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Biomedical subjects

W W Peck

Publications and source records attributed to W W Peck.

At least 19 recordsLinked to original sources

Cervical paraspinal calcification in collagen vascular diseases.

Although soft-tissue calcification is common in collagen vascular disease, paraspinal calcification in the cervical spine has not been described before. We studied five women with large, lobulated, predominantly homogeneous calcific masses centered on synovial articulations in the neck. Changes consisting of either osteolysis or erosions were evident. All patients had radiculopathy, focal pain, or stiffness. In two patients, the presence of hydroxyapatite crystals was confirmed on biopsy. Symptomatic cervical paraspinal calcifications in patients with collagen vascular disease cause large soft-tissue masses that mimic tumoral calcinosis.

Aged↗

High-resolution MR imaging of pituitary microadenomas at 1.5 T: experience with Cushing disease.

The MR images of 27 patients with clinically and biochemically suspected Cushing disease were evaluated retrospectively in a blinded fashion. The MR interpretation was compared with detailed operative diagrams and operative and pathologic reports. The examinations were performed on a 1.5-T MR system with thin-section sagittal and coronal T1-weighted (short TR/TE) images. Each pituitary half was considered separately (54 "halves"). Twenty-one pituitary halves were considered to have glandular abnormalities on MR. Compared with surgical findings, 17 MR findings were true positives and four were false positives (one pars intermedia cyst, three normal tissue). Of the 33 pituitary halves considered normal on MR, 26 were true negatives and seven were false negatives. MR had an overall sensitivity of 71% and a specificity of 87% for these adrenocorticotropic hormone (ACTH)-secreting pituitary adenomas. A focal glandular hypointensity identified on coronal images was the most sensitive predictor of adenoma location. Sagittal images were not useful in either detection or localization. Upward convexity of the gland and deviation of the stalk were less useful indicators. Abnormalities of the sellar floor were the least reliable. In comparison with the capabilities of CT detection of microadenomas described in the current literature, it appears that high-field thin-section MR of the sella is the most sensitive imaging method for preoperative localization of ACTH-secreting adenomas in patients with Cushing disease.

Adenoma↗

Hyperparathyroidism: comparison of MR imaging with radionuclide scanning.

Twenty-three patients with hyperparathyroidism were evaluated preoperatively with magnetic resonance (MR) imaging. Twenty patients also underwent thallium-201/technetium-99m scintigraphy. Of 22 patients with primary hyperparathyroidism, 12 had persistent or recurrent disease. One had secondary hyperparathyroidism due to end-stage renal disease. MR imaging allowed accurate localization of abnormal parathyroid glands in 64% evaluated prospectively and 82% evaluated retrospectively. Scintigraphy allowed localization of 60% evaluated prospectively and 70% retrospectively. The two imaging modalities together allowed detection of 68% evaluated prospectively and 91% retrospectively. MR imaging allowed detection of two of five mediastinal adenomas evaluated prospectively and four of five retrospectively. In patients who underwent both imaging studies, MR was more successful in those with previous neck surgery (73% evaluated prospectively and 91% retrospectively) than in those with no prior surgery (57% prospectively and 71% retrospectively). Scintigraphy allowed accurate localization in 64% evaluated prospectively and 64% retrospectively in patients with previous surgery versus 57% prospectively and 86% retrospectively in patients with no prior neck surgery. Four false-positive results were obtained with MR imaging and three with scintigraphy. MR imaging was useful for parathyroid localization in patients with hyperparathyroidism, particularly in patients requiring additional surgery.

Adult↗

Rathke cleft cysts: CT, MR imaging, and pathologic features.

