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Biomedical subjects

J Senges

Publications and source records attributed to J Senges.

At least 127 records · Page 7Linked to original sources
PubMed1995

[The T-wave shock: a new reliable method for induction of ventricular fibrillation in ICD testing].

During ICD-implantation it is necessary to induce ventricular fibrillation several times to determine the defibrillation threshold. In third generation ICDs there are several options to induce ventricular fibrillation. We want to present a new method, called T-wave-shock, which is first available in the PCD Jewel 7219 (Medtronic). The T-wave-shock is the delivery of a low-energy-shock into the vulnerable period after ventricular stimulation with a basic cycle-length. We applied the T-wave-shock in 46 consecutive ICD-recipients intraoperatively and at the pre-hospital-discharge test. The method is highly effective when applying the shock into the ascending part of the T-wave (98% of the patients were inducible), and the duration of cardial and cerebral ischemia during induction is short (between 3.1 and 3.8 s). This raises defibrillation efficacy.

Adult↗
PubMed1995

[Takayasu arteritis--a rare differential diagnosis in aortic dissection. A case report].

A 36-year-old woman was delivered to our hospital with suspected aortic dissection from an outlying hospital in May 1994. She reported a history of acute and persistent thoracic and epigastric pain. The physical examination revealed a minor senso-motorical palsy of the left side as residuum after minor strokes occurring 12/93 and 4/94. Also, a marked hypertension (170/100 mm Hg) was present. The hematologic and blood chemical values were normal with a white cell count of 12,000, an erythrocyte sedimentation rate (ESR) of 19 mm/h and a c-reactive protein (CRP) of 2.2 mg/dl. The electrocardiogram was normal. Transthoracic- and transesophageal-echocardiography (TTE, TEE) revealed an eccentric thickening of the whole wall of the descending aorta up to the bifurcation with a stenosis at the side of the diaphragma. Those findings were confirmed by computed tomography. Because of the acute onset of symptoms and the results of the imaging procedures aortic dissection de Bakey type III was diagnosed and the patient was treated with beta-blockers. Symptoms were relieved over the following days. After 2 days a pleuric effusion developed and all inflammatory tests rose (fibrinogen 780 mg/dl, ESR 80 mm/hr, CRP 16 mg/dl). At this time the differential diagnosis of an arteritis was considered. A new TEE-study demonstrated no change, but now more attention was given to the fact that no dissection membrane could be visualized and all wall structures were thickened. In combination with the history of cerebral infarction due to carotid obstruction and the elevated laboratory values the diagnosis of Takayasu-aortitis was established and corticoid therapy was started. Within a few weeks the arterial changes diminshed markedly and the woman became free of symptoms. This case demonstrates the rare situation of an arteritis mimicking aortic dissection, in which the clinical course revealed the true diagnosis.

Adult↗
PubMed1994

Intraindividual comparison of diltiazem and verapamil on induction of paroxysmal supraventricular tachycardia.

The effects of i.v. diltiazem (0.25 mg/kg) and i.v. verapamil (0.15 mg/kg) were studied in 18 patients with recurrent paroxysmal supraventricular tachycardia (SVT) who underwent serial electrophysiological studies. In 10 of 18 patients with extranodal accessory pathways the effects of diltiazem and verapamil were similar in comparable plasma concentrations. SVT was prevented in 10/10 cases after diltiazem and 9/10 cases after verapamil, furthermore there as an increase in antegrade refractoriness of the normal AV nodal pathway of 22 and 27%, respectively; accessory pathway refractoriness and conduction remained unchanged in both drugs. In 8 of 18 patients with dual AV nodal pathways diltiazem was significantly less effective as compared to verapamil (p < 0.02) regarding prevention ov SVT (3/8 vs. 8/8 cases) and increase in the antegrade refractoriness of the slow AV nodal pathway (+21 vs. +34%). However, both drugs produced equivalent slowing of antegrade AV nodal conduction and a similar increase in antegrade refractoriness of the fast AV nodal pathway. In all 18 patients, the site of action of both drugs was the antegrade limb, regardless of SVT mechanism. The data suggest that the two calcium antagonists are equipotent in AV reentrance but verapamil may offer greater benefit in AV nodal reentrance than diltiazem.

Adult↗
PubMed1992

[Intravenous thrombolysis in acute myocardial infarct: optimization of the therapeutic strategy by informing the patients and physicians].

Intensive education of patients and physicians helps to increase the incidence of thrombolytic therapy in patients with myocardial infarction. Important factors in this process are: 1. Reduced delays in patients' awareness of the severity of his symptoms, 2. shorter time periods from patients' hospital admission to the initiation of thrombolytic therapy, 3. more indications by educated physicians with a higher degree of precision, and 4. reduced catalogue of contraindications.

