Breast uptake of technetium-99m MDP during radionuclide angiography.
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Biomedical subjects
Publications and source records attributed to S Port.
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Multiple defibrillations by the automatic implantable cardioverter/defibrillator (AICD) have been reported to result in localized epicardial damage. No data exist, however, regarding whether this damage can be detected in the clinical setting or whether it interferes with the detection of true myocardial infarction. Forty-nine patients who received defibrillations by patch electrodes were studied prospectively. We attempted to document the presence of myocardial injury with the following three commonly used modalities for the detection of myocardial infarction: serial electrocardiographic changes, serial creatine phosphokinase (CPK) and CPK-MB release, and technetium 99m pyrophosphate scanning. Fifteen patients received defibrillations by AICD patches at the time of AICD generator replacement. Nine patients received defibrillations at the time of new AICD lead placement. The average total energy delivered was 85 +/- 29 J. None of these patients had detectable myocardial injury. Ten patients had defibrillations by the AICD patches at the time of bypass operation. One patient in this group developed acute myocardial infarction in the inferior wall after posterior descending coronary bypass operation, as detected by electrocardiogram, 99mTc pyrophosphate scanning, and CPK-MB analysis. Fifteen patients were evaluated for spontaneous AICD discharges. Thirteen had a maximum of five consecutive shocks, and cumulative energy delivered was not greater than 330 J. None of these patients had detectable injury. Two patients had CPK-MB release of 15.3% and 7.5%, respectively. One of these patients had a positive 99mTc pyrophosphate scan. These two patients received 12 and 17 rapid and consecutive AICD discharges, respectively, with cumulative delivered energy of 360 and 510 J, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
Previous reports have shown that TI-201 myocardial imaging with either an oral or intravenous administration of dipyridamole is a suitable diagnostic examination for patients at risk for coronary artery disease who cannot perform treadmill exercise. To compare the incidence of complications associated with these two routes of drug administration, the records of 78 oral and 97 intravenous dipyridamole TI-201 imaging studies were reviewed. The oral administration is associated with a significantly higher incidence of nausea (15% vs. 4%). Despite the higher incidence of nausea, the percentage of patients having one or more dipyridamole-induced symptoms was no greater for the oral (29%) than for the intravenous (37%) administration. Intravenous administration produced both a significantly higher incidence of atypical angina (14% vs. 4%) and a significantly greater increase in heart rate (16.6 vs. 10.2 beats per minute). No patient in either the oral or intravenous dipyridamole protocols had life-threatening arrhythmias or myocardial infarctions. In clinical practice, the difference in complications associated with the oral and intravenous administration of dipyridamole for TI-201 imaging is not significant.
In contrast to young persons, normal elderly persons who undergo symptom-limited dynamic exercise demonstrate a decrease in left ventricular (LV) contractile performance characterized by a decrease in LV ejection fraction. To test the hypothesis that physical conditioning can be achieved in older persons and produces improvement in the exercise-induced decrease in LV ejection fraction observed during normal aging, we examined 24 normal elderly persons (mean age 72.0 years) before and after a 12-week program of physical training. The subjects had been screened for evidence of cardiovascular disease including rest and exercise stress electrocardiograms. All subjects underwent rest and exercise upright sitting radionuclide angiocardiography before and after the training program. The subjects achieved cardiovascular training effects as measured by increased functional capacity and decreased double product at one-half the maximum work load attained at the initial stress test. A significant increase occurred after training in the cardiac index response to exercise (p less than 0.02) and in the augmentation of the end-diastolic volume index produced by exercise (p less than 0.05). However, the exercise-induced decrease in LV ejection fraction and increase in LV end-systolic volume index remained unaltered by training. In conclusion, although older persons can achieve overall training effects from a program of physical conditioning, the age-associated differences in LV contractile performance remained unchanged. Our data suggest that deconditioning is not a significant contributor to the decline in LV contractile performance in the elderly.
