Neonatal surgery casebook. Congenital aplasia of iliac veins.
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Biomedical subjects
Publications and source records attributed to S Katz.
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Coronary reperfusion in myocardial infarction improves infarct zone motion, but its effect on the global ejection fraction has been less consistent. The directional movement of the ejection fraction is determined by the opposing influences of improved infarct zone motion and diminishing hyperkinesia in the noninfarct zone. Noninfarct zone hyperkinesia has been attributed to catecholamine stimulation, the Frank-Starling mechanism or intraventricular interactions that unload noninfarcted segments. To investigate the influence of catecholamine stimulation, 9 men presenting with a first myocardial infarction (mean age 53 +/- 13 years) were studied. Coronary reperfusion was accomplished less than 4 hours after the onset of myocardial infarction. Radionuclide ventriculography was then performed before and immediately after the intravenous administration of 15 mg of metoprolol. End-diastolic volume did not change, but end-systolic volume increased 28% after metoprolol (p = 0.041). The ejection fraction decreased from 55 +/- 13% before metoprolol to 45 +/- 14% after its administration (p = 0.002). There was no effect of intravenous metoprolol on infarct zone motion, whereas motion in the noninfarcted segment decreased (p = 0.002). The patients underwent repeat ventriculography after receiving metoprolol, 100 mg orally twice a day for 9 days. Infarct zone motion improved (p less than 0.002) and the ejection fraction increased to 55 +/- 12% (p less than 0.02). Normal zone motion did not change. Thus, compensatory hyperkinesia is at least in part caused by catecholamine stimulation. Conclusions regarding the effects of reperfusion on global ventricular performance can be influenced by the timing of ejection fraction determinations relative to metoprolol therapy.
We have compared the effect of ursodeoxycholic acid with placebo on the clinical state, blood liver chemistries and serum and urinary bile acids in four patients with primary biliary cirrhosis. All parameters were evaluated monthly, and bile acid composition was measured by capillary gas-liquid chromatography. At the time of admission, all patients showed intense pruritus, and their serum alkaline phosphatase, AST and ALT levels were elevated 4.3, 2.7 and 2.3 times over control values. Serum bile acids were elevated almost 38-fold with 2.5 times more cholic acid than chenodeoxycholic acid. Urinary bile acid output was elevated 28 times the control values, and 36% were 1 beta-hydroxycholic acid, 1 beta-hydroxydeoxycholic acid and hyocholic acid (3 alpha,6 alpha, 7 alpha-trihydroxy-5 beta-cholanoic acid). Three months of placebo administration did not significantly affect the clinical or biochemical presentations, and the serum and urinary bile acid composition did not change. In contrast, ursodeoxycholic acid feeding (12 to 15 mg per kg per day) for 6 months abolished pruritus in two and lessened itching in two subjects and reduced serum alkaline phosphatase, AST and ALT levels by 21, 35 and 47%, respectively. The mean values for the total serum bile acid concentrations in these patients declined 26% from the pretreatment value, but the proportion of ursodeoxycholic acid increased from 3 to 40% of the total bile acids; thus, total fasting serum endogenous bile acid levels decreased almost 50%. Similar changes were noted in the urinary bile acids, in which ursodeoxycholic acid became the major bile acid, and approximately 18% were hydroxylated at C-1, C-6 and C-21.(ABSTRACT TRUNCATED AT 250 WORDS)
Left ventricular performance was studied during isometric exercise in 17 patients with severe congestive heart failure, combining invasive hemodynamic and echo-Doppler techniques. Isometric exercise at 30% of maximum resulted in a decrease in stroke volume index (27.4 +/- 7.1 to 22.7 +/- 7.4 ml/m2), with a significant increase in heart rate from 81 +/- 10 to 92 +/- 14 beats/min and in systemic vascular resistance from 1827 +/- 527 to 2372 +/- 737 dyne.sec.cm-5. A significant rise in pulmonary capillary wedge pressure (18 +/- 9 to 31 +/- 10 mm Hg) was associated with a marked increase in mitral regurgitant volume (14 +/- 11 to 27 +/- 15 ml), calculated as the difference between total stroke volume obtained by two-dimensional echocardiography and forward stroke volume measured by pulsed Doppler at the aortic anulus. During isometric exercise, left ventricular end-diastolic and end-systolic volumes did not change markedly, but the total stroke volume tended to increase from 62 +/- 13 to 67 +/- 13 ml. The increase in mitral regurgitant volume induced by isometric exercise was correlated with the fall in forward stroke volume (r = 0.7, p less than 0.01). Thus a rise in systemic arterial pressure induced by isometric exercise is associated with a decrease in cardiac performance attributable to redistribution of total left ventricular output with an increase in mitral regurgitation and a simultaneous decrease in forward cardiac output.
