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Biomedical subjects

M Schlepper

Publications and source records attributed to M Schlepper.

At least 37 records · Page 2Linked to original sources
PubMed1994

[The clinical significance of the ajmaline test in the noninvasive diagnosis of the Wolff-Parkinson-White syndrome].

A knowledge of electrophysiological parameters of accessory atrioventricular conduction pathways, such as effective refractory time and high conduction capacity in atrial fibrillation, make it possible to detect those patients who are at risk of life-threatening ventricular tachyarrhythmias. One criterion to identify these electrophysiological parameters is persistent pre-excitation after intravenous administration of ajmaline in Wolff-Parkinson-White (WPW) syndrome. Sensitivity and specificity of the ajmaline test in detecting patients at risk of life-threatening ventricular tachyarrhythmias were evaluated in 58 consecutive patients (22 females, 36 males; mean age 40.2 +/- 13 years) with the WPW syndrome. Pre-excitation was blocked after ajmaline in 43 patients (74%), pre-excitation persisting in 15 (26%). In 26 of the 43 patients with blocked pre-excitation the ajmaline test indicated short effective refractory time (< 270 ms) of the accessory pathway, and a high conduction capacity in 19 (minimal pre-excitation R-R interval during atrial fibrillation of < 250 ms). Sensitivity of the ajmaline test in the detection of a short refractory time was 33.3%, specificity 89.4%, while the corresponding values were 40.6% and 92.3% for the detection of accessory pathways with high conduction capacity in atrial fibrillation. These data show that the ajmaline test is not useful for estimating the electrophysiological characteristics of the accessory pathways. It is thus of only subordinate diagnostic value in predicting how much patients with the WPW syndrome are at risk of serious ventricular tachyarrhythmias.

Adult↗
PubMed1994

Effect of biphasic waveform pulse on endocardial defibrillation efficacy in humans.

Several clinical studies have proved increased defibrillation efficacy for implantable cardioverter defibrillators with biphasic pulse waveforms compared to monophasic pulse waveforms. This difference in defibrillation efficacy depends on the type of defibrillation lead system used. The influence of biphasic defibrillation pulse waveforms on the defibrillation efficacy of purely endocardial defibrillation lead systems has not yet been sufficiently examined, we, therefore studied 30 consecutive patients with drug refractory ventricular tachyarrhythmias during the implantation of a cardioverter defibrillator. After implanting an endocardial "integrated" sensing/defibrillation lead we performed a prospective randomized comparison of the defibrillation efficacy of monophasic and biphasic defibrillation waveform pulses. For endocardial defibrillation with the biphasic waveform the mean defibrillation threshold was 12.5 +/- 4.9 joules and for the monophasic waveform 22.2 +/- 5.6 joules (P < 0.0001). There was a decrease in the required defibrillation energy of biphasic defibrillation in 29/30 patients. Thus considering purely endocardial defibrillation a statistically significant and clinically relevant increase in defibrillation efficacy can be demonstrated for biphasic defibrillation waveform pulses.

Defibrillators, Implantable↗
PubMed1994

[Subtypes of muscarinic receptors--aspects of their physiologic significance for controlling heart rate in the human].

The cDNAs for five different muscarinic cholinoceptors have been cloned. The biochemical and physiological relevance of the m1, m2 and m3 receptors is understood in many aspects. The pharmacological defined M1, M2 and M3 related to antagonists binding studies closely correspond with those cloned. We compared effects of atropine and of the subtype selective M-cholinoceptor antagonists pirenzepine and AF-DX 116 in humans. Dose- or time-response curves have been established for heart rate. Plasma samples were drawn in parallel with the effect measurements and analysed for drug concentrations. Subtype-selective radioceptor assays of the samples served to estimate the respective receptor occupancy in vivo. After low dosis of pirenzepine (M1-selective blockade) a negative chronotropic effect on heart rate could be observed. After high doses of pirenzepine or atropine (M-unselective blockade) the wellknown tachycardia appeared in parallel with occupancy of both the M2 and M3 subtypes. AF-DX 116 induced a tachycardia without a decrease of salivary flow in agreement with its selectivity profile (M2 > M1 > M3). Gastric emptying was only slightly inhibited by AF-DX 116 but nearly completely by a very high dose of pirenzepine blocking M1-, M2- and M3-cholinoceptors. The negative chronotropic effect on heart rate of a low dose of pirenzepine (M1 selective) was multi-folded by pretreatment with isoprenaline but disappeared during bicycle exercise. The implications of the functional M cholinoceptor heterogeneity in humans revealed by antagonists are discussed according to its possible importance for the control of autonomous nerve system.

