Supravalvular tricuspid ring and Ebstein's anomaly in congenitally corrected transposition.
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Adolescent↗
Biomedical subjects
M Ritter
Publications and source records attributed to M Ritter.
Congenital cleft of the anterior tricuspid leaflet with severe tricuspid regurgitation in adults.
OBJECTIVES AND BACKGROUND: Severe primary tricuspid regurgitation in the adult is a rare finding. This study describes the diagnostic findings and the treatment of an isolated congenital cleft of the anterior leaflet of the tricuspid valve as the morphologic substrate for severe tricuspid regurgitation. METHODS: The clinical, echocardiographic findings and the follow-up findings of five patients (all male, 20 to 56 years old) with this disorder are described. Four of the five patients underwent cardiac surgery that confirmed the diagnosis. RESULTS: In three of five patients, exertional fatigue was the limiting symptom (New York Heart Association functional classes II and III). The clinical findings included a holosystolic murmur and supraventricular arrhythmias in all patients. Cardiac catheterization, performed in four patients, yielded the incorrect diagnosis of Ebstein's anomaly in three. In one patient the cleft was associated with an atrial septal defect of the secundum type. In four of five patients successful reconstruction of the tricuspid valve with a DeVega annuloplasty was performed. One patient had a partial excision of the right atrium, and one had a closure of a coexisting atrial septal defect. One patient refused operation. CONCLUSIONS: Tricuspid valve anomalies can be accurately identified by Doppler echocardiography. Surgical repair is the treatment of choice in patients with severe tricuspid regurgitation due to a congenital cleft of the anterior leaflet of the tricuspid valve.
Adult↗
[Pathophysiology, prevention and therapy of altitude pulmonary edema].
Alveolar hypoxia and resulting tissue hypoxia initiates the pathophysiological sequence of high altitude pulmonary edema (HAPE). Very rapid ascent to high altitude without prior acclimatization results in HAPE, even in subjects with excellent tolerance to high altitude. Upon acute altitude exposure, HAPE-susceptible individuals react with increased secretion of norepinephrine, epinephrine, renin, angiotensin, aldosterone and atrial natriuretic peptide. In response to exercise at high altitude, subjects developing acute mountain sickness and HAPE secrete more aldosterone and antidiuretic hormone than subjects who remain well. This results in sodium and water retention, reduction of urine output, increase in body weight and development of peripheral edemas. The hypoxic pulmonary vascular response is enhanced in HAPE-susceptible subjects, thus favouring the development of severe pulmonary hypertension on exposure to high altitude. It has been postulated that uneven pulmonary vasoconstriction enhances filtration pressure in non-vasoconstricted lung areas, leading to interstitial and alveolar edema. The high protein content of the edema fluid in HAPE characterizes this edema as a permeability edema. The prophylactic administration of nifedipine prevents the exaggerated pulmonary hypertension of HAPE-susceptible subjects upon rapid ascent to 4559 m and thus prevents HAPE in most cases. This finding illustrates the crucial role of hypoxic pulmonary hypertension in the development of HAPE. The causal treatment of HAPE is descent, evacuation and administration of oxygen. Treatment of HAPE patients with nifedipine results in a reduction of pulmonary artery pressure, clinical improvement, increased oxygenation, decrease of the alveolar arterial oxygen gradient and progressive clearing of pulmonary edema on chest x-ray. Thus nifedipine offers a pharmacological tool for the treatment of HAPE.
Aldosterone↗
Effects of bradykinin on cell volume and intracellular pH in NIH 3T3 fibroblasts expressing the ras oncogene.
