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Biomedical subjects

B Lüderitz

Publications and source records attributed to B Lüderitz.

At least 289 records · Page 16Linked to original sources
PubMed1993

Pneumocystis carinii infections in HIV-infected hemophiliacs during aerosolized pentamidine prophylaxis.

The frequency, presentation, diagnosis and clinical course of Pneumocystis carinii infections (PCI) were studied during aerosolized pentamidine prophylaxis (AP) and its impact on the spectrum of AIDS-related and other pulmonary infections in HIV-infected hemophiliacs. We conducted an open study on primary (PP) and secondary (SP) AP. Breakthrough P. carinii infections (BPCI) and other infectious complications were analyzed retrospectively. Hemophiliacs without prior P. carinii pneumonia (PCP) who had been reluctant to any prophylaxis and who developed PCP served as control group. Statistical analysis of the efficacy of prophylaxis was performed by calculating confidence intervals of binomial p. Of 73 hemophiliacs (56 on PP and 17 on SP) 10 developed BPCI (7 in PP and 3 in SP) during a mean observation time of 14.9 months (range 0.5-30); total 13.6% (6.7%; 23.7%), PP 12.5% (5.1%; 24%), SP 17.6% (3.7%; 43.4%), confidence intervals at a level of 95%. Three BPCI presented atypically with cavitation (1), pneumothorax (2), Pneumocystis pleuritis (1), dissemination (2) as compared to none in the control group. Sensitivity of bronchoalveolar lavage (BAL) was 88.9%, specificity 100% (both 100% in the control group). PCP was the leading AIDS manifestation (21.3%), CNS manifestations taken together were more frequent (36.2%). Bacterial pneumonia was the most frequent respiratory infection. One patient of the study group with recurrent pneumothorax possibly died of BPCI as compared to no BPCI-related deaths in the control group. Efficacy of prophylaxis in hemophiliacs was comparable to other risk groups. AP alone may be insufficient for the control of PCI in patients with long-term profound immunodeficiency, especially in SP. 30% of BPCI presented atypically.(ABSTRACT TRUNCATED AT 250 WORDS)

AIDS-Related Opportunistic Infections↗
PubMed1993

[Effect of frequent ventricular extrasystole on brain circulation in patients with coronary heart disease].

Animal experiments using the microsphere method indicate a 8% reduction of mean cerebral blood flow during parasystolic rhythm induced by ventricular pacing in comparison to a control group with sinus rhythm. The parasystolic rhythm causes changes of systemic arterial blood pressure, which are comparable to the hemodynamic effects of frequent premature ventricular contractions. Because a reduction of cerebral blood flow induced by frequent premature ventricular beats can be assumed by the results of the laboratory investigations, cerebral blood flow was determined in a clinical study in 19 coronary artery disease patients and in 11 healthy, age-adjusted volunteers using the 133Xenon-inhalation method, in order to investigate the effect of ventricular ectopics on cerebral perfusion. Simultaneously Holter monitoring was performed during cerebral blood flow measurements. Cerebral blood flow was estimated by the initial slope index, which is calculated from the early decay of the clearance curve, and by the mean cerebral blood flow index, which is calculated by the stochastic method. Grey matter blood flow is estimated by the two-compartment analysis. Cerebral blood flow in coronary artery disease patients is reduced versus controls. The initial slope indices were 45.2 +/- 5.1 s-1 and 57.4 +/- 7.2(-1), respectively (p < 0.01). In patients with frequent ventricular ectopic activity (739/h) an additional reduction of cerebral blood flow was observed. The initial slope index was 42.6 +/- 6.3 s-1 (p < 0.01). The reduction of cerebral blood flow in coronary artery disease patients is partially due to the coincidence of coronary and cerebral artery disease. Frequent ventricular premature contractions might cause an additional reduction.

Adult↗
PubMed1993

[Current treatment of supraventricular tachycardia: drug therapy].

