Search PubMed⌕ Search

Biomedical subjects

L Seipel

Publications and source records attributed to L Seipel.

At least 127 records · Page 7Linked to original sources
PubMed1988

[Cardiac side effects of anti-arrhythmia agents].

Antiarrhythmic drugs have typical cardiac side effects. These effects are due to their electrophysiological action on the one hand and to the negative inotropy on the other. These electrophysiological effects can cause a depression of sinus node function and/or AV conduction leading to severe bradycardia or asystole. However, the proarrhythmic effects of these drugs are clinically more important, especially the induction of ventricular tachycardia and "torsades". The incidence of these proarrhythmic effects is at least 5% of all patients treated. Patients with reduced ventricular function, "malignant" ventricular arrhythmias, and QT prolongation are especially endangered. Proarrhythmic effects may occur after the first dose. However, in most instances the risk is increased with higher dosage. The hemodynamic effects of antiarrhythmic drugs are especially important in patients with reduced cardiac function. The negative inotropy of antiarrhythmic drugs is often counterbalanced by the simultaneous decrease in blood pressure leading to an afterload reduction. Antiarrhythmic drugs causing an increase in systemic resistance may have a more pronounced depressive effect on cardiac function. However, if the acute treatment of severely ill patients in the CCU is excluded, the negative inotropy of antiarrhythmic drugs is not such an important problem as the proarrhythmic effect. As a consequence, antiarrhythmic treatment should be restricted to severely symptomatic patients on the one hand and to those with arrhythmias of prognostic importance on the other. In addition, the patient's treatment should be carefully controlled, especially during the early phase of treatment with antiarrhythmic drugs.

Anti-Arrhythmia Agents↗
PubMed1988

[Experimental studies of the hemodynamics of disopyramide in comparison with quinidine].

The haemodynamic effects of quinidine and disopyramide i.v. were investigated in 79 rats. Measurements were performed in the intact circulation (LVP, AoP, dp/dtmax). Myocardial function was examined independently of circulatory changes by isovolumetric registrations (peak LVP). Animals with NaCl infusion served as controls. After infusion of 5 mg/kg (10 mg/kg) quinidine, we obtained a reduction (p less than 0.05) in the left ventricular pressure to 81.6 +/- 3.1% (82.6 +/- 3.7%), in the mean aortic pressure to 70.7 +/- 3.4% (79.3 +/- 6.7%), in dp/dtmax to 73.9 +/- 5.6% (72.8 +/- 6.2%), and in the heart rate to 69.7 +/- 7.4% (69.9 +/- 5.4%). Isovolumic pressure maxima after quinidine were not different from the controls (90.7 +/- 2.4% and 93.6 +/- 1.5% respectively vs. 96.1 +/- 1.0%). 1 mg/kg disopyramide caused no significant haemodynamic changes. 2 mg/kg disopyramide led to a slight increase in dp/dtmax (107.2 +/- 5.6%, N.S.), while 4 mg/kg disopyramide had a tendency to reduce the left ventricular pressure (88.5 +/- 6.2%), mean aortic pressure (80.5 +/- 14.8%) and dp/dtmax (75.1 +/- 8.0%). After 4 mg/kg disopyramide, the isovolumic maxima were reduced. Our results indicate that the haemodynamic side effects of class-I antiarrhythmic drugs are different. Quinidine i.v. caused a reduction in pressures and heart rate, but had no influence on the isovolumic pressure maxima. Disopyramide i.v., on the other hand, had no significant haemodynamic effects in clinical doses. After high (not clinically used) doses of disopyramide (4 mg/kg), which also led to high plasma levels, myocardial performance was depressed.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

[Phenotypic heterogeneity of cardiac myxomas].

Histogenesis of cardiac myxoma is still unclear. Beside endothelial cells a variety of different cell types were detected in this benign cardiac tumor. Cryostat sections of four myxomas were analysed in the indirect immunoperoxidase technique using monoclonal antibodies (MoABs) directed against MHC class I and II antigens, as well as different surface determinants specific for endothelial cells or monocytes/macrophages. Tumor cells forming cell clusters and blood vessel like structures differed in their expression of endothelial antigens suggesting cellular heterogeneity within single and different myxomas. Like in fetal cardiac tissue vascular channels rarely carried HLA-class II antigens. Tumor cells carrying antigens of monocytes/macrophages, as well as intracellular alkaline phosphatase of endothelial cells could represent subpopulations of an early differentiation stage. This analysis further supports previous hypothesis of an endothelial origin of myxomas.

