New-onset Afib in a Patient with CKD: A Case-based Quiz

May 9, 2017
Payal Kohli, MD
Payal Kohli, MD

Mr Smith is 66-years-old. How would you treat his arrhythmia? What would you choose for anticoagulation?

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Mr. Smith is a 66-year-old man with a history of hypertension, chronic kidney disease (CrCl 45 mL/min), and diet-controlled type 2 diabetes (T2DM), who is seeing you today for recent-onset atrial fibrillation (AF). He was diagnosed with AF about 6 weeks ago when he went to his primary care doctor after an upper respiratory illness for which he had been taking around-the-clock over-the-counter decongestant medications. He was started by your partner, who was covering your pager that day, on diltiazem XR 120 mg and warfarin.

Today, his heart rate is 118 beats/min, blood pressure 132/84 mm Hg and his ECG shows he is in AF. He reports persistent fatigue and mild constipation since the initiation of diltiazem and asks for your recommendation.

1. Which of the following would you do next?

A. Stop diltiazem. No alternative medication needed as he has paroxysmal atrial fibrillation.

B. Switch the diltiazem to metoprolol.

C. Switch the diltiazem to digoxin.

D. Start amiodarone.

E. Refer the patient for an ablation as he is symptomatic with his atrial fibrillation.

Answer, discussion, and next question>>

 

The correct answer is: B. Switch the diltiazem to metoprolol.

The patient could be fatigued due to AF with rapid ventricular rate (he is poorly rate-controlled today) or due to medication side effects. Mr Smith is also reporting constipation, which could be a result of calcium channel blocker use. In addition, diltiazem is sometimes less effective than a beta blocker. So an alternative nodal agent would be most appropriate. In this patient with chronic kidney disease, digoxin is a poor choice. And, given his young age, one would want to avoid amiodarone until all other less toxic choices have been exhausted. As he has not achieved adequate rate control, it is not clear whether his symptoms are from his AF or his rapid ventricular rate. Once rate control has been achieved and if the patient remains symptomatic, then one can consider rhythm control options.

 

Patient history, con'td: Mr. Smith returns for a 4-week follow up and is feeling better, with less fatigue. His heart rate is 82 beats/min today. You are looking over his laboratory values and see that his INRs have been widely variable.

2. What is the appropriate next step?

A. Stop warfarin and start a direct oral anticoagulant (DOAC).

B. Liberalize the INR goal range from 2-3 to 1.5 to 3.5 to allow more time in therapeutic range.

C. Refer the patient for a Watchman (left atrial appendage occlude device) as he is a poor candidate for oral anticoagulation.

D. None of the above.

Answer, discussion, and next question>>

 

The correct answer is A. Stop warfarin and start a DOAC.

In this patient with widely variable INRs and a low time in therapeutic range (TTR), a DOAC is a good option for maintaining adequate therapeutic anticoagulation. It is the wide variability of INRs (too low or too high) that increases the risk of embolism and bleeding. There is no data for a wider range of INR being effective in prevention of thromboembolism. The standard range is 2-3. The Watchman device is mainly indicated for patients who have a contraindication to prolonged oral anticoagulation. It is not a therapy for patients who have trouble achieving INR goals with warfarin. Since this patient has chronic kidney disease, the dosing of the DOAC will have to be adjusted according to glomerular filtration rate.

3. Which of the following DOACs would be the LEAST desirable choice for this patient?

A. Pradaxa (dabigatran)

B. Xarelto (rivaroxaban)

C. Eliquis (apixaban)

D. Savaysa (edoxaban)

Answer and discussion>>

 

The correct answer is D. Savaysa (edoxaban)

According to a study of the ENGAGE-TIMI 48 trial, there was an apparent decrease in relative efficacy to prevent thromboembolism at higher levels of CrCl (CrCl ≤ 50 mL/min) with a HR 0.87 compared with HR 0.78 for CrCl > 95 mL/min. However, in this analysis, bleeding rates were lower at all levels of CrCl and therefore, the net clinical outcomes were still statistically more favorable across all CrCl (p-interaction was not significant). Nevertheless, in patients with mild renal impairment who receive dose edoxaban 60 mg daily or 30 mg daily (for CrCl 30-50 ml/min) the relative efficacy of edoxaban is lower than in those with normal renal function and this may not be the best DOAC choice.

 

Reference: Bohula EA, Giugliano RP, Ruff CT, et al. Impact of renal function on outcomes with edoxaban in the ENGAGE AF-TIMI 48 Trial. Circulation. 2016;134:24-36.