Active lifestyles may delay the onset of the functional consequences of chronic disease, potentially increasing active life expectancy. We analyzed the Longitudinal Study of Aging (LSOA) to test the hypothesis that elders participation in an active lifestyle prevents loss of function. Focusing on the cohort aged 70-74 who reported being able to carry 25 lb, walk 1/4 mile, climb 10 steps and do heavy housework without help and without difficulty at baseline, decline was defined as no longer being able to perform these tasks independently and without difficulty 2 years later. Using multivariate logistic regression, results reveal that those who did not report regularly exercising or walking a mile were 1.5 times more likely to decline than those who did, controlling for reported medical conditions and demographic factors. Similar findings (with different models) were observed for both men and women. Findings suggest the potential value of programs oriented toward the primary prevention of functional decline.
A case of a girl who developed severe dysphagia from an aggressive fibromatosis involving the cervical esophagus is reported. A 3 x 4 cm unencapsulated fibrous tumor was completely excised with the involved esophageal wall. The esophageal defect was bridged by an inverted skin tube with good functional and cosmetic results. Eight years later the patient is disease-free. Primary radical excision is the treatment of choice of aggressive fibromatosis.
This paper describes current efforts to construct a set of innovative educational and skill building materials targetted at groups of persons with HIV infection, those at risk for HIV, their families and friends, and health professionals. The ENCOUNTERS family of interactive simulations is designed to provide participants with the necessary communication and behavioral skills to deepen their understanding of HIV, to improve their interaction with others in their interpersonal environment, and to more effectively manage stress generated by HIV concerns The ENCOUNTERS family of simulations are built on the principles of role play, but adds to them principles of simulation gaming. The former technique is strengthened by offering active participation for all group members, increased structure, and the opportunity for participants to take different perspectives on an issue of concern in a supportive small group environment.
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When a single-lumen urethral catheter (catheter coudé) is applied for bladder catheterization in the female, secure fixation of such a catheter may present a problem. A simple method for fixation of a single-lumen urethral catheter in the female is described.
Cardiac performance and mitral regurgitation were measured by Doppler echocardiography and right heart catheterization in 12 patients with severe congestive heart failure who performed isometric exercise during control and intravenous administration of dobutamine and nitroglycerin. During control isometric exercise, mitral regurgitant volume increased from 18 +/- 13 to 31 +/- 17 ml (p less than 0.01), while forward stroke volume, by both thermodilution and Doppler echocardiography, substantially decreased. At rest, dobutamine decreased mitral regurgitant volume from 18 +/- 13 to 11 +/- 10 ml (p less than 0.05), while forward stroke volume increased from 46 +/- 13 to 55 +/- 15 ml (p less than 0.05). During isometric exercise, dobutamine tended to decrease mitral regurgitant volume (24 +/- 12 vs. 31 +/- 17 ml; NS) when compared with control exercise. At rest, nitroglycerin decreased mitral regurgitant volume from 18 +/- 13 to 11 +/- 11 ml (p less than 0.05), while forward stroke volume, by both thermodilution and Doppler echocardiography, substantially increased. Similarly, during isometric exercise, nitroglycerin decreased mitral regurgitant volume from 31 +/- 17 to 20 +/- 14 ml (p less than 0.05), while significantly increasing forward stroke volume. At control rest, the median mitral regurgitant fraction was 24% for the 12 patients. Neither dobutamine nor nitroglycerin changed significantly forward stroke and mitral regurgitant volumes at rest and during isometric exercise in the six patients with resting mitral regurgitant fraction below the median. In contrast, dobutamine and nitroglycerin significantly decreased mitral regurgitant volume and increased forward stroke volume both at rest and during isometric exercise in the six patients with mitral regurgitant fraction greater than the median.(ABSTRACT TRUNCATED AT 250 WORDS)
We studied the effect of omega-3 fatty acid (omega 3FA) treatment on plasma lipids and cardiomyopathy in the diabetic rat. The omega 3FA preparation used was Promega. Male Wistar rats (250-275 g) were rendered diabetic by streptozocin (STZ; 55 mg.kg-1). Nondiabetic control rats received the vehicle alone. Two weeks after STZ or vehicle injection, control and diabetic rats were randomly assigned to either a treated or untreated group. Promega was administered at a dose of 0.5 ml.kg-1.day-1 by oral gavage for 4 wk, after which the rats were decapitated, plasma collected, and isolated working heart performance studied. Promega treatment did not affect plasma glucose, triglyceride, or cholesterol concentrations of either the control or diabetic rats. Cardiac performance was assessed by measuring the left ventricular response to changing left atrial filling pressures (7.5-20 cm H2O). The treatment had no effect on peak left ventricular developed pressure (LVDP) or maximal rate of change of left ventricular pressure during systole (+dP/dtmax) or diastole (-dP/dtmax) in the nondiabetic control rats. LVDP and +/- dP/dt were significantly improved (P less than .05) in the treated diabetic rats compared with untreated diabetic rats, although cardiac performance did not improve to the nondiabetic level. Cardiac sarcoplasmic reticulum (SR) calcium transport activity was not affected by the treatment in the control rats but was significantly improved (P less than .05) in the treated diabetic rats. These data suggest that omega 3FA treatment partially blocks the development of experimental diabetic cardiomyopathy, possibly by affecting SR calcium transport activity.