Adult↗
PubMed1987

[Digitalis therapy in medical practice. Research on indications and dosage criteria in general practice].

Two hundred digitalized patients under nine freely practising physicians were investigated. One hundred and ninety-six patients received digoxin or one of its derivatives. Of these, 50% did not have therapeutic serum glycoside concentrations, 48% were in the mostly subtherapeutic range and 2% were in the potentially toxic range. Signs of glycoside intoxication were not found. A substantiated indication for glycoside therapy was found in the final analysis in 55% of the patients. In 128 patients, the methyldigoxin dose calculated (0.16 +/- 0.030 mg/d) was markedly in excess of that actually prescribed (0.13 +/- 0.050 mg/d; p less than 0.001), so that there were indications of a general underdigitalization. In addition, it was not possible to anchor the restrictive kidney function as a reason for reduction of digoxin dosage in the prescription behavior. In the long run, only 36% of the patients with justified indication and therapeutic serum glycoside concentration as well as (with reservations) the 3% with potentially toxic serum glycoside concentration profited from the glycoside therapy.

Atrial Fibrillation↗
PubMed1987

[Percutaneous transluminal coronary angioplasty and aortocoronary bypass surgery in unstable angina pectoris and coronary multivessel disease].

In 113 patients demonstrating the clinical syndrome of unstable angina, acute-stage coronary angiography revealed multivessel disease. Acute PTCA of the ischaemia-related coronary artery or bypass grafting was performed depending on angiographic criteria. Of the total of 68 patients in whom PTCA was performed, 45 had two-vessel disease (2 vd) and 23 three-vessel disease (3 vd). 12 of the 45 patients with bypass operation had a left main stem stenosis, whereas 33 had three-vessel disease. The primary success rate of PTCA was 81%, 89% in patients with 2 vd and 70% in patients with 3 vd. Acute post-PTCA bypass grafting was necessary in 2 patients having 2 vd and in 5 patients suffering from 3 vd. 5 of the 68 patients treated with PTCA developed a transmural myocardial infarct and one patient died after PTCA and emergency bypass surgery. 8 of the 45 operated patients had a perioperative or postoperative myocardial infarct and 5 patients died intraoperatively or postoperatively. The overall morbidity was 11.5%, and the mortality of hospitalised patients was 5.3% (6/113). Combination of PTCA with emergency bypass grafting offers a new and effective treatment with an acceptable risk even in multivessel disease patients and in those having unstable angina pectoris. The additional use of PTCA definitely improves therapeutic management in this high-risk population.

Angina Pectoris↗
PubMed1987

Phosphocreatine and adenine nucleotides in postasphyxial hearts with normal basal function and normal oxygen demand.

We investigated whether there is a relationship between the prolonged dysfunction after myocardial ischaemia and the postischaemic phosphocreatine overshoot phenomenon. In 16 open-chest rats 3 periods of 4 minutes of oxygen deficiency were performed and basal haemodynamic variables and the myocardial oxygen demand were determined during the recovery period. At the end of the 20 minutes recovery period, left ventricular pressure, dp/dtmax, ejection fraction, and myocardial oxygen demand were completely recovered. High energy phosphate levels, however, were still altered. The sum of adeninenucleotides was decreased to 78 +/- 4% of control (mean +/- SEM, p less than 0.05). The level of phosphocreatine was markedly elevated to 162 +/- 14 (mean +/- SEM). The persistence of the phosphocreatine overshoot phenomenon, while basal function was already normalized, indicates that a reduced function and thus a reduced energy demand of the contractile apparatus are not the cause of the phosphocreatine overshoot. We found no close relationship between high energy levels and basal function or oxygen demand in myocardium after mild oxygen deficiency.

Adenine Nucleotides↗
PubMed1987

Changes in haemodynamics and left ventricular function during intravenous nifedipine infusion with and without additional propranolol in patients with coronary artery disease. A randomized, placebo controlled trial.

