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Biomedical subjects

J Brachmann

Publications and source records attributed to J Brachmann.

At least 55 records · Page 3Linked to original sources
PubMed1994

Cardiac late potentials for diagnosis in heart disease.

In recent years abundant information has been obtained about the relationship of heart disease and cardiac late potentials. Non-invasive recordings of ventricular late potentials are useful in risk stratification of various clinical conditions, in particular, in patients following myocardial infarction. Here a close correlation has been established between cardiac late potentials and spontaneous or induced sustained ventricular tachycardias using programmed electrical stimulation. Cardiac late potentials also appear to be associated with arrhythmic events in patients with cardiomyopathies, and following unsuccessful antitachycardia surgery. Furthermore, recording of abnormal late potentials are associated both with acute rejection after cardiac transplantation and unsuccessful thrombolytic therapy after myocardial infarction. Interestingly, antiarrhythmic drugs have no clear effect on cardiac late potentials.

Arrhythmias, Cardiac↗
PubMed1994

Electrophysiological mechanisms of action of ethmozine that explain its antiarrhythmic efficacy in the late stage of experimental myocardial infarction in dogs.

The effects of intravenous ethmozine (3 mg.kg-1) on electrophysiological parameters of ischaemically damaged myocardium and induced ventricular tachyarrhythmias were studied by programmed stimulation in 17 conscious dogs with 4 to 8 day-old ligation of the left anterior descending coronary artery. Ethmozine showed a beneficial effect on sustained ventricular tachycardia by suppressing its inducibility in five of 14 animals or by slowing its rate in six of 14 animals. Ethmozine prolonged the ventricular effective refractory period in normal and infarcted myocardium, and impaired depressed conduction in ischaemically damaged tissue. The latter was indicated by significant lengthening of late potentials recorded from the infarction zone. The QT interval was only slightly increased with ethmozine. Our findings indicate an antiarrhythmic action of ethmozine in the late stage of myocardial infarction. Major mechanisms accounting for its efficacy may predominantly be associated with marked depression of slow conduction in the infarction zone, as well as with prolongation of ventricular refractoriness without significant changes of ventricular repolarization.

Animals↗
PubMed1994

Differential effects of the new class III agent dofetilide on potassium currents in guinea pig cardiomyocytes.

The electrophysiologic effects of dofetilide (UK 68,798), a new class III antiarrhythmic drug were investigated on the following currents in guinea pig left ventricular cardiomyocytes by whole-cell patch-clamp technique: (a) delayed rectifier potassium current with its fast component (IKr) and its slow component (IKs), (b) inward rectifier potassium current (IK1), (c) fast sodium current (INa), and (d) L-type calcium current (ICa). Dofetilide in 10(-6) M reduced the amplitude of IKr to 61% of control currents, as measured by 200-ms test pulses and analysis of the deactivating tail currents of IKr. On the deactivating tail currents of IKs, dofetilide caused no significant amplitude change, but time constants of deactivation became 2.3 times slower, as measured by 2,000-ms test pulses and analysis of the deactivating tail currents of IKs. When the concentration of dofetilide was increased, these effects were more pronounced. Rapid application of the substance to the cells showed that IKr was reduced in the first minute to 60% of control currents. For complete current suppression, at least 3 min were necessary. The suppression effect remained unchanged during a 10-min washout phase. Dofetilide had no effect on IK1. Neither were amplitudes and Hodgkin-Huxley parameters of sodium current influenced by dofetilide. Calcium currents were not blocked by dofetilide. Dofetilide is not only a highly selective blocker of IKr, but also delays deactivation of IKs.

Animals↗
PubMed1994

Acute efficacy and chronic follow-up of patients with non-thoracotomy third generation implantable defibrillators.