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The current therapeutic interest in specific phosphodiesterase (PDE) inhibition involves patients with severe congestive heart failure (CHF) whose symptoms are not controlled by diuretics, nitrates, angiotensin converting enzyme (ACE) inhibitors, and digitalis. Maximal exercise capacity is limited in these patients by an inadequate rise in cardiac output and a fixed capacity to dilate the skeletal muscle vasculature, which is perhaps compounded by disorders of the skeletal muscle metabolism. To improve maximal exercise capacity, the increase in cardiac performance produced by specific phosphodiesterase inhibitors must, in turn, reverse the abnormalities present in the periphery, and more specifically augment the capacity to dilate the skeletal muscle vasculature. Increased vasodilatory response to maximal exercise probably depends on the regression of structural changes in the skeletal muscle vasculature. Such regression may be mediated by a reduction in neurohormonal vasoconstrictor stimuli and/or chronic augmentation in resting limb blood flow. Submaximal exercise capacity, at work loads equivalent to less than 70% of peak aerobic capacity, appears to be directly limited by depressed cardiac output and high sympathetic vasoconstrictor activity. Specific phosphodiesterase inhibition, which consistently increases left ventricular performance during exercise, is more likely to improve exercise capacity at submaximal work loads than at maximal work loads.
The literature on the effectiveness of facial surgery for persons with Down syndrome was reviewed. Research based on impressions of involved persons (e.g., parents and doctors) generally provided evidence for the surgery's effectiveness. However, studies that used before-after research designs, control groups, indirect measures, and ratings of less involved persons were less supportive of the operation's positive effects. Certain of these studies indicated that the operation failed to achieve its goals. Furthermore, in evaluations of the operation, investigators generally did not critically examine the assumptions upon which the operation is based and the professional and social implications of facial surgery for persons with Down syndrome.
In the period from January 1986 to July 1988, Blastocystic hominis was found in moderate and numerous quantities in 103 (1.6%) of 6,262 stool specimens examined in our laboratory. There was no significant association of the detection of B. hominis with travel history or symptoms. Indeed, 20 patients (36%) with moderate to heavy infections had no gastrointestinal symptoms, and three symptomatic patients did not show clinical improvement after elimination of the parasite. Reexamination of stool samples revealed that eight untreated patients had spontaneous disappearance of B. hominis. We conclude that B. hominis probably is not responsible for clinical symptoms when detected, and additional investigations should be pursued for other etiologies of the patient's symptoms.
We have studied the effect of ursodeoxycholic acid on the serum and urinary bile acids in seven patients with moderate to severe primary biliary cirrhosis. Bile acids were characterized by gas-liquid chromatography-mass spectrometry and quantified by capillary gas-liquid chromatography. Serum bile acids were elevated 26-fold over control values, with 2.2 times more cholic acid than chenodeoxycholic acid. Urinary bile acid output was elevated 22-fold over control values with a cholic acid:chenodeoxycholic acid ratio of 1.6. In addition, lithocholic acid, deoxycholic acid, ursodeoxycholic acid, 1 beta-hydroxycholic acid, 1 beta-hydroxydeoxycholic acid, and hyocholic acid were identified in both serum and urine; the proportions of the 1- and 6-hydroxylated bile acids were much higher in urine than in serum of the patients (32.1% versus 4.2%). Three months of placebo administration did not change the serum and urinary bile acid composition. In contrast, ursodeoxycholic acid feeding (12-15 mg/kg body weight per day) for 6 months resulted in a 25% decline in the total serum bile acid concentration from the pretreatment values. The proportion of ursodeoxycholic acid increased from 2.1 to 41.2% of total bile acids, so that total fasting serum endogenous bile acid levels decreased 62.4%. Ursodeoxycholic acid feeding substantially increased urinary bile acid output, with ursodeoxycholic acid comprising 58.1%. The proportion of 1- and 6- hydroxylated endogenous bile acids was reduced by 45.5% from pretreatment levels and approximately 4.5% of the urinary bile acids were omega-muricholic acid, 1 beta-hydroxyursodeoxycholic acid, and 21-hydroxyursodeoxycholic acid. These results demonstrate significant changes in the serum and urinary bile acid pattern in primary biliary cirrhosis during ursodeoxycholic acid treatment. The beneficial effect of ursodeoxycholic acid may be due to reduction of the hydroxylated derivatives of endogenous bile acids together with the appearance of hydroxylated derivatives of ursodeoxycholic acid or it may be due to displacement of the more hydrophobic endogenous bile acids by the hydrophilic ursodeoxycholic acid.
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