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Biomedical subjects

L Bruch

Publications and source records attributed to L Bruch.

At least 19 recordsLinked to original sources
PubMed2003

[Structure of the Australian system of 'Diagnosis Related Groups' regarding cardiovascular diseases and corresponding cost weights in Germany].

BACKGROUND: An adapted system of 'Diagnosis Related Groups' (DRG's) will be introduced for Germany at the beginning of 2003. This article focuses on the structure of the Australian DRG system (AR-DRG 4.1) regarding the diseases of the cardiovascular system and corresponding cost weights in Germany (G-DRG 1.0). METHODS: Cardiac diagnoses, procedures and cost weights (with a different base rate) were compared between the Australian and German DRG's. RESULTS: Categories and procedures for diagnostics and therapies are shown regarding coronary interventions, electrophysiological strategies including implantation of pacemakers and cardioverter/ defibrillators, hybrid treatment modalities, transcatheter closure of interatrial/-ventricular communications as well as interventions during intensive care treatment.

Angioplasty, Balloon, Coronary↗
PubMed2001

Neuropathological correlates of dysarthria in progressive supranuclear palsy.

BACKGROUND: The dysarthria of progressive supranuclear palsy consists of prominent hypokinetic and spastic components with less prominent ataxic components. OBJECTIVE: To correlate the types of dysarthria with neuropathological changes in patients with progressive supranuclear palsy. DESIGN AND METHODS: In 14 patients with progressive supranuclear palsy, we correlated the perceptual speech findings with the neuropathological findings. A dysarthria assessment was performed a mean +/- SD of 31 +/- 15 months (range, 10-53 months) before death. The deviant speech dimensions were rated on a scale of 0 (normal) to 3 (severe). The neuropathological examination consisted of semiquantitative analysis of neuronal loss and gliosis by investigators (A.A.F.S., and L.A.B.) blinded to the clinical findings. Correlation and linear regression analysis were used to correlate the severity of the hypokinetic, spastic, and ataxic components with the degree of neuronal loss and gliosis in predetermined anatomical sites. RESULTS: All patients had hypokinetic and spastic dysarthria, and 9 also had ataxic components. The severity of the hypokinetic components was significantly correlated with the degree of neuronal loss and gliosis in the substantia nigra pars compacta (r = 0.61, P =.02) and pars reticulata (r = 0.64, P =.01) but not in the subthalamic nucleus (r = 0.51, P =.07) or the striatum or globus pallidus (/r/<0.34, P>.20). The severity of the spastic and ataxic components was not significantly correlated with the neuropathological changes in the frontal cortex (r = 0.20, P =.50) and cerebellum (/r/<0.28, P>.33), respectively. CONCLUSION: The hypokinetic dysarthria of progressive supranuclear palsy may result from degenerative changes in the substantia nigra pars compacta and pars reticulata and not from changes in the striatum or globus pallidus.

Aged↗
PubMed2001

Transcatheter closure of muscular ventricular septal defects in two patients after myocardial infarction.

Acquired muscular ventricular septal defects (MVSD) after myocardial infarction (MI) can lead to right heart failure and cardiogenic shock with high mortality. Early surgical therapy is often difficult to perform but can reduce the mortality. The closure of congenital septal defects is performed with high safety. Therefore, the interventional closure of an acquired post-MI VSD might be feasible and of potential benefit. To date, experiences with closure of post-MI MVSDs are minimal. We report on two patients with post-MI VSD.

Aged↗
PubMed2000

Effects of iloprost inhalation on exercise capacity and ventilatory efficiency in patients with primary pulmonary hypertension.

BACKGROUND: The continuous infusion of prostacyclin has been shown to improve exercise capacity and survival in patients with primary pulmonary hypertension (PPH). Inhalation of iloprost, a stable analog of prostacyclin, might be an alternative therapy for PPH, selectively acting on the pulmonary vascular bed through ventilation-matched alveolar deposition of the drug. We investigated the short-term effects of iloprost inhalation on exercise capacity and gas exchange in patients with PPH. METHODS AND RESULTS: In 11 patients with PPH, we performed 2 consecutive cardiopulmonary exercise tests before and after the inhalation of 17 microgram of iloprost. Patients had marked pulmonary hypertension (mean pulmonary artery pressure 65 mm Hg), and inhalation resulted in a decrease in pulmonary vascular resistance (1509 versus 1175 dyne. s(-1). cm(-5), P<0.05). Arterial blood gases remained unchanged (PaO(2) 69.3 versus 66.8 mm Hg; PaCO(2) 29.6 versus 28.8 mm Hg). Iloprost significantly (P<0.05) improved exercise duration (379 versus 438 seconds), peak oxygen uptake (12.8 versus 14.2 mL. kg(-1). min(-1)), VE-versus-V CO(2) slope (58 versus 51.4). CONCLUSIONS: The present data show that iloprost inhalation exerts pulmonary vasodilatation and improves symptoms and exercise capacity in patients with PPH. The data also suggest that iloprost inhalation is a suitable treatment for PPH. Whether these effects are maintained during long-term treatment and are paralleled by improvement in prognosis remains to be determined.

