ABSTRACT
Reinjection of 201Tl is used for improved detection of viable myocardium. Prospectively the effect of the redistribution time after injection for the quantification of the definitive perfusion defect size in multivessel coronary heart disease and severely impaired left ventricular function was examined. Thirty patients were included preoperatively before CABG. The study was performed with 80-90 MBq 201Tl-Cl and reinjection (40-50 MBq). Imaging was performed after an exercise test and 3 hours afterwards. Thereafter, the reinjection dose was given and repeated studies were performed 10 minutes, 2 hours, and 20 hours later. Defect sizes were compared with the 3-hour rest-study without reinjection. Imaging studies were repeated postoperatively. The defect size was expressed as % of left ventricular total myocardium. Perfusion defect sizes were as follows: post-stress study (27%), 3 hour rest-study (17%), post-reinjection-10 min (12%), 2 hours (9%), and 20 hours (7%). Compared with the 3 hour rest-study, the perfusion defect was reduced only in 7/30 patients in the study immediately after reinjection. In the delayed studies, defect sizes were markedly smaller (p < 0.05) both in studies 2 hours and 20 hours after reinjection. In 15/30 patients there was a marked reduction of 50% of defect sizes in the study 2 hours post-reinjection vs the 3 hour rest-study. The residual defects at 2 hours after reinjection were identical to the postoperative defect sizes (10%). Further prolongation of the redistribution time to 20 horus caused an additional small reduction in defect size only in two patients compared with the 2-hour post-reinjection images (n.s.). Using a marker as 201Tl with redistribution characteristics, the redistribution time after reinjection is of utmost importance to correctly identify the definitive size of the perfusion defect vs viable myocardium in patients with multivessel disease. A delay of 2 hours for redistribution after the reinjection most correctly corresponds to the postop defect size; a longer redistribution time did not provide additional advantages.
ABSTRACT
Episodes of sustained paroxysmal supraventricular tachycardias can be terminated by antiarrhythmic drugs given intravenously. The cardiodepressive effects of these drugs are an important limitation of this therapeutic procedure. The dose-dependent circulatory and myocardial effects of the nucleoside adenosine (0.5, 2.0, 5.0 mg/kg/minute) and the class I antiarrhythmic drug ajmaline (1.0, 2.0, 4.0 mg/kg) were investigated in 73 open-chest rats. Hemodynamic measurements in the intact circulation and isovolumic registrations (peak isovolumic left ventricular systolic pressure and peak isovolumic dP/dtmax) were compared with saline controls. Adenosine has a short-lasting, negative, chronotropic effect that causes a dose-dependent reduction of cardiac output (-34%, -54%, -65% vs control). The peak isovolumic left ventricular systolic pressure (LVSP) is not changed significantly by adenosine (-6%, -4%, +5% vs control). The negative chronotropic effect of ajmaline with consecutive reduction of cardiac output is less pronounced (cardiac output: -18%, -20%, -38% vs control). The highest dose of ajmaline causes a significant reduction of peak isovolumic LVSP (-2%, -1%, -7% vs control). Adenosine has an impressive negative chronotropic effect with a consequent marked decrease of cardiac output. The reduction of cardiac output by adenosine is more pronounced compared with ajmaline. Nevertheless, adenosine has-in contrast to ajmaline-no cardiodepressive effects in vivo.
