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M Ritter

Publications and source records attributed to M Ritter.

At least 109 records · Page 6Linked to original sources
PubMed1995

[Severe aortic stenosis without left-ventricular hypertrophy: associated variables and prognosis following aortic valve replacement].

The purpose of the present study in patients with severe aortic stenosis was to assess prevalence, predictors and course after aortic valve replacement in patients without left ventricular hypertrophy according to echocardiographic mass criteria (LVH). 90% had LVH compared with 10% without. The following variables were associated with absence of LVH: younger age, low body surface area, and increased cardiac index. In patients with LVH, ventricular adaptation following aortic valve replacement was adequate more often than in those without. Six-month mortality following aortic valve replacement was insignificantly lower in patients with LVH (7.6%) than in those without it (12.5%, p = 0.10).

Aged↗
PubMed1995

[Rare association of a coronary fistula with a fusiform aneurysm of the superior vena cava: diagnosis via transesophageal echocardiography and MRI].

A congenital fistula of the left circumflex coronary artery with large aneurysmal sacculations and drainage into the vena cava superior is reported in an asymptomatic black adult female. An indicator dilution curve excluded a significant left-to-right shunt. In addition, the patient had a large fusiform aneurysm of the superior vena cava with maximal extension in the anterior upper mediastinum. Transesophageal Doppler echocardiography and magnetic resonance imaging were complementary diagnostic tools, the first for clearly visualizing coronary anatomy and shunt, the second for accurate imaging of the aneurysmal vena cava superior in the upper mediastinum.

Adult↗
PubMed1995

[Abnormalities of the atrial septum in adults: kind, prevalence and clinical relevance].

UNLABELLED: To classify interatrial septal anomalies in adults, 24,458 Doppler-echocardiographic studies performed between 1. 1. 1987 and 31. 12. 1992 were reviewed. Patients below 16 years of age or with complex congenital heart disease, or after surgical closure of an atrial septal defect, were excluded. Additionally, all 823 transesophageal echocardiographies done between 1. 1. 1993 and 31. 12. 1994 were analyzed to see whether a patent foramen ovale was present. Among 294 patients with interatrial septal anomalies (prevalence 1.2%; male:female = 1:1.4), 298 congenital anomalies of the interatrial septum were detected. 63% of interatrial septal anomalies constituted newly detected anomalies. Age ranged from 16 to 84 (median 43) years. In 21% of the patients the left-to-right shunt was > or = 50% (QP/QS > or = 2). In 25% pulmonary hypertension was present and 25% of the patients underwent surgery. A patent foramen ovale was present in 0.16% of all transthoracal and in 5.7% of all transesophageal echocardiographies. Secundum defects constituted 46%, atrial septal aneurysms 24%, patent foramen ovale 13%, atrioventricular canals 11%, and superior sinus venosus defects with anomalous pulmonary venous return 6% of all diagnoses. Associated anomalies were mitral valve prolapse in 14%, pulmonary valve stenosis in 3%, left-sided persistent vena cava superior and Chiari network in 2% each, anomalous pulmonary venous return, ventricular septal defect, bicuspid aortic valve, and Ebstein's anomaly in 1% each. 4% of the patients showed further cardiac lesions. CONCLUSIONS: Anomalies of the interatrial septum in adults were frequent and often newly detected. In a high percentage of patients with interatrial septum the left-to-right shunt was hemodynamically relevant.

Adolescent↗
PubMed1995

[Severe, predominantly aortic stenosis without left ventricular hypertrophy (LVH): effect of LVH definition].

210 out of approximately 16,000 Doppler echocardiographic examinations between 1989 and 1992 at the University Hospital of Zurich, Switzerland, produced the diagnosis of severe, longstanding and predominant aortic stenosis with a mean transvalvular pressure gradient of > or = 50 mm Hg. These patients, who had no significant valvular heart disease other than aortic stenosis and no coronary artery disease, were investigated for the prevalence and for existing gender predominance of absent left ventricular hypertrophy (LVH) using eight different, clinically established and validated definitions for LVH. 4 to 44% of all study patients were found to have absent LVH depending on how LVH was defined. There was no gender predominance in patients without LVH if a gender-specific LVH definition was used. Defining absent LVH as LV mass index < 109 g/m2 body surface area (for women) and < 134 g/m2 body surface area (for men) combined with relative LV wall thickness < 0.45, the prevalence of absent LVH amounted to 4% (9/210 patients). The majority of patients had concentric LVH (132/210), 57/210 patients had excentric LVH, and 12/210 had concentric LV remodeling. There was a significant inverse association between the time elapsed since diagnosis of aortic stenosis and the finding of absent LVH. However, average duration since diagnosis of aortic stenosis in patients without LVH was quite long averaging 3.2 years. Therefore, factors other than duration of the disease and not investigated in this study seem to be more closely related to the absence of LVH.

