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Biomedical subjects

D Baumgart

Publications and source records attributed to D Baumgart.

119 records · Page 7Linked to original sources
PubMed1989

[Surgical therapy of life-threatening tachycardic cardiac arrhythmias in children].

Surgical techniques for tachyarrhythmias refractory to medical treatment are used with increasing frequency. Among 211 patients undergoing antiarrhythmic surgery 10 children (2 to 14 years old) were operated by electrophysiologically directed procedures. 7 patients suffered from WPW syndrome, 2 from focal atrial tachycardias and 1 from recurrent ventricular tachycardia following the repair of Fallot's tetralogy. In all cases preoperative electrophysiologic study and intraoperative mapping preceded operative ablation. Surgical treatment consisted of interruption of the bundle of Kent (3 right-sided, 2 left-sided, 3 septal), ablation of the atrial focus (1 right-sided, 1 left-sided) and right ventricular outflow tract incision. In 7 operations cryo-techniques were added. 2 children with WPW syndrome had two interventions because of tachycardia recurrences due to multiple accessory pathways. In 1 case a VVI-pacemaker was implanted postoperatively due to complete atrioventricular block. Another 2 children with prolonged postoperative bradycardia received a pacemaker prophylactically. Only the child with previous tetralogy of Fallot is still under antiarrhythmic medication while all other children are free of tachycardiac episodes. Our data confirm the efficacy of surgical treatment of tachyarrhythmias in children thereby abolishing the need for life-long antiarrhythmic medication.

Adolescent↗
PubMed1988

Surgical alternatives in the treatment of life-threatening ventricular arrhythmias.

We present our experience in the treatment of life-threatening ventricular tachycardia using electrophysiologically guided surgery (97 patients), automatic implantable cardioverter defibrillator (AICD) (42 patients), and orthotopic heart transplantation (15 patients). Eighty-three percent of these patients had ischemic and 17%, nonischemic heart disease. Our results of electrophysiologically directed surgery show an early mortality of 10% and a recurrence of 5% in the ischemic group. In the nonischemic group, the recurrence was 45%. The AICD was implanted in 31 patients with ischemic heart disease, in 5 with ventricular dysplasia, and in 6 with dilative cardiomyopathy, the ejection fractions ranging from 12% to 65%, with a mean of 30%. Early and late mortalities were 5% and 19%, respectively. The AICD was effective in all patients. Survival rate at 1 year was 83% +/- 6.4%. Thirteen of 15 patients have survived heart transplantation for 3-20 months (mean: 11 months). Ejection fractions prior to transplantation ranged from less than 10% to 34% (mean: 16%). We conclude that electrophysiologically guided surgery is highly effective in most cases of ischemia-related ventricular tachycardia. The AICD is considered a palliative alternative in patients with either poor ventricular function, no electrophysiological substrate, or multimorphological tachycardia. Heart transplantation has to be considered especially in young patients in whom progression of the underlying disease can be anticipated. Bridging by AICD is possible when transplantation is not immediately available or recommendable.

Adolescent↗
PubMed1987

[Ectopic atrial tachycardia: surgical therapy (case report and review of the literature)].

Focal atrial tachycardia with frequencies up to 200/min in an 11-year-old girl had been resistant to drugs over a period of 5 years. An electrophysiological study demonstrated a left atrial ectopic tachycardia. Intraoperative epicardial mapping localized the automatic focus at the base of the left atrial appendage. Excision of the appendage and cryoablation of the adjacent area were performed using cardiopulmonary bypass. Histological examination of the excised tissue showed no specific alterations aside from islets of fatty tissue. The girl has been in sinus rhythm and has shown no tachycardias during the 6 months following the operation. Review of the literature covering 17 cases of right and 12 cases of left atrial focal tachycardia indicates excision of the atrial tissue in combination with cryoablation to be the treatment of choice to ensure success.

Child↗
PubMed1986

Successful surgical treatment of focal atrial tachycardia--a case report and review of the literature.

Focal atrial tachycardia with frequencies up to 200/min in an 11-year-old girl had been resistant to drugs over a period of 5 years. An electrophysiological study demonstrated a left atrial ectopic tachycardia. Intraoperative epicardial mapping localized the automatic focus at the base of the left atrial appendage. Excision of the appendage and cryoablation of the adjacent area were performed using cardiopulmonary bypass. Histologic examination of the excised tissue showed no specific alterations aside from islets of fatty tissue. The girl has been in sinus rhythm and has shown no tachycardias during the 6 months following the operation. A review of the literature, covering 17 cases of right and 12 cases of left atrial focal tachycardia, indicates excision of the atrial tissue in combination with cryoablation to be the treatment of choice to ensure success.