Non-thoracotomy implantation of implantable cardioverter defibrillators (ICDs) has simplified the process of device insertion, promising to decrease associated procedural complications while providing sudden death protection at least equal to epicardial systems. This study presents the acute and chronic results of 110 patients who underwent attempted non-thoracotomy ICD implantation with the Medtronic Transvene lead system and PCD model 7217 or 7219. Of the 110 patients attempted, 100 (91%) had the system successfully implanted without the need for an epicardial patch. One patient died 1 week postoperatively of septic shock related to the implantation (0.9% perioperative mortality). During follow-up of 16 +/- 11 months, 45% of the patients had an event detected as ventricular tachycardia; 26% of these detections were felt clinically to be due to supraventricular rhythms. Of the remainder, 87% were successfully treated with the first VT therapy, and 98% were terminated by the final therapy; 66% of the patients had at least one episode of ventricular fibrillation, of which 5% were felt to be inappropriate detections; 85% of the appropriate episodes were successfully treated with the first VF therapy, and all were converted by the final therapy. Total mortality at 6, 12, and 24 months was 3%, 11%, and 19% respectively. Only one patient had sudden cardiac death, occurring at 13 months postimplant. Overall, the non-thoracotomy lead system for this ICD displayed infrequent implant complications and proved to be reliable at terminating arrhythmias and maintaining a low rate of sudden cardiac death in this high risk population.

Adult↗
PubMed1994

Lidocaine converts inducible ventricular fibrillation into sustained ventricular tachycardia in conscious dogs with recent myocardial infarction.

The aim of the present study was to investigate the effect of lidocaine (L) on ventricular tachyarrhythmias with special reference to ventricular fibrillation (VF). Myocardial infarction (MI) was created in 39 dogs by doubly ligating the left anterior descending (LAD) coronary artery. All animals surviving the infarction (n = 33) were subjected to programmed ventricular stimulation 7.6 +/- 3.2 days later. Local electrical activity was recorded from the subepicardium of the left ventricular wall by means of a specially designed composite electrode. L (2 and 4 mg/kg i.v.) facilitated the induction of sustained monomorphic ventricular tachycardia (sVT) in 8 dogs with nonsustained polymorphic ventricular tachycardia (nsVT) in the control. In 13 dogs developing sVT during control stimulation, L slowed the rate of tachycardia in 8 animals (first-dose effect), while it abolished arrhythmia induction in 5 animals (second-dose effect). It was interesting that L (2 mg/kg) abolished reproduction of control VF in 12 animals by converting it into sVT. L significantly depressed conduction and prolonged ventricular refractoriness in the infarction zone. The results suggest that L facilitates induction of sVT in conscious dogs with recent MI, thereby decreasing susceptibility of infarcted myocardium to aggressive polymorphic nsVT or VF. The capability of L to exacerbate slow conduction in the infarction zone seems not to favor the development of VF during this stage of MI.

Animals↗
PubMed1994

[Arrhythmogenic right ventricular disease].

In patients with arrhythmogenic right ventricular disease (ARVD), life threatening ventricular tachyarrhythmias and sudden cardiac death mostly occur in adolescence, or in young adults before the age of 40. In the right ventricle, progressive fibrolipomatous replacement of the ventricular myocardium is pathognomonic. In severe cases progressive congestive right heart failure can develop although mild forms are extremely difficult to recognized. In most cases the disease can be diagnosed only by elaborate investigation. Right ventricular cineangiography, myocardial biopsy, MRI, and electrophysiological investigation are the most important diagnostic procedures. If the disease is diagnosed in an early stage the risk of life-threatening arrhythmias can be reduced by carefully selected antiarrhythmic therapy.

Adolescent↗
PubMed1994

[Electrophysiological effects of antiarrhythmic drug UK-68798 on different AV nodal cells in rabbit heart].

By means of microelectrode techniques the electrophysiological effects of a new class III antiarrhythmic agent, UK-68798 (Dofetilide), were investigated on atrionodal (AN), nodal (N), nodal-His (NH) and His (H) cells in the AVN area of rabbit heart. UK-68798 (5 x 10(-9) to 5 x 10(-6) mol/L) had no effect on APA and RP of the 4 kinds of cells but caused a dose-dependent decrease in AVN spontaneous rhythm without changing the A-H conduction time. APD50 and APD90 were prolonged markedly by the drug in a dose-dependent manner. Among the 4 kinds of cells, N cell had the highest percentage increment in APD, indicating a prominent sensitivity to the drug. For example, at 5 x 10(-6) mol/L, the prolongation percentages of APD90 are: 95 +/- 26% (N), 75 +/- 22% (AN), 63 +/- 26% (H), 46 +/- 26% (NH). The effective refractory periods (ERP) of the 4 kinds of cells were lengthened also in a dose-dependent manner, while the ERP increment percentages (delta ERP%) of the 4 kinds of cells did not show significant difference. However, ERP corresponding repolarization membrane potentials (ERP-RMP) of the 4 kinds of cells were not affected by the drug. The above results suggested that though ERP increased in parallel with APD prolongation, the homogeneous delta ERP% and unchanged ERP-RMP values of the 4 kinds of cells would prevent the AVN area from becoming a source of reentry arrhythmias under the action of UK-68798.