Atropine↗
PubMed1994

[Anti-ischemia effects of gallopamil and esmolol in an intra-individual comparison in patients with coronary heart disease].

To compare the hemodynamic, antiischemic, metabolic, and neurohumoral effects of intravenous esmolol (beta 1 blocking agent) and gallopamil (verapamil-like calcium channel blocker), 14 patients with angiographically proven CAD and reproducible ST segment depression were studied at rest and during exercise under control conditions and after an intravenous bolus injection of esmolol (0.5 mg/kg/1 min, followed by an infusion with 0.2 mg/kg/min) or gallopamil (0.025 mg/kg/3 min). In contrast to gallopamil, esmolol significantly reduced systolic blood pressure (175.7 vs. 160 mm Hg) and heart rate (107.4 vs. 96.9 min-1) during exercise as well as cardiac output (11.57 vs. 9.38 l/min) and significantly enhanced systemic vascular resistance both at rest (1241 vs. 1479 dynes.s.cm-5) and during exercise (805 vs. 947 dynes.s.cm-5). On the other hand, exercise filling pressures and lactate levels (3.66 vs. 3.05 mmol/l) were significantly reduced by gallopamil only. Thus, the significant improvement of exercise tolerance by both esmolol and gallopamil is based on different mechanisms of action: esmolol improves myocardial ischemia by appreciably reducing myocardial oxygen consumption, whereas gallopamil primarily improves oxygen supply and ventricular performance. Plasma catecholamines, atrial natriuretic factor, and aldosterone levels as well as plasma renin activity were identically influenced by esmolol and gallopamil, respectively. A reflex activation of the sympathetic system did not occur.

Adrenergic beta-Antagonists↗
PubMed1994

Steady-state plasma concentrations of propafenone--chirality and metabolism.

In a selected group of 86 patients (60 males, 26 females) with symptomatic ventricular arrhythmias, possible interactions between metabolic and chiral effects at steady-state were investigated by comparing the plasma levels of propafenone, its major metabolites and the 2 structural isomers. The antiarrhythmic drug propafenone is metabolized--besides a minor dealkylation pathway--mainly via 5-hydroxylation. It is a well-known phenomenon that this oxidative pathway is not shared by all individuals to the same extent. We were able to verify among our subjects the portion of so-called poor metabolizers reported in the literature for the total population. Propafenone was administered as a slow release formulation at 3 different dose regimens (2 x 225 mg, 2 x 325 mg and 2 x 425 mg). The crude drug is a racemic mixture of equal amounts of R- and S-forms. During treatment, the plasma S and R ratio was shifted towards the S-isomer due to preferential clearance of the R-form. It was further found that neither a genetic disposition (gender, metabolic phenotype) nor age or the dose applied had any influence on the measured plasma isomer ratio.

Adult↗
PubMed1994

[Indications and contraindications for therapy with implantable cardioverters/defibrillators].