First-pass radionuclide angiocardiography was used to access the left ventricular response to submaximal exercise in 150 patients with coronary artery disease (CAD). To test the hypothesis that resting systolic left ventricular function as determined by left ventricular ejection fraction (LVEF) was a predictor of the hemodynamic response to exercise, the study group included patients with a wide range of resting LVEF (0.12-0.82). The influences of resting LVEF, resting end-diastolic volume, the number of diseased vessels, exercise end point and exercise double product on the change in LVEF (delta LVEF) during exercise were tested using multiple linear regression analyses. Resting LVEF was a highly significant predictor of the delta LVEF (p = 0.0001). Exercise duration was not related to either the resting LVEF or the delta LVEF. For the 112 patients in whom coronary anatomy was known, resting LVEF retained its significance as a predictor of delta LVEF (p = 0.002) even after adjustment for the significance of the extent of CAD (p = 0.0007) and the exercise end point (p = 0.06). Patients with normal resting LVEF showed the most profound decreases in LVEF, the highest frequency of new regional dysfunction and the largest relative increase in end-diastolic volume during exercise. As rest LVEF decreased, the magnitude of the delta LVEF and the frequency of new regional dysfunction decreased. Therefore, left ventricular function at rest is an important determinant of the direction and magnitude of change in left ventricular function during exercise.
Rest and exercise radionuclide angiocardiographic measurements of left ventricular function were obtained in 496 patients who underwent cardiac catheterization for chest pain. Two hundred forty-eight of these patients also had an exercise treadmill test. An ejection fraction less than 50% was the abnormality of resting left ventricular function that provided the greatest diagnostic information. In patients with normal resting left ventricular function, exercise abnormalities that were optimal for diagnosis of coronary artery disease were an injection fraction at least 6% less than predicted, an increase greater than 20 ml in end-systolic volume and the appearance of an exercise-induced wall motion abnormality. The sensitivity and specificity of the test were lower in patients who were taking propranolol at the time of study and in patients who failed to achieve an adequate exercise end point. In the 387 patients with an optimal study, the test had a sensitivity of 90% and a specificity of 58%. Radionuclide angiocardiography was more sensitive and less specific than the exercise treadmill test. The high degree of sensitivity of the radionuclide test suggests that it is most appropriately applied to patient groups with a high prevalence of disease, including those considered for cardiac catheterization.
To assess the effects of age on the left ventricular ejection fraction (LVEF), we performed radionuclide angiocardiography at rest and during upright bicycle exercise in 77 healthy volunteers 20 to 95 years of age. Radionuclide measurements included left ventricular ejection fraction, end-diastolic volume, and regional wall motion. Age did not appear to influence any of these indexes at rest. However, during exercise the ejection fraction was less than 0.60 in 45 per cent of subjects over age 60 as compared with 2 per cent of younger subjects (P < 0.001). In addition, there was a decline in the change in LVEF (exercise LVEF minus rest LVEF) with increase in age (r = -0.71). Wall-motion abnormalities during exercise occurred with increasing frequency in patients who were 50 and older. In the older subjects these age-related changes in ejection fraction during exercise were not associated with differences in end-diastolic volume or blood pressure.
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To determine if abnormalities in left ventricular function precede angina pectoris and electrocardiographic evidence of myocardial ischemia, we used radionuclide angiocardiography to measure left ventricular ejection fraction, volumes, cardiac output and wall motion in 10 normal subjects and 25 patients with coronary artery disease at rest and during two levels of upright bicylce exercise. In the patients with coronary artery disease, the first radionuclide study during exercise was performed before and the second after the onset of ST-segment depression. In all normal subjects, the ejection fraction increased more than 5%, the end-diastolic volume increased less than 25% and the end-systolic volume decreased from rest to both levels of exercise. Wall motion was normal at rest and increased with exercise. No patient with coronary artery disease had chest pain or ST-segment depression during the first level of exercise. The ejection fraction either decreased or increased less than 5% in 18 patients, the end-diastolic volume increased more than 25% in nine, the end-systolic volume increased in 19 and a segmental contraction abnormality developed in 14. Hemodynamic and wall motion abnormalities occurred in all patients during the second level of exercise when ST-segment depression was present. During exercise in patients with coronary artery disease, abnormalities in left ventricular function frequently develop before angina pectoris and electrocardiographic evidence of myocardial ischemia.