BCECF fluorescence has been applied to determine intracellular pH (pHi) in NIH 3T3 fibroblasts expressing the Ha-ras oncogene (+ras) and otherwise identical cells not expressing the oncogene (-ras). In +ras cells, pHi is significantly more alkaline (6.79 +/- 0.03 n = 12) than in -ras cells (6.64 +/- 0.02, n = 8). Bradykinin (100 nmol/l) leads to intracellular alkalinization in both +ras (to 6.96 +/- 0.04, n = 12) and -ras cells (to 6.85 +/- 0.02, n = 8). The effect of bradykinin is completely abolished in the presence of dimethylamiloride (100 mumol/l), which does not modify pHi in the absence of bradykinin. Similar to bradykinin, cell shrinkage by addition of 15 mmol/l NaCl to the extracellular fluid leads to intracellular alkalinization (by 0.08 +/- 0.01, n = 15). Cell volume is significantly greater in +ras cells (2.7 +/- 0.4 pl, n = 15) than in -ras cells (2.2 +/- 0.4 pl, n = 15). Bradykinin leads to cell shrinkage in both +ras cells (by 7 +/- 1%, n = 17) and -ras cells (by 5 +/- 1%, n = 15). The effect of bradykinin on cell volume can be reversed by the reduction of extracellular NaCl concentration by 15 mmol/l NaCl in +ras cells and by 7 mmol/l NaCl in -ras cells. This maneuver completely abolishes (in -ras cells) or blunts (in +ras cells) the alkalinizing effect of bradykinin. In conclusion, +ras cells are more alkaline than -ras cells. Bradykinin leads to further intracellular alkalinization by activation of the Na+/H(+)-exchanger, at least in part secondary to hormone-induced cell shrinkage.
3T3 Cells↗
[Cor triatriatum in adulthood: Doppler echocardiographic diagnosis. Case report of an asymptomatic adult].
Cor triatriatum is a rare cardiac malformation occurring in about 0.1% of all congenital heart disease. As symptoms are usually present soon after birth, diagnosis in adulthood is extremely rare. We describe a case of a 33-year-old asymptomatic woman who was referred for echocardiographic examination because of a postural variable systolic click. The anatomy of the malformation and the hemodynamics of the left atrium were accurately assessed by means of conventional transthoracic Doppler echocardiography. The antero-inferior course of the intraatrial membrane inserting proximal to the left atrial appendage was documented in multiple perpendicular planes of examination. All pulmonary veins drained correctly into the proximal compartment of the left atrium. Additionally, a small atrial septal defect communicated between the distal compartment of the left atrium and the right atrium. Using pulsed wave Doppler, no site of pressure gradient could be detected between the two compartments of the left atrium. Thus, conventional transthoracic Doppler echocardiography represents an adequate tool for assessing cor triatriatum in adults. The patient refused transesophageal echocardiography.
Adult↗
Effects of inhibitors and ion substitutions on oscillations of cell membrane potential in cells expressing the RAS oncogene.
Previous studies revealed that in NIH fibroblasts expressing the ras oncogene but not in other NIH fibroblasts, bradykinin leads to sustained, calcium dependent oscillations of cell membrane potential by repetitive activation of calcium-sensitive K+ channels. The present study has been performed to test for ion and inhibitor sensitivity of these oscillations. Both, Lys-bradykinin (kallidin) and bradykinin, but not any shorter peptide tested, maintained the oscillations. The oscillations are abolished in the presence of the K+ channel blocker barium (10 mmol/l). The amplitude but not the frequency of the oscillations is dependent on the extracellular potassium concentration. The oscillations are not dependent on the presence of extracellular sodium, bicarbonate or chloride. The oscillations are abolished in the absence of extracellular calcium and their frequency is significantly decreased at reduced extracellular calcium (to 0.2 mmol/l). The oscillations are not inhibited by acute administration of ouabain (0.1 mmol/l), by dimethylamiloride (100 mumol/l), furosemide (1 mmol/l) and hydrochlorothiazide (100 mumol/l), by cobalt (100 mumol/l), zinc (100 mumol/l), gadolinium (100 mumol/l), verapamil (10 mumol/l) and diltiazem (10 mumol/l), but are abolished in the presence of 100 mumol/l lanthanum, 1 mmol/l cadmium, 10 mumol/l nifedipine, 25 mumol/l SK & F 96365 and 200 mumol/l TMB-8. Stimulation of calcium entry by 10 nmol/l ionomycin is frequently followed by oscillations of cell membrane potential even in the absence of bradykinin. In conclusion, in cells expressing the ras oncogene bradykinin leads to sustained activation of calcium channels at the cell membrane, which cause oscillations of the cell membrane potential by triggering intracellular calcium release.