Child, Preschool↗
PubMedDate not supplied

Characterization of the inotropic and arrhythmogenic action of the sodium channel activator BDF 9148: a comparison to its S-enantiomer BDF 9196, to its congener DPI 201-106, to norepinephrine, and to ouabain.

Positive inotropic substances which enhance the myocardial cAMP level or inhibit the Na+/K(+)-ATPase are known for their proarrhythmic side-effects. This study was performed to investigate the inotropic and arrhythmogenic action of the Na(+)-channel activator BDF 9148 (racemate) in comparison to its S-enantiomer BDF 9196, its congener DPI 201-106 (racemate), to norepinephrine, and to ouabain. In 30 open-chest dogs, the effects of these substances on the first derivative of left ventricular pressure (dP/dt, Millar-tip catheter) and anterior systolic wall thickening (AWT, sonomicrometry) were studied. Concomitantly, myocardial excitability, conduction times, and refractory period were assessed with a transmural, three-dimensional, 16-electrode array in the anterior wall. For the study of the Na(+)-channel activators, alpha- and beta-adrenergic and muscarinic receptors were blocked. A first set of measurements was performed during normoperfusion with administration of BDF 9148 (1 mg/kg, n = 8), BDF 9196 (0.5 mg/kg, n = 8), and DPI 201-106 (1 mg/kg, n = 8), respectively. A second set of measurements was performed with administration of the threefold dosage of either substance. With a severe stenosis on the left anterior descending coronary artery, a final set of measurements was performed, again using the higher dosage of either substance. For the study of norepinephrine (0.5 micrograms/kg/min i.v., n = 6) and ouabain (40 micrograms/kg i.v., n = 4), measurements were performed during normoperfusion in additional animals. Under normal conditions, either Na(+)-channel activator induced increases in dP/dtmax (lower dosage: 45-84%, higher dosage: by 93-117%) and AWT (lower dosage: by 24-37%, higher dosage: by 19-56%). Under ischemic conditions, either drug increased dP/dtmax by 60-98% and AWT by 45-102%. Excitability, conduction times, and refractory period did not change significantly in response to the Na(+)-channel activators, neither under normal nor under ischemic conditions. There was no significant difference in the incidence of spontaneous ventricular extrasystoles before and after administration of either Na(+)-channel activator. In contrast, an equi-inotropic dosage of norepinephrine (increases in dP/dtmax by 148% and AWT by 42%) increased excitability, decreased conduction times and refractory period, and increased the incidence of spontaneous ventricular extrasystoles. Ouabain induced only a moderate increase in dP/dtmax by 56% and AWT by 24%, but elicited sustained and complex ventricular arrhythmias. Excitability was markedly increased, whereas conduction times and refractory period changed only little.(ABSTRACT TRUNCATED AT 400 WORDS)

Analysis of Variance↗
PubMedDate not supplied

Neuronal control of coronary blood flow.

Controversies on acetylcholine-induced increases or decreases in coronary blood flow arise from obvious species differences, the role of endothelium in mediating vascular smooth muscle responses, and the marked negative chronotropic and inotropic effects of acetylcholine. In man, there appears to be a predominant dilation of intact epicardial coronary arteries and a constriction of artherosclerotic segments. However, at present there is no evidence for a vagal initiation of myocardial ischemia. Coronary vascular beta-adrenergic receptors mediate dilation, but appear to be functionally insignificant during sympathetic activation. The beta-adrenergic mechanism contributing to myocardial ischemia are indirect, mediated by a tachycardia-related redistribution of blood flow away from the ischemic myocardium. alpha-Adrenergic receptors mediating epicardial coronary artery constriction in experimental studies appear not to be responsible for the initiation of ischemia in patients with angina at rest. However, alpha-adrenergic constriction of coronary resistance vessels resulting in the precipitation of post-stenotic myocardial ischemia was demonstrated in experimental studies and recently confirmed in patients with effort angina. Non-adrenergic, non-cholinergic neurotransmitters exist; however, their role in regulating coronary blood flow remains entirely unclear.

Acetylcholine↗
PubMedDate not supplied

Three-dimensional analysis of regional mechanical function, blood flow and electrophysiological parameters during early myocardial ischemia in dogs.

