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Biomedical subjects

L C Becker

Publications and source records attributed to L C Becker.

205 records · Page 12Linked to original sources

Combined corrections for attenuation, depth-dependent blur, and motion in cardiac SPECT: a multicenter trial.

BACKGROUND: The diagnostic accuracy of cardiac single photon emission computed tomography (SPECT) is limited by image-degrading factors, such as heart or subject motion, depth-dependent blurring caused by the collimator, and photon scatter and attenuation. We developed correction approaches for motion, depth-dependent blur, and attenuation and performed a multicenter validation. METHODS AND RESULTS: Motion was corrected both transversely and axially with a cross-correlation technique. Depth-dependent blurring was corrected by first back-projecting each projection and then applying a depth-dependent Wiener filter row by row. Attenuation was corrected with an iterative, nonuniform Chang algorithm, based on a transmission scan-generated attenuation map. We validated these approaches in 112 subjects, including 36 women (20 healthy volunteers, 8 angiographically normal patients, and 8 patients with coronary artery disease [CAD] found by means of angiography) and 76 men (23 healthy volunteers, 10 angiographically normal patients, and 43 patients with CAD found by means of angiography). Either technetium 99m or thallium 201 was used for emission; either gadolinium 153 or Tc-99m was used for transmission. Images were reconstructed and blindly interpreted with a 5-point scale for receiver operating characteristic analysis in 2 ways: motion correction plus a Butterworth filter, and combined motion and blur and attenuation corrections. The interpretation by means of consensus was for the overall presence of CAD and vascular territory. The receiver operating characteristic curves for overall presence and each of the 3 main coronary arteries were all shifted upward and to the left and had larger areas under the curve, for combined corrections compared with motion correction and Butterworth. Sensitivity/specificity for motion correction and Butterworth were 84/69, 64/71, 32/94, and 71/81 overall for the left anterior descending, the right coronary artery, and circumflex territories, respectively, compared with 88/92, 77/93, 50/97, and 74/95, respectively, for the combined corrections. CONCLUSIONS: The proposed combined corrections for motion, depth-dependent blur, and attenuation significantly improve diagnostic accuracy, when compared with motion correction alone.

Coronary Disease↗

Augmentation of myocardial ischemia by low level carbon monoxide exposure in dogs.

This study was conducted to determine whether low level exposure to carbon monoxide would increase myocardial ischemia associated with acute myocardial infarction. An hour after coronary artery ligation, eleven anesthetized dogs underwent five sequential respiratory exposures to 5,000 ppm carbon monoxide, producing mean blood carboxyhemoglobin levels of 4.9% to 17.0%. Ischemia, as indicated by the amount of S-T segment elevation in epicardial electrocardiograms, increased significantly at the lowest carboxyhemoglobin level and increased further with increasing carbon monoxide exposure. These changes occurred in the absence of altered heart rate, blood pressure, left atrial pressure, cardiac output, or blood flow to ischemic myocardium. Flow to non-ischemic myocardium increased with carbon monoxide exposure, the percentage increase being approximately double the increase in carboxyhemoglobin level. Thus, low level exposure to carbon monoxide can significantly augment ischemia in acute myocardial infarction, apparently through a reduction in oxygen supplied to ischemic tissue. The data suggest that hypoxia induced by carbon monoxide exposure is more severe than can be accounted for by a simple reduction in oxygenated hemoglobin.

Animals↗

Performance of a computerized CCU arrhythmia monitor system.

Experience gained during clinical trials at Johns Hopkins University Hospital has led to refinements in a commercial arrhythmia monitoring system. The performance capabilities and limitations are described for normal Coronary Care Unit use. The system evaluation spanned a time period of over 16 months and included 3,176 monitored patient days. The majority of both false and true arrhythmia alarms was found to be produced by two small, statistically independent segments of the patient population.

Arrhythmias, Cardiac↗

The Psychophysiological Investigations of Myocardial Ischemia (PIMI) study: objective, methods, and variability of measures.