Animals↗
Altered cell volume regulation in ras oncogene expressing NIH fibroblasts.
Expression of the Ha-ras oncogene has been reported to stimulate the dimethylamiloride sensitive Na+/H+ exchanger and Na+,K+,2Cl- cotransport, both transport systems which are involved in cell volume regulation. The present study has been performed to test for an influence of ras oncogene expression on cell volume regulation in NIH 3T3 fibroblasts expressing the Ha-ras oncogene (+ ras). As controls served NIH 3T3 fibroblasts not expressing the ras oncogene (-ras). In isotonic extracellular fluid, the cell volume of + ras cells (2.70 +/- 0.08 pl) is significantly greater than the cell volume of -ras cells (2.04 +/- 0.10 pl). Both, + ras and -ras cells exhibit a regulatory cell volume increase in hypertonic extracellular fluid and a regulatory cell volume decrease in hypotonic extracellular fluid. The regulatory cell volume decrease is inhibited by 1 mmol/l quinidine and barium, the regulatory cell volume increase is inhibited in -ras and +ras cells by dimethyl-amiloride (100 mumol/l) and, only in +ras cells, by furosemide (100 mumol/l) and bumetanide (10 mumol/l). In conclusion, expression of the ras oncogene leads to a shift of the set point for cell volume regulation to greater cell volumes, which may contribute to the activation of the Na+/H+ exchanger and Na+,K+,2Cl- cotransport.
3T3 Cells↗
Acute tricuspid papillary muscle rupture following blunt chest trauma.
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Acute Disease↗
Work-health relationships in middle-aged and elderly residents of a Jerusalem community.
Work-health relationships were examined cross-sectionally in 1886 men and women aged greater than or equal to 50 years in Jerusalem in 1985-1987, in the third round of a multipurpose longitudinal community health study. The main occupational variables were employment status, reasons for not working, and satisfaction with work. Sex and age were controlled in all comparisons. Workers were clearly healthier than nonworkers with respect to general, physical and emotional health, and people who had given up work were less healthy than those still working, whether they had stopped for health reasons, only because of their age, or only for extrinsic reasons (retrenchment or dismissal). Workers who expressed satisfaction with their work were healthier than others, the odds ratio in favour of good general health being 2.4 at 50-64 and 2.5 at greater than or equal to 65 years of age. The associations between job satisfaction and health remained apparent when education and origin were controlled. Multivariate analyses suggested that the associations were not spurious ones attributable to proneness to report both dissatisfaction and ill-health. Job dissatisfaction was not significantly associated with angina pectoris, possible myocardial infarction, or hypertension. Taken at their face value, the findings support the impact of job satisfaction or its determinants on the health of middle-aged and elderly men and women. The associations will be re-appraised in the longitudinal analysis of the study data.
Aged↗
A simplified index of physical health for use in epidemiological studies.
A battery of simple questions designed to measure physical health, in terms of ability to perform physical activities, was appraised in 1839 men and women aged greater than or equal to 50 years in a community survey in Jerusalem. The number of "Yes" answers to six questions, five of which could be skipped if the first one was answered positively, was found to be a satisfactory index, with a high degree of consistency-reliability in the total sample (Cronbach's alpha coefficient = 0.97) and in subgroups categorized by sex, age, education, or father's region of birth. The index constituted an excellent Guttman scale (coefficient of reproducibility = 0.96, coefficient of scalability = 0.94), indicating that the score serves both as a measure of physical health and as an indication of the profile of capabilities. Associations with age and other variables conformed with expectations, attesting the construct validity of the index.
Aged↗
Prevention and treatment of high altitude pulmonary edema by a calcium channel blocker.