Aged↗
PubMed1995

Antisense oligonucleotides suppress cell-volume-induced activation of chloride channels.

Cell volume regulation is an essential feature of most cells. After swelling in hypotonic media, the simultaneous activation of potassium and chloride channels is believed to be the initial, time-determining step in cell volume regulation. The activation of both pathways is functionally linked and enables the cells to lose ions and water, subsequently leading to cell shrinkage and readjustment of the initial volume. NIH 3T3 fibroblasts efficiently regulate their volume after swelling and bear chloride channels that are activated by decreasing extracellular osmolarity. The chloride current elicited in these cells after swelling is reminiscent of the current found in oocytes expressing an outwardly rectifying chloride current termed ICln. Introduction of antisense oligodeoxynucleotides complementary to the first 30 nucleotides of the coding region of the ICln channel into NIH 3T3 fibroblasts suppresses the activation of the swelling-induced chloride current. The experiments directly demonstrate an unambiguous link between a volume-activated chloride current and a cloned protein involved in chloride transport.

Animals↗
PubMed1995

Pseudoaneurysm following aortic homograft: clinical implications?

OBJECTIVE: To determine the prevalence of pseudoaneurysm formation after aortic (left ventricular outflow tract) homograft implantation and to evaluate predisposing factors. METHODS: Echocardiographic data were analysed in 30 patients for evidence of pseudoaneurysm formation after homograft implantation. Pseudoaneurysm was characterised as a perfused echo-free space between the homograft and the native aortic wall communicating with the left ventricular outflow tract. Clinical data were analysed for potential predisposing factors for pseudoaneurysm formation. RESULTS: Pseudoaneurysms were found in 22 of 30 patients. Mean age, length of follow up after surgery, aortic systolic pressure gradient (15 (SD 12) v 10 (4) mm Hg), aortic root diameter, and size of the homografts were comparable in patients with and without pseudoaneurysm. preoperative infection, operating techniques, and whether first or reoperation did not affect pseudoaneurysm formation. However, pseudoaneurysms were often localised at the site of an abscess or a paravalvular leak after eradicated prosthetic valve endocarditis. CONCLUSIONS: (1) Doppler echocardiography demonstrates that pseudoaneurysm formation is common after aortic homograft implantation. (2) A prospective study is needed to clarify the prognostic importance of pseudoaneurysms. (3) The high incidence of pseudoaneurysm formation may lead to an improvement of surgical technique (application of fibrin glue).

Adult↗
PubMed1995

Detection of DNA methylation in the calcitonin gene in human leukemias using differential polymerase chain reaction.

One of the earliest events in the multistep process of malignant transformation is a change in the methylation pattern of certain genes. DNA methylation is usually detected by Southern blotting after restriction digest with methylation-sensitive endonucleases. Calcitonin gene hypermethylation has been described in a variety of human malignancies including lymphomas and leukemias. Here we report a technique based on the semi-quantitative differential polymerase chain reaction (PCR) which is capable of detecting subtle changes in the methylation pattern of the human calcitonin gene. This technique is based on two principles: (i) simultaneous coamplification of the target gene (5'-region of the calcitonin gene) and a reference gene for quantitative purposes; and (ii) simultaneous coamplification of a competitor with identical primer-binding sites as the target gene to control for proper restriction digest. Using this technique, we investigated calcitonin gene methylation in a variety of human cell lines, primary leukemias and normal human blood donors. The data revealed good correlation with standard Southern blotting. Weak calcitonin gene methylation was found in all normal blood donors tested (n = 14). In contrast, strong calcitonin gene methylation was detected in most acute leukemias (five of 10 acute myeloid leukemias (AML); six of seven acute lymphoblastic leukemias (ALL)). These data show that this technique can reliably be used to quantitate gene methylation and indicate that there exists heterogeneity with regard to methylation status in different leukemias, suggesting that hypermethylation of the calcitonin gene may play a role in the transformation process of some, but not all, human leukemias. Furthermore, differential PCR may facilitate determination of calcitonin gene methylation in clinical or archival tumor samples.

Base Sequence↗
PubMed1995

[Traumatic aortic rupture: diagnosis using biplanar transesophageal echocardiography].

