Failure of follow-up gallium single-photon emission computed tomography and fluorine-18-fluorodeoxyglucose positron emission tomography to predict the deterioration of a patient with cardiac sarcoidosis.

Although gallium-67-citrate (67Ga) scanning and single-photon emission computed tomography (SPECT) are useful in the assessment of disease activity in cardiac sarcoidosis, a patient with cardiac sarcoidosis in whom SPECT imaging with 67Ga failed to predict the deterioration in the clinical course is presented. A 53-year-old woman diagnosed with cardiac sarcidosis had 67Ga scanning and 67Ga SPECT, both of which showed abnormal high uptake. After treatment with corticosteroid, there was an apparent improvement in the 67Ga SPECT findings, and the dose of the corticosteroid was reduced. Subsequently, the disease activity of the cardiac sarcoidosis was thought to be well controlled, because abnormal uptake was not found on repeat 67Ga SPECT. However, 4 years after initial diagnosis, thinning at the basal ventricular septal wall and complete atrioventricular block were noted. Despite repeating the evaluation with 67Ga SPECT and additional fluorine-18-fluorodeoxyglucose positron emission tomography (18FDG PET) after discovering this progression, neither of these examinations showed any abnormality. Unfortunately, in this patient, the disease activity of cardiac sarcoidosis was underestimated by the diagnostic imaging modalities.

A case of the toxicity of pilsicainide hydrochloride with comparison of the serial serum pilsicainide levels and electrocardiographic findings.

We treated an 88-year-old man with aortic valvular stenosis/insufficiency and paroxysmal atrial fibrillation, who developed ventricular tachycardia due to pilsicainide toxicity. He was treated at the outpatient clinic of his local hospital, and was administered pilsicainide (100 mg/day) for atrial fibrillation. The electrocardiographic findings on admission to our hospital indicated wide QRS with frequent episodes of ventricular tachycardia. We diagnosed him as having pilsicainide toxicity because of a low cardiac output and renal dysfunction. His creatinine level was 2.4 mg/dL and the serum pilsicainide level was 2.42 microg/mL on admission. Fluid infusion and continuous hemodiafiltration were performed to achieve an early reduction in the serum pilsicainide level. His serum pilsicainide concentration was significantly decreased by these treatments, and the prolongation of the QTc and ventricular tachycardia improved in parallel to the decrease in the serum pilsicainide level. The changes in the serum pilsicainide level showed a significant positive correlation with the changes in the electrocardiographic findings (PQ, QRS, ST intervals, and QTc). Pilsicainide should be administered with great care to elderly patients, especially patients with cardiac dysfunction and renal dysfunction. Estimation of the serum level may be possible from the electrocardiographic findings if the pilsicainide toxicity occurs.