Don't forget bleeding risk in AF

"First do not harm."

By Ahmed Adlan
11 October 2016

ABBREVIATIONS 

COPD, chronic obstructive pulmonary disorder; CRP, C-reactive protein; ECG, electrocardiogram; Hb, haemoglobin; INR, international normalised ratio; JVP, jugular venous pressure; MI, myocardial infarction.

Case

A 76 y old lady with multi-morbidity (ischaemic heart disease with prior coronary artery bypass graft, moderate aortic stenosis, permanent atrial fibrillation on warfarin, chronic kidney disease stage 4, severe COPD) was admitted under the surgical team with right upper quadrant pain. Investigations revealed gallstones. During the admission she developed acute chest pain with breathlessness. Serial ECG showed rate controlled atrial fibrillation with no dynamic changes. Serial Troponin enzymes were elevated with a 50 % rise. Clinical examination revealed moderate aortic stenosis, raised JVP and crackles in the lung bases. Chest radiograph confirmed pulmonary oedema. Blood tests showed normocytic anaemia (Hb 100 g/L), WBC 9 x 10^9 /L, CRP <5 mg/L and INR 2.4. 

A diagnosis of acute coronary syndrome, complicated by pulmonary oedema was made (non ST-elevation MI).

Question. 

Appropriate management includes treatment of pulmonary oedema and:

1. Triple therapy. Aspirin, Clopidogrel and Warfarin for one year.

2. Dual antiplatelets, no Warfarin. Stop Warfarin and start Aspirin, Clopidogrel and enoxaparin (treatment dose 1mg/kg bid).

3. Double therapy. Continue Warfarin but add Clopidogrel for 1 year.

4. Triple therapy. Aspirin, Clopidogrel and Warfarin but stop Aspirin after 6 weeks, and stop Clopidogrel after 1 year. 

5. Warfarin only. Urgent coronary angiogram and perform revascularisation as appropriate. 

Answer

3. 

Explanation 

This patient has a very high bleeding risk which must always be taken into account when prescribing antiplatelet and anti-thrombotic agents. Options 1 and 4 are not recommended due to the high bleeding risks associated with triple therapy for such a long duration (HASBLED score is 5). Option 2 is not suitable because discontinuing warfarin would place the patient at an increased risk of ischemic stroke and thromboembolism (CHADSVASc score is 5). Additionally there is no value in giving enoxaparin when the patient is already therapeutically anticoagulated with warfarin. Option 5 would not be suitable as the patient has pulmonary oedema and is not yet fit for angiography. 

Current European guidelines support early coronary angiography in high risk patients with atrial fibrillation and acute coronary syndrome, to assess coronary anatomy and suitability for revascularisation (1). If revascularisation is to be considered then option 5 would be reasonable. Options 3 and 4 are reasonable following surgical or percutaneous revascularisation, respectively. 

Option 3 is the most reasonable treatment if a conservative (non-revascularisation) strategy is to be employed. 

In this particular case a conservative approach would be reasonable with double therapy for a year (Clopidogrel or Aspirin, and Warfarin), followed by warfarin lifelong. Given the significant comorbidities surgical revascularisation would almost certainly be ruled out. Coronary angiography would not be advised until the pulmonary oedema has resolved. However it may be reasonable to assess suitability for percutaneous revascularisation, if the patient was symptomatic. If percutaneous coronary intervention is performed then triple therapy maybe given for 6 weeks, followed by double therapy for a year  followed by monotherapy with warfarin lifelong. 

CHADSVASc stroke risk and HAS-BLED bleeding risk scores. 

Learning points

When assessing patients with acute coronary syndrome it is vitally important to assess bleeding risk. 

In cases of acute coronary syndrome and atrial fibrillation with high stroke risk one must balance the risks and benefits of antiplatelet and antithrombotic therapy.

References

1. 2015 ESC guidelines for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation. Eur Heart January 2016; 37: 267-315.