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Biomedical subjects

B Lüderitz

Publications and source records attributed to B Lüderitz.

At least 361 records · Page 20Linked to original sources
PubMed1987

[Combination of sotalol with the class I B substances mexiletine or tocainide in complex ventricular extrasystole].

In 34 patients with ventricular tachyarrhythmias the effect of the antiarrhythmic therapy of sotalol (160-320 mg p.o.) in combination with the type-I-B-agent mexiletine (600-800 mg p.o.) or tocainide (800-1200 mg p.o.) was studied by Holter monitoring. In all patients 2.2 +/- 1.1 drugs trials had failed, including amiodarone in 8 patients and beta blocking substances in 15 patients. The combination of sotalol with mexiletine or tocainide reduced ventricular ectopic beats by 79% and complex ventricular arrhythmias (pairs and salvoes) by 85%. A significant reduction of ventricular ectopic beats (greater than 80%) was reached in 74% of the patients, of pairs and salvoes (greater than 90%) in 79%. There was no difference in the antiarrhythmic efficacy between the combination of sotalol/mexiletine and sotalol/tocainide. Intervals of the resting ECG or laboratory values did not change significantly. In 5 patients with sotalol/tocainide and 1 patient with sotalol/mexiletine, side effects were observed which necessitated discontinuation of the treatment. The results show that sotalol, in combination with mexiletine or tocainide, has a potent antiarrhythmic effect in patients with otherwise drug-refractory ventricular arrhythmias.

Adult↗
PubMed1987

[Inhibition of flecainide resorption by activated charcoal].

The effect of orally administered activated charcoal on plasma concentrations of flecainide were studied in eight volunteers (24-38 years of age). A single dose of 200 mg flecainide were given at 3 days: control (day 1); simultaneous application of flecainide and 30 g charcoal (day 2); application of 30 g charcoal 90 min after flecainide (day 3). Plasma concentrations were determined by HPLC after 2, 4 and 6 h. Absorption of flecainide was almost completely prevented, when flecainide and charcoal was ingested immediately. When charcoal was taken 90 min after flecainide, the following flecainide plasma levels were found: after 2 h 231 +/- 62 ng/ml (266 +/- 30 ng/ml control; n.s.), after 4 h 199 +/- 49 ng/ml (232 +/- 27 ng/ml control; P less than 0.05) and after 6 h 155 +/- 42 ng/ml (231 +/- 51 ng/ml control; P less than 0.01). Charcoal seems to be effective in prevention of the absorption of flecainide. A drug interaction may occur if charcoal is given therapeutically, for example in hypercholesterolaemia. Charcoal may be indicated as an additional treatment of flecainide intoxication.

Administration, Oral↗
PubMed1987

[Quantifying aortic valve insufficiency by digital subtraction aortography].

The purpose of this study was to assess the contribution of digital subtraction angiography (DSA) to the quantification of aortic valve regurgitation in 21 patients undergoing heart catheterization. The digital image subtraction was used for densitometric evaluation. The regurgitation was derived from the distribution of contrast volumes during diastole in aortic and left ventricular "regions of interest". DSA-measurements were compared with results of conventional cineangiography. Results showed the following correlation between DSA measurements and cineangiographic estimates (grades I-III): regurgitation 1.7-9.8% in grade I (n = 11), 8.9-22.3% in grade II (n = 5), 31.7 and 32.5% in grade II-III (n = 2), 37-42.4% in grade III (n = 3). DSA and digital densitometry seem to be valuable methods for the quantification of regurgitation. Concerning quantitative measurements in left heart catheterization the digital subtraction aortography is superior to conventional cineangiography and will be helpful to characterize patients with aortic regurgitation more completely.

Adult↗
PubMed1987

[Evaluation of aortic valve insufficiency using color Doppler echocardiography].

UNLABELLED: Colour flow mapping Doppler echocardiography is a new, noninvasive method for studying the direction and velocity of blood flow within the cardiac chambers. In order to estimate the sensitivity and specificity of this method in the evaluation of aortic regurgitation, 44 patients were examined consecutively. In 24 patients, aortic valve incompetence was proven by angiography; in 20 patients aortography revealed no regurgitation. Quantification of the severity of aortic insufficiency was performed by grading the amount of colour of the regurgitant flow (grade I-IV) and comparing it with the angiographic data. In 43 out of 44 patients diagnostic images could be obtained with colour flow mapping Doppler echocardiography. With this method aortic insufficiency was detected in all cases (sensitivity 100%). The specificity was 97% (one false positive diagnosis). For quantification of the severity of regurgitation agreement with the angiographic findings was obtained in 18 out of 24 cases. In the remaining 6 patients the difference was one grade. CONCLUSION: Colour flow mapping Doppler echocardiography is an important advance in the noninvasive preoperative diagnostics of aortic incompetence.