Despite all advances in the diagnostic and therapy of cardiovascular diseases the mortality from malignant ventricular tachyarrhythmias is still a major health problem. In addition to established therapeutic strategies in the prevention of sudden cardiac death such as antiarrhythmic drug treatment, catheter ablation or antiarrhythmic surgery the implantable cardioverter/defibrillator was introduced to clinical practice in 1980. The number of 50,000 overall implants reflects the current clinical status of the therapy with implantable cardioverters/defibrillators. Significant technical improvements in the defibrillator therapy may contribute to an increase in therapy acceptance. These advances include the introduction of nonthoracotomy lead systems, enhanced defibrillation efficacy, full programmable devices providing tiered electrical therapy, improved diagnostic Holter functions and enhanced arrhythmia detection algorithms. The major present goals of defibrillator therapy are, detection and termination of malignant ventricular tachyarrhythmias, reduction of sudden cardiac death, reduction in patient's mortality and improvement in quality of life. The efficacy and safety of defibrillator therapy to prevent sudden arrhythmic death has been proven in several large clinical investigations. The annual sudden cardiac death mortality is < 2% even in high-risk patient populations. Compared to sudden cardiac death rate there is a much higher rate of overall cardiac mortality because a defibrillator is not able to prevent nonarrhythmic cardiovascular deaths. There is a clinical impression that cardiovascular mortality is lower in patients treated with an implantable cardioverter/defibrillator compared to patients treated with other therapies. However there are no results from controlled studies providing scientific evidence that defribillator therapy can reduce overall cardiovascular mortality.(ABSTRACT TRUNCATED AT 250 WORDS)

Contraindications↗
PubMed1994

[The anti-ischemic effect of phosphodiesterase III inhibitors].

When enoximone is acutely administered to patients with stable angina and angiographically proven relevant coronary stenosis i.v. application of 0.75 mg/kg exhibits pronounced antiischemic effects. This could be observed in patients during exercise and in those in whom the ischemia was provoked by rapid cardiac stimulation. The antiischemic effects were documented by relief of symptoms, reduction of ST-depression, improvement of impaired myocardial wall motion, decrease to normalization of pathologically elevated filling pressure, amelioration of coronary blood flow as evidenced by myocard scintigraphy and washout time of an intracoronarily injected echo-contrast medium. There was also a definite improvement of ischemia-caused mitral regurgitation. Similar observations were found when the drug was injected in the diseased coronary arteries in a small dose (0.075 mg/kg) so that peripheral effects were not present. In comparison to the Ca(++)-blocker Gallopamil the antiischemic effects of Enoximone were more pronounced, a synergistic action was, however, observed. Negative dromotropic effects of Gallopamil could be abolished by Enoximone. With oral administration of the drug over a period of one week antiischemic effects could also be documented with Holter monitoring as well as during exercise. There was a reduction of ST-depression both at spontaneously occurring ischemic episodes and during exercise, in the number and duration of episodes of silent ischemia, particularly, however, a decrease in symptomatic episodes. In none of the patients under study proarrhythmic effects were observed.

Administration, Oral↗
PubMed1994

[Neurohumoral and hemodynamic effects in combination therapy of enoximone and dopamine].