Recurrent supraventricular arrhythmias are associated with palpitations, weakness, syncopes, etc. Pharmacological treatment with antiarrhythmic agents aims to interrupt the tachyarrhythmia episodes (acute therapy) and to stabilize sinus rhythm thereafter (chronic therapy). Due to the newer curative options (transvenous ablation), the segment for the pharmacological therapy is shrinking. Treatment with antiarrhythmic agents is still indicated, if the recurrence of tachycardia episodes can be sufficiently controlled by a well-tolerated antiarrhythmic regimen. In the cohort of atrial fibrillation, total mortality and mortality from cardiovascular causes were increased under the influence of quinidine. The risk must, therefore, be weighed against the anticipated benefit from as well as the likelihood of arrhythmia suppression, before treating a patient with class I antiarrhythmic drugs. In some cases, reduction of ventricular rate by calcium antagonists will be the better choice. In case of recurrent atrial fibrillation without or with minimal structural abnormalities, propafenone or flecainide are recommended. Sotalol, and in rare cases amiodarone, will be applied in coronary artery disease. Atrial fibrillation of recent onset may be interrupted by bolus injection of ajmaline, propafenone, or flecainide. In case of impaired cardiac function, intravenous amiodarone can be applied safely. In summary, the scientific basis for the treatment of supraventricular tachycardias has been strengthened by clinical trials. Careful evaluation of the individual patient is warranted prior to institution of the pharmacological treatment.

Anti-Arrhythmia Agents↗
PubMed1993

[Risks and side effects in treatment of supraventricular tachycardia].

Many new antiarrhythmic drugs effective in supraventricular tachyarrhythmia are now available. Since these compounds may lead to serious side-effects, the correct indication for the antiarrhythmic treatment has to be given regarding the ratio of risk and benefit. There is no doubt that aggravation of arrhythmia i.e. acceleration of tachycardia or even degeneration into ventricular flutter (including torsades-de-pointes tachycardia) and fibrillation may be related to the cardiac diagnosis depending on the extent of disease or left ventricular dysfunction and the presenting arrhythmia and possibly the electrophysiological effects of the drug. In general, negative inotropic effects of antiarrhythmic substances are overestimated; they may even be neglected as long as the antiarrhythmic agent leads to effective suppression of the symptomatic ventricular tachyarrhythmia. The best and most important consequence of the CAST study (Cardiac Arrhythmia Suppression Trial) showing an increase in mortality with antiarrhythmic drugs compared with placebo should be that physicians handle antiarrhythmic drugs now with more care than before. The problems with risks and side-effects in antiarrhythmic drug therapy of supraventricular arrhythmias underline the requirement for careful cardiological evaluation and monitoring in all patients receiving such drugs.

Anti-Arrhythmia Agents↗
PubMed1993

Semiquantitation of aortic regurgitation by pulsed Doppler examination of the subclavian artery velocity contour.

The reflux of aortic regurgitation causes an increased and longer diastolic reverse flow in the aorta and its branching vessels as compared to the normal flow contour. The changes of the aortic flow are related to the severity of aortic regurgitation and can be demonstrated by Doppler ultrasound. As Doppler examinations are often restricted in the aorta, a prospective study was designed to determine the feasibility and accuracy of Doppler measurements in the subclavian artery for the identification of severe forms of aortic regurgitation. Fifty-five patients with and 40 patients without aortic regurgitation were examined both by aortography and pulsed Doppler flow analysis of the subclavian artery. Two age groups were differentiated: patients below and those over 60 years of age, respectively. A high quality Doppler signal was recorded in all patients. In patients below 60 years, the best predictors of severe aortic regurgitation proved to be a pandiastolic reverse flow and an increased regurgitant fraction (77%) with a sensitivity of 100% and specificity of 75% and 92%, respectively. Since a pandiastolic reverse flow was detected in most patients in the control group over 60 years, it was not indicative of aortic regurgitation in these cases. However, an increased maximal diastolic velocity (> -37 cm/s) identified severe forms of aortic regurgitation in this age group with a sensitivity of 89% and a specificity of 100%. Therefore, severe forms of aortic regurgitation may be reliably identified by analysing the subclavian artery Doppler spectrum. In conclusion, the method is a useful adjunctive technique to other Doppler echocardiographic methods to assess the severity of aortic regurgitation.

Adult↗
PubMed1992

Effects of chronic amiodarone therapy on defibrillation threshold.