Adult↗
PubMed1987

[Fungal endocarditis of the tricuspid valve in Crohn disease].

In a 59-year-old patient with Crohn's disease, tricuspid valve endocarditis caused by candida albicans was observed. Prior to fungal endocarditis a treatment with prednisone and azathioprine was performed. The patient had severe embolic pneumonia with abscesses. Following the echocardiographic examination, the infected valve was replaced by a Hancock bioprosthesis. Despite high dose antifungal chemotherapy the patient died. Septic disorders in patients with Crohn's disease, who are treated with prednisone and azathioprine, can be caused by fungal endocarditis and should be investigated by echocardiography.

Candidiasis↗
PubMed1987

[Automatic implantable cardioverter-defibrillator (AICD) and antitachycardia pacemaker (Tachylog 651) in the treatment of ventricular tachyarrhythmias].

For the electrotherapy of refractory ventricular tachycardia the automatic implantable cardioverter-defibrillator (AICD) and antitachycardia pacemaker are available. The long-term use of antitachycardia pacing is still limited by the potential risk of acceleration to ventricular fibrillation. To combine the advantages of antitachycardia pacing with back-up defibrillation, we evaluated the use of an antitachycardia pacemaker with the automatic defibrillator. The AICD was implanted in 13 patients with a mean age of 62 years (from 46 to 75 years); six of them with recurrent ventricular tachycardia (170 +/- 16 per minute) which could reliably be terminated by overdrive pacing, received also an antitachycardia pacemaker (Tachylog 651). The underlying cardiac disease was coronary heart disease in 11 patients and cardiomyopathy in 2 cases. All patients had survived 1 to 6 cardiac arrests and had not responded to 6 +/- 1.5 antiarrhythmic drugs. For antitachycardia pacing we used burst stimulation with 4 to 6 stimuli and coupling intervals from 260 to 300 ms. During the follow-up period of 12 +/- 2 months, 83% of 744 tachycardias could be terminated by burst stimulation, according to the diagnostic data of the pulse generator. If the pacemaker failed to terminate or in case of acceleration (three patients), the automatic countershock of the AICD (5-42 per patient) restored sinus rhythm. In seven patients with high rate tachycardia, 2 to 69 AICD discharges occurred. No patient died suddenly, but three died due to underlying disease and one because of a pneumonia postoperatively. Future antitachycardia devices should be flexible with regard to detection and termination modes, combining antitachycardia pacing with back-up defibrillation.

Electric Countershock↗
PubMed1987

[Therapy refractory sinus tachycardia following polytrauma].

The course of a 20-year-old patient with head injury and fractures of the ribs is reported, in whom sinus tachycardia has now persisted for three years. Antiarrhythmic treatment with calcium antagonists, beta-blocking agents and digitalis did not reduce the rate of the tachycardia. Contusio cordis, as well as different mechanisms of arrhythmias after cerebral trauma are discussed.

Adult↗
PubMed1987

[Cardiology].

Explore the source record for details and available documents.

Cardiology↗
PubMed1986

[Increase in liver circulation with nifedipine].

The hepatic hemodynamic effect of 20 mg sublingual nifedipine was evaluated in 15 patients (13 men, 2 women) during heart catheterization. The liver blood flow was measured 10 min after administration of nifedipine by continuous thermodilution (Baim coronary sinus flow analyzer). Nifedipine was associated with a decrease in systolic blood pressure (from 156 +/- 14 to 138 +/-13 mmHg), an increase in heart rate (from 73 +/- 13 to 81 +/- 8.6 beats/min), and increase in cardiac output (from 6.0 +/- 1.6 to 6.5 +/- 1.3 l/min). In 2/15 patients no significant change was derived. The liver blood flow increased in 13/15 patients from 218 +/- 171.7 to 336.7 +/- 247.7 ml/min (22%-194%, P less than 0.01). The study demonstrates that the vasodilation of nifedipine involves the hepatic circulation. If the hepatic clearance of drugs is high and flow dependent, nifedipine-induced increase of hepatic blood flow may impair drug clearance.

Adult↗
PubMed1986

[Acceleration of amiodarone elimination by cholestyramine].