Twelve patients with severe heart failure (NYHA class III-IV) were investigated by intraindividual comparison for the hemodynamic and neurohumoral effects of dopamine (3 and 6 micrograms/kg/min), enoximone (8 micrograms/kg/min), and the combination of both medications (dopamine 3 micrograms/kg/min+enoximone 8 micrograms/kg/min) using right heart catheterization. The duration of active treatment was 8 h for each substance with a subsequent washout time of 16 h. Dopamine led to a dose-dependent increase in cardiac index of 10-13% and 18-37% under 3 and 6 micrograms/kg/min, respectively (p < 0.001). Enoximone monotherapy produced a comparable increase in cardiac index between 27 and 32% (p < 0.001). Enoximone, but not dopamine, resulted in a significant decrease in mean pulmonary artery pressure (21-26%; p < 0.01), pulmonary capillary wedge pressure (24-30%; p < 0.01), and right atrial mean pressure (26-28%; p < 0.001). The systemic vascular resistance was without significant changes at low-dose dopamine therapy, decreased by 10-19% insignificantly at a dose of 6 micrograms/kg/min, and reached the level of significance with enoximone therapy (-20 to -25%; p < 0.001). There was a highly significant decrease by 49-55% in systemic vascular resistance with enoximone (p < 0.001), in contrast to dopamine. Heart rate and blood pressure remained without significant changes at low-dose dopamine, with the heart rate increasing significantly by 25% at a dose of 6 micrograms/kg/min within the first 2 h (p < 0.01). Enoximone produced a heart rate increase by 8-13% (being significant after 2 h; p < 0.05) with no changes in blood pressure. The combination therapy with dopamine and enoximone led to an additive increase in cardiac index by 35-43% (p < 0.001), a decrease in right atrial mean pressure by 28-36% (p < 0.01), a decrease in systemic vascular resistance by 27-30% (p < 0.01) and in pulmonary vascular resistance by 46-51%. An additive effect on heart rate was not observed. The respective monotherapies with low-dose dopamine and enoximone had no remarkable effect on plasma catecholamines, while dopamine at a dose of 6 micrograms/kg/min and combination therapy led to a significant increase in noradrenaline levels. There was a highly significant decrease in the plasma concentration of the atrial natriuretic factor under enoximone and combination therapy (p < 0.001) as well as a significant decrease in aldosterone (0 < 0.05).(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1994

[Doppler and echocardiography parameters in detection of acute graft rejection after heart transplantation].

Due to the invasive nature of myocardial biopsies, a complication rate of up to 2.5%, and the limitations, e.g., at focal distribution of rejection, there is a continuous need for reliable, non-invasive parameters in recognizing moderate (grade 2) and severe (grade 3) acute cardiac allograft rejections in patients treated with cyclosporine A. 64 biopsies of 20 patients with previous heart transplantations in the past 3 weeks to 36 months (mean 11 months) were compared prospectively to Doppler and echocardiographic results. Parameters of systolic function such as percent fractional shortening (FS) and systolic wall thickness of the posterior wall (SWT) remained without significant changes at grade 2 and grade 3 rejections. The same is valid for relaxation parameters such as maximum velocity of posterior wall reduction (PTR), the time interval of endsystole to maximum velocity of posterior wall reduction (tES-PTR), and the isovolumic relaxation time (IVRT). Left-ventricular filling parameters such as maximum early diastolic flow velocity (VEmax) increased significantly from 73.3 +/- 15.2 cm/s in the rejection-free interval (grade 0) to 103.9 +/- 15.0 cm/s at grade 2 rejection and 101.1 +/- 9.2 cm/s at grade 3 rejection (both p < 0.001). A sensitivity of 50% and a negative predictive value of 77% are, however, too low to diagnose or exclude a moderate or severe acute rejection in the individual case.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗
PubMed1993

Rapid and sensitive assay of dobutamine in plasma by high-performance liquid chromatography and electrochemical detection.

A sensitive and specific high-performance liquid chromatographic method with electrochemical detection was developed for measuring dobutamine in human plasma samples. Following an external standard method, 0.1 ml of EDTA-glutathione plasma was diluted on ice with 0.2 ml of a 5% trichloracetic acid solution. The mixture was centrifuged, filtered, and 30 microliters were injected. Assessment was done by electrochemical detection. The assay was linear from 1 to 400 ng/ml plasma. For determination of dobutamine we also used a liquid-liquid extraction method routinely applied for plasma catecholamines. Liquid-liquid extraction requires application of 100-1000 microliters of plasma. The standard curve was linear from 0.1 to 600 ng/ml. Absolute recovery of dobutamine was 90 +/- 3% with the liquid-liquid extraction procedure and 91 +/- 3% with the protein precipitation method. For both methods dobutamine was separated on Nova-Pak C18 columns. The mobile phase used was 0.1 molar phosphate buffer-acetonitrile (80:20, v/v) with 1-octanesulfonic acid and triethylamine as ion-pair reagents. The pH was adjusted to 2.7.