Administration, Inhalation↗
PubMed2000

Relationship between impaired pulmonary diffusion and cardiopulmonary exercise capacity after heart transplantation.

STUDY OBJECTIVES: Diffusion impairment and reduced performance in cardiopulmonary exercise testing (CPX) have been found in patients after heart transplantation. The pathogenesis of these abnormalities is unclear. In particular, the contribution of pulmonary interstitial changes has not yet been verified. DESIGN: We analyzed pulmonary function tests, high-resolution CT (HRCT), echocardiography, left heart catheterization, and CPX in transplanted patients. PATIENTS: Forty long-term survivors were studied at a median of 47 months (range, 12 to 89 months) after heart transplantation. RESULTS: Diffusion was impaired in 40% (transfer factor for carbon monoxide) or 82.5% (carbon monoxide transfer coefficient) of the patients. Diffusion impairment was caused by a decreased diffusing capacity of the alveolar capillary membrane in 89% and/or by a decreased blood volume of the alveolar capillaries in 46% of cases. In five patients (12.5%), CT revealed interstitial lung changes. These patients did not have different values of diffusion capacity. Maximal oxygen uptake and ventilatory efficiency during exercise (minute ventilation/carbon dioxide output slope) were impaired in 92% and 46% of the cases, respectively. CONCLUSIONS: Our data show that the diffusion abnormalities are caused by an impaired diffusion status of the alveolar capillary membrane. Interstitial changes detectable in HRCT were found not to be involved in this process. The reduced performance in CPX in our long-term survivors is caused by pulmonary perfusion abnormalities and low tidal volume, which is due to the deconditioning of respiratory muscle, rather than by interstitial changes or diffusion abnormalities.

Adult↗
PubMed2000

Comparison of the relaxation effect in vitro of nitroglycerin vs. fenoterol on human myometrial strips.

AIMS: Substance dose-related comparison of relaxation effect of nitroglycerin (GTN) and the beta 2-mimetic substance fenoterol in human myometrial tissue. METHODS: Test criterion is the isometric force development of isolated human myometrial strips. These muscle strips were removed from the lower uterine segment at cesarean section. Fenoterol in concentrations of 3 x 10(-8)-10(-5) mol/l or GTN in concentrations of 1.7 x 10(-8)-5.8 x 10(-4) mol/l were applied to the 2 x 2 x 10-mm strips, which were fixed and maintained in tissue baths. The curves were plotted on line. The integral or the "area under the curve" (AUC) served as the parameter for muscle strip activity. RESULTS: A total of 100 strips from 20 patients were used. GTN demonstrated a significant relaxation effect in the in vitro model on human myometrial strips from pregnant women already treated with oxytocin. The effect was able to be enhanced to a point where oxytocin-induced contractions were completely absent. A relatively clear connection was demonstrated between dose and effect whereby increased muscle relaxation resulted at increased concentrations. Compared to GTN application, muscle strip relaxation was less pronounced under fenoterol; a complete inhibition of myometrial activity was not achieved under fenoterol. CONCLUSIONS: With respect to relaxation of the myometrial tissue samples the NO donor GTN is at least as potent as the standard tocolytic agent fenoterol in the in vitro model.

Adrenergic beta-Agonists↗
PubMed1999

Pulmonary artery stenosis 5 years after single lung transplantation in primary pulmonary hypertension.

This is a case report about a 56-year-old female patient with primary pulmonary hypertension who underwent single, right lung transplantation. Five years postoperatively she developed signs of right heart failure. History and physical examination suggested pulmonary artery stenosis. Diagnosis was confirmed by pulmonary angiography. Percutaneous placement of a balloon expandable stent normalized pulmonary artery pressure.

Blood Pressure↗
PubMed1998

Pituitary adenylate cyclase activating peptides relax human pulmonary arteries by opening of KATP and KCa channels.