The authors retrospectively reviewed the clinical, computed tomography (CT), and magnetic resonance (MR) imaging findings in seven patients with pathologically proved Rathke cleft cysts. All the cysts were located in the anterior sella turcica or the anterior suprasellar cistern. Five cysts had both intra- and suprasellar components, one was entirely intrasellar, and the other was predominantly suprasellar in location. The size of the cysts ranged from 8 to 20 mm. CT scans demonstrated low-density homogeneous lesions in four cases. On MR images of three of these four cases, the cysts had the same intensity as cerebrospinal fluid on T1- and T2-weighted images, while in the fourth case, the cyst was hyperintense on the T1-weighted images. In the remaining three cases, CT showed slight hyperdensity relative to brain parenchyma, suggestive of contrast enhancement. MR showed signal heterogeneity of these lesions with focal components of diminished signal intensity of T2-weighted images. These same foci appeared iso- to slightly hyperintense on T1-weighted images.

Adult↗

Analysis of phase-angle histograms from equilibrium radionuclide studies: correlation with semiquantitative grading of wall motion.

Quantitative wall motion assessment from gated radionuclide left ventriculograms using phase analysis was studied in 14 subjects (6 normal volunteers and 8 patients with previous acute myocardial infarction). The standard deviation and skewness of the phase-angle histograms were determined from both global and segmental left ventricular (LV) regions of interest (septal, apical and posterolateral). Studies were performed at rest, after administration of atropine and after combined administration of phenylephrine and atropine. Both the standard deviation and skewness showed significant correlations with semiquantitative wall motion scoring. From the global analyses, the highest correlations were found after atropine administration (r = 0.86, p less than 0.001 for standard deviation and r = 0.72, p less than 0.001 for skewness). Nevertheless, deterioration in global wall motion scores correlated poorly with directional changes in standard deviation (r = 0.06, difference not significant) or skewness (r = 0.33, p less than 0.05). No significant correlation between skewness or change in skewness and wall motion scores were found with the segmental analyses. The maximal correlation between segmental standard deviation and segmental wall motion grading was again noted after atropine administration (r = 0.68, p less than 0.001), but deterioration in grading did not correlate with similar deterioration of the standard deviation (r = -0.05, difference not significant). Based on 90% confidence limits for normal standard deviation and skewness, an abnormal standard deviation (greater than 14.5) identified 13 of 28 wall motion disorders (sensitivity 46%), whereas an abnormal skewness (greater than 1.4) identified 1 of 28 wall motion disorders (sensitivity 4%).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Effects of beta-adrenergic blockade on the natural progression of myocardial infarct size and compensatory hypertrophy.

Using contrast-enhanced computed tomography, the effects of beta-adrenergic blockade were assessed on experimentally produced myocardial infarcts in dogs evaluated serially over the course of approximately 1 month. Infarct size, initial perfusion defect (jeopardized segment) and noninfarcted muscle mass were studied in two groups of conditioned mongrel dogs. Group 1 (n = 11) served as the control group and Group 2 (n = 10) was pretreated with propranolol (2 mg/kg). Each animal in the propranolol-treated group was given identical amounts of the agent twice daily for 7 days after coronary occlusion. Both groups developed increases in the noninfarcted muscle mass of the left ventricle (compensatory hypertrophy). The mean increase averaged 19.8% over 30 days when the two groups were included together. Infarct size was smaller in the propranolol-treated group, and averaged 28% less (p less than 0.05) than that of the control group 30 days after initial myocardial infarction. Thus, pharmacologic interventions were shown by computed tomography to alter the size of an acute experimental myocardial infarct, particularly when examined over the time course of infarct healing. Moreover, compensatory hypertrophy occurred in both the control and propranolol-treated groups.

Animals↗

In vivo assessment by computed tomography of the natural progression of infarct size, left ventricular muscle mass and function after acute myocardial infarction in the dog.