Acute aortic rupture is a typical consequence of severe blunt chest trauma often associated with rapid deceleration in car accidents. Initial diagnostic findings are often misleading and multiorgan injuries add to the diagnostic complexity; therefore, the natural history of acute rupture is usually fatal during the first 24 h after injury if left untreated. Prompt and simple diagnosis is, hence, of paramount importance for successful treatment of acute aortic rupture. Transesophageal echocardiography, particularly with a biplane or multiplane probe, currently represents the diagnostic tool of choice to meet these criteria; because of its high sensitivity and specificity transesophageal echocardiography will replace aortography as "gold standard" for diagnosis of acute aortic rupture. We report on a 47-year-old woman with severe blunt thoraco-abdominal trauma resulting from a car accident; at hospital admission abdominal injuries were predominant and diagnosis of an acute rupture of the descending thoracic aorta was made only about 18 h after admission using biplane transesophageal echocardiography. Emergency surgical revision confirmed the diagnosis of complete transsection of the descending thoracic aorta immediately after the origin of the left subclavian artery; the site of transsection was surrounded by a large hematoma. Despite successful reconstruction of the descending thoracic aorta by means of graft interposition, a recurrent local bleeding event lead to complete circulatory destabilization and, finally, to the death of the patient.

Aortic Rupture↗
PubMed1995

Antiviral drugs from the nucleoside analog family block volume-activated chloride channels.

BACKGROUND: The antiviral drugs AZT and acyclovir are generally used in the treatment of infections with human immunodeficiency virus (HIV) and herpes simplex virus (HSV). These substances are known to impede virus replication by premature nucleic acid chain termination. It is not yet clear, however, if this is the sole mechanism responsible for the antiviral and/or the numerous side effects observed in patients treated with these agents. We investigated the swelling-induced chloride current in fibroblasts, which we demonstrated is closely related or identical to a cloned epithelial chloride channel, ICln: This chloride channel can be blocked by nucleotides. MATERIALS AND METHODS: Electrophysiological, fluorescence optical, and volume measurements were made to determine the effect of nucleoside analogs on the swelling-dependent chloride current (ICl) in NIH 3T3 fibroblasts and in human T cell lymphoma (H9) cells and the cAMP-dependent chloride current in CaCo cells. RESULTS: AZT and acyclovir block the swelling-dependent chloride current and the chloride flux in fibroblasts, and the regulatory volume decrease (RVD) and ICl in H9 cells. This immediate effect can be substantially reduced by the simultaneous incubation of the cells with thymidine-5'-diphosphate (TDP) or uridine, both of which are by themselves unable to affect ICl. CONCLUSIONS: We show here a novel molecular mechanism by which antiviral drugs of the nucleoside analog family could lead to impairments of the kidney, bone marrow, gastrointestinal, and neuronal functions, and how these side effects could possibly be restricted by the presence of TDP or uridine.

3T3 Cells↗
PubMed1995

Effects of calcium channel blockers on NIH 3T3 fibroblasts expressing the Ha-ras oncogene.

NIH 3T3 fibroblasts expressing the ras oncogene (+ras cells) respond to bradykinin, bombesin or serum with sustained oscillations of cell membrane potential reflecting oscillations of intracellular calcium activity and subsequent activation of calcium-sensitive K+ channels. In contrast, identical cells not expressing the oncogene (-ras cells) respond to bradykinin with a single, transient hyperpolarization of the cell membrane. Furthermore, +ras cells are characterized by a serum-independent proliferation, an increase in cell volume and a marked reorganization of the cytoskeleton. It has been shown previously that the calcium channel blocker nifedipine, but not verapamil and diltiazem, inhibits oscillations of cell membrane potential as well as proliferation. In this study, we have examined the effect of several calcium channel blockers (bepridil, nifedipine, verapamil, diltiazem) on the proliferation, volume and cytoskeletal reorganization of +ras cells. Bepridil (10 mumol/l), which is also shown here to inhibit oscillations of cell membrane potential, and nifedipine (10 mumol/l) caused a decrease in cell number, whereas verapamil and diltiazem (10 mumol/l each) resulted in growth rates which did not differ from untreated +ras cells. The increase in cell volume as observed in untreated +ras cells was also observed for cells treated with verapamil and diltiazem, whereas cell volumes of +ras cells treated with bepridil and nifedipine were markedly reduced and similar to the values obtained for -ras cells. In addition, bepridil and nifedipine markedly inhibited cytoskeletal rearrangement, i.e depolymerization of actin-containing stress fibers. This inhibitory effect was not observed for verapamil and diltiazem.(ABSTRACT TRUNCATED AT 250 WORDS)

3T3 Cells↗
PubMed1994

[Stress echocardiography: development and significance].