The haemodynamic effects of a combined intravenous treatment of nifedipine and propranolol in ten patients with coronary artery disease compared to a single treatment with nifedipine or placebo were investigated. Nifedipine infusion resulted in a reduction of left ventricular (LV) afterload and LV volumes with an increase in heart rate and EF and no change of the double product, coronary sinus flow, LV diastolic parameters and dp/dtmax. Addition of propranolol lowers myocardial oxygen demand by reducing heart rate and dp/dtmax together with a sustained afterload reduction with no change in LV volumes and EF. The vasodilatatory action of nifedipine pretreatment balanced the negative effects of acute beta-receptor blockade on LV function and allows the reduction of myocardial oxygen demand without a deterioration of LV function.

Angiography↗
PubMed1987

Influence of sampling site and flow area on cardiac output measurements by Doppler echocardiography.

In 40 patients cardiac output was simultaneously determined by pulsed Doppler echocardiography and thermodilution (range 4.0 to 10.2 liters/min). The sample volume was located in the center of the mitral anulus, at the tips of the mitral leaflets and in the center of the aortic anulus. Circular cross-sectional areas of the mitral anulus, aortic anulus and aortic bulbus were calculated from M-mode and two-dimensional echocardiographic diameters. The varying short axis of the elliptical mitral opening area was obtained from the diastolic leaflet separation in the M-mode, and the long axis was derived from the maximal mitral orifice area or mitral anulus diameter. Cardiac output was calculated by multiplying time-velocity integrals with the different areas and heart rate. Doppler flow measurements correlated significantly with the thermodilution method (r = 0.79 to 0.93). Flow measurements at the aortic anulus were most accurate (r = 0.93, SEE = 0.589 liter/min) if the annular area was derived from the M-mode tracing. Measurement of the anulus in the apical five chamber view yielded a significant underestimation and the area of the aortic bulbus provided an overestimation of cardiac output. Left ventricular inflow was underestimated at the mitral leaflet tips and overestimated at the mitral anulus. The accuracy of pulsed Doppler cardiac output measurements strongly depends on the assumed flow area and sampling site. Both should be determined at the same level in the inflow or outflow tract of the left ventricle. Measurement of cardiac output in the center of the aortic anulus provided the highest accuracy.

Adolescent↗
PubMed1987

Myocardial and circulatory effects of inosine.

The action of inosine (2.5, 5, or 10 mg.kg-1.min-1 iv) was investigated in open chest rats (n = 46) and guinea pigs (n = 16). Left ventricular and aortic pressures, dP/dtmax, and stroke volume were measured. Additionally, isovolumic peak pressure and peak dP/dtmax were measured during short occlusions of the aorta for assessing myocardial performance independent of circulatory changes. In rats inosine caused a dose dependent decrease in dP/dtmax (-5%, -21%, -40% of preinfusion values), heart rate (-7%, -23%, -55%), and mean aortic pressure. Additionally, a subgroup of seven rats was paced at their initial preinfusion heart rate, but independently from the heart rate there was a reduction in dP/dtmax (-15%). The isovolumic measurements confirmed the negative inotropic effect of inosine in rats. Peak dP/dtmax was reduced to 85% of preinfusion values with a dose of 2.5 mg.kg-1 min-1 (to 70% of preinfusion values with 10 mg.kg-1.min-1). Similarly, the maximum isovolumic pressure for a defined filling volume was decreased by 30 mmHg (at 350 microliter; 5 mg.kg-1.min-1; p less than 0.05). The mean aortic pressure decreased with 2.5 mg.kg-1.min-1 inosine indicating vasodilative properties. In contrast to the significant effects in rats even 10 mg.kg-1.min-1 inosine did not have an effect on heart rate, mean aortic pressure, or dP/dtmax in guinea pigs. The isovolumic peak left ventricular pressure in guinea pigs was also unchanged after inosine infusion. Thus the haemodynamic effects of inosine were species dependent.

Animals↗
PubMed1987

Diagnosis and quantification of aortic regurgitation by pulsed Doppler echocardiography in patients with mitral valve disease.