In a prospective and parallel, randomized study, the long-term stability of epicardial defibrillation threshold was evaluated in 22 patients, using a patch-patch lead configuration at the time of implantation and generator replacement. The concomitant antiarrhythmic drug treatment consisted of either mexiletine (720 mg/day) or amiodarone (400 mg/day) and was administered to patients in a randomized and parallel manner. During a mean follow-up of 24 +/- 6 months, the defibrillation threshold increased significantly from 14.3 +/- 2.8 to 17.9 +/- 5.3 J (p < 0.05) for the entire patient group. The increase in the chronic defibrillation threshold was due to a marked increase in defibrillation energy needs in the subgroup of patients receiving amiodarone. Whereas no significant change in the defibrillation threshold was documented in the subgroup of patients receiving mexiletine, the mean defibrillation threshold increased from 14.1 +/- 3.0 to 20.9 +/- 5.4 J (p < 0.001) in those receiving amiodarone. In all patients with increased defibrillation thresholds, reevaluation showed a reduction in the defibrillation threshold after discontinuation of antiarrhythmic drug therapy. The only variable associated with an increase in the chronic defibrillation threshold was amiodarone treatment. These findings suggest that the defibrillation threshold should be measured at each generator replacement and in case of a change in antiarrhythmic drug treatment. In particular, if amiodarone treatment is initiated, it is recommended that the defibrillation threshold should be reevaluated to ensure an adequate margin of safety.

Amiodarone↗
PubMed1992

Pharmacologic treatment of supraventricular tachycardia: the German experience.

Tachyarrhythmias that originate above the bifurcation of the bundle of His or in tissue proximal to it are classified as supraventricular tachyarrhythmias (SVTs). Primary treatment of SVT tries to influence the underlying disease. Symptomatic therapy is subdivided into drug therapy, electrotherapeutic tools (e.g., antitachycardia pacemakers, catheter ablation), and antiarrhythmic surgery. Antiarrhythmic agents that slow conduction and suppress premature beats are efficient for emergency and long-term treatment of SVTs. We evaluated some of the most relevant antiarrhythmic drugs in SVT, including propafenone, diprafenone, cibenzoline, sotalol, and diltiazem; in addition, usage and efficacy of quinidine/verapamil, disopyramide, amiodarone, ajmaline, adenosine, and flecainide are summarized. In 1990, the case load of supraventricular arrhythmias per physician in Germany was more than 30 patients seen per month. About 50% of them were treated with drug therapy; i.e., approximately 17 patients were treated with antiarrhythmic drugs per month per physician for supraventricular arrhythmias. The most important antiarrhythmic agents used in Germany are propafenone (40%), combination of quinidine and verapamil (23%), sotalol (12%), disopyramide (6%), flecainide (6%), and other (13%).

Anti-Arrhythmia Agents↗
PubMed1992

Hemodynamic effects of amiodarone during acute and chronic treatment in patients with recurrent sustained ventricular tachycardia.

In 15 patients with recurrent ventricular tachycardia, the hemodynamic effects of amiodarone were evaluated under oral loading (1000 mg/day for 14-16 days) and during chronic treatment (600 mg/day for a further 10 weeks). In all patients, coronary artery disease was present with a mean ejection fraction of 37%+/- 10%. The cardiac output during the sinus rhythm, as determined by thermodilution, did not change significantly during loading with amiodarone. During ventricular tachycardia, the cardiac output increased from 3.7 +/- 1.3 to 4.5 +/- 1.6 1/min under the influence of amiodarone in 5 patients. Echocardiographic measurements of the left ventricle dimensions did not show a directed change of the enddiastolic and endsystolic diameters and the fraction shortening at the end of the loading period and after 3 months of maintenance therapy. No negative inotropic effect of amiodarone could be demonstrated in patients with recurrent ventricular tachycardia and impaired left ventricular function due to coronary artery disease.

Aged↗
PubMed1992

Electrophysiological and haemodynamic effects of lidocaine and ajmaline in the management of sustained ventricular tachycardia.

The electrophysiological and haemodynamic effects of lidocaine (100 mg) and ajmaline (50 mg) were evaluated while attempting to interrupt sustained ventricular tachycardia. The study was performed as a prospective, non-blinded, randomized investigation in 61 patients. Lidocaine terminated ventricular tachycardia in four of 31 patients, ajmaline in 19 of 30 patients (P less than 0.001). QRS and RR intervals during ventricular tachycardia were prolonged by ajmaline from 164 +/- 28 ms to 214 +/- 49 ms and from 371 +/- 86 ms to 479 +/- 137 ms (P less than 0.001), respectively; lidocaine did not influence these parameters. The duration of the return cycles after termination of ventricular tachycardia did not differ between the two groups. Lidocaine did not change cardiac output during ventricular tachycardia whereas cardiac output increased significantly under ajmaline from 3.5 +/- 1.21.min-1 to 5.5 +/- 1.91.min-1 (P less than 0.001). It is concluded that anti-arrhythmic agents such as ajmaline, which slow conduction velocity and prolong refractoriness, are more effective than lidocaine in the medical treatment of haemodynamically stable, sustained ventricular tachycardia.