BACKGROUND: Pituitary adenylate cyclase activating peptides (PACAPs) are potent endothelium independent dilators of human coronary arteries; however, their effects on human pulmonary arteries are unknown. METHODS: The vasorelaxant effects of PACAP27 on human pulmonary segmental arteries were studied and the specific potassium (K+) channel regulatory mechanisms in the vasorelaxant effects were tested by means of isometric contraction experiments. RESULTS: PACAP27 produced dose dependent relaxations of 10 microM rings preconstricted with prostaglandin F2 alpha (PGF2 alpha) with half maximal relaxation (IC50) at 17 nM. Pretreatment of the vessels with the ATP sensitive K+ (KATP) channel blocker glibenclamide (1 microM) or with the Ca2+ activated K+ (KCa) channel blocker iberiotoxin (100 nM) inhibited the PACAP27 induced relaxation. CONCLUSIONS: These results provide evidence that PACAPs are potent vasodilators of human pulmonary arteries and that this relaxation might be mediated by opening of KATP and KCa channels.

Analysis of Variance↗
PubMed1995

Effects of prostaglandin E1, prostaglandin E0 and SPM 206 on isolated human coronary arteries.

The effects of PGE1, PGE0 and the stable PGE1-analogue SPM 206 on human epicardial coronary arteries were studied in vitro. The tension of the isolated arterial rings was measured isometrically. After precontraction, concentration-response curves with the compounds were performed. PGE1 and SPM 206 elicited concentration-dependent relaxations which are counteracted by a contractile action in higher concentrations. In PGE0, the contractile action occurred even in lower concentrations. This contraction was antagonized by the selective thromboxane A2 antagonist SQ 29,548, resulting in an equipotent relaxation for all three compounds.

Alprostadil↗
PubMed1995

Pituitary adenylate cyclase activating peptides are endothelium-independent dilators of human and porcine coronary arteries.

The PACAPs have been shown to be potent vasodilators in different animal species. Data in humans are still lacking. Therefore we investigated the effects of PACAP 38, PACAP 27 and VIP on isolated human and porcine coronary arteries (HCA and PCA). Our data show, that the PACAPs are endothelium-independent vasorelaxants, which in HCA are slightly more potent than VIP. The N-terminal shortened peptides PACAP 6-38 and PACAP 6-27 also show relatively potent vasorelaxant effects, acting as partial agonists. Glibenclamide, a selective inhibitor of ATP-sensitive potassium channels, partially reverses the effects of the PACAPs, indicating an involvement of these channels in the mechanism of action.

Animals↗
PubMed1994

Acute influence of beta-adrenergic antagonists on left ventricular diastolic function: contrasting results after administration of celiprolol and metoprolol.

Various beta-adrenergic receptor antagonists have different effects on myocardial function. A clinical study was performed in 30 patients with symptomatic coronary artery disease and systemic hypertension to compare the effects of single intravenous doses of 0.15 mg/kg celiprolol (n = 16) (third generation beta-blocking agent) and metoprolol (n = 14) (second generation) on left ventricular diastolic function. Parameters derived from pressure, volume, flow, time intervals and their combination were used to characterise diastolic function. After celiprolol administration, parameters of diastolic myocardial function improve (dp/dtip-; relaxation time constant T1, peak filling rate PFR; first-third filling rate FF1/3 or diastolic wall stress-time integral Sigdiasc) or remain unchanged. In contrast, after metoprolol administration parameters of diastolic function seem to be deteriorated (dp/dtip-, T1; Sigdiasc). This indicates an improvement in myocardial relaxation and filling under the influence of celiprolol but not under metoprolol. The left shift of the pressure-volume loops after celiprolol (n = 13), in contrast to metoprolol, supports this interpretation. Celiprolol did not show any deterioration of diastolic function in patients with coronary heart disease and arterial hypertension under these acute conditions.

Adrenergic beta-Antagonists↗
PubMed1993

Diastolic heart function--pathophysiology, characterization, and therapeutic approaches.

In recent years diastolic cardiac function has attracted increasing attention since parameters of diastolic function were found to be altered earlier or more specifically than parameters of systolic function. Diastolic cardiac function is determined by both active (muscular relaxation, redistribution of calcium, synchronization, etc.) and passive (myocardial structure, fibrosis, etc.) factors. As a consequence, a comprehensive assessment of diastolic cardiac function cannot be based on one single parameter. For a complete analysis of diastolic function it is necessary to perform invasive diagnostic procedures involving the measurement of atrial and ventricular pressures, as well as the registration of volume changes with a high time resolution. In addition, it is necessary to measure wall thickness and ventricular configuration, so that apart from filling parameters the stress-strain relationship can be obtained. Noninvasive techniques (Doppler echocardiography, radionuclear ventriculography, apexcardiography) may suggest alterations in diastolic function as well. They ought to be complemented by additional diagnostic procedures (pulmonary pressure, stress testing, etc.). Therapy must consider potentially harmful effects on diastolic function parameters, particularly if changes in myocardial oxygen consumption may result (heart rate, parietal wall stress). Calcium antagonists (verapamil, diltiazem, nifedipine), phosphodiesterase inhibitors (milrinone), beta-adrenergic agonists and antagonists with vasodilating effects (e.g., celiprolol) all have beneficial effects on diastolic myocardial function. A range of diastolic function parameters is being reviewed in the following paper. Their role in the estimation of cardiac function and their responsiveness to therapy in hypertrophy, cardiomyopathy, and coronary heart disease is being discussed.

