation, use a 60 IU/kg loading dose (maximum 4,000 IU) followed by 12 IU/kg/h (maximum 1,000 IU/h), titrating to an aPTT of 60-80 seconds. For PCI in patients without prior anticoagulant therapy, use 70-100 U/kg to achieve an activated clotting time of 250-300 seconds; patients previously anticoagulated may receive additional UFH to the same ACT target. [7]

DAPT reduces recurrent ischemic events and stent thrombosis after ACS or PCI, but antithrombotic intensity must be balanced against bleeding. In patients with concomitant atrial fibrillation requiring oral anticoagulation after ACS or PCI, avoid assuming that prolonged triple therapy is necessary; randomized evidence and subsequent analyses compare oral anticoagulant plus a single antiplatelet agent with triple-antithrombotic strategies. [1][10][12]
- If fibrinolytic therapy is used, the ACS guideline specifies UFH 60 IU/kg bolus (maximum 4,000 IU), then 12 IU/kg/h (maximum 1,000 IU/h), titrated to therapeutic aPTT. [7]
- Classify the event mechanism before labeling recurrent symptoms as type 1 ACS; type 2 MI, MINOCA, and SCAD require different diagnostic and therapeutic frameworks. [7]

*ACS anticoagulation targets when unfractionated heparin is selected. [7]*

| Clinical use | UFH regimen | Monitoring target |
| --- | --- | --- |
| Initial ACS therapy | 60 IU/kg bolus, maximum 4,000 IU; then 12 IU/kg/h, maximum 1,000 IU/h [7] | aPTT 60-80 seconds [7] |
| PCI without prior anticoagulation | 70-100 U/kg initial bolus [7] | ACT 250-300 seconds [7] |
| PCI after prior anticoagulant therapy | Additional UFH as needed [7] | ACT 250-300 seconds [7] |

## Select testing for symptomatic chronic coronary disease

Choose testing to answer whether symptoms reflect obstructive anatomy, inducible ischemia, or an alternative cause.

In stable or recurrent anginal syndromes, use noninvasive testing when the result will change medical therapy, revascularization planning, or the diagnostic label. Routine screening for coronary heart disease in asymptomatic persons is unlikely to change management or the intensity of risk-factor reduction, so it should not substitute for direct preventive treatment. [3]

CCTA is useful when exclusion of obstructive CAD is the principal diagnostic objective. In intermediate-risk chest-pain populations, reported CCTA sensitivity is approximately 91%-99% and negative predictive value 93%-97% for CAD detection. A comparative meta-analysis found greater sensitivity for coronary CT than stress-testing strategies but substantial heterogeneity, supporting patient-specific modality selection rather than a universal first test. [20][18]

After an equivocal exercise treadmill ECG, CCTA can resolve uncertainty about coronary anatomy because the test has strong negative predictive performance for CAD. Conversely, functional testing provides an ischemia-focused answer; select it when documenting exercise-induced ischemia would direct management more clearly than anatomic exclusion alone. [20]

Reserve invasive coronary angiography for patients in whom anatomy is needed to guide revascularization or to clarify an ischemic cause of heart failure. In chronic coronary disease with heart failure, noninvasive ischemia testing or CCTA may be appropriate in selected circumstances, while invasive angiography can identify coronary anatomy and direct subsequent treatment. [12]
- Do not use screening testing in an asymptomatic patient merely to decide whether to intensify conventional risk-factor reduction. [3]
- Use CCTA preferentially when a high-sensitivity anatomic rule-out is needed after uncertain exercise ECG results. [20]
- Use invasive angiography when the anticipated result would determine revascularization feasibility or clarify an ischemic contribution to heart failure. [12]

### Physiologic clarification after CCTA

When CCTA demonstrates intermediate anatomic stenosis and functional significance remains uncertain, CT-derived fractional flow reserve may be used where available. In a contemporary photon-counting CCTA series, FFR-CT of 0.80 or greater was interpreted as negative for functionally significant stenosis; this threshold should be applied within an integrated anatomic and clinical assessment rather than as an isolated indication for invasive angiography. [6]