Action Potentials↗
PubMed1994

[The implantable cardioverter/defibrillator (ICD). Developments up to the present time and future perspectives].

The implantable cardioverter/defibrillator is gaining increasing significance in the therapy of life-threatening ventricular arrhythmias. Independently, the team of Mirowski and the team of Schuder started to develop experimental automatic implantable defibrillators in the seventies. In 1980, the first human implant of an automatic defibrillator was done by Levi Watkins together with the team of Mirowski in Baltimore, USA. Since 1989 implantable cardioverter/defibrillators exhibit multiple functions among which are high energy defibrillation therapy, low energy cardioversion, antitachycardia pacing, permanent and post therapy antibradycardia pacing, diagnostic counters, and device status parameters. This offers a markedly improved technical device to the patients. Evaluation of the patient's diagnostic counters provide a detailed overview about the patient's arrhythmia history and information for optimizing antitachycardia pacing therapy and additional antiarrhythmic drug therapy. The availability of non-thoractomy transvenous lead systems and biphasic shock forms allows the insertion of the device without open chest surgery and even without subcutaneous leads resulting in low mortality rates and an exclusively transvenous system. Single-lead unipolar devices are currently investigated in clinical trials. Future development of atrial sensing lead systems may further reduce inappropriate shock therapy triggered by sinus tachycardia or atrial tachyarrhythmias, e.g. atrial fibrillation, and may be used for dual chamber stimulation. Hemodynamic sensors for determining the severity of the arrhythmia are currently under experimental evaluation. Possible prognostic indications of ICD therapy in patients without a history of malignant arrhythmias are currently studied in several prospective trials. All new directions hold promise to expand and improve the use of ICDs in patients at risk for sudden cardiac death.

Death, Sudden, Cardiac↗
PubMed1994

[Heart rhythm after conversion of ventricular tachyarrhythmia by internal shock delivery].

The purpose of this retrospective study is the analysis of dysrhythmias following internal cardioversion/defibrillation of ventricular tachycardia (VT) or fibrillation (VF) and to discuss their relevance to the therapy with automatic implantable devices. Therefore, 304 internal conversions of VT/VF during and/or after implantation of automatic defibrillators were evaluated in 51 patients. Significant post-shock arrhythmias (bradycardia, atrial fibrillation, non-sustained VT of > or = 10 cycles) were absent after 89% of internal shocks. Pauses of > 2 s were observed in 2/9 patients without VVI-back-up pacing. The heart rate was > or = 50 bpm in 10/51 patients. Atrial fibrillation occurred in 7 patients. Non-sustained, mostly polymorphic VT consisting of > or = 10 cycles followed 18/304 (6%) internal shocks in 13 patients. The VT rate was > or = 200/min in 17/18 episodes and triggered an inadequate shock once. The incidence of non-sustained VT post-shock was unrelated to shock energy, type, and duration of the converted arrhythmia. In conclusion, automatic implantable devices should provide back-up pacing. Tachycardic rhythms can mislead automatic interpretation of the effect of internal shocks.

Adult↗
PubMed1994

Effects of dihydropyridine calcium-antagonists on intracellular action potentials of rabbit sinus node, atrium and atrioventricular node. Comparison of felodipine with nifedipine.

The effects of the new dihydropyridine Ca-antagonist felodipine (CAS 72509-76-3) (3 x 10(-9) mol/l - 10(-6) mol/l) on intracellular action potentials of the rabbit sinus node and atrium were studied. Results were compared to the effects of nifedipine (10(-8) mol/l - 3 x (-10) mol/l). Additionally, rate-dependent effects of both substances on AV nodal conduction time were assessed. The data demonstrate a concentration-dependent reduction of sinus nodal automaticity due to depression of phase 4 automaticity concomitant with a reduction of the maximum upstroke velocity of the sinus action potential by both substances. Felodipine was about one half order of magnitude more potent than nifedipine. Both substances exerted little effects on action potentials in atrial cells. Felodipine and nifedipine led to a concentration and frequency-dependent ("use-dependent") retardation of AV nodal conduction. Again felodipine was about one half order of magnitude more potent than nifedipine.