Quantification of myocardial infarct (MI) size is of prognostic importance in patients with acute ischemic damage. Evaluation of the efficacy of interventions for salvage of ischemic myocardium depends on the accurate estimation of the ischemic area and a knowledge of the natural progression of the infarct. Computerized transmission tomography (CTT) is a reliable in vivo technique for estimating infarct size. We serially studied 8 dogs over approximately 1 month after occlusion of the left anterior descending coronary artery using both ungated and prospectively electrocardiogram-gated CTT. Scans were obtained 20 minutes after occlusion and then several more times until the dogs were killed. Using the ungated CTT scans, infarct size increased from 0 to 4 days (+ 65 +/- 20%, mean +/- standard error of the mean, p less than 0.05), then progressively decreased. The initial perfusion defect overestimated the eventual MI size at 1 month by 33 +/- 15% (p less than 0.05). The MI size at necropsy correlated well (r = 0.98, p less than 0.001) with CTT MI size determined just before sacrifice. Non-infarcted left ventricular (LV) muscle mass increased significantly (27 +/- 7% greater at 1 month compared with day 0, p less than 0.01) over time, presumably representing compensatory LV hypertrophy. The LV muscle mass at necropsy correlated well (r = 0.94, p less than 0.001) with CTT LV muscle mass just before sacrifice.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Use of computerized tomography to assess myocardial infarct size and ventricular function in dogs during acute coronary occlusion and reperfusion.

Prospectively ECG-gated and nongated computed tomography (CT) can be used to assess global and regional left ventricular (LV) function and to measure myocardial infarct (MI) size. In the current study, CT was used to assess the effects of coronary occlusion and reperfusion in 16 dogs. Ten dogs were subjected to permanent occlusion of the proximal left anterior descending coronary artery and 6 dogs were reperfused after a 2-hour period of total coronary occlusion. Gated scans were used to quantitate the extent of wall thickening in the ischemic zone and to assess changes in mid-LV cross-sectional chamber area at end-diastole and end-systole. Nongated scans were used to estimate the size of the initial perfusion defect during contrast injection shortly after coronary occlusion and the size of the MI as indicated by delayed enhancement of the infarct 10 to 30 minutes after cessation of contrast administration. Neither group showed significant changes in end-diastolic chamber area during acute occlusion or 3 days later. Both groups showed a significant deterioration in percent change in chamber area both early after coronary occlusion and 3 days later; however, in the permanent occlusion group, percent wall thickening in the ischemic zone decreased from 46.2 +/- 16.5% (mean +/- standard deviation) to 1.6 +/- 9.0% during acute occlusion (p less than 0.01) and thickening remained depressed 3 days later (2.4 +/- 10.1%, p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗

Sustained venous occlusion plethysmography: effects on protein osmotic pressure, intravascular volume, and capillary filtration.

In six acutely anesthetized, mechanically ventilated mongrel dogs, we evaluated sequential changes (over 30 minutes) of sustained forelimb venous occlusion (occlusion pressures 30 to 65 mm Hg) on strain gauge dimension, radionuclide blood pool emissions, and venous, subcutaneous, and intramuscular pressures (Wick technique). Forelimb intravascular volume (assessed by decay-corrected radionuclide counts/unit time) changed by a mean of only -1.2 +/- 2.8% (+/- SEM) and thus was ignored in the calculation of filtration rate. Forelimb (distal to the occlusion site) hematocrit changed insignificantly (45.3 +/- 1.4% at the control point to 48.2 +/- 1.1% at 30 minutes), colloid osmotic pressure rose slightly 19.4 +/- 1.4 mm Hg to 22.7 +/- 1.6 mm Hg, p less than 0.01), and serum osmolality remained unchanged. During sustained occlusion, venous pressure remained constant, subcutaneous pressure rose (-0.7 +/- 1.2 mm Hg control vs 0.5 +/- 1.4 mm Hg at 30 minutes, p less than 0.05), and intramuscular pressure also rose (-0.4 +/- 1.1 mm Hg to 2.6 +/- 1.6 mm Hg, p less than 0.01). Driving pressure, defined by venous pressure - oncotic pressure less the average of intramuscular and subcutaneous pressure declined slightly over the 30 minutes of the study (27.8 +/- 5.5 mm Hg to 23.3 +/- 1.3 mm Hg, p less than 0.05). The relationship between either the initial driving pressure or the initial difference between venous and protein osmotic pressure correlated (r = 0.83 for both) well with strain gauge estimates of capillary fluid flux (evaluated by the change in forelimb strain gauge dimension over time and given as cc/100 cc forelimb volume/min).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Intravascular and extravascular pulmonary fluid volumes during acute experimental pericardial tamponade.

