Q. What is Atrial Fibrillation ?
As the left atrial size increase and atrial wall gets fibrosed, depolarization wave fronts get fragmented and atrial fibrillation sets in. Atrial fibrillation eventually develops in majority of patients with tight mitral stenosis. Initially it may be paroxysmal but later it becomes persistent and then chronic. Fast ventricular rate decreases diastolic filling time that would increase the mean left atrial pressure. Loss of atrial contraction also contributes to increase in mean left atrial pressure. This would lead to worsening of clinical picture due to increased pulmonary wedge pressure and development of pulmonary edema. Very often patient who has been stable deteriorates following the onset of AF and becomes symptomatic necessitating surgery or balloon valvuloplasty.
Left atrial dilatation and stasis due to fibrillation causes development of atrial and atrial appendage thrombus. Incidence of thrombo embolic complications in AF due to rheumatic mitral stenosis is 17 times more than that seen in lone atrial fibrillation. Not uncommonly systemic embolization is a presenting symptom in patients with atrial fibrillation. All patients with atrial fibrillation with or without presence of documented left atrial clot or systemic embolization should receive oral anticoagulants. Even when the atrial fibrillation is intermittent, oral anti coagulants should be given. Also in patients with dilated left atrium more than 5 cm oral anti coagulation is considered even when there is no documented atrial fibrillation. Onset of atrial fibrillation is not related to the severity of mitral stenosis since many other co morbid conditions can generate atrial fibrillation. Presence of atrial fibrillation but not the severity of mitral stenosis determines the indication for oral anticoagulants.
Attempts to regain sinus rhythm either by pharmacological means or by electric cardio version often fails if the underlying disease is not tackled. Any attempt to regain sinus rhythm should be made only after excluding left atrial appendage clots. When amiodarone is given to a patient with atrial fibrillation and undiagnosed left atrial clot, sinus rhythm may suddenly be regained and embolization may occur with disastrous consequences. Hence one should be careful in starting amiodarone in a patient with mitral stenosis and atrial fibrillation. It is better to control ventricular rate by other means before starting amiodarone even when the patient is very sick. Trans esophageal echocardiogram is mandatory before starting amiodarone to a patient with mitral stenosis and AF. As far as possible, in patients with mitral stenosis sinus rhythm should be maintained. The best way of achieving this is by relief of mitral stenosis itself. After relieving mitral stenosis, if the patient has atrial fibrillation attempts should be made to regain sinus rhythm. Usually such attempts made before relieving mitral stenosis are futile or will not be long lasting. At the time of surgical correction either by way of open mitral valvotomy or mitral valve replacement surgeon should do maze procedure to regain sinus rhythm. If sinus rhythm is not regained after surgery or balloon mitral valvotomy, patient may be stared on amiodarone after excluding clots in left atrial appendage or left atrium. If after two weeks of treatment with amiodarone sinus rhythm is not regained one should attempt synchronized DC version after excluding left atrial thrombus. DC version may be ineffective when given without pretreatment with amiodarone. DC version should be given cautiously in sick patients with tight mitral stenosis as sometimes it may worsen patient's condition and precipitate pulmonary edema. It has been shown that long term out come with mitral valve replacement is better in those in whom sinus rhythm has been restored than when mere rate control was achieved.