*Test selection for suspected chronic obstructive CAD. [3][12][18][20]*

| Clinical question | Useful test strategy | Decision implication |
| --- | --- | --- |
| Asymptomatic patient without a management-changing indication | Avoid routine CAD screening [3] | Treat established risk factors directly because screening results are unlikely to change prevention intensity [3] |
| Need to exclude obstructive CAD | CCTA [18][20] | High sensitivity and negative predictive value support an anatomic rule-out approach [20] |
| Equivocal exercise treadmill ECG | CCTA [20] | Clarifies coronary anatomy when exercise ECG leaves diagnostic uncertainty [20] |
| Heart failure with possible ischemic cause | Noninvasive ischemia testing, CCTA, or invasive angiography according to the question [12] | Use invasive angiography when coronary anatomy will direct treatment [12] |

## Build secondary prevention around antiplatelet and lipid-lowering therapy

Chronic coronary disease requires event prevention even when symptoms are controlled or revascularization has been performed.

For chronic coronary disease without an indication for oral anticoagulation, prescribe low-dose aspirin 81 mg daily (acceptable range 75-100 mg) to reduce atherosclerotic events. The decision changes when long-term oral anticoagulation is required, because antithrombotic combinations after PCI or ACS require individualized bleeding-versus-thrombotic assessment. [9][1][2]

After PCI for chronic coronary disease, use DAPT with aspirin and clopidogrel for 6 months, then continue single antiplatelet therapy. In selected patients with a drug-eluting stent who have completed 1-3 months of DAPT, P2Y12-inhibitor monotherapy for at least 12 months is reasonable when reducing bleeding risk is a priority. [9]

Use statin-based lipid lowering as secondary prevention in obstructive CAD; randomized trials have demonstrated reductions in recurrent cardiovascular events and mortality. In post-ACS patients, adding ezetimibe 10 mg to simvastatin 40 mg reduced relative MACE risk by 6.4% versus simvastatin alone in IMPROVE-IT; benefit was similar among participants with baseline LDL-C of 50-70 mg/dL and those with LDL-C of at least 70 mg/dL. [8][10]

For patients with chronic coronary disease and symptoms suggestive of stable angina undergoing outpatient angiography, an hs-cTnI concentration above 10 ng/L identified a higher-risk group in a prospective cohort. Troponin was independently associated with MI or cardiovascular death over a median 2.4 years, but this observational risk marker should complement—not replace—clinical assessment, coronary anatomy, and standard secondary prevention. [19]
- Default chronic coronary disease antiplatelet regimen without oral anticoagulation: aspirin 81 mg daily. [9]
- Default post-PCI chronic coronary disease regimen: aspirin plus clopidogrel for 6 months, followed by single antiplatelet therapy. [9]
- Consider P2Y12 monotherapy after 1-3 months of DAPT in selected drug-eluting-stent recipients when bleeding reduction outweighs the value of continued aspirin. [9]
- Consider intensifying statin-based therapy with ezetimibe after ACS; the cited trial used simvastatin 40 mg plus ezetimibe 10 mg. [10]

*Antiplatelet decisions in chronic coronary disease. [9]*

| Scenario | Recommended or reasonable regimen | Key tradeoff |
| --- | --- | --- |
| CCD without an oral-anticoagulant indication | Aspirin 81 mg daily (75-100 mg) [9] | Reduces atherosclerotic events [9] |
| CCD after PCI | Aspirin plus clopidogrel for 6 months, then single antiplatelet therapy [9] | Balances MACE reduction with bleeding risk [9] |
| Selected DES recipient after 1-3 months of DAPT | P2Y12-inhibitor monotherapy for at least 12 months is reasonable [9] | May reduce bleeding risk [9] |

## Use revascularization for a defined clinical objective

PCI or CABG should follow a demonstrable anatomic and clinical rationale, not angiographic disease alone.

