# Resolution of long-standing persistent atrial fibrillation after coronary revascularization: a case report on this rare reversible cause of atrial fibrillation

## TL;DR

A man with long-term atrial fibrillation and heart disease regained normal heart rhythm after a procedure to improve blood flow to the heart, suggesting that heart artery blockage can cause atrial fibrillation.

## Contribution

This case report presents a rare instance where atrial fibrillation was reversed through coronary revascularization without ablation or antiarrhythmic drugs.

## Key findings

- A patient with long-standing atrial fibrillation spontaneously converted to sinus rhythm after PCI for coronary artery disease.
- Left ventricular function normalized within a month following the procedure.
- The case suggests ischaemia may be a reversible cause of atrial fibrillation in some patients.

## Abstract

Atrial fibrillation (AF) commonly coexists with coronary artery disease (CAD) due to overlapping risk factors. Although ischaemia can promote atrial arrhythmogenesis, sustained restoration of sinus rhythm after revascularization alone is unusual.

A 55-year-old man with hypertension and long-standing persistent AF (three years) was referred for pulmonary vein isolation. Echocardiography showed mild LV dysfunction (LVEF 48%) and basal septal thinning. Rest 99mTc-sestamibi myocardial perfusion SPECT (MPS) demonstrated moderate apical and mild to moderate inferior wall defects; 18F-FDG PET/CT with myocardial suppression showed no focal myocardial FDG uptake to suggest active inflammation. Coronary angiography demonstrated critical proximal LAD stenosis (95%) and minor RCA disease (30%). Following LAD PCI (3 mm × 15 mm DES), the patient spontaneously converted to sinus rhythm within two hours and has remained in sinus rhythm for 6 months without antiarrhythmic drugs. LV function normalized at 1 month.

AF usually arises from pulmonary-vein triggers acting on a remodelled atrial substrate; chronic comorbidities (hypertension, obesity, diabetes, sleep apnoea), accelerated fibrosis, conduction slowing, and re-entry. CAD is prevalent in AF cohorts (17–46.5%), reflecting shared risk profiles and potential ischaemic effects on the atria. Experimental work shows atrial ischaemia shortens refractoriness, increases dispersion of repolarization, and heightens AF inducibility. Coronary occlusion (particularly RCA) facilitates both triggers and substrate. Clinically, reports conflict on whether coronary artery disease worsens post-ablation outcomes: large registries found no independent association between CAD burden and AF recurrence, while other studies observed higher recurrence in CAD with benefit from revascularization prior to ablation. Our case adds a rare but persuasive datapoint: ischaemia-driven AF that terminated immediately after PCI without ablation or antiarrhythmics, followed by durable sinus rhythm and rapid left ventricular recovery—features that argue causality.

In atrial fibrillation patients with coexisting CAD, ischaemia may be a reversible driver of arrhythmia. This case demonstrates immediate and sustained restoration of sinus rhythm after PCI without antiarrhythmics or ablation. Incorporating ischaemia evaluation into pre-ablation assessment may avert invasive procedures and optimize outcomes in selected individuals.