Peptide radiopharmaceuticals in nuclear medicine.

This article reviews the labelling of peptides that are recognised to be of interest for nuclear medicine or are the subject of ongoing nuclear medicine research. Applications and approaches to the labelling of peptide radiopharmaceuticals are discussed, and drawbacks in their development considered.

Head-to-head comparison between technetium-99m-sestamibi and thallium-201 tomographic imaging for the detection of coronary artery disease using combined dipyridamole-exercise stress.

AIM: The purpose of this study was a head-to-head comparison of tomographic imaging (SPECT) with technetium-99m (Tc-99m)-sestamibi and thallium-201 (Tl-201) using dipyridamole-low-level bicycle exercise stress for the assessment of coronary artery disease. METHODS: We studied 38 consecutive patients referred for the evaluation of chest pain who had undergone coronary angiography. The patients were randomly allocated to Tc-99m-sestamibi SPECT followed by Tl-201 SPECT or vice versa. The accuracy of both tracers in detecting significant coronary artery disease (> 50% luminal stenosis) was 87% (95% confidence interval 72-96%). Only two patients were classified differently by the two methods. RESULTS: On a segmental basis, good agreement was found between Tc-99m-sestamibi and Tl-201 for both the localization and the nature of perfusion defects (reversible or persistent) identified (Cohen's kappa = 0.67). CONCLUSION: No clinically relevant differences in diagnostic accuracy were demonstrated between Tc-99m-sestamibi and Tl-201 SPECT using combined dipyridamole-exercise stress for the evaluation of coronary artery disease.

Acute effects of intravenous nisoldipine on left ventricular function after acute myocardial infarction.

Nisoldipine is a calcium antagonist with potent coronary vasodilating effects in patients with chronic stable angina pectoris. In an initial study we showed that intravenous nisoldipine, given 24-72 hours after uncomplicated myocardial infarction, was a safe and feasible intervention that had beneficial effects on global and regional myocardial function. We subsequently studied the acute effects of nisoldipine in six patients within 24 hours (mean 14 +/- 4 hours) after the onset of myocardial infarction. Nisoldipine was administered as a 4.5 micrograms/kg intravenous bolus over 3 minutes, followed by intravenous infusion of 0.2 microgram/kg over 60 minutes. Radionuclide angiography, cardiac output, and intraarterial blood pressure measurements were performed before and during nisoldipine. Left ventricular ejection fraction increased from 48.3 +/- 10.3% to 55.3 +/- 11.8% (p = 0.034) during nisoldipine infusion. Regional wall motion score changed during nisoldipine infusion from 3.3 +/- 2.5 to 1.8 +/- 2.6 (p = 0.027). Cardiac output increased from 5.5 +/- 1.0 to 7.3 +/- 1.3 l/min (p = 0.0001). Heart rate increased from 78 +/- 12 to 88 +/- 11 min-1 (p = 0.004). Mean arterial blood pressure decreased from 92 +/- 20 to 79 +/- 13 mmHg (p = 0.038). The rate-pressure product did not change significantly during nisoldipine infusion. It is concluded that nisoldipine improves global and regional left ventricular function in patients with acute myocardial infarction within the first 24 hours.

The acute effects of intravenous nisoldipine on left ventricular function within 24 h after acute myocardial infarction.

Nisoldipine is a calcium antagonist with potent coronary vasodilating effects in patients with chronic stable angina pectoris. We studied the acute effects of nisoldipine in six patients within 24 h (mean 14 +/- 4 h) after the onset of myocardial infarction. Nisoldipine was administered as a 4.5 micrograms kg-1 intravenous bolus over 3 min followed by intravenous infusion of 0.2 microgram kg-1 min-1 during 60 min. Radionuclide angiography, cardiac output and intra-arterial blood pressure measurements were performed before and during nisoldipine. Left ventricular ejection fraction increased from 48.3 +/- 10.3% to 55.3 +/- 11.8% (P = 0.034) during nisoldipine infusion. Regional wall motion score changed during nisoldipine infusion from 3.3 +/- 2.5 to 1.8 +/- 2.6 (P = 0.027). Cardiac output increased from 5.5 +/- 1.0 to 7.3 +/- 1.3 l min-1 (P = 0.0001). Heart rate increased from 78 +/- 12 to 88 +/- 11 beats.min-1 (P = 0.004). Mean arterial blood pressure decreased from 91.7 +/- 20.2 to 78.7 +/- 13.1 mmHg (P = 0.038). The rate-pressure product did not change significantly during nisoldipine infusion. It is concluded that nisoldipine improves global and regional left ventricular function in patients with acute myocardial infarction within the first 24 h. Our findings suggest that this effect is achieved without increasing myocardial oxygen demand.

Automatic region of interest determination in dual photon absorptiometry of the lumbar spine.

In a heuristic approach, the authors developed an algorithm for automatic region-of-interest (ROI) determination in bone mineral density (BMD) measurements of the lumbar spine. First, the algorithm detects the boundaries of the spine utilizing simple smoothing and gradient operators followed by a dynamic programming technique. Second, it selects L2, L3, and L4 from the spine by examining the BMD values along lines that are orthogonal to the local direction of the spine. The algorithm was tested in studies of a spine phantom, normal subjects (30), and patients (94). In all but two patient studies of severely affected spines the contours were detected correctly. The ROI determination was performed satisfactorily in all studies of the phantom, normals, and patients that had no spinal fractures. The coefficient of variation (CV) in the phantom studies was equal to 0.7%. In duplicate studies of 15 normal subjects and nine patients, the CV was equal to 1.0 and 2.7%, respectively. Compared to manual determination of the ROI, the precision of BMD measurements was clearly improved by the automatic procedure.

Short-term and long-term changes of left ventricular volumes during rate-adaptive and single-rate pacing.

To evaluate the adaptation of the heart to exercise during pacing, 15 patients with permanent endocardial pacemakers were studied; nine patients had atrioventricular universal (DDD) pacemakers (Symbios 7005) and six patients had activity detecting rate-responsive ventricular (VVIR) pacemakers (Activitrax 8403). Left ventricular function in each patient during rate variable pacing was compared to ventricular function during VVI single-rate pacing. End-systolic and end-diastolic volume changes during exercise were measured by radionuclide angiography and the amount of volume change was used to assess left ventricular function. Both short-term (within 4 hours) and long-term measurements (after at least 4 weeks) were made at rest and at 50% of the maximal exercise capacity in DDD or VVIR mode and were compared with VVI single-rate pacing. All patients, when changed from DDD or VVIR mode to VVI single-rate pacing showed a significant increase of the end-diastolic volume during exercise, which increased even more after long-term VVI pacing. During long-term rate variable pacing, there was no increase of the end-diastolic volume during exercise. DDD or VVIR pacing initially showed a substantial increase of the end-systolic volume during exercise combined with a decrease of left ventricular ejection fraction, suggesting a decrease of the left ventricular contractility. After 4 weeks, contractility improved both with DDD and VVIR pacing. We conclude that short-term DDD and VVIR pacing induces a temporary impairment of left ventricular function that improves after 4 weeks, whereas long-term VVI pacing is associated with left ventricular dilatation even at moderate levels of exercise.