Coronary Syndrome and Atrial Fibrillation

English | 中文 | हिन्दी | Español | Français | العربية | Português | Русский | Deutsch | 日本語 | 한국어 | Italiano | Türkçe | Polski | Slovak

Chronic coronary syndrome (CCS)

• A slowly developing (over years) stenosis of a coronary artery or arteries causing myocardial ischaemia.
• The myocardium gradually adapts to slowly progressive stenosis, but this creates a substrate for atrial fibrillation (AF).
• Most commonly results from slow progression of atherosclerotic plaques within the coronary artery lumen.
• CCS most commonly presents clinically as:
• Stable angina pectoris
• CCS is considered severe (risk of sudden cardiac death >3 % per year) if CT coronary angiography shows:
• >50 % stenosis of the left main coronary artery
• >70 % stenosis with three-vessel coronary disease
• >70 % stenosis with two-vessel disease including the proximal LAD (Left Anterior Descending artery)
• >70 % stenosis of the proximal LAD

Acute coronary syndrome (ACS)

• A sudden reduction or interruption of blood flow through a coronary artery or arteries.
• ACS does not occur because a stenosis reaches a certain threshold (e.g. 70–80 %), but when an acute reduction in flow occurs, which may develop even with an acute 50 % stenosis.
• Most commonly results from rupture of an atherosclerotic coronary plaque with subsequent acute formation of a platelet thrombus.
• The thrombus then causes an acute stenosis (narrowing) or occlusion (closure) of the arterial lumen.
• Acute ischaemia develops, which provides a substrate for AF.
• ACS most commonly presents clinically as:
• Unstable angina pectoris – mainly due to acute stenosis
• NSTEMI (Non-ST-Elevation Myocardial Infarction) – mainly due to acute stenosis
• STEMI (ST-Elevation Myocardial Infarction) – mainly due to acute occlusion

Type 1 myocardial infarction

• Results from rupture of an atherosclerotic plaque and subsequent thrombosis at the rupture site within the coronary artery lumen. Patients often have pre-existing coronary stenoses (>50 %). Type 1 MI most commonly presents as:
• NSTEMI
• STEMI

Type 2 myocardial infarction

• Myocardial infarction without direct acute coronary thrombosis, due to a supply–demand mismatch in oxygen delivery and consumption.
• It may occur, for example, during an episode of tachy-AF and anaemia, when the coronary circulation cannot supply sufficient oxygen to the myocardium. Type 2 MI most commonly presents clinically as:
• NSTEMI

Revascularization is restoration of blood flow across a stenosis or occlusion of a coronary artery. Revascularization methods include:

• Percutaneous coronary intervention (PCI) – balloon dilatation of the stenosis/occlusion followed by stent implantation in most cases. PCI is the most common revascularization method:
  • STEMI: ~85–90 %
  • NSTEMI: ~60–70 %
  • CCS: ~30–40 %
• Surgical revascularization (CABG – Coronary Artery Bypass Graft) – surgical creation of a bypass around a coronary stenosis/occlusion using a graft (internal mammary artery or great saphenous vein). Used mainly for critical left main stenosis or multivessel coronary disease:
  • STEMI: <5 %
  • NSTEMI: ~5–10 %
  • CCS: ~10–15 %
• Pharmacological revascularization (thrombolysis) – administration of a fibrinolytic to dissolve an acute thrombus in a coronary artery. Used only where PCI is not available:
  • STEMI: ~5–10 %
  • NSTEMI: 0 %
  • CCS: 0 %

ACS is an acute critical condition that may trigger or worsen an AF episode.

The incidence of new-onset AF within 24 hours after ACS is 2–23 %.

• These patients did not have AF before ACS, but AF develops during ACS.

10–15 % of patients with AF undergo PCI for coronary artery disease.

Tachy-AF (ventricular rate >100/min) may cause type 2 myocardial infarction.

Patients with ACS and AF require combined antithrombotic therapy:

• In ACS, a platelet thrombus forms – antiplatelet therapy is administered
• In AF, a fibrin thrombus forms – anticoagulation therapy is administered

NOAC – Non-vitamin K Oral Anticoagulant, P2Y12 – P2Y12 adenosine diphosphate (ADP) receptor inhibitor (e.g. Clopidogrel, Prasugrel, Ticagrelor), CCS – Chronic coronary syndrome, PCI – Percutaneous coronary intervention (coronary angioplasty with stent)

ACS after PCI requires antiplatelet therapy; therefore, patients with AF (if they require anticoagulation therapy) and ACS after PCI require:

• TAT – most commonly (NOAC + clopidogrel + aspirin), or
• DAT – most commonly (NOAC + clopidogrel)

In ACS and AF, NOAC (not warfarin) are preferred as anticoagulation therapy.

