<![CDATA[Idiopathic pulmonary fibrosis (IPF) and supraventricular arrhythmias (SVAs) share a profound pathophysiological connection beyond incidental comorbidity. This review synthesizes current evidence demonstrating how progressive pulmonary fibrosis creates an arrhythmogenic cardiac substrate through three interdependent pathways. Pulmonary hypertension imposes chronic pressure overload on the right heart, leading to right atrial dilation, interstitial fibrosis, gap junction dysfunction, and electrical remodeling, creating conditions for re-entrant circuits. Chronic hypoxemia induces intracellular calcium overload, after-depolarizations, and sympathetic overactivity, providing functional arrhythmogenic triggers independent of structural remodeling. 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, are strongly associated with IPF's cardiopulmonary pathophysiology. This integrated perspective challenges clinicians to view IPF not as an isolated lung disease but as a systemic syndrome with significant cardiac implications. However, current evidence is largely observational, and further prospective studies are needed to establish screening and management guidelines.]]>
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