Chromatography, High Pressure Liquid↗
PubMed1993

A familial hypertrophic cardiomyopathy locus maps to chromosome 15q2.

We report that a gene responsible for familial hypertrophic cardiomyopathy (FHC) in a kindred with a mild degree of cardiac hypertrophy maps to chromosome 15q2. The gene encoding cardiac actin, located on chromosome 15q, was analyzed and excluded as a candidate for FHC at this locus. Two additional families with typical FHC were studied and the disorder in one also maps to the chromosome 15q2 locus. The maximum combined multipoint logarithm of odds score in the two linked families is 6.02. Although these two kindreds reside in the same country, we believe that their disorder is caused by independent mutations in the 15q2 locus because of the clinical and genotypic differences between affected individuals. Mutations in at least four loci can cause FHC: chromosomes 14q1 (beta cardiac myosin heavy chain gene), 1q3, and 15q2 and another unidentified locus, suggesting substantial genetic heterogeneity.

Adolescent↗
PubMed1993

High PAI activity with correlation to triglyceride and HDL cholesterol values in patients with coronary artery disease with no difference in survivors of myocardial infarction.

The fibrinolytic capacity of blood depends mainly on the amount of tissue-type plasminogen activator (t-PA) activity and plasminogen activator inhibitor type-1 (PAI-1) activity. Previous studies linked high PAI activity or low t-PA activity with the development of atherosclerosis and thromboembolic diseases. Yet, there are conflicting reports in the literature as to whether there is higher PAI activity in patients with myocardial infarction (MI) than in patients with coronary artery disease (CAD) without previous MI. In this retrospective study, t-PA activity, t-PA antigen, and PAI activity before and after a venous occlusion test (VOT) of 10 min were assessed in 109 patients with angiographically documented CAD, in two subgroups of CAD patients with (n = 66) or without (n = 43) previous MI, and in subgroups of CAD patients according to their triglyceride levels and other risk factors. The mean values of t-PA activity in the whole patient group showed a 100-fold increase and a 3.1-fold increase in t-PA antigen after VOT (0.03 +/- 0.03 to 3.0 +/- 6.8 U/ml and 16.5 +/- 6.9 to 51.0 +/- 25.4 ng/ml, p < 0.05). PAI activity was 24.4 +/- 11.0 before and 19.6 +/- 13.2 U/ml after VOT. Within the CAD group, no difference was found between patients without MI and survivors of previous MI in PAI activity before VOT (24.6 +/- 10.7 vs. 24.3 +/- 11.3 U/ml) and after VOT (19.0 +/- 12.1 vs 20.0 +/- 14.0 U/ml), or t-PA activity before (0.03 +/- 0.01 vs. 0.04 +/- 0.04 U/ml) and after VOT (2.8 +/- 7.0 vs. 3.2 +/- 6.7 U/ml). In 39.4% of CAD patients elevated plasma PAI activity before VOT (> 25 U/ml) was found. This subgroup of patients represented the highest PAI activity after VOT (p < 0.05), the lowest t-PA activity after VOT (p < 0.001), and the highest triglyceride levels (p < 0.05). In 11% of the patients, a small increase in t-PA activity (less than 0.5 U/ml) after VOT was seen. This group showed the lowest t-PA antigen after VOT (p < 0.001) and the highest fibrinogen level (p < 0.05). Both subgroups showed the same distribution among patients with and without MI. CAD patients with triglyceride levels over 200 mg/dl had the highest PAI activity values before VOT (28.3 +/- 11.8 U/ml; p < 0.01) and after VOT (24.9 +/- 13.2 U/ml; p < 0.01), resulting in low t-PA activity after VOT (p < 0.01).(ABSTRACT TRUNCATED AT 400 WORDS)

Cholesterol, HDL↗
PubMed1993

Tedisamil (KC 8857) is a new specific bradycardic drug: does it also influence myocardial contractility? Analysis by the conductance (volume) technique in coronary artery disease.

