Sudden Coma Immediately after Percutaneous
Balloon Mitral Valvuloplasty

Dear Editor:

Despite the fact that percutaneous mitral valvuloplasty (PMV) is a safe and effective therapy for the treatment of mitral valvular stenosis, one of the most important immediate complications of this procedure is systemic embolization (calcic or thrombotic). The incidence of cerebral embolization ranges from 0.5–5% of all PMV, although clinical expression is slightly symptomatic.¹ We report an extremely rare clinical presentation of a neurological complication after a PMV.
Case Description. A 50-year-old female was referred to our hospital for percutaneous balloon mitral valvuloplasty due to severe mitral stenosis associated with New York Heart Association (NYHA) class III dyspnea. The patient also had a personal history of type 2 diabetes mellitus and atrial fibrillation treated with chronic oral anticoagulant therapy. Prior to this procedure, a transesophageal echocardiogram (TEE) revealed no thrombi in the left atrium or appendage, and the Wilkins score was 6 (no valve calcification). Anticoagulation levels were optimal before the PMV with an INR up to 2.5. Percutaneous valvuloplasty was performed using the Inoue technique (Figure 1) with a good final result: increase in valvular area until 1.5 cm² and a decrease in the pressure gradient to 4 mmHg. A dose of 5,000 IU of unfractionated heparin was administered during the procedure. However, immediately after the procedure, the patient had sudden diplopia and dizziness, with a rapidly progressive loss of consciousness, reaching a comatose status within a few minutes. Initial neurological examination suggested an acute vertebrobasilar artery territory stroke confirmed by an urgent transcranial Doppler, and no evidence of intracranial hemorrhage was confirmed by urgent cerebral computed tomography (CT). Intravenous fibrinolytic therapy with recombinant tissue plasminogen activator (alteplase) was initiated 50 minutes after the onset of symptoms. The patient’s neurological condition improved during the next 24 hours with a complete recovery of consciousness and the only residual neurological deficit was a vertical light paralysis. Nine days later, a new cerebral CT already revealed acute ischemic left talamus-subtalamic and right occipital strokes (Figure 2).
Discussion. Cerebral embolization after a PMV is an immediate complication particularly related to the presence of atrial fibrillation or left appendage thrombus, the severity of mitral stenosis, the grade of valve calcification, an incorrect anticoagulation management and an excessive manipulation of the catheter in the left atrium during the technique.^2,3 On the other hand, acute basilar artery embolism is especially associated with cardiac arrhythmias, whereas there are very few reported cases in direct relation with a cardiac catheterization. Clinical presentation of this embolic cerebral location is an acute loss of consciousness followed by other multiple neurologic symptoms without a significant motor or sensory affectation. When the basilar artery stroke has an embolic origin, outcome is usually good and mortality is low.⁴ The most effective treatment of this kind of stroke is intravenous or intra-arterial thrombolysis.⁵
In short, we describe an acute basilar artery stroke that presented like a sudden coma immediately after a PMV. This unusual complication appeared despite a complete preliminary valvular examination and strict anticoagulation management before and during the procedure. In fact, our patient had a favorable valvular anatomy, a previous EET showed no intracardiac thrombi, the anticoagulation levels before and during the PMV were always in adequate ranges and there were no special difficulties in catheter manipulation during the technique. This case illustrates the importance of careful monitoring in the first hours after PMV in order to quickly detect possible immediate complications and treat them rapidly, as happened in our case, because we cannot predict these complications from preliminary examination with certainty.

Javier Escota-Villanueva, MD, María R. Ortas-Nadal, MD, José R. Ruiz-Arroyo, MD, Antonio Peleato-Peleato, MD Department of Cardiology, Haemodynamic Laboratory, University Hospital “Lozano Blesa,” Av. San Juan Bosco 15 50005 Zaragoza, Spain. E-mail: jaescota@yahoo.es