Myasthenia gravis (MG) is an autoimmune disease that mainly affects the neuromuscular junction. Patients are grouped according to the serological conditions, symptoms, age at onset, and thymic involvement.[1] Coexisting conditions such as secondary autoimmune disease,[2] thymoma, cardiac disease, and therapy-induced disorders represent a major challenge in the treatment of MG patients. In treating MG, medications such as pyridostigmine, corticosteroids, and other immunosuppressants are given. In addition, a thymectomy is conducted if concurrent thymoma, early onset MG without thymoma, or generalized MG with acetylcholine receptor antibodies in late onset group is present.[3] When myasthenic crisis occurs, immune globulin or plasma exchange plays a pivotal role in intensive care. Atrial fibrillation (AF) is one of the most clinically significant cardiac arrhythmias that poses a threat to the cardiovascular system. A 5-fold increased risk for stroke, a 2-fold increased risk for all-cause mortality, and subsequent cardiomyopathy have been reported.[4] The interplay between MG and the cardiac arrhythmia is postulated by different mechanisms. Autonomic dysfunction may play a role in inducing arrythmia. In MG patient, parasympathetic cardiac impairment was found, and the associated baroreflex sensitivity was decreased. Dysfunction in the baroreflex mechanism may leads to dizziness, syncope, atrioventricular block, and even lethal atrial fibrillation.[5] Critical arrhythmias such as ventricular and supraventricular arrhythmias as well as QTc prolongation, have also been reported.[6] In another recent study, myocardial inflammation was suggested to facilitate AF. Cardiomyositis is a rare but fatal complication reported in thymoma MG and late-onset MG in patients who present with anti kv-1.4 muscle antibodies,[7] while one older population study stated that MG is associated with a lower incidence of cardiac-related deaths.[8] A dog model aimed at studying AF found that cholinergic stimulation is the main factor in the development of spontaneous AF. The acetylcholinesterase inhibitor, which is commonly used to treat MG inhibits the breakdown of acetylcholine, thereby increasing both the level and duration of the acetylcholine effect in the autonomic ganglia and the neuromuscular junction.[9] However, augmentation of vagal tone causes a nodal conduction block and atrial arrhythmias.[10,11] One case series found that new-onset AF can occur during myasthenic crisis. However, to the best of our knowledge, there is no epidemiologic evidence to support this result. Thus, we performed a nationwide population-based cohort study to analyze the subsequent risk of AF in people with a history of MG.

So a lot of ppl have heart issues in addition to; however, sometimes when the lungs do not get enough air, the heart beats faster to try and compensate. That’s what I’ve been dealing with.

I have a maternal hereditary factor too. Thank you for the above information.