To determine whether inotropism influences the bradycardic action of tedisamil, hemodynamic assessment was performed in 13 patients with ischemic coronary artery disease including analysis of end-systolic pressure-volume relationships after an infusion of tedisamil, 0.3 mg/kg, at rest, and during paced tachycardia stress. Slope Emax fell by 14% at rest (13 patients) and by 10% during tachycardia (6/13 patients), whereas loops of end-systolic pressure-volume relationships moved rightward; all parameter changes indicated a lack of significant inotropism loss with tedisamil (p > 0.05). Although the mean heart rate decreased from 77.5 to 64.7 beats/min and QTc duration increased by 14% (p < 0.05), filling pressure and dp/dtmin remained unchanged and vascular resistance increased by 30%. Parameters of left ventricular pump function (ejection fraction, stroke volume, left ventricular efficiency) decreased slightly (between 3% and 13%), whereas left ventricular volumes increased (end-diastolic volume by 6%, end-systolic volume by 23%). The respective parameter changes during tachycardia were comparable in tendency, and angina could no longer be induced during postdrug pacing stress. We concluded that the bradycardic effects of tedisamil are selectively generated without impairing either ventricular pump function or contractility in a clinically relevant fashion, whereas the postdrug anginal threshold appears elevated. Thus tedisamil can be used safely in ischemic coronary artery disease.

Aged↗
PubMed1993

123I-metaiodobenzylguanidine scintigraphy in the detection of irregular regional sympathetic innervation in long QT syndrome.

Twelve patients with the long QT syndrome were studied to determine the usefulness of 123I-metaiodobenzylguanidine (MIBG) single-photon emission tomography (SPECT) at 2 h and 6 h after injection; the results were compared to 10 healthy volunteers (controls). Uptake of MIBG in the left ventricle at 2 h after injection was significantly reduced in patients with the long QT syndrome (1.43 +/- 0.13 vs 1.66 +/- 0.15 in controls, heart-to-mediastinum ratio, P < 0.002) and washout after 6 h was faster on a planar view image. Decreased MIBG uptake could be observed preferentially in the anterior and lateral walls near the apex. The half-time values of MIBG washout from the left ventricle were significantly reduced in the long QT syndrome (6.4 +/- 1.5 h) compared to controls (16.7 +/- 15.3 h, P < 0.002). In three cases, the same pattern of disturbed activity distribution was maintained even after surgical left cardiac sympathetic denervation. The present results strongly support the hypothesis that an inhomogenous regional distribution of sympathetic nerve terminals accompanied by an overall reduction in their absolute number may play an important role in the pathogenesis of the long QT syndrome. Additional functional disturbances, possibly related to the uptake of catecholamines in the left ventricle may coexist with regional inhomogeneity of nerve terminals. The differences observed from one case to the other may be related to the variation in severity of the disease. MIBG SPECT imaging seems an interesting new tool for the quantitative assessment of presynaptic sympathetic nerve terminal disturbances in the left ventricle of patients with the long QT syndrome.

3-Iodobenzylguanidine↗
PubMed1993

[Stored intracardiac electrograms: accuracy of arrhythmia classification in patients with cardioverter/defibrillator system].

A cardioverter/defibrillator that is capable of storing endocardial electrograms before and after electrical device therapy was implanted in 29 patients presenting drug refractory ventricular arrhythmias. During a follow-up period of 7.5 +/- 4.6 months 15/29 patients (51%) experienced a total number of 112 pulse generator discharges. In 104 arrhythmia episodes the stored electrogram was analyzed. Morphological criterias of the stored electrogram as detectable P-waves and changes in the QRS-morphology during tachycardia compared to sinus rhythm served for classification of the documented arrhythmia. The analysis of the stored electrogram established a definitive diagnosis of the arrhythmia and allows to distinguish supraventricular arrhythmias from ventricular arrhythmias in every episode. 72/104 (69.2%) of the discharges were classified as appropriate, 32/104 (30.8%) of the device discharges were not appropriate and caused by atrial fibrillation and flutter, sinustachycardia and AV-nodal reentrant tachycardia. In two patients device discharges caused by a sensing malfunction ot the pulse generator was detected by the analysis of the stored electrogram. The new diagnostic feature of stored electrogram shows a high accuracy of rhythm classification and represents a major advance in the treatment with cardioverter/defibrillators.