High altitude pulmonary edema (HAPE) is characterized by marked pulmonary hypertension. Treatment of 6 subjects suffering from radiographically documented HAPE with the calcium channel blocker nifedipine, lowered pulmonary artery pressure and resulted in clinical improvement, better oxygenation, reduction of alveolar-arterial oxygen gradient and a progressive clearing of alveolar edema on chest x-ray. This amelioration occurred despite continued exercise at an altitude above 4000 m and without supplementary oxygen. Prophylactic application of nifedipine slow release preparation, 20 mg every 8 hours, prevented HAPE in 9 out of 10 subjects with a history of radiographically documented HAPE upon rapid ascent and subsequent stay to an altitude of 4559 m. Seven of 11 comparable subjects who received placebo developed pulmonary edema at 4559 m. As compared with the subjects who received placebo, those who received nifedipine had a significantly lower mean systolic pulmonary artery pressure, alveolar-arterial pressure gradient of oxygen and symptom score of acute mountain sickness at 4559 m. Thus nifedipine offers a potential emergency treatment of HAPE when descent or evacuation is impossible and oxygen is not available. Prophylactic administration of nifedipine prevents HAPE in susceptible subjects. High pulmonary artery pressure has an important role in the pathogenesis of HAPE.
Acute Disease↗
Myocardial oxygen consumption in aortic valve disease with and without left ventricular dysfunction.
OBJECTIVE: To assess whether and to what extent myocardial oxygen consumption is modified by hypertrophy and alterations in contractility in patients with aortic valve disease and to evaluate the influence of regression of left ventricular hypertrophy and improvement of contractility on myocardial oxygen consumption after successful aortic valve replacement. DESIGN: A cohort analytical study to investigate the influence of the "explanatory" variables of myocardial oxygen consumption by multiple regression analysis. A comparison of myocardial oxygen consumption in preoperative patients with that after operation in a group with comparable severity of aortic valve disease before operation (analysis of covariance). PATIENTS: In six controls and in 43 patients with aortic valve disease and normal coronary arteries standard haemodynamic variables were measured, left ventricular biplane cineangiography performed, and coronary sinus blood flow measured by thermodilution. The patients were divided into three groups: 19 preoperative patients with normal ejection fraction (greater than or equal to 57%) (group 1); nine preoperative patients with reduced ejection fraction (less than 57%) (group 2); 16 postoperative patients (one with preoperative and postoperative measurements (group 3). Postoperative evaluation was performed 12-51 months after surgery. MAIN OUTCOME MEASUREMENTS: Myocardial oxygen consumption/100 g left ventricular muscle mass and its suspected "explanatory" variables--that is, peak systolic left ventricular circumferential wall stress, heart rate, contractility (assessed by left ventricular ejection fraction), and left ventricular muscle mass index. RESULTS: Multiple regression analysis showed that the product of peak systolic stress and heart rate (p less than 0.0001) and ejection fraction (p less than 0.03) were positively correlated with myocardial oxygen consumption/100 g and that left ventricular muscle mass index (p less than 0.002) was negatively correlated with myocardial oxygen consumption/100 g (r = 0.72; n = 50 measurements). Myocardial oxygen consumption per 100 g at a given stress-rate product was higher in the controls than in group 1 (hypertrophied ventricles with normal ejection fraction) and was also higher in group 1 than in group 2 (hypertrophied ventricles with reduced ejection fraction). In a subgroup of the postoperative patients with complete regression of hypertrophy and normalisation of contractility, myocardial oxygen consumption per 100 g at a given stress-rate product was indistinguishable from that in controls. CONCLUSIONS: When the actual stress-rate product was used as an index of overall left ventricular performance the results suggested that mechanical efficiency was increased in hypertrophied ventricles especially when contractility was decreased. These changes in mechanical efficiency seemed to be reversible during the postoperative course when muscle mass and contractility returned to normal.
Aged↗
Anesthetic effects on pulmonary allergic responses in rats: changes in sensitivity to serotonin.
