The following 3 forms of atrial fibrillation are distinguished:
• paroxysmal: duration not more than 2 days, spontaneous cessation of an attack;
• persistent: duration exceeds 7 days, arrhythmia can be eliminated;
• permanent: lasting more than one year, usually not stopped.
Atrial fibrillation associated with vagotonia usually appears at night or at rest, while with sympathicotonia, atrial fibrillation appears as a result of physical or psycho-emotional stress.
Atrial fibrillation is usually caused by an organic lesion of the heart, for example, ischemic heart disease, hypertension, mitral stenosis or mitral insufficiency, dilated or hypertrophic cardiomyopathy. There are also cases of idiopathic atrial fibrillation (atrial fibrillation, in 15% of cases). Patients with atrial fibrillation often complain of palpitations, a feeling of lack of air, interruptions in the work of the heart, and general weakness.
From a pathophysiological point of view, the occurrence of atrial fibrillation can be explained as follows. Flicker usually occurs in the PL, in particular due to the focal trigger activity of the atrium wall near the mouths of the pulmonary veins. Multiple paths of re-entry of excitation waves lead to arrhythmias, electrical tissue restructuring and structural changes. As a result, the atria lose their ability to contract and expand.
Blood stasis in the enlarged and non-contractile left atrium (LP) increases the risk of thromboembolism by 5-7 times compared with the risk of this complication in the population. Thromboembolism occurs in 20% of patients with atrial fibrillation, and in 80% of cases thromboembolism of cerebral arteries is observed. To reduce the risk of this complication, patients with atrial fibrillation are prescribed anticoagulants.