Pulmonary congestion is usually absent in cardiac tamponade. To examine the effects of experimental pericardial tamponade on pulmonary fluid volumes, we studied 14 anesthetized dogs with indicator-dilution techniques to measure extravascular (EVLW) and intravascular (PBV) pulmonary fluid volumes. Seven dogs were studied at two levels of tamponade and seven were studied during two levels of left atrial (LA) hypertension produced with an LA balloon. EVLW and PBV were measured in both groups at control state and then at two levels of elevated LA pressure (P). When LAP was raised by the balloon, PBV rose with the increase in LAP (4.9 +/- 2 cc/kg control at LAP 1.2 +/- 1.0 mm Hg versus 6.8 +/- 2.1 cc/kg at LAP 8.4 +/- 1.4 mm Hg and 6.8 +/- 2.1 cc/kg at LAP 14.7 +/- 2.0 mm Hg; both intervention PBV values p less than 0.01 vs control). During tamponade, PBV did not change (4.1 +/- 1.1 cc/kg at LAP 1.3 +/- 2.2 mm Hg control versus 4.4 +/- 1.0 cc/kg at LAP 7.4 +/- 1.4 mm Hg and 4.8 +/- 1.3 cc/kg at LAP 12.7 +/- 2.8 mm Hg). EVLW changes were similar during elevation of LAP in both groups (tamponade dogs 7.1 +/- 2.6 cc/kg, 7.1 +/- 1.6 cc/kg and 8.9 +/- 2.1 cc/kg, respectively; and LA hypertension dogs 6.9 +/- 2.5 cc/kg, 7.3 +/- 2.0 cc/kg, and 8.0 +/- 2.0 cc/kg, respectively. We conclude that during cardiac tamponade there is little change in PBV in response to rises in LAP. This is significantly different from the changes seen when increasing LAP by inflating an LA balloon, where fluid is shifted from the peripheral to the central circulation. EVLW changes were similar for the two methods during elevation of LAP.

Animals↗

Nuclear magnetic resonance analysis of acute and chronic myocardial infarction in dogs: alterations in spin-lattice relaxation times.

The purpose of this study was to evaluate the effects of acute and chronic ischemic injury on myocardial spin-lattice relaxation times (T1) in dogs. Ligation of the left anterior descending coronary artery was performed on 23 dogs which were divided into four experimental groups and killed at 3 hours (n = 6), 4 days (n = 6), 21 days (n = 5), and 56 days (n = 6) after coronary occlusion. T1 was measured in vitro with a 2.5 kg nuclear magnetic resonance (NMR) spectrometer using tissue from ischemic and control areas of the myocardium. Both the 3-hour and 4-day groups showed prolongations in T1 (p less than 0.01) for tissue from the ischemic area. In the 21-day group, two infarcts showed an increase in T1, two showed a decrease in T1, and one showed no significant change. The 56-day old infarcts had a lower mean value for T1 than control myocardium (p less than 0.01). The differences in myocardial water content between control and infarcted myocardium were found to parallel changes in T1 values in each experimental group. Pathologic examination of the myocardial scar from 21- and 56-day-old infarcts revealed extensive fibrosis in the infarcts with lower T1 values and tissue water contents than control myocardium. We conclude that myocardial edema in 3-hour and 4-day-old infarcts results in association with prolongations in T1. Twenty-one-day-old infarcts may be edematous (with increased T1) or fibrotic (with T1 values lower than normal myocardium), while 56-day-old infarcts are fibrotic and have shorter T1 values than normal myocardium.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Right ventricular mural thrombus caused by myocardial infarction diagnosed by computed tomography.