In eleven patients serum levels of amiodarone and its desethyl metabolite were determined after a single dose of 400 mg amiodarone given with and without subsequent administration of colestyramine. In addition, the elimination half-life was measured in three patients after discontinuation of long-term amiodarone therapy. Mean serum levels of amiodarone at 7 1/2 hours after dosing (n = 11) were 0.42 +/- 0.11 micrograms/ml without colestyramine and 0.21 +/- 0.14 micrograms/ml with colestyramine (P less than 0.01). Elimination half-life after discontinuing long-term amiodarone therapy (n = 3) was 23 1/2, 29 and 32 days, respectively (half-life in eight controls: 35-58 days). The results indicate that colestyramine significantly reduces the enterohepatic circulation of amiodarone. Therefore, colestyramine should be capable of accelerating the regression of dose-dependent side-effects of amiodarone by enhancing its elimination.

Adult↗
PubMed1986

[Indoramin in severe cardiac insufficiency. Acute hemodynamic effectiveness].

Systemic peripheral resistance, right and left heart pressures, cardiac output and left ventricular ejection fraction were measured in 12 patients with severe heart failure (stages III-IV of the NYHA), before and after intravenous injection of indoramin (0.2-0.4 mg/kg bodyweight). Peripheral resistance decreased from a mean of 2738.5 to 1294.4 dyn X s X cm-5 (P less than 0.001), mean pulmonary artery pressure from 39.4 to 21.4 mm Hg (P less than 0.001), mean aortic pressure from 105.3 to 86.0 mm Hg (P less than 0.001), left ventricular end-diastolic pressure from 35.3 to 18.3 mm Hg (P less than 0.001), arterio-venous oxygen difference from 36.1 to 25.4% (P less than 0.001), while cardiac output rose from 2.1 to 3.3 l X min-1 X m-2 (P less than 0.001), and the ejection fraction increased from 29.0 to 42.5% (P less than 0.001). Heart rate remained nearly unchanged. There were no significant side effects, such as hypotension or arrhythmias. The results indicate that the parenteral injection of indoramin favourable influences haemodynamic parameters of patients in severe heart failure.

Adult↗
PubMed1986

Indoramin in severe congestive heart failure.

The acute and chronic effects of indoramin, a new alpha 1-adrenoceptor antagonist with vasodilating properties, were examined in patients with severe congestive heart failure (New York Heart Association class III or IV). In the acute phase, indoramin, 0.2-0.4 mg/kg body weight, was given intravenously to 12 patients, and systemic peripheral resistance, right and left heart pressures, cardiac output, and left ventricular ejection fraction were determined. After indoramin, hemodynamic parameters improved significantly without heart rate changes. At peak effect (10-20 min), there were significant (p less than 0.001) decreases in mean arterial pressure from 105.3 +/- 20.4 to 86.0 +/- 16.8 mm Hg, mean pulmonary artery pressure from 39.4 +/- 10.4 to 21.4 +/- 5.8 mm Hg, total systemic peripheral resistance from 2,738.5 +/- 660 to 1,294.4 +/- 314 dyn s/cm-5, and left ventricular end-diastolic pressure from 35.3 +/- 6.8 to 18.3 +/- 4.7 mm Hg. There were increases (p less than 0.001) in cardiac index from 2.1 +/- 0.73 to 3.3 +/- 0.88 L/min/m2 of body surface area and in left ventricular ejection fraction from 29.0 +/- 6.4 to 42.5 +/- 4.6%. The arteriovenous oxygen difference fell from 36.1 +/- 6.4 to 25.4 +/- 3.8% (p less than 0.001); heart rate did not change significantly (73.3 +/- 5.4 beats/min control; 76.3 +/- 7.9 beats/min after indoramin). Eight patients were studied in the chronic phase. There were no significant changes in systolic or diastolic blood pressure and heart rate in the supine or upright position.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1986

Current concepts in the treatment of cardiac arrhythmias.

Attention has been paid to the recognition of patients at risk of sudden cardiac death. Whereas the long-term prognosis of healthy subjects with frequent and complex ventricular premature complexes is similar to that of the normal population, coronary patients with frequent and complex ectopy are at high risk of sudden cardiac death; in this group, recent myocardial infarction and impaired left ventricular function increase the likelihood for sudden death. In a similar way, patients with idiopathic dilated cardiomyopathy and reduced left ventricular function, in whom frequent episodes of ventricular tachycardias or ventricular pairs are detected, are at high risk of sudden death. These patient groups with left ventricular impairment may potentially be treated with the alpha 1-antagonist indoramin, which has exhibited antiarrhythmic properties in animal experiments. In a therapeutic dose, indoramin prohibited reflex tachycardia but did not show any additional electrophysiologic effects. Therefore, no adverse effects on sinus node function or on atrioventricular conduction, or intraventricular conduction must be expected during therapy with indoramin.

Adolescent↗