When chronic coronary disease coexists with ischemic cardiomyopathy, distinguish CABG-eligible disease from PCI-amenable disease before projecting a survival or heart-failure benefit. In evidence summarized by the chronic coronary disease guideline, an invasive treatment strategy reduced cardiovascular death or MI in a cited population, whereas REVIVED-BCIS2 found no reduction in all-cause death or heart-failure hospitalization with PCI plus medical therapy versus medical therapy alone among 700 patients with LVEF 35% or less and PCI-amenable chronic coronary disease. [12]

For chronic coronary disease with heart failure, use invasive coronary angiography when it will establish revascularization suitability or clarify the cause of heart failure; otherwise, noninvasive ischemia evaluation or CCTA may answer the clinical question with less procedural exposure. [12]

After PCI, align the antiplatelet plan with stent-related thrombotic risk and bleeding risk before discharge. DAPT lowers recurrent ischemic events and stent thrombosis, but abbreviated DAPT followed by P2Y12 monotherapy is an evidence-based bleeding-reduction option only for selected drug-eluting-stent recipients who have completed the initial 1-3-month DAPT course. [1][9]
- Do not infer that PCI improves survival or prevents heart-failure hospitalization in every patient with LVEF 35% or less and PCI-amenable chronic CAD; REVIVED-BCIS2 did not show that benefit. [12]
- Use angiography when revascularization selection is the unresolved decision, not solely because chronic CAD is present. [12]

*Revascularization decisions in chronic coronary disease with reduced ejection fraction. [12]*

| Clinical setting | Evidence-based interpretation | Next decision |
| --- | --- | --- |
| CCD, LVEF 35% or less, anatomy amenable to PCI | PCI plus medical therapy did not reduce all-cause death or heart-failure hospitalization versus medical therapy in REVIVED-BCIS2 (38.0% vs 37.2%). [12] | Do not use PCI solely to expect reduction in those outcomes; define symptom, ischemia, or anatomic objectives. [12] |
| Heart failure with uncertain ischemic etiology | Noninvasive modalities or CCTA may be appropriate; invasive angiography can define coronary anatomy and direct therapy. [12] | Choose the least invasive test that answers whether revascularization assessment is needed. [12] |

## Do not stop the evaluation at nonobstructive epicardial disease

Persistent angina with nonobstructive anatomy requires consideration of vasomotor and nonatherosclerotic mechanisms.

When symptoms persist despite nonobstructive epicardial anatomy, consider vasospastic angina rather than escalating therapy solely for fixed obstructive CAD. The chronic coronary disease guideline defines epicardial spasm as more than 90% reduction in coronary diameter after intracoronary acetylcholine compared with baseline resting diameter after intracoronary nitroglycerin. [9]

If myocardial infarction occurs with nonobstructive coronary arteries or in the setting of suspected SCAD, classify the mechanism before assigning standard type 1 ACS secondary-prevention and revascularization assumptions. The ACS guideline explicitly identifies MINOCA and SCAD as conditions covered in separate guidance. [7]
- A greater than 90% acetylcholine-provoked epicardial diameter reduction meets the guideline definition of epicardial coronary spasm. [9]
- MINOCA and SCAD should trigger mechanism-specific evaluation rather than reflex application of the type 1 AMI pathway. [7]

*Phenotypes that change the coronary disease pathway. [7][9]*

| Phenotype | Discriminator | Management implication |
| --- | --- | --- |
| Type 1 AMI | Plaque rupture, erosion, or dissection mechanism addressed by ACS guidance [7][15] | Use ACS-directed antithrombotic and reperfusion decision pathways [7] |
| MINOCA or SCAD | Mechanism differs from routine type 1 AMI pathway [7] | Use separate diagnostic and management frameworks [7] |
| Vasospastic angina | More than 90% epicardial diameter reduction after intracoronary acetylcholine challenge [9] | Recognize epicardial spasm rather than attributing symptoms exclusively to fixed CAD [9] |

## References
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## Editorial note

Prepared from cited clinical literature using Astra's research workflow. Verify recommendations against current guidance and patient-specific factors.