The preferred P2Y12 inhibitor is clopidogrel (not ticagrelor and prasugrel).

Combination of anticoagulation therapy (warfarin or NOAC) with (ticagrelor or prasugrel) is not recommended,

• due to high bleeding risk

During DAT (warfarin + antiplatelet therapy)

• a target INR 2–2.5 (not 2–3) should be considered to reduce bleeding risk.

Preferred DAT in AF after ACS or after PCI is:

• Apixaban + clopidogrel

During TAT and DAT, proton pump inhibitors (pantoprazole) are recommended for prevention of gastrointestinal bleeding.

In patients with AF and stable CCS, anticoagulation therapy alone is recommended (not DAT).

Anticoagulation and antiplatelet therapy in atrial fibrillation	Class
In combination therapy (OAC + antiplatelet therapy), NOAC (not warfarin) are preferred as OAC due to lower bleeding risk and better thromboembolism prevention.	I
If the patient is taking (rivaroxaban + antiplatelet therapy), rivaroxaban dose reduction 20 mg → 15 mg once daily may be considered to reduce bleeding risk.	IIa
If the patient is taking (dabigatran + antiplatelet therapy), dabigatran dose reduction 150 mg → 110 mg twice daily may be considered to reduce bleeding risk.	IIa
If the patient is taking (warfarin + antiplatelet therapy), a target INR 2–2.5 may be considered to reduce bleeding risk.	IIa

OAC - Oral anticoagulation, NOAC – Non-vitamin K Oral Anticoagulant (Dabigatran, Rivaroxaban, Apixaban, Edoxaban)

Acute coronary syndrome and atrial fibrillation	Class
In patients with AF and ACS after PCI (low ischaemic risk), the following is recommended: Triple therapy (NOAC + clopidogrel + aspirin) for < 1 week, then discontinue aspirin. Then dual therapy (NOAC + clopidogrel) and discontinue clopidogrel after 12 months. Then continue NOAC.	I
In patients with AF and ACS after PCI (high ischaemic risk), the following is recommended: Triple therapy (NOAC + clopidogrel + aspirin) for < 1 month, then discontinue aspirin. Then dual therapy (NOAC + clopidogrel) and discontinue clopidogrel after 12 months. Then continue NOAC.	IIa

NOAC – Non-vitamin K oral anticoagulants (Dabigatran, Rivaroxaban, Apixaban, Edoxaban), ACS – Acute coronary syndrome, PCI – Percutaneous coronary intervention

High ischaemic risk after percutaneous coronary intervention (PCI)
History of stent thrombosis (despite adequate antiplatelet therapy)
Stent implantation in the last remaining patent coronary artery
Diffuse coronary artery disease (especially in patients with diabetes mellitus)
Chronic kidney disease creatinine ≥133 µmol/L (CrCl <60 ml/min)
Implantation of ≥3 stents
Treatment of ≥3 coronary lesions
Treatment of a bifurcation with 2 stents
Total stent length >60 mm
Treatment of CTO (Chronic Total Occlusion)

Chronic coronary syndrome and atrial fibrillation	Class
In patients with AF and CCS after PCI (low ischaemic risk), the following is recommended: Triple therapy (NOAC + clopidogrel + aspirin) for < 1 week, then discontinue aspirin. Then dual therapy (NOAC + clopidogrel) and discontinue clopidogrel after 6 months. Then continue NOAC.	I
In patients with AF and CCS after PCI (high ischaemic risk), the following is recommended: Triple therapy (NOAC + clopidogrel + aspirin) for < 1 month, then discontinue aspirin. Then dual therapy (NOAC + clopidogrel) and discontinue clopidogrel after 6 months. Then continue NOAC.	IIa

NOAC – Non-vitamin K oral anticoagulants (Dabigatran, Rivaroxaban, Apixaban, Edoxaban), CCS - Chronic coronary syndrome, PCI – Percutaneous coronary intervention

Duration of antiplatelet therapy after ACS with atrial fibrillation	Class
In stable patients after ACS with AF, antiplatelet therapy is not recommended beyond 12 months.	III