Aged↗
PubMed1987

Amiodarone in patients with recurrent sustained ventricular tachyarrhythmias: results of programmed electrical stimulation and long-term clinical outcome in chronic treatment.

Thirty-three patients with clinically recurrent ventricular tachyarrhythmias were treated with amiodarone (200 to 600 mg/day) during a mean follow-up period of 23.7 months. Prior to amiodarone therapy, sustained ventricular tachycardia or ventricular fibrillation was initiated in all patients at control electrophysiologic study; patients failed a mean of 5.7 drugs, as assessed by programmed electrical stimulation. At electrophysiologic study after a loading phase (1000 mg/day for 10 days), 10 patients had no inducible ventricular tachycardia, nine patients had nonsustained ventricular tachycardia, 13 patients had persistent sustained ventricular tachycardia, and one patient had ventricular fibrillation. Patients were continued on amiodarone alone regardless of the findings at the electrophysiologic study, and during follow-up patients with no inducible sustained ventricular tachycardia or fibrillation on amiodarone had no recurrent arrhythmias or sudden death. Six of 14 patients (43%) with sustained ventricular tachyarrhythmias still inducible had recurrent ventricular tachycardia/fibrillation, and four of them died suddenly (29%). Programmed electrical stimulation predicts a good clinical long-term outcome during amiodarone therapy. Patients with persisting fast tachyarrhythmias (cycle length less than or equal to 300 msec) on amiodarone and a low ejection fraction (less than 35%) seem to have a higher incidence of sudden death. In these patients, therapeutic approaches such as antiarrhythmic surgery or implantation of antitachycardia devices should be considered.

Amiodarone↗
PubMed1987

Effects of intravenous disopyramide and quinidine on normal myocardium and on the characteristics of arrhythmias: intraindividual comparison in patients with sustained ventricular tachycardia.

Intraindividual comparison of the acute response to intravenous quinidine and to intravenous disopyramide was performed in 27 patients with sustained ventricular tachycardia (VT) who underwent serial electrophysiological studies. In each patient, sustained VT could be reproducibly initiated by programmed ventricular stimulation during control studies. Quinidine and disopyramide prevented inducibility of sustained VT in 7 and 8 of the 27 patients, respectively. Six patients were concordant responders to both drugs and 18 patients were concordant non-responders resulting in a total of 24 patients (89%) who had a concordant result (P less than 0.01). In the 18 non-responders with inducible sustained VT after both drugs, quinidine and disopyramide caused qualitatively and quantitatively similar changes in the characteristics of the VT: prolongation of the interval between the initiating extrastimulus and the first beat of VT by 36 and 39%, and an increase in VT cycle length by 21 and 29%, respectively. The QRS morphology of VT was concordantly altered in 13 of these 18 patients (72%). In all 27 patients, quinidine and disopyramide caused a quantitatively similar prolongation of ventricular refractoriness by 12 and 14%, of the QRS duration by 14 and 13% and of the QTc interval by 13 and 13%, respectively. The clinical data obtained at comparable plasma concentrations confirm the experimental presumption that quinidine and disopyramide have qualitatively and quantitatively similar electrophysiological effects not only on normal myocardium but also on the characteristics of VT, resulting in a significant concordance of antiarrhythmic responses.

Adult↗
PubMed1986

Effect of sotalol, aprindine and the combination aprindine-sotalol on monophasic action potential duration.

The effects of sotalol, aprindine and the combination aprindine-sotalol in the intact dog heart were evaluated during constant atrial pacing with the use of monophasic action potential (MAP) recording. A first group of five dogs was given 1.5 mg kg-1 body weight of sotalol, followed by a second infusion of 1.5 mg kg-1 30 min later. Both doses of sotalol produced a statistically significant increase in right atrial MAP duration at 50% of repolarization (RAMAP50) and right ventricular MAP duration at 90% of repolarization (RVMAP90). To a second group of six dogs aprindine 1 mg kg-1 and aprindine 2 mg kg-1 were administered intravenously. The infusion of aprindine did not alter right atrial and right ventricular MAP duration. The addition of 1.5 mg kg-1 of sotalol to the dogs pretreated with aprindine 2 mg kg-1 resulted in a 25% increase in RAMAP50 and a 21% prolongation of RVMAP90. In summary, sotalol lengthens atrial and ventricular monophasic action potential duration and still prolongs repolarization of monophasic action potentials after previous administration of aprindine. A combination of sotalol, a beta-adrenergic blocker possessing class III efficacy, with a class I antiarrhythmic agent may be useful with respect to their electro-physiological action.