Exercise electrocardiography is still the primary method used in the non-invasive assessment of coronary artery disease. Stress echocardiography is now being increasingly used as a more sensitive adjunct technique to assess ischemia. Ischemia provoked by stress can induce reversible wall motion abnormalities which are disclosed by cross-sectional 2-dimensional echocardiography and standard projections. The types of stress used are physical exercise (bicycle, treadmill), atrial pacing or pharmacologic stimulation. In the latter, the catecholamine dobutamine has emerged as preferable to the vasodilators dipyridamole and adenosine. The diagnostic accuracy of dobutamine stress echocardiography is comparable to that of bicycle or treadmill exercise echocardiography, but dobutamine stress echocardiography is technically simpler and can be performed in patients unable to exercise. Its sensitivity in diagnosing ischemic or viable myocardium is comparable to that of nuclear methods, MRI or PET. In contrast to nuclear methods, stress echocardiography is however free of radiation. In the assessment of patients with coronary artery disease, stress echocardiography has been shown to be valuable for diagnosis, preoperative risk stratification and determination of prognosis. Furthermore, low dose dobutamine echocardiography can be used to detect viable myocardium. Despite these very promising aspects of the method, there are recognized disadvantages and limitations: stress echocardiography is very time-consuming and operator-dependent; its sensitivity correlates strongly with the number of studies performed; analysis of wall motion is performed qualitatively on a purely subjective level, and hence lacks the objectivity of a quantitative approach. These factors emphasize the need for intensive research to render stress echocardiographic analysis more objective. Automatic boundary detection of left ventricular endocardium, color-Doppler-based tissue imaging and three-dimensional reconstruction offer interesting perspectives in rendering the subjective more objective.

Adenosine↗
PubMed1994

The effect of LDL apheresis on progression of coronary artery disease in patients with familial hypercholesterolemia. Results of a multicenter LDL apheresis study.

This study investigated the effect of extracorporal lipid-lowering therapy by low-density lipoprotein (LDL) apheresis on coronary artery disease in a population characterized by early development and rapid progression of atherosclerosis. We treated 32 patients aged between 15 and 63 years with drug-refractory familial hypercholesterolemia, treated once a week by immuno-specific LDL apheresis for 3 years in a controlled prospective and non-randomized trial; 25 patients (14 females and 11 males) completed the study. Noninvasive data were obtained by physical examination, 12-lead ECG and exercise testing. Invasive cardiological data were obtained by cardiac catheterization according to a standardized protocol in four cardiological centers. Left ventricular ejection fraction was calculated using planimetry. Coronary stenoses were measured quantitatively in 23 defined coronary segments by a panel of four investigators with an electronic digital caliper. In addition, overall coronary atherosclerosis was visually qualified. Final decisions on a classification into one of three groups (regression, no change, progression) of coronary atherosclerosis were based on panel consensus. Six cardiac events occurred throughout the study: percutaneous transluminal coronary angioplasty in one patient, coronary bypass grafting in three and two deaths. Statistical analysis of exercise testing yielded no significant change for maximum power and work capacity during the study period. Hemodynamic data revealed no significant change; mean ejection fraction was calculated as 65.8 +/- 15.9% at study entry and 67.0 +/- 12.7% at completion. Quantitative measurement of 111 circumscribed coronary stenoses showed a mean stenosis degree of 45 +/- 26% at entry cineangio-film and 43 +/- 22% at final cineangio-film demonstrating no significant change.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1994

Effects of urea on K+ fluxes and cell volume in perfused rat liver.

Exposure of the perfused rat liver to a perfusate made hyperosmotic by the presence of 200 mmol l-1 glucose led, as expected, to marked, transient hepatocellular shrinkage followed by volume-regulatory net K+ uptake. However, even after this volume-regulatory K+ uptake had ceased, the liver cells are still slightly shrunken. Withdrawal of glucose from the perfusate resulted in marked transient cell swelling, net K+ release from the liver and restoration of cell volume. However, when the Krebs-Henseleit perfusate was made hyperosmotic by the presence of urea (20-300 mM), there was no immediate decrease in liver mass, yet a slight and persistent cell shrinkage developing 2 min after the onset of exposure to urea. Surprisingly, urea induced concentration-dependent net K+ efflux from the liver and removal of urea net K+ reuptake from the inflowing perfusate. The urea (200 mM)-induced net K+ release resembled that observed following a lowering of the influent [NaCl]: making the perfusate hypoosmotic (245 mosmol l-1, by reducing influent [NaCl] by 30 mM) gave roughly the same K+ response as hyperosmotic exposure (505 mosmol/l) resulting from the presence of 200 mM urea. The urea-induced K+ efflux was not inhibited in the presence of ouabain (1 mM), or in Ca(++)-free perfusion, but was modified in the presence of quinidine (1 mM) or Ba++ (1 mM). The direction in which the liver was perfused had no effect on the urea-induced net K+ release.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