Subsequent to observations that pulmonary responses to antigen challenge are of different magnitudes in sensitized rats that are anesthetized with different drugs, we conducted studies to test whether the alterations in responses were due to changes in airway responsiveness to cholinergic or serotonergic challenge, opioid-receptor mediated events, or changes in mast cell mediator release. Immunoglobulin E-sensitized rats anesthetized with ketamine/urethan had larger changes in lung resistance and plasma histamine after pulmonary antigen challenge compared with rats anesthetized with fentanyl-droperidol. Blockade of opioid receptors with naloxone did not affect the responses. In unsensitized rats, airway responses to aerosolized methacholine were similar for the two anesthetics, indicating unchanged smooth muscle responsiveness; however, airway responses to intravenous serotonin were enhanced by ketamine and ablated by droperidol. We conclude that ketamine- and droperidol-induced alterations of pulmonary allergic responses are due to changes in sensitivity to serotonin and in mast cell mediator release. We speculate that mast cell mediator release may be modulated by a serotonin receptor-linked mechanism.
Airway Resistance↗
Active autoimmune gastritis without total atrophy of the glands.
To date, autoimmune gastritis has been diagnosed for the most part only when total atrophy of the oxyntic glands is detected. On the basis of 40 patients without total atrophy of the glands, and with parietal cell antibodies in the serum, we show that the diagnosis of type A gastritis is also possible in the pre-atrophic stage. The histological criteria for the diagnosis of active autoimmune gastritis without total atrophy of the glands are 1. usually dense, diffuse locally emphasized lymphocytic infiltration of the lamina propria between the glands in the oxyntic mucosa, 2. focal destruction of individual glands in the corpus of the stomach by lymphocytes, and 3. reactive pseudohypertrophy of the parietal cells. A comparison with a group of patients with autoimmune gastritis and total atrophy of the glands shows that in active autoimmune gastritis, too, women are more frequently affected than men (in both groups, the sex ratio is approximately 3:1). Patients without atrophy of the glands are, on average, about 12 years younger than those with "burnt out" type A gastritis (average age 69.98:57.80 years). While in the case of burnt out type A gastritis, no colonisation with Helicobacter pylori was to be found, such colonisation was demonstrated for the corpus mucosa in 22.5%, and for the antral mucosa in 15.0%. In 27.5% a minimal or low-grade inactive superficial gastritis, as may be seen after eradication of Helicobacter pylori, was additionally diagnosed in the antrum. A knowledge of the histological appearance of the pre-atrophic stage of type A gastritis might be of importance for the possible prevention of pernicious anaemia.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Cell membrane potential oscillations induced by kinins in fibroblasts expressing the Ha-ras oncogene.
In NIH-3T3 fibroblasts expressing the ras oncogene (+ras) bradykinin (BK) elicits sustained oscillations (1/min) of cell membrane potential (PD) due to oscillations of intracellular calcium activity with subsequent activation of calcium sensitive K+ channels. In NIH-3T3 fibroblasts not expressing the oncogene (-ras), BK leads to a single transient hyperpolarization of the cell membrane, not followed by oscillations. The oscillations of cell membrane potential require the presence of extracellular calcium and are abolished by K+ channel blocker barium (1 mmol/l), as well as by calcium channel blockers cadmium (1 mmol/l), lanthanum (0.1 mmol/l) and nifedipine (10 mumol/l). However, the oscillations are not modified by 1 mumol/l nifedipine, or by other calcium channel blockers, such as verapamil (10 mumol/l) or diltiazem (10 mumol/l). Cell proliferation is inhibited by nifedipine (10 mumol/l) but not by verapamil or diltiazem, indicating that the oscillations of intracellular calcium are a prerequisite for the growth factor independent proliferation of ras oncogene expressing cells.
3T3 Cells↗
Well-differentiated thymic carcinoma. An organotypical low-grade carcinoma with relationship to cortical thymoma.
Based on a study of 26 cases, the well-differentiated thymic carcinoma is described as a distinct organotypical carcinoma of the thymus with low-grade malignancy. It is characterized by a predominance of epithelial cells with usually low mitotic rate, an epidermoid differentiation with slight to moderate cytological atypia, the constant presence of interepithelial immature cortical thymocytes, lobular growth, and formation of epithelial palisades around perivascular spaces. The tumor occurs at age 14 to 76 years in both sexes. An association with myasthenia gravis is found in 77% of the patients, and 83% of the tumors show invasion of adjacent organs or endothoracic metastasis at primary operation. This rate is higher than in cortical thymomas (47%) but lower than in other thymic carcinomas (92%). Two of 18 patients with follow-up died of tumor recurrence and pleural metastasis. Well-differentiated thymic carcinoma can be related to cortical thymoma by common morphological features and a similar immunophenotype of epithelial cells. It must be differentiated from the lymphocyte-depleted cortical thymomas after corticosteroid treatment and from the benign epithelial-rich medullary thymomas.
