Linking Idiopathic Pulmonary Fibrosis to Supraventricular Arrhythmias – A Literature Review

Abstract

Idiopathic Pulmonary Fibrosis (IPF) and supraventricular arrhythmias (SVAs) share a profound pathophysiological connection that extends beyond incidental comorbidity. This review synthesizes current evidence demonstrating how progressive pulmonary fibrosis creates an arrhythmogenic cardiac substrate through a triad of interconnected pathways. The development of pulmonary hypertension (PH) imposes mechanical stress on the right heart, leading to right atrial dilation, interstitial fibrosis, and electrical remodeling. Chronic hypoxemia induces calcium handling abnormalities and sympathetic activation, while systemic inflammation directly modulates ion channel function and promotes profibrotic signaling. These mechanisms collectively transform the atrial myocardium into a vulnerable environment where re-entrant circuits and triggered activity persist. The resulting SVAs particularly atrial fibrillation and flutter represent not merely associated conditions but direct consequences of IPF's cardiopulmonary pathophysiology. Ultimately, this integrated perspective challenges clinicians to view IPF not as an isolated lung disease, but as a systemic syndrome with significant cardiac implications.