OBJECTIVE: This study evaluated physiological, neuroendocrine, and psychological status and functioning of patients with coronary artery disease in order to clarify their role in the expression of symptoms during myocardial ischemia (MI), and to establish repeatability of responses to mental stress. Design and methods of the study are presented. METHODS: One hundred ninety-six coronary artery disease patients were examined during physical and mental stress tests in four hospitals. Eligibility criteria included narrowing of at least 50% in the diameter of at least one major coronary artery or verified history of myocardial infarction, and evidence of ischemia on an exercise treadmill test. Psychological, biochemical, and autonomic function data were obtained before, during, and after exposure to mental and exercise stressors during 2 or 3 half-days of testing. Ventricular function was assessed by radionuclide ventriculography, and daily ischemia by ambulatory electrocardiography. Sixty patients returned for a short-term mental stress repeatability study. Twenty-nine individuals presumed to be free of coronary disease were also examined to establish reference values for cardiac responses to mental stress. RESULTS: Study participants were 41 to 80 years of age; 83 (42%) had a history of MI, 6 (3%) of congestive heart failure, and 163 (83%) of chest pain; 170 (87%) were men; and 90 (46%) had ischemia accompanied by angina during exercise treadmill testing. Ischemia during ambulatory monitoring was found in 35 of 90 (39%) patients with and 48 of 106 (45%) patients without angina during exercise-provoked ischemia. Intraobserver variability of ejection fraction changes during bicycle exercise and two mental stress tests (Speech and Stroop) was good (kappa = 1.0, .90, and .76, respectively; percent agreement = 100, 97.5, and 93.8%, respectively). Variability of assessed wall motion abnormalities during bicycle exercise was better (kappa, agreement = 85%) than during Speech or Stroop kappa and .57, percent agreement = 70% and 82.5%, respectively). CONCLUSIONS: Study design, quality control data, and baseline characteristics of patients enrolled for a clinical study of symptomatic and asymptomatic myocardial ischemia are described. Lower repeatability of reading wall motion abnormalities during mental stress than during exercise may be due to smaller effects on wall motion and lack of an indicator for peak mental stress.

Adult↗

Racial differences in low-density lipoprotein particle size in families at high risk for premature coronary heart disease.

OBJECTIVE: Although small, dense low-density lipoprotein (LDL) has been implicated in atherogenesis and coronary heart disease (CHD) events, little is known about possible racial differences in LDL particle size. This study was designed to examine racial differences in the prevalence of small, dense LDL among 159 African-American and 477 White siblings of persons with premature (<60 years of age) CHD. METHODS AND RESULTS: This study examined fasting levels of total cholesterol, LDL cholesterol, high-density lipoprotein cholesterol, apolipoprotein B (ApoB), apolipoprotein A-1, and triglycerides, as well as factors known to be associated with small, dense LDL, including age, sex, obesity, hypertension, and diabetes. Relative LDL particle size was defined by the LDL cholesterol to ApoB ratio. Direct measurement of LDL particle size was obtained by proton NMR spectroscopy in a subset of 64 siblings. Despite similar levels of total and LDL cholesterol, White siblings were more likely to have low LDL cholesterol to ApoB ratios, indicative of atherogenic small, dense LDL, compared with African-American siblings. Multiple logistic regression analysis predicting the presence of LDL cholesterol/ApoB < or = 1.0 demonstrated that race (P = .009), triglyceride level (P = .0001), and diabetes (P = .02) were independent predictors, controlling for age and all other variables. Direct measurement of LDL particle size by NMR spectroscopy supported these findings. CONCLUSION: These findings provide the first known evidence that White individuals from a population at high risk for premature CHD have a greater probability of having a preponderance of small, dense LDL particles than do African Americans, independent of triglyceride levels, and despite comparable levels of total and LDL cholesterol.

Adult↗

Prevalence of hypercholesterolemia among siblings of persons with premature coronary heart disease. Application of the Second Adult Treatment Panel guidelines.

