In a 71‑year‑old woman taking dapagliflozin (Farxiga) with a heart rate of 55 beats per minute, should the medication be discontinued or what evaluation is indicated for the bradycardia?

Dapagliflozin (Farxiga) Should Be Continued in a 71‑Year‑Old Woman with a Heart Rate of 55 Beats Per Minute

A heart rate of 55 beats per minute in a patient taking dapagliflozin does not require discontinuation of the medication, because dapagliflozin does not cause bradycardia and the observed heart rate is likely unrelated to the SGLT2 inhibitor. 1

Dapagliflozin Does Not Affect Heart Rate

• Dapagliflozin has no significant effect on heart rate, blood pressure, or potassium levels, distinguishing it from medications that directly modulate cardiac conduction or autonomic tone 1
• The drug's mechanism—inhibition of renal sodium‑glucose cotransporter‑2—does not involve cardiac ion channels, beta‑adrenergic receptors, or calcium channels that regulate heart rate 2
• In large randomized trials (DAPA‑HF, DELIVER, DAPA‑CKD), dapagliflozin was not associated with bradycardia or heart block as an adverse event 3, 4, 5

Evaluation of Bradycardia in This Patient

Before attributing the heart rate of 55 to any medication, systematically review the patient's complete drug list and clinical context:

• Identify concomitant medications that cause bradycardia:

  • Beta‑blockers (metoprolol, carvedilol, bisoprolol) are the most common culprits in heart‑failure patients and can produce heart rates in the 50–60 range 6
  • Non‑dihydropyridine calcium‑channel blockers (diltiazem, verapamil) slow AV nodal conduction 6
  • Digoxin, amiodarone, ivabradine, and certain antiarrhythmic agents (procainamide, sotalol) all list bradycardia as a known side effect 6
  • Clonidine and other centrally acting antihypertensives may reduce heart rate 6

• Assess whether the bradycardia is symptomatic:

  • A heart rate of 55 beats per minute is physiologically normal for many individuals, especially those on guideline‑directed medical therapy for heart failure 6
  • Bradycardia becomes clinically significant only when it causes dizziness, lightheadedness, syncope, fatigue, or signs of hypoperfusion 6
  • If the patient is asymptomatic and hemodynamically stable, no intervention is required 6

• Obtain a 12‑lead electrocardiogram to exclude second‑ or third‑degree heart block, which would necessitate pacemaker evaluation rather than drug discontinuation 6

• Check thyroid function and electrolytes (potassium, magnesium) if bradycardia is new or unexplained, as hypothyroidism and electrolyte disturbances can slow heart rate 6

Management Algorithm

1. Continue dapagliflozin at the current dose (10 mg daily) because it provides robust cardiovascular and renal protection and does not cause bradycardia 1, 3, 4

2. If the patient is symptomatic (e.g., dizziness, fatigue, syncope):

   • Reduce the dose of beta‑blocker or other bradycardic agents rather than stopping dapagliflozin 6
   • Consider temporary discontinuation of digoxin or ivabradine if these are part of the regimen 6
   • Evaluate for drug interactions (e.g., amiodarone plus beta‑blocker) that may potentiate bradycardia 6

3. If the patient is asymptomatic:

   • No dose adjustment is needed for any medication, including dapagliflozin 6
   • Monitor heart rate at follow‑up visits to ensure it does not fall below 50 beats per minute or become symptomatic 6

4. If second‑ or third‑degree heart block is present on ECG:

   • Refer for pacemaker evaluation rather than discontinuing dapagliflozin, because the conduction abnormality is unrelated to the SGLT2 inhibitor 6

Common Pitfalls to Avoid

• Do not discontinue dapagliflozin solely because of a heart rate of 55 beats per minute; the drug does not cause bradycardia and stopping it will forfeit significant mortality and morbidity benefits 1, 3, 4

• Do not attribute bradycardia to dapagliflozin without first reviewing beta‑blockers, calcium‑channel blockers, digoxin, amiodarone, and other rate‑lowering agents 6

• Do not reduce beta‑blocker doses preemptively in asymptomatic patients with heart rates in the 50–60 range, as this is an expected and beneficial effect of guideline‑directed therapy 6

• Do not withhold dapagliflozin in elderly patients or those with mild bradycardia, because age and baseline heart rate do not modify the drug's cardiovascular and renal benefits 1, 4

Evidence Supporting Continuation of Dapagliflozin

• In the DAPA‑HF trial, dapagliflozin reduced cardiovascular death or worsening heart failure by 26 % (HR 0.74,95 % CI 0.65–0.85) in patients with heart failure and reduced ejection fraction, with no increase in bradycardia 3

• In the DELIVER trial, dapagliflozin reduced cardiovascular death or worsening heart failure by 18 % (HR 0.82,95 % CI 0.73–0.92) in patients with heart failure and preserved ejection fraction, again without bradycardia as an adverse event 5

• In the DAPA‑CKD trial, dapagliflozin reduced the composite of sustained eGFR decline, end‑stage kidney disease, or cardiovascular/renal death by 39 % (HR 0.61,95 % CI 0.51–0.72), with no reported bradycardia 1

• Subgroup analyses by age (including patients ≥75 years) showed consistent benefits without excess bradycardia or other cardiac conduction abnormalities 4