Ajmaline↗
PubMed1992

Long-term therapy of antitachycardia pacing for supraventricular tachycardia.

Long-term antitachycardia pacing therapy with the InterTach 262-12 and 262-16 was evaluated in 32 consecutive patients (mean age 50 +/- 13 years) with recurrent, drug refractory supraventricular tachycardia. AV nodal reentrant tachycardia was present in 20 patients, Wolff-Parkinson-White syndrome in ten patients, and a reentrant tachycardia due to Mahaim fibers in one patient. During follow-up of 39 +/- 17 months, 250 persistent tachycardia episodes occurred in 22 patients. By adjusting detection and termination mode, recurrent supraventricular tachycardia could be controlled in 19 of 32 patients (60%) by antitachycardia pacing alone. Concomitant antiarrhythmic drug therapy was required in ten of 32 patients (30%). During follow-up antitachycardia pacing became ineffective in three patients (10%). Thus, chronic antitachycardia pacing proved to be safe and effective in selected patients with drug refractory supraventricular tachycardia and could significantly improve quality of life by rapid termination of recurrent supraventricular tachycardia episodes.

Algorithms↗
PubMed1992

Failure of an implantable cardioverter-defibrillator to redetect ventricular fibrillation in patients with a nonthoracotomy lead system.

BACKGROUND: Shock delivery of an implantable defibrillator may cause a change in the amplitude of endocardial electrograms and impair the detection of ventricular fibrillation. Thus, the effects of shock discharges on the amplitude of endocardial electrograms were evaluated in five patients undergoing implantation of a cardioverter-defibrillator in combination with a new nonthoracotomy lead system. METHODS AND RESULTS: At implant, bipolar endocardial electrograms were recorded before each shock application, during ventricular fibrillation, during redetection of ventricular fibrillation in case the applied shock was ineffective, and at intervals of 5, 10, 20, 30, 60, and 120 seconds after each shock delivery. The amplitude of the endocardial electrograms decreased from 10.5 +/- 3.8 mV during sinus rhythm to 6.3 +/- 1.9 mV during initial ventricular fibrillation and declined to 2.2 +/- 1.3 mV during redetection of ventricular fibrillation. After successful termination, the following bipolar electrograms could be obtained at the predetermined intervals: 1.9 +/- 1.2 mV, 3.1 +/- 1.8 mV, 4.5 +/- 1.9 mV, 6.5 +/- 2.9 mV, 9.5 +/- 3.3 mV, and 10.4 +/- 3.8 mV. At predischarge testing, failure of redetection of ventricular fibrillation could be documented in two patients, requiring rescue external defibrillation in both cases to restore sinus rhythm. CONCLUSIONS: These findings demonstrate that the implantable cardioverter-defibrillator did not ensure reliable redetection of ventricular fibrillation in patients using the implanted nonthoracotomy lead system. Thus, the potential risk of sudden cardiac death may persist in these patients despite defibrillator therapy.

Cardiomyopathy, Dilated↗
PubMed1992

[Combination anti-arrhythmic drug therapy].

Antiarrhythmic treatment with single agents is often ineffective and can be limited by dose-dependent side-effects. Therefore, combinations of antiarrhythmic drugs in smaller and well-tolerated doses are advocated in cases refractory to single antiarrhythmic drugs. Basically, substances belonging to the same electrophysiologic class should not be combined. A combination of beta-adrenoreceptor blockers with class I antiarrhythmic drugs may be effective, mainly in cases in which the arrhythmia is dependent on adrenergic stimulation. As shown in our study, the combination of class III and I B-substances can be useful in some cases, from the electrophysiological and clinical points of view. Among the successful combinations of this type are amiodarone and mexiletine, sotalol and mexiletine, and sotalol and tocainide. In patients refractory to amiodarone alone or to a combination with mexiletine, the combined treatment with amiodarone and class-I-C drugs such as flecainide and encainide prolongs the cycle length of ventricular tachycardia, but does not suppress induction of ventricular tachycardia during programmed stimulation. Combination therapy with amiodarone and encainide is associated with a remarkable incidence of proarrhythmic effects. Nevertheless, a combination of antiarrhythmic drugs improves efficacy of therapy in selected patients. However, a close monitoring is mandatory because of the risk of proarrhythmia.

Amiodarone↗