BACKGROUND: Increased blood cholesterol, specifically high low-density lipoprotein cholesterol, increases risk for coronary heart disease (CHD). Persons with a positive family history of premature CHD also are at markedly increased risk. OBJECTIVE: To examine the prevalence of hypercholesterolemia based on the second report of the National Cholesterol Educational Program Adult Treatment Panel (ATP II) guidelines in the asymptomatic healthy siblings of people with premature CHD. METHODS: A total of 668 asymptomatic healthy siblings (354 men and 314 women) underwent screening for risk factors for CHD. Siblings were categorized into treatment categories for primary prevention defined by ATP II. The percentage who were candidates for intervention were compared with the published national estimates for those without CHD from the third National Health and Nutrition Examination Survey (NHANES III). RESULTS: Based on ATP II guidelines, 65% of the asymptomatic adult siblings required fasting lipoprotein analysis compared with 33% of adults without CHD in the national reference population. Of the siblings who met the criteria for fasting lipoprotein analysis, most (56%) were candidates for dietary therapy, more than twice the proportion of adults from NHANES III. The percentage of the siblings who qualified for drug intervention and dietary therapy was 3 times greater than the national sample, 33% vs 11%, respectively. Assuming a 10% hypothetical reduction in low-density lipoprotein cholesterol levels as the result of dietary modification, the proportion of the sibling sample who were possible candidates for drug therapy was 20%, still 4 times that predicted for the national sample. CONCLUSIONS: These results underscore the need for aggressive detection and treatment of hypercholesterolemia in this easily identifiable high-risk population of siblings of people with premature CHD.

Adult↗

Cardiac sympathetic nerve function assessed by [131I]metaiodobenzylguanidine after ischemia and reperfusion in anesthetized dogs.

BACKGROUND: Accumulation of 131I-labeled metaiodobenzylguanidine ([131I]MIBG), a radiolabeled norepinephrine analog, is reduced in infarcted myocardium, suggesting loss of cardiac sympathetic nerve viability. Histopathologic studies, however, indicate that the nerve endings ae morphologically intact. Experiments were therefore designed to determine the mechanism of reduced MIBG accumulation. METHODS AND RESULTS: Desipramine, a specific blocker or neuronal norepinephrine reuptake, was used to separate the portions of total myocardial [131I]MIBG accumulation attributable to neuronal and nonneuronal uptake mechanisms. Sixteen dogs underwent circumflex coronary artery occlusion for 60 minutes followed by a 5-hour reperfusion. [131I]MIBG was injected intravenously 1 hour after reperfusion. The left ventricle was removed and incubated in triphenyltetrazolium chloride to identify infarcted and viable myocardium within the zone at risk. Preliminary studies in sham-operated dogs showed that pretreatment with desipramine (5 mg/kg) reduced [131I]MIBG accumulation 4 hours after injection to 38.9% of untreated controls. Chemical sympathectomy by topical phenol resulted in a similar decrease in [131I]MIBG accumulation (to 45.7% of normal), and desipramine did not produce further inhibition of [131I]MIBG accumulation over that produced by phenol alone, indicating that the inhibitory effect of desipramine on neuronal accumulation of [131I]MIBG was essentially complete. In dogs undergoing ischemia-reperfusion, myocardial samples from infarcted and viable postischemic areas showed 64.5% +/- 11.85 and 84.7% +/- 9.1% of normal [131I]MIBG activity, respectively (both, p < 0.01 vs normal area, n = 9). With desipramine pretreatment (n = 7), accumulation of [131I]MIBG decreased in all areas. Neuronal accumulation was reduced uniformly in infarcted, viable postischemic, and normal areas by 30% to 35% compared with sham-operated controls. In contrast, nonneuronal accumulation was only 39.3% in infarcted areas and 84.6% in viable postischemic areas compared with normal areas, and these decreases accounted entirely for the reduced total [131I]MIBG accumulation. CONCLUSIONS: Reduced [131I]MIBG accumulation in infarcted myocardium after 60 minutes of ischemia and 5 hours of reperfusion is attributable to a deficit in nonneuronal accumulation and not to decreased accumulation by sympathetic nerves.

3-Iodobenzylguanidine↗