Understanding the pathophysiology of atrial fibrillation is still lacking (AF). Given that this arrhythmia can coexist with a number of pathological conditions (such as mitral valve disease, hyperthyroidism, hypertension, coronary artery disease, etc.) and can also occur in a healthy heart, a condition known as "lone AF," current research points to a multifactorial pathogenesis for AF. It has been demonstrated that triggers coming from both PVs and non-PV sites account for the majority of cases of paroxysmal AF. Ectopic foci, however, might not necessarily be required for the onset and upkeep of AF. Decreased wavelength alone (a product of refractory period and conduction velocity) permitted the maintenance of several concurrent re-entry circuits, resulting in the formation of AF. The idea of electrical remodelling and the variations in ion channel number and function that go along with it have been linked to the progression of the illness and the idea that "AF begets AF." The persistence of the arrhythmia, or so-called chronic AF, has been linked to the presence of a vulnerable atrial structural substrate with areas of conduction block, which causes spatial separation of the wavelets and encourages re-entry. Atrial remodelling, which occurs in chronic AF, makes wave propagation more complex, multiplies sites with the highest dominant frequency (known as rotors), and moves these sites from the PV region towards the left atrium (LA) and/or right atrium. It is still unknown, nevertheless, whether the structural remodelling with interstitial fibrosis and myolysis features or a rise in autonomic tone are pro-fibrillatory variables or whether AF can be created or produced as a symptom of advanced age or underlying cardiac disease