Minimally invasive resection of a right atrial mass in a cardiac transplant recipient: a case report.

Intracardiac thrombus formation usually occurs in the left-sided cavities of the heart, most frequently in the presence of atrial fibrillation or cardiomyopathy. We report the case of an initially unclear mass developing in the right atrium (RA) of a heart transplant recipient, which was subsequently resected via a minimally invasive surgical approach. Access via right anterior minithoracotomy using videoscopic assistance allowed for uncomplicated RA thrombectomy in the presented case, avoiding reentry sternotomy with the potential risk of cardiac injury and without aortic cross-clamping or cardioplegic arrest. The patient is doing fine with excellent graft function at the latest follow-up 4 months after minimally invasive thrombectomy and 30 months after cardiac transplantation. To the best of our knowledge, this is the first report describing minimally invasive resection of a right atrial thrombus in a heart transplant recipient.

Transcatheter aortic valve implantation in a heart transplant recipient: a case report.

Transcatheter aortic valve implantation (TAVI) has evolved into a feasible therapeutic option for the management of selected patients with severe aortic stenosis and high or prohibitive risk for standard surgery. Symptomatic severe aortic stenosis occasionally occurs in the allograft long after heart transplantation. Because of specific characteristics and comorbidities of heart transplant recipients, these patients may be considered candidates for this less invasive approach. We report a first case of successful transapical TAVI in a heart transplant recipient with symptomatic severe calcific aortic valvular disease and relevant comorbidities long after heart transplantation.

Frequency-dependent effect of quinidine, mexiletine, and their combination on postrepolarization refractoriness in vivo.

Combination therapy with mexiletine and quinidine has been shown to enhance antiarrhythmic efficacy. To assess further the underlying electrophysiological mechanism, the effect of therapeutic concentrations of mexiletine and quinidine, and of their combination, on action potential duration (at the level of 90% repolarization, APD90), effective refractory (ERP), and the relationship between these two parameters (ERP-APD90) was determined in 21 in vivo canine hearts. The frequency dependence of these effects was assessed over a range of paced steady-state cycle lengths from 250-600 ms. A modified contact electrode technique allowed measurements of both APD90 and ERP simultaneously and at the same ventricular site. In the drug-free state, both APD90 and ERP shortened linearly with shorter cycle lengths, maintaining a constant relationship (ERP-APD90) difference = -9 +/- 2 ms) at all cycle lengths. Quinidine prolonged APD90 by a near constant amount of 11 +/- 1 ms over the entire range of cycle lengths, while mexiletine tended to shorten it. Both mexiletine and quinidine increased ERP and ERP-APD90 in a rate-dependent fashion, the effect increasing with shorter cycle lengths. When used in combination, mexiletine attenuated the lengthening effect of quinidine on APD90 but augmented the rate-dependent increase in ERP, thereby producing greater postrepolarization refractoriness than either drug alone. This effect may explain the clinically favorable antiarrhythmic efficacy of mexiletine and quinidine combination therapy.