Thrombi of the left ventricle are common sequelae to acute anterior myocardial infarctions that involve the apex of the heart and produce akinetic or dyskinetic wall thickening patterns. While infarctions of the right ventricle are being increasingly recognized in the setting of inferior myocardial infarcts, little data on in vivo clot formation in the right ventricle of the heart are available in these patients. In the current study we were able to demonstrate a right ventricular mural thrombus using gated computed tomography of the heart. Although an abnormality in the right ventricle extending from the septal margin of the ventricle into the outflow tract could be identified with standard blood pool computed tomographic images and from cross sectional echocardiograms, only with cardiac gating could the relationship between the mass (thrombus) and the noncontractile section of the right ventricular myocardium be clearly identified. We conclude that cardiac gating may help in the evaluation of cardiac masses, and in particular cardiac thrombi. This will be particular valuable in the setting of recent or remote infarction, as the relationship between wall-motion abnormalities and thrombus formation has been well documented.

Adult↗

Effects of transient coronary ischemia and reperfusion on myocardial edema formation and in vitro magnetic relaxation times.

The effects of transient ischemia and reperfusion on regional myocardial function, salvage and swelling have been systematically analyzed in experimental canine preparations. The results of these interventions on myocardial in vitro measurements of magnetic relaxation times (T1 = magnetization recovery, T2 = spin echo) are of significant importance with respect to future nuclear magnetic resonance tomographic imaging. Thus, using a pulsed magnetic resonance spectrometer (10.7 MHz), myocardial tissue samples from two groups of dogs were evaluated. In group 1 (n = six dogs), the left anterior descending artery was occluded for 3 hours before sacrifice; in group 2 (six dogs), 3 hours of occlusion was followed by 1 hour of reperfusion. Multiple tissue samples from normal and ischemic (or ischemic and reperfused) myocardium were obtained for measurement of T1, T2 and % water content (wet weight--dry weight/wet weight). Water content increased with ischemia (78 +/- 4%) and reperfusion (81 +/- 4%) (both p less than 0.01 versus control values). Values for T1 increased with ischemia (598 +/- 39 versus 487 +/- 23 ms in normal tissue from the same heart, p less than 0.01). Even greater T1 changes occurred in the animals with reperfusion (654 +/- 52 ms, p less than 0.01 versus the intra-animal control values). Changes in T2 were similar but less marked (ischemic zone 43.9 +/- 1.0 versus 41.2 +/- 1.0 ms in nonischemic tissue in the corresponding heart, p less than 0.05; reperfusion zone 48.3 +/- 3.5 versus 41.9 +/- 2.3 ms in the normal zone, p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Myocardial infarct size determined by computed transmission tomography in canine infarcts of various ages and in the presence of coronary reperfusion.

Thirty-one dogs underwent in vivo scanning with computed transmission tomography; 15 dogs were studied within 7 days (mean 4) after coronary occlusion, 10 dogs 21 to 25 days (mean 28) after occlusion and 6 dogs 4 days after coronary reperfusion of a 2 to 3 hour coronary ligation. Ungated scans (1 cm in depth) of the left ventricle were obtained from apex to base to determine infarct size. In all animals with documented (postmortem) infarction (n = 26), contrast medium caused delayed enhancement of the entire infarct or the periphery of the infarct. Infarct size was calculated from scans showing contrast enhancement of the infarct. Infarct size was also determined from the postmortem heart using histochemical morphometry (nitroblue tetrazolium) and then compared with infarct size derived from tomography using the outer margin of the contrast-enhanced periphery of the infarct as the border of the infarct. Infarct size calculated by the tomographic technique (excluding the animals without an infarct) correlated well with infarct size determined at autopsy (r = 0.90, p less than 0.001). The tomographic estimate (18.2 +/- 11.3 g) of infarct size was similar to autopsy values (18.6 +/- 11.8 g, p = NS). Thus, ungated computed transmission tomographic imaging of the heart can reliably estimate infarct size in a variety of potential clinical circumstances, particularly when the area of rim enhancement of the infarct is included within the presumed infarct region.

Animals↗