Adrenergic beta-Antagonists↗
PubMed1991

Antiplatelet, antineutrophil and vasodilating properties of 13,14-dihydro-PGE1 (PGE0)--an in vivo metabolite of PGE1 in man.

The actions of the in vivo metabolite of PGE1, 13,14-dihydro-PGE1 (PGE0), on platelet and neutrophil (PMN) function and vessel tone were studied in vitro. PGE0 inhibited aggregation, ATP release and thromboxane generation by human platelets (IC50 10-100 nmoles/l). The compound also inhibited superoxide anion generation and lysosomal enzyme release from human PMN. PGE0 was equipotent to PGE1 in both systems, while 15-keto-PGE1 was ineffective in platelets but produced some inhibition in PMN. These inhibitory effects of PGE0 and PGE1 were paralleled by concentration-dependent increases in cyclic AMP in platelets and PMN. Both compounds were also potent relaxants of several arterial preparations in the rabbit at comparable concentrations. In general, the vasorelaxing properties of PGE0 were somewhat lower and the contractile effects somewhat stronger in comparison to PGE1. These data demonstrate a significant and concentration-dependent inhibition of receptor-mediated activation of human platelets and PMN by PGE0. The molar potency of the compound is comparable to that of PGE1. Generation of PGE0 from infused PGE1 may contribute to the clinical efficacy of PGE1 in treatment of severe peripheral arterial occlusive disease.

Alprostadil↗
PubMed1991

[The pharmacology of 13,14-dihydro-PGE1 in comparison with PGE1].

This study investigates the effects of 13,14-Dihydro-PGE1 (PGE0) in comparison to PGE1 on human platelets, human polymorphonuclear granulocytes (PMN) and a number of vessel preparations of different species. The potency of PGE0 in inhibition of platelet and neutrophil activation is similar to PGE1. The vascular action differs. At a comparable molar potency, PGE0 showed stronger contractile and less relaxing effects than PGE1. The biological activities of PGE0 may contribute to the in vivo effects of PGE1 in treatment of peripheral arterial occlusive disease, in particular at high-dose i.v. administration.

Alprostadil↗
PubMed1990

[Determination of pressure-volume relations from ventriculographs using catheter tip manometers].

The evaluation of cardiac function alone from pressure and volume data can lead to misinterpretations. By linking of pressure and volume data a variety of new parameters can be calculated. Computer techniques allow the evaluation not only of cardiac work, but also of acceleration work and the efficiency of heart power. As an example of double blind study with CHD patients the measurement of such parameters under invasive diagnostics is demonstrated, facilitating a detailed evaluation of cardiac function.

Adrenergic beta-Antagonists↗
PubMed1990

[Acute changes of coronary and global hemodynamics in patients with angina pectoris and arterial hypertension caused by celiprolol and metoprolol].

In 30 hypertensives with angina pectoris the acute action of beta-blockers Celiprolol and Metoprolol on the global and coronary haemodynamics was tested within cardiac catheter diagnostics. In accordance with no long-term effects Metoprolol acts negatively inotrope, chronotrope as well as pre- and post-load increasing. Celiprolol lowered the pre- and postload, and increased the cardiac output, but did not influence the heart rate. Both medicaments increased coronary flow and myocardiac oxygen consumption. From the mentioned effects important conclusions for therapy with both Beta-blockers can be derived.

Adrenergic beta-Antagonists↗
PubMed1989

[The effect of ionic and nonionic contrast media (amidotrizoate, iopromide) on cardiac function (contractility, relaxation, perfusion)].

In 30 patients the influence of ionic (Amidotrizoate) and non-ionic (Iopromide) contrast agents on the heart parameters contractility, relaxation, perfusion and the rate of extrasystoles was investigated. They were significantly less influenced by Iopromide than by Amidotrizoate. A negative inotropic action was detectable only for Amidotrizoate. It is concluded that non-ionic contrast media should be used especially for critical patients.

Coronary Circulation↗