Action Potentials↗
PubMed1994

Time-frequency analysis of ventricular late potentials.

The time-frequency characteristics are studied of averaged and filtered ECG records from 21 patients with sustained ventricular tachycardia and 29 healthy control subjects. Simulated data as well as real ECG records reveal the detection accuracy of the wavelet transform of signals with late potentials. The wavelet-transforms of preprocessed ECG signals are plotted in the time-frequency plane. These representations of the signals are well suited to describe the different characteristics of the patients and healthy subjects. A quantitative discrimination was performed with a sensitivity of 90% and a specificity of 72% by the energy underneath the squared modulus of the time-frequency distribution plots of the computed wavelet transforms.

Cardiac Pacing, Artificial↗
PubMed1993

Endocarditis caused by a Leptotrichia buccalis-like bacterium in a patient with a prosthetic aortic valve.

The isolation of a Leptotrichia buccalis-like bacterium from the blood of a patient with endocarditis associated with a prosthetic aortic valve is reported. The organism was isolated from different blood cultures. It was similar but not completely identical to Leptotrichia buccalis. The microbiological identification was confirmed independently by three laboratories, including two reference institutions. The case and the characteristics of the microorganism are reported.

Aged↗
PubMed1993

In-hospital experience with multiprogrammable implantable antitachycardia/antifibrillation devices.

Multiprogrammable, automatic internal defibrillators with (n = 45) and without (n = 15) antitachycardia pacing features were implanted in 60 consecutive patients with refractory, malignant ventricular tachycardia (VT) (n = 42) or fibrillation (VF) (n = 18). Left ventricular (LV) ejection fraction was reduced to 39% +/- 12% as a result of structural heart disease in 56 patients. The complexity of the systems caused no additional risks to the surgical procedure or postoperative management. VT/VF detection parameters were individually adjusted to the arrhythmia type (detection cycle length 323 +/- 40 ms in patients with VF vs 405 +/- 40 ms for VT patients, P < 0.05) and incidence (longer detection periods if frequent nonsustained VT was also present). Shock energy was reduced in patients with VT as compared to VF (11J vs 24J, P < 0.05). Antitachycardia pacing was activated in 19/28 (68%) patients with well tolerated VT. Signal, telemetry, as detected by the device, combined with programmability allowed the device to be checked for correct decisions (these were inappropriate in four patients in three of whom corrections were non-invasive) prior to discharge. In conclusion, in the automatic tachyarrhythmia control devices we studied, programmability and flexibility appeared to be clinically safe and useful. Prolonged observation periods are required, however, to evaluate the true clinical safety and persistent efficacy of device programmability and flexibility.

Algorithms↗
PubMed1993

Acute and chronic antiarrhythmic efficacy of d-sotalol in patients with sustained ventricular tachyarrhythmias.

To evaluate the clinical efficacy of d-sotalol, 84 patients with a history of sustained ventricular tachycardia (VT) or ventricular fibrillation (VF), who had inducible sustained VT/VT at baseline electrophysiologic study (EPS), were investigated after intravenous (IV) d-sotalol (1.5-2.5 mg.kg-1). A total of 29 additional patients received only oral d-sotalol, (400-600 mg.day-1). Acute success of antiarrhythmic therapy was defined as suppression of inducible sustained VT/VF. The overall success rate of IV d-sotalol was 38% (32/84) after a mean of 4.3 drugs failed to suppress inducibility. A 78% success rate (31/40) was demonstrated in patients who were also assessed after oral d-sotalol. Torsade de pointes type VT was seen in one patient. After 1 year, only 16% of patients with a positive EPS had a recurrence compared to 43% of patients with a negative EPS (P < 0.05). Estimated survival rates were 95 and 88% after 1 and 2 years of follow-up, respectively. Only five of 56 patients discontinued d-sotalol therapy because of adverse effects. IV d-sotalol appears to be an effective antiarrhythmic agent. Its long-term efficacy is predictable on the basis of therapy guided by electrophysiologic testing in patients with refractory ventricular tachyarrhythmias. The efficacy of d-sotalol seems comparable to that reported for d,l-sotalol.

Cardiac Pacing, Artificial↗
PubMed1993

Comparative effects of d-sotalol and l-sotalol on the atrioventricular node of the rabbit heart.