Adolescent↗
Omeprazole-induced pseudohypertrophy of gastric parietal cells.
Paraffin-embedded and haematoxylin-eosin-stained sections of biopsy material obtained from patients taking omeprazole reveal a characteristic "hypertrophy" of the parietal cells; these are taller than the chief cells, and project, with convexly bulging apical cell membrane, into the lumen of the body glands, producing a serrated internal gland profile. We have found this phenomenon in 92.9% of 198 patients with non-operated stomachs. After Billroth I or II resection, this phenomenon was found in the body mucosa of the stomach remnant in only 35.3% of the cases (n = 17). The specificity of the diagnosis "hypertrophy" of the parietal cells under omeprazole therapy was 89.4%, the sensitivity 91.0%. A comparative morphometric analysis in forceps biopsy material investigated after paraffin and epoxide embedding, showed that this "hypertrophy" was a pseudohypertrophy. Apparently, as a result of an increase in intracytoplasmic secretory canaliculi, the gastrin-stimulated parietal cell shrinks less than the non-stimulated parietal cell. This pseudohypertrophy of the parietal cells can readily be used to monitor the compliance of the patient prescribed omeprazole. A question that has yet to be clarified is how quickly pseudohypertrophy develops, and how long it takes to regress after discontinuation of omeprazole. The phenomenon can also be seen in active autoimmune gastritis with no atrophy of the gland, since the parietal cell antibody also binds selectively to the proton pump of the parietal cell.
Cell Membrane↗
Prevention of high-altitude pulmonary edema by nifedipine.
BACKGROUND: Exaggerated pulmonary-artery pressure due to hypoxic vasoconstriction is considered an important pathogenetic factor in high-altitude pulmonary edema. We previously found that nifedipine lowered pulmonary-artery pressure and improved exercise performance, gas exchange, and the radiographic manifestations of disease in patients with high-altitude pulmonary edema. We therefore hypothesized that the prophylactic administration of nifedipine would prevent its recurrence. METHODS: Twenty-one mountaineers (1 woman and 20 men) with a history of radiographically documented high-altitude pulmonary edema were randomly assigned to receive either 20 mg of a slow-release preparation of nifedipine (n = 10) or placebo (n = 11) every 8 hours while ascending rapidly (within 22 hours) from a low altitude to 4559 m and during the following three days at this altitude. Both the subjects and the investigators were blinded to the assigned treatment. The diagnosis of pulmonary edema was based on chest radiography. Pulmonary-artery pressure was measured by Doppler echocardiography and the difference between alveolar and arterial oxygen pressure was measured in simultaneously sampled arterial blood and end-expiratory air. RESULTS: Seven of the 11 subjects who received placebo but only 1 of the 10 subjects who received nifedipine had pulmonary edema at 4559 m (P = 0.01). As compared with the subjects who received placebo, those who received nifedipine had a significantly lower mean (+/- SD) systolic pulmonary-artery pressure (41 +/- 8 vs. 53 +/- 16 mm Hg, P = 0.01), alveolar-arterial pressure gradient (6.6 +/- 3.8 vs. 11.8 +/- 4.4 mm Hg, P less than 0.001), and symptom score of acute mountain sickness (2.0 +/- 0.7 vs. 3.9 +/- 1.9, P less than 0.01) at 4559 m. CONCLUSIONS: The prophylactic administration of nifedipine is effective in lowering pulmonary-artery pressure and preventing high-altitude pulmonary edema in susceptible subjects. These findings support the concept that high pulmonary-artery pressure has an important role in the development of high-altitude pulmonary edema.
Adult↗