UNLABELLED: To test the ability of pulsed Doppler echocardiography (PDE) to detect and quantify aortic regurgitation (AR), 55 consecutive patients (14-74 years) with aortic and mitral valve disease were examined clinically and by echocardiography before cardiac catheterisation. The severity of AR was determined angiographically (I-IV) and compared to the extent of the regurgitant jet in the left ventricle measured by PDE. In 13 of 55 patients (3 with mitral stenosis, 3 with mitral incompetence, 3 with combined mitral lesions, 3 with aortic stenosis, one with aortic and mitral stenosis) neither angiography nor PDE showed AR (specificity 100%). Apart from 3 patients with poor echo quality PDE correctly detected AR in 39 of 42 patients (sensitivity 93%). Clinical examination (62%), mode M.mode (62%) and both methods combined (81%) were significantly less sensitive than PDE, especially in mild AR (P less than 0.008). The PDE degree of AR closely correlated with angiography (corrected contingency coefficient 0.91). Differentiation between AR III and IV was not possible. Mitral valve disease did not affect quantification of AR (n = 20 patients). CONCLUSIONS: Pulsed Doppler echocardiography is better than auscultation and M-mode echocardiography in the diagnosis of aortic regurgitation, especially in grades I and II. PDE can reliably discriminate between three degrees of aortic regurgitation (I-III). Mitral valve disease does not affect quantification of aortic regurgitation by PDE.

Adolescent↗
PubMed1987

Negative inotropic effect of class-I-antiarrhythmic drugs: comparison of flecainide with disopyramide and quinidine.

An important side-effect of antiarrhythmic drugs is their negative inotropic action. To investigate this after i.v. administration we compared the newer class-I-antiarrhythmic drug flecainide (2 mg, 4 mg and 8 mg kg-1) with disopyramide (1 mg, 4 mg and 8 mg kg-1), quinidine (5 mg and 10 mg kg-1) and saline (controls). Isovolumic measurements of ventricular function by short aortic crossclamping were performed in 82 open-chest rats and peak left ventricular isovolumic pressure (LVSP) and peak isovolumic dp/dt max were determined 5 and 15 minutes after intravenous drug injection. All drugs decreased isovolumic indices of myocardial function dose-dependently. Flecainide reduced peak isovolumic LVSP and dp/dt max only after 8 mg kg-1 (to 85 +/- 3% and 45 +/- 5%, resp., means +/- SE, P less than 0.01), 2 mg kg-1 and 4 mg kg-1 had no significant effect. Disopyramide influenced myocardial function already at 4 mg kg-1 (peak LVSP 88 +/- 4%, P less than 0.05, peak dp/dt max 64 +/- 7%, P less than 0.01, means +/- SE), 8 mg kg-1 had an even more marked depressive effect (peak LVSP 81 +/- 4%, peak dp/dt max 50 +/- 8%, means +/- SE, P less than 0.01). 5 mg kg-1 and 10 mg kg-1 quinidine both decreased peak LVSP and peak dp/dt max (91 +/- 3% and 92 +/- 1%, resp., and 80 +/- 5% and 74 +/- 6% means +/- SE, P less than 0.05). Thus, disopyramide had the most marked negative inotropic potential of the investigated class-I-antiarrhythmic drugs.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

[Clinical value of Doppler echocardiography in the determination of shunt size in atrial septal defect of adult patients].

The purpose of this study was to assess the clinical utility of pulsed Doppler echocardiography in the determination of shunt flow magnitude in adults with an atrial septal defect. Therefore, in 24 unselected, consecutive adult patients with an ostium-secundum type atrial septal defect, and in 16 patients without heart disease, Doppler echocardiography was performed to measure blood flow in the right and left ventricular outflow tract. In eight patients with an atrial septal defect, pulmonary flow measurement was impossible because of pulmonary insufficiency or poor visualization of the pulmonary annulus. The ratio between the pulmonary (Qp) and systemic blood flow (Qs) was between 0.83 and 1.13 in the control group and between 1.31 and 4.46 in patients with an atrial septal defect. In the control group the correlation between Qs and Qp was r = 0.96 (SEE = 0.417 l/min, y = 1.05x - 0.21). The correlation between Qp/Qs, determined by oximetry and pulsed Doppler echocardiography in patients with an atrial septal defect, was significant (r = 0.82, SEE = 0.54). Systematic differences between invasive and non-invasive shunt calculations did not occur. Thus, pulsed Doppler echocardiography is clinically useful in the determination of shunt flow magnitude in about two thirds of adult patients with an atrial septal defect and provides precise information for the decision for conservative or operative treatment.

Adult↗
PubMed1987

[Comparison of Doppler echocardiographic methods of determining cardiac minute volume].