The purpose of this study was to compare the dose-dependent effects of d-sotalol and l-sotalol (3 x 10(-7) M to 10(-4) M) on electrophysiological parameters in isolated preparations of the rabbit atrioventricular (AV) node. Standard microelectrode techniques were used in recording transmembrane action potentials from cells of the upper and lower AV node. Twelve New Zealand white Rabbits of either sex weighing between 1.5 and 2.6 kg were used. In both cell types studied, d-sotalol as well as l-sotalol prolonged action potential duration to the same extent. No significant effects were observed with either isomer on maximum diastolic potential, action potential amplitude, or maximum upstroke velocity of the action potential (Vmax). The rate of spontaneous discharge in AV nodal cells was decreased to the same extent by both isomers; this effect was caused by action potential prolongation; no effect on the rate of diastolic depolarization or Vmax was observed. Both d-sotalol and l-sotalol prolonged AV nodal conduction to the same degree by lengthening the action potential duration in AV nodal cells. The effects of 10(-4) M d-sotalol on AV nodal reentrant tachycardia were studied in one preparation in which AV nodal reentrant tachycardias could reproducibly be initiated by atrial premature stimulation. d-Sotalol abolished the occurrence of this tachycardia by lengthening refractoriness in AV nodal cells; this effect can be ascribed to a Class III antiarrhythmic effect.

Action Potentials↗
PubMed1993

Effects of prenylamine and AQ-A 39 on reentrant ventricular arrhythmias induced during the late myocardial infarction period in conscious dogs.

The effects of prenylamine (PNL) and AQ-A 39 on sustained ventricular tachycardia (SVT) were studied by programmed stimulation in conscious dogs 4-10 days after ligation of the left anterior descending (LAD) coronary artery. In 8 of 16 dogs developing SVT in the control, PNL (3 mg/kg intravenously, i.v.) suppressed inducibility of SVT and slowed the rate of tachycardia in 6 other animals. In a separate group of 10 dogs with inducible SVT, AQ-A 39 (4 mg/kg i.v.) abolished elicitation of tachycardia in 3 dogs and decreased its rate in 6 other dogs. Neither drug affected normal conduction significantly, but PNL impaired slow conduction in the infarct zone, as indicated by prolongation of late potential. Both agents increased the effective refractory period (ERP) of infarcted and normal ventricular myocardium and prolonged the corrected QT interval. PNL and AQ-A 39 exert notable efficacy in preventing infarcted heart from severe ventricular arrhythmias. Prolongation of ventricular refractoriness and repolarization, as well as decreased slow conduction in ischemically damaged myocardium, are major mechanisms accounting for the effectiveness of these drugs against ventricular arrhythmias.

Animals↗
PubMed1993

Heart rate variability in time and frequency domains: effects of gallopamil, nifedipine, and metoprolol compared with placebo.

OBJECTIVE: To assess the effects of three different antianginal drugs on heart rate, blood pressure, and heart rate variability. DESIGN: Randomised, single blind, placebo controlled, cross over study. SETTING: University hospital. PARTICIPANTS: Nine healthy male volunteers. INTERVENTIONS: Oral administration of either 50 mg gallopamil, 20 mg nifedipine, 100 mg metoprolol, or placebo according to a random crossover plan. MAIN OUTCOME MEASURES: Time intervals between consecutive R waves in electrocardiograms measured with an accuracy of 5 ms from digital Holter recordings. Blood pressure monitored continuously by finger plethysmography. RESULTS: Metoprolol lowered heart rate from 62(6) to 51(5) beats/min (p = 0.003) after 78(23) minutes. Nifedipine provoked reflex tachycardia from 56(5) to 94(18) beats/min (p < 0.001) at 10(3) minutes after treatment followed by an exponential decline in heart rate to baseline values with a time constant of 34(7) min in seven subjects but 83 minutes in one volunteer. One subject showed no exponential decline in heart rate. Nifedipine significantly lowered the supine mean arterial pressure from 86(6) to 67(6) mm Hg (p = 0.004) after 11(2) minutes, indicating an acute reduction in arterial resistance. Gallopamil did not significantly change mean heart rate or blood pressure. In the sitting position three hours after administration gallopamil and metoprolol significantly lowered power spectral density in the low frequency band (0.03 Hz to 0.15 Hz) compared with placebo (p < 0.05). Nifedipine did not produce such an effect. CONCLUSIONS: Gallopamil and metoprolol both inhibit cardiac sympathetic activation compared with placebo, whereas nifedipine causes reflex sympathetic activation.

Adult↗