Aged↗
PubMed1993

[Cardioverter-defibrillator implantations without thoracotomy: clinical experience with various electrode configurations and defibrillation wave forms of an endocardial/subcutaneous defibrillator system].

Twenty-seven consecutive patients with refractory ventricular arrhythmias were investigated for implantation of an nonthoracotomy cardioverter-defibrillator lead system. Supply with a nonthoracotomy lead system could be achieved in 25 of 27 patients (92.5%), while implantation proved impossible in two patients due to elevated defibrillation thresholds. After implantation of an endocardial defibrillation electrode no differences were found compared to the implantation of an endocardial defibrillation electrode with a subcutaneous chest wall defibrillation patch with regard to the defibrillation thresholds obtained for monophasic defibrillation waveform. Supply with an endocardial defibrillation lead system was successful in 18 of 25 patients (72%). Ten consecutive patients with implantation of an endocardial defibrillation lead system alone were compared for defibrillation efficacy following monophasic and biphasic defibrillation waveforms. Defibrillation with biphasic waveforms led to a decrease in the necessary defibrillation energy from 19 J (4.6 J) to 10 J (4.0 J). There was occurrence of refractory ventricular fibrillation that could not be controlled by endocardial and transthoracic defibrillation in two patients during the intraoperative testing of defibrillation thresholds. In both cases these arrhythmias could be terminated by the described method of endocardial/extrathoracic defibrillation (200 J). Further perioperative complications were not observed. Over a mean follow-up of 6.8 (1-17) months all patients demonstrated regular functioning of the cardioverter-defibrillator. Dislocation of defibrillation electrodes did not occur. Implantation of a cardioverter-defibrillator can be performed without thoracotomy in the majority of cases. The use of defibrillator systems with biphasic waveform widens the scope for implantation of nonthoracotomy defibrillating lead systems.

Adult↗
PubMed1993

[Is the bradycardic effect of tedisamil at the expense of the loss of the inotropic effect? A pressure-volume analysis with the conductance (volume) catheter technique in patients with coronary artery disease].

UNLABELLED: To exclude or prove potential inotropic influences from tedisamil's bradycardiac effects, our hemodynamic evaluation in 13 patients (pat.) with coronary artery disease (CAD) included analyses of end-systolic pressure-volume relationships (ESPVR) after tedisamil, 0.3 mg/kg infusion at rest and during tachycardia induced by atrial pacing. Slope Emax [mm HG/ml] fell by 14% at rest (13 pat.) and by 10% during paced tachycardia (6/13 pat.) while loops of ESPVR tended to move rightward towards larger volumes (p > 0.05): all parameter changes indicated lack of significant inotropy loss with tedisamil. While mean heart rate decreased from 77.5 to 64.7 b/min and QTc duration increased by 14% (p < 0.05), filling pressure as well as dP/dtmin remained unchanged and vascular resistance rose by 30%. Parameters of LV-pump function (ejection fraction, stroke volume) decreased slightly (between 3 and 13%), while LV-volumes increased (end-diastolic by 6%, end-systolic by 23%). The respective parameter changes during paced tachycardia were comparable in tendency. CONCLUSION: Tedisamil's bradycardic effects are selectively generated without impairing either ventricular pump function or contractility in a clinically relevant fashion. Thus, tedisamil can be used safely in CAD.

Aged↗