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A 52-year-old male patient presented with resistant congestive heart failure. Echocardiographic findings revealed increased right ventricular (RV) wall thickness in conjunction with concentric left ventricular (LV) hypertrophy, LV systolic dysfunction and a granular sparking myocardial appearance. Doppler assessment showed a restrictive LV and RV diastolic filling pattern. These echocardiographic features combined with low voltage of the electrocardiogram is highly suggestive of cardiac amyloidosis. The diagnosis was confirmed by cardiac catheterization and endomyocardial biopsy.

To evaluate the effect of ionic contrast medium on plasma atrial natriuretic peptide (ANP) and its contributing factors, we measured plasma ANP, serum osmolality, pulmonary capillary wedge pressure (PCWP), femoral artery systolic pressure (FASP), and heart rate before and after left ventriculography with Rayvist in 13 patients suspected of coronary artery disease. The control values of plasma ANP, serum osmolality, and PCWP were 20.3 +/- 5.1 pg/ml, 293.5 +/- 1.5 mosm/kg, 6.6 +/- 0.8 mm Hg, respectively. Rayvist produced a significant increase in plasma ANP, serum osmolality, and PCWP at 1 minute (26.0 +/- 6.3 pg/ml, p < 0.05; 300.7 +/- 1.9 mosm/Kg, p < 0.001; 10.7 +/- 1.3 mm Hg, p < 0.001) and 5 minutes (27.3 +/- 6.3 pg/ml, p < 0.01; 296.8 +/- 1.9 mosm/Kg, p < 0.001; 10.4 +/- 1.7 mm Hg, p < 0.01) post left ventriculography. The FASP decreased significantly at 1 minute, followed by an insignificant increase at 5 minutes. The heart rate increased significantly at 1 minute but no significant change was noted at 5 minutes. We conclude that plasma ANP increases significantly after left ventriculography with Rayvist and its response may be related to left ventricular filling pressure and serum osmolality, but not to FASP or heart rate.

The electrophysiologic effects of intravenous verapamil (0.15 mg/kg) and oral sustained-release verapamil (verapamil-SR) (240 mg once daily for 7 days) were studied in 17 patients with paroxysmal supraventricular tachycardia (SVT). Ten patients had atrioventricular (AV) nodal reentrant tachycardia and 7 had AV reciprocating tachycardia involving an accessory AV pathway. Both preparations significantly prolonged anterograde effective refractory period of the AV node and depressed the retrograde AV nodal conduction system. The sinus cycle length, and atrial and ventricular effective refractory periods were prolonged after oral verapamil-SR. Furthermore, oral verapamil-SR depressed retrograde accessory pathway conduction which was not interfered with by intravenous verapamil. Intravenous verapamil and oral verapamil-SR prevented induction of sustained SVT in 12 of 17 (71%) and 10 of 17 (59%) patients, respectively. Follow-up study with oral verapamil-SR 240 mg once daily in 15 patients for 19 +/- 6 months revealed that among the 8 patients without induction of sustained SVT, 7 have been free of symptomatic arrhythmia; only 1 patient had occasional SVT attacks. For the 7 patients with induction of sustained SVT, 3 patients failed to respond to oral verapamil-SR, 1 patient became symptom free, and the remaining 3 patients had less frequent SVT attacks. Thus, immediate intravenous verapamil testing predicts the electrophysiologic results of oral verapamil-SR therapy, and oral verapamil-SR once daily may be used for long-term prophylaxis of SVT with better patient compliance.