Animals↗
PubMed1985

The conduction and cardiac sympathetic systems: metabolic aspects.

Compared with the myocardium, glycolytic enzymes are reduced by 50% and mitochondrial enzymes and space by 70% in the conduction system of the calf heart. In addition, on the basis of adenosine triphosphate activities energy demands are reduced by more than 50%; this is in parallel with the reduction in myofibrillar space. The increased tolerance of the conduction system against ischemia can be explained by a reduction of energy demands and a higher proportion of (anaerobic) glycolytic as opposed to aerobic mitochondrial energy production. Among the structures of the conduction system, the sinoatrial and atrioventricular nodes are markedly susceptible to hypoxia in contrast to atrial conduction and ventricular conduction by way of the His-Purkinje system. In the isolated perfused rat heart, an increased net release of noradrenaline during the first 10 minutes of ischemia is only noted after sympathetic stimulation. During this phase, catecholamine overflow is limited by the activity of the neuronal reuptake. At a later second phase, from 15 to 40 minutes after the onset of ischemia, the mechanism of noradrenaline net release is carrier-mediated efflux inhibited by neuronal uptake blocking agents. During the third phase of ischemia, after about 40 minutes, spontaneous noradrenaline release is greatly augmented, probably as a result of leakage caused by membrane damage.

Animals↗
PubMed1985

Contribution of delayed ventricular repolarization to the anti-arrhythmic efficacy of sotalol.

Eighteen patients with sustained ventricular tachycardia underwent serial electrophysiological studies to establish the therapeutic efficacy of sotalol as compared to other available anti-arrhythmic agents. One or more acutely effective drug was found in 14 of the 18 patients (78%). Sotalol was tested in all 18 patients and was effective in 12 of them (67%). For assessment of the prophylactic efficacy of other anti-arrhythmic agents, an average of 3.5 additional studies per patient were performed resulting in successful prevention of ventricular tachycardia in a total of 10 of 63 (16%) additional trials. Nine patients were placed on chronic oral therapy with sotalol. In these nine patients long-term prophylaxis against ventricular tachycardia was documented over a mean follow-up period of 9.6 months (range 2-18 months). The study suggests that sotalol can provide effective prophylaxis against ventricular tachycardia in a significant proportion of patients refractory to other available drugs and that this prophylactic efficacy is predominantly due to its Class III anti-arrhythmic properties. Experimental studies were performed in eight conscious dogs 3-7 days following proximal LAD ligation. Epicardial recordings were obtained using implanted composite electrodes. Sotalol prevented sustained VT by a predominant increase in refractoriness of the infarcted zone. In vitro, sotalol caused a significant prolongation of the action potential of epicardial and endocardial fibres within both the infarcted and noninfarcted myocardium. Refractoriness of epicardial ventricular fibres was significantly more prolonged in ischemically damaged cells as compared to normal fibres.

Animals↗
PubMed1985

Intraindividual comparison of intravenous ajmaline and quinidine in patients with sustained ventricular tachycardia: effects on normal myocardium and on arrhythmia characteristics.

Intraindividual comparison of the acute response to intravenous quinidine and to intravenous ajmaline was performed in 23 patients with sustained ventricular tachycardia (VT) who underwent serial electrophysiological studies. In each patient, sustained VT could be reproducibly initiated by programmed ventricular stimulation during control studies. Inducibility of sustained VT was prevented after quinidine in 6 of the 23 patients (26%) and after ajmaline in 8 of the same 23 cases (35%). Agreement between the effects of both drugs was not significant: 2 patients had a similar response to both quinidine and ajmaline and 11 patients did not have a response to either of the two drugs, resulting in a total of only 13 patients (57%) who had a similar response to both drugs. In the 11 non-responders with inducible sustained VT before and after both drugs, quinidine and ajmaline caused qualitatively and quantitatively similar alterations of VT characteristics including a significant prolongation of the interval between the initiation extrastimulus and the first beat of VT by 38 and 42% (P less than 0.01), an increase in VT cycle length by 15 and 22% (P less than 0.01) and a prolongation of the QRS duration during VT by 15 and 18% (P less than 0.01), respectively. In all 23 patients, quinidine and ajmaline caused a quantitatively similar prolongation of ventricular refractoriness by 11 and 9% (P less than 0.05), of the QRS duration at sinus rhythm by 10 and 15% (P less than 0.01) and of the QTc interval by 13 and 10% (P less than 0.05), respectively. Thus, ajmaline and quinidine appear to have similar electrophysiological effects on both normal myocardium and on indirect parameters of reentry; in individual patients with sustained VT, however, such electrophysiological similarities do not result in significant agreement of preventive responses.

Adult↗