CAR-10. Procainamide-associated heart valve thrombus: "in the thick of it".

Long-term procainamide administration has been previously shown to be associated with circulating antiphospholipid antibodies. Antiphospholipid antibodies are a well known cause of venous and arterial thrombosis, and rarely, intracardiac thrombosis. In a review of the available literature we were unable to locate a single report of intracardiac thrombus in association with procainamide-induced antiphospholipid syndrome. A 67-year-old white male underwent a transthoracic echocardiogram for symptoms of exertional dyspnea. He was found to have a small mass attached to posterior leaflet of tricuspid valve, confirmed by transesophageal echocardiogram. The differential diagnosis included a tumor, vegetation or a thrombus. His past medical history revealed paroxysmal atrial fibrillation for which he had been on chronic procainamide therapy for eight years. He denied any history of previous thromboembolic phenomenon, immunologic or bleeding disorders. Lab data revealed activated partial thromboplastin time (PTT) prolonged at 103 which did not correct on mixing studies. Platelets were noted to be low at 131,000. A procoagulant laboratory evaluation ensued which showed a significantly elevated level of anticardiolipin antibodies. The patient was started on full dose warfarin therapy and the procainamide was discontinued. A follow up echocardiogram 1 month later confirmed resolution of the mass consistent with a diagnosis of thrombus Labs showed significant improvement of PTT and normalization of the platelet count. The antiphospholipid (aPL) syndrome is defined as the presence of any of a heterogenous group of antibodies, all directed at phospholipids or phospholipid-binding proteins, in association with venous or arterial thrombosis or recurrent pregnancy losses. Thrombocytopenia is often present. A VAMC study of 66 patients in 1997 showed that 21% of patients taking procainamide had elevated levels of aPL antibodies as opposed to none of the control group. Our case demonstrates it is very important that patients who take medication that are recognized to cause coagulation abnormalities, have regular follow up including lab evaluation. This is especially true in the case of patients with arrhythmia, who are at higher risk for thromboembolic events.

Scott Duffy, Silvestre Cansino, Imran Arif. Department of Cardiovascular Medicine, Joan C. Edwards School of Medicine, Huntington, WV.