ACS – Acute coronary syndrome

Antithrombotic therapy in ACS, CCS, and atrial fibrillation	Class
NOAC (not warfarin) are the preferred anticoagulation therapy in combination with antiplatelet therapy.	I
NOAC doses are reduced according to standard NOAC dose-reduction criteria.	I
During treatment with (warfarin + antiplatelet therapy), a target INR 2–2.5 may be considered.	IIa
During warfarin therapy (without antiplatelet therapy), a target INR 2–3 is recommended.	I
The preferred P2Y12 inhibitor in combination with anticoagulation therapy is clopidogrel (not ticagrelor or prasugrel).	IIa

ACS – Acute coronary syndrome, CCS - Chronic coronary syndrome, NOAC – Non-vitamin K oral anticoagulants (Dabigatran, Rivaroxaban, Apixaban, Edoxaban)

All of the following patients:

• Have known AF and are on long-term anticoagulation therapy (NOAC or warfarin), or
• Have newly diagnosed AF (during ACS or PCI) with an indication for anticoagulation therapy (NOAC or warfarin).

ACS after PCI (Low ischaemic risk)
Example: A patient with AF (on NOAC) had an infarction (STEMI or NSTEMI), was transferred to a cardiac centre where PCI was performed with implantation of 1 stent in the circumflex artery.

ACS after PCI (High ischaemic risk)
Example: A patient with AF had an infarction (STEMI or NSTEMI), was transferred to a cardiac centre where PCI was performed with implantation of 3 stents.

CCS after PCI (Low ischaemic risk)
Example: A patient with AF (on NOAC) had stable angina pectoris and significant coronary stenosis (>70 %) on CT coronary angiography; PCI was performed with implantation of 1 stent in the right coronary artery.

CCS after PCI (High ischaemic risk)
Example: A patient with AF (on NOAC) had stable angina pectoris; coronary angiography showed 3 severe stenoses (>70 %), and 3 stents were implanted during PCI.

Stable CCS
Example: A patient with AF (on NOAC) has CCS with non-significant coronary stenosis (<50 %), not indicated for PCI.

In patients after PCI, bleeding risk is assessed using the ARC-HBR (Academic Research Consortium – High Bleeding Risk) score.

• It indicates whether shortening (not discontinuation) of antithrombotic therapy duration after PCI may be considered.
• The ARC-HBR score is positive if the patient has ≥1 major criterion or ≥2 minor criteria.
• Positive ARC-HBR score:
• Risk of major bleeding 4–9 % within 1 year after PCI
• Shortening of antithrombotic therapy after PCI may be considered
• TAT (1 week → 3–7 days)
• TAT (1 month → 1–4 weeks)
• DAT (12 months → 6–12 months)
• Negative ARC-HBR score:
• Risk of major bleeding ~1–3 % within 1 year after PCI
• Antithrombotic therapy is not shortened

ARC-HBR score (Bleeding risk)
Major criteria (1 is sufficient) Active bleeding Previous intracranial bleeding Intracranial tumour or arteriovenous malformation Recent intracranial event (<6 months) Long-term oral anticoagulation (NOAC or warfarin) Thrombocytopenia <100 × 109/L Haemoglobin <11 g/dL or transfusion within the last 4 weeks Severe chronic kidney disease (eGFR <30 ml/min) Severe liver disease with portal hypertension
Minor criteria (≥2 required) Age ≥75 years Mild to moderate chronic kidney disease (eGFR 30–59 ml/min) Haemoglobin: men 11–12.9 g/dL, women 11–11.9 g/dL Chronic therapy with steroids or NSAIDs: ibuprofen, diclofenac, naproxen, indomethacin, ketorolac History of non-intracranial bleeding (>12 months)

ARC-HBR - Academic Research Consortium – High Bleeding Risk. PCI - Percutaneous coronary intervention. NOAC – Non-vitamin K Oral Anticoagulant (Dabigatran, Rivaroxaban, Apixaban, Edoxaban). eGFR = estimated Glomerular Filtration Rate. NSAIDs - non-steroidal anti-inflammatory drugs

ARC-HBR - Academic Research Consortium – High Bleeding Risk. PCI - Percutaneous coronary intervention. DAT - Dual Antithrombotic Therapy. TAT - Triple Antithrombotic Therapy.

These guidelines are unofficial and do not represent formal guidelines issued by any professional cardiology society. They are intended for educational and informational purposes only.