Atrial Fibrillation Triggered by Adenosine During Fractional Flow Reserve Measurement: Common Arrhythmia in an Uncommon Scenario

Dear Editor,

Recently, we came across the development of new-onset atrial fibrillation (AF) while performing fractional flow reserve (FFR) for the two patients with borderline lesions of the left anterior descending (LAD) and right coronary arteries (RCA). The use of adenosine for the termination of supraventricular tachycardia is a common indication. The hemodynamic evaluation of a coronary lesion prior to revascularization has grown after the publication of the FAME and FAME 2 trials.^{1, 2} In the catheterization laboratory, intracoronary or intravenous adenosine is used to document the significance of borderline lesions as a vasodilator. Transient bradyarrhythmia is known as an adverse effect. The development of AF following intracoronary or intravenous infusions of adenosine is a rare occurrence.^{3, 4}

Case 1

A 48-year-old male, hypertensive, chronic alcoholic, and tobacco chewer, was admitted for 2 months with complaints of recent onset effort angina. He was on treatment for alcoholic optic neuritis. Initial evaluation of electrocardiography revealed T-wave inversions in inferolateral leads. Echocardiography revealed mild concentric left ventricular hypertrophy with normal left ventricular systolic and diastolic functions. Cardiac manufacturers were unremarkable. He was subjected to coronary angiography, which demonstrated single-vessel intermediate, 60%–70% lesion of the distal segment of the RCA. As a result, for the FFR, intracoronary adenosine doses of 90 mcg and 120 mcg were given in succession. The FFR was non-significant (0.93). The patient developed AF with a fast ventricular rate (150–160 beats per minute). He was asymptomatic, and his hemodynamics were normal. As intravenous metoprolol 5 mg failed to restore normal sinus rhythm, a bolus dose of 150 mg intravenous amiodarone was given, followed by an infusion. After 8 hours, the patient’s sinus rhythm returned to normal. He was discharged the next day on aspirin 75 mg once daily, metoprolol succinate 25 mg once daily, and atorvastatin 40 mg at bedtime because his FFR was >0.8.

Case 2

A 67-years old, male, hypertensive and diabetic, general physician, got admitted for coronary angiography for exertional breathlessness over last 6-months despite good control of cardiovascular risk factors. He is on active treatment of bronchial asthma. He demonstrated intermediate lesion of proximal segment of the LAD and the need for FFR to document the significance of the lesion was discussed with him. The FFR was 0.82, indicating that aggressive medical management was recommended. Intracoronary adenosine was injected 120 mcg followed by 160 mcg, which lead to development of atrial fibrillation with fast ventricular rate. Intravenous diltiazem could not revert to normal sinus rhythm, intravenous bolus of amiodarone (150 mg) followed by infusion could establish normal sinus rhythm after 6 hours. He was discharged next day with prescription of metoprolol 25 mg twice daily, rosuvastatin 40 mg at bed time, aspirin 75 mg once daily.

Adenosine and Atrial Fibrillation: Electrophysiological Correlation

Adenosine and its ability to cause cardiac arrhythmia are already well-established. The correlation with AF induction after adenosine myocardial perfusion stress testing has been verified by adenosine infusions used for diagnosing significant coronary artery disease. ⁵ As a function of this category, adenosine is both capable of reducing atrial intervals and shortening its action potential and refractory periods, rendering the atrial myocardium more vulnerable to arrhythmia activation. No occurrence of this complication linked to the FFR evaluation is currently recorded. ⁶ Furthermore, research connects adenosine administration to the development of PACs, which is associated with the development of AF.

There is no recorded prevalence of this complication associated with FFR measurement at this time; nonetheless, the morbidity attributed to AF renders this an essential side effect to evaluate during the functional assessment of intermediate coronary lesions. It is unknown whether this consequence is much more common with intracoronary or intravenous adenosine treatment. Furthermore, the effect of intracoronary adenosine dosage, delivery to the left or right coronary system, coronary dominance, and the proportion of ischemic myocardium on the onset of AF is unclear.

A very unusual consequence of intracoronary adenosine injection during daily catheterization room procedures, such as the measurement of FFR, has been documented in these clinical instances. It is important to keep in mind the possibility of atrial fibrillation being induced during an FFR assessment in light of its expanding usage.