In 40 patients without valvular disease, cardiac output was determined by pulsed Doppler echocardiography and thermodilution simultaneously. The sample volume was located in the center of the mitral valve ring, at the tips of the mitral leaflets and in the left ventricular outflow tract, directly proximal to the aortic valve leaflets. Circular cross-sectional areas of the mitral valve ring, aortic ring and bulbus of the aorta were calculated from the M-mode and two dimensional echocardiographic diameters. The mitral orifice was assumed to be an ellipse with varying short axes, determined as the mean diastolic leaflet separation in the M-mode and a constant long axis, derived from the maximal mitral orifice area or mitral ring diameter. Cardiac output was calculated by multiplying time-velocity integrals with different areas and heart rate. Cardiac output, measured by the thermodilution technique, ranged from 4.0 l/min to 10.2 l/min. Cardiac output determined by the different Doppler methods correlated significantly with the thermodilution measurements. Cardiac output measurements in the left ventricular outflow tract provided the best correlation coefficient (0.93) and a standard error of the estimate of 0.589 l/min, when the circular flow area was derived from the M-mode echo of the aortic ring.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1986

[Biatrial myxomas--a diagnostic challenge].

Like isolated cardiac myxoma, biatrial myxoma may manifest itself only by extracardiac symptoms over a prolonged period. A 24-year-old patient presented over seven years a history of repeated arthalgia with concomitant anaemia, elevated blood sedimentation rate, positive antistreptolysin test and electrophoretic signs of inflammation. A discrete systolic sound on auscultation gave rise to an echocardiographic examination which revealed a biatrial myxoma.

Adult↗
PubMed1986

Treatment of non anti-GBM-antibody mediated, rapidly progressive glomerulonephritis by plasmapheresis and immunosuppression.

A retrospective study was conducted to evaluate the efficacy of plasmapheresis in combination with different immunosuppressive drugs ("pulse" therapy, azathioprine or cyclophosphamide together with steroids) in nine patients presenting with rapidly progressive glomerulonephritis (RPGN) not mediated by antibody to glomerular basement membrane. Six of these patients had to be initially dialysed. All patients underwent renal biopsy, which revealed that seven patients had a minimum of 80% crescents and five had interstitial fibrosis. Recovery of renal function was observed in seven patients (78%). All patients without interstitial fibrosis were recompensated for at least 14 months after the acute onset of RPGN. Those who presented with interstitial fibrosis declined to endstage renal failure after 13 months requiring chronic hemodialysis treatment or cadaveric kidney transplantation. On the basis of these findings interstitial fibrosis seems to be a limiting factor for the prognosis of non-anti-GBM-antibody mediated RPGN.

Adult↗
PubMed1986

[Modification of hemodynamics by intravenous administration of flecainide].

We investigated the influence of the new class-I antiarrhythmic drug flecainide on myocardial performance and hemodynamic parameters in Wistar rats (2 mg, 4 mg, 8 mg flecainide/kg). Left ventricular and aortic pressures, dp/dt max, cardiac output and additionally isovolumic left ventricular maxima curves were registered 5 min and 15 min after flecainide (n = 28) or saline (controls; n = 12) i.v. infusion (7 min). 2 mg and 4 mg flecainide/kg had no significant effect on isovolumic indices. 5 min after infusion of 8 mg flecainide/kg peak isovolumic left ventricular pressure was reduced by 84.9 +/- 2.6% vs. 95.6 +/- 1.1% (NaCl), mean +/- SEM (p less than 0.01) and peak isovolumic dp/dt max by 44.5 +/- 4.5% vs. 91.5 +/- 3.6% (NaCl), mean +/- SEM (p less than 0.01). Flecainide caused a significant reduction of heart rate (81.9 +/- 4.7%, 2 mg flecainide/kg vs. 95.4 + 2.5% (NaCl), an AV-block occurred only after administration of 8 mg/kg. Mean aortic pressure was decreased after 4 mg and 8 mg flecainide/kg. 8 mg flecainide/kg significantly reduced the cardiac output (73.1 +/- 7.7%, p less than 0.05). 15 min after 2 mg and 4 mg flecainide/kg infusion the determined parameters were normalized, only a dose of 8 mg/kg caused a prolonged hemodynamic depression. Our results demonstrate that in clinically used dosages no hemodynamic side-effects are detectable. A significant reduction of isovolumic indices of myocardial performance occurs only after infusion of 8 mg flecainide/kg. A transfer of laboratory experiments to the clinical situation is only possible with limitations, but our data might indicate that the myocardial and hemodynamic side-effects of flecainide are relatively small at therapeutic dosages.

Animals↗