Ventricular arrhythmias are primarily responsible for sudden cardiac death early after the onset of acute myocardial ischemia. We designed an experimental model to simultaneously characterize regional myocardial function, myocardial blood flow, and electrophysiological parameters, and to determine predisposing factors for the development of early ventricular arrhythmias (EVA). The left circumflex coronary artery was occluded in six anesthetized (n = 2 piritramide/N2O, n = 4 chloralose/urethane) mongrel dogs. Systolic wall thickening (%WT) in a control zone and in the central ischemic zone was measured with sonomicrometry and regional myocardial blood flow (RMBF) with colored microspheres. Excitability and relative refractory period at the stimulus electrode and conduction times to all other electrodes were determined with a three-dimensional transmural multi(16)-electrode assay using a computer algorithm. In three of six dogs spontaneous EVA occurred 4 to 6 min after coronary occlusion, degenerating to ventricular fibrillation in two of these dogs. The three dogs developing EVA were not distinguished from those not developing EVA, neither by the kind of anesthesia nor by ischemic % WT (-6.6 +/- 3.8 [SD] vs -7.8 +/- 1.6, ns). Also, dogs with and without EVA did not differ significantly in excitability and relative refractory period. In contrast, dogs with EVA were characterized by a greater mass of severely ischemic myocardium, i.e., exhibiting a RMBF reduction to less than 0.1 ml/(min.g) (18 +/- 3 g vs 7 +/- 4 g, p less than 0.05), and by an increase in subendocardial conduction times of greater than 100% above the respective pre-ischemic values (120 +/- 18% vs 66 +/- 9%, p less than 0.05). Dogs with and without EVA were not as clearly distinguished by the increases in subepicardial (81 +/- 22% vs 46 +/- 15%, ns) and transmural (98 +/- 31% vs 67 +/- 14%, ns) conduction times. The development of EVA is associated with a greater mass of severely ischemic myocardium and a greater increase in subendocardial conduction times.

Animals↗
PubMedDate not supplied

Tomographic left ventricular volume determination in the presence of aneurysm by three-dimensional echocardiographic imaging. I: Asymmetric model hearts.

To improve the accuracy of measurements of left ventricular volume in the presence of an aneurysm, we used three-dimensional echocardiographic imaging to analyze the shape of left ventricles in 23 asymmetric model hearts with eccentric aneurysms of different sizes, shapes, and localizations. A standard 3.75 MHz ultrasound probe with a rotation motor device was used to obtain a three-dimensional data set. By rotating the probe stepwise 1 degree, 180 radial ultrasound pictures were digitized. On the basis of the three-dimensional data set, the following parameters were determined and compared with the dimensions of the model hearts obtained by direct measurement: total left ventricular volume (LVV), aneurysm volume, area of the aneurysm's base, the longest aneurysm long diameter, and the longest aneurysm cross diameter. In addition, quantification of LVV by three-dimensional echocardiography was compared with biplane two-dimensional echocardiographic measurement according to the disk method. Good agreements were found for LVV measured by both techniques, three-dimensional echocardiographic and direct measurement (mean of differences = 0.91 ml; SD of differences = +/- 6.23 ml; line of regression y = 1.07 x - 14.24 ml; r = 0.968; standard error of the estimate [SEE] = +/- 6.17 ml), aneurysm volume (mean of differences = 0.43 ml; SD of differences = +/- 2.14 ml; line of regression y = 1.05 x - 0.81 ml; r = 0.996; SEE = +/- 1.96 ml), area of the aneurysm's base (mean of differences = 0.24 cm2; SD of differences = +/- 1.72 cm2; line of regression y = 1.02 x - 0.02 cm2; r = 0.981; SEE = +/- 1.75 cm2), the longest aneurysm long diameter (mean of differences = -0.26 mm; SD of differences = +/- 1.60 mm; line of regression y = 0.97 x + 1.34 mm; r = 0.996; SEE = +/- 1.54 mm), and the longest aneurysm cross diameter (mean of differences = 1.35 mm; SD of differences = +/- 3.94 mm; line of regression y = 0.95 x + 3.17 mm; r = 0.941; SEE = +/- 3.99 mm). In contrast, in these extremely asymmetric-shaped model hearts, agreement between biplane two-dimensional echocardiographic and both direct LVV measurement (mean of differences = 7.8 ml; SD of differences = +/- 20.8 ml; line of regression y = 1.48 x - 92.45 ml; r = 0.874; SEE = +/- 18.36 ml) and three-dimensional echocardiographic measurements (mean of differences = -7.6 ml; SD of difference = +/- 18.1 ml; line of regression y = 0.59 x + 80.98 ml; r = 0.908; SEE = +/- 10.36 ml) was poor. Thus tomographic three-dimensional echocardiography allowed accurate volume determination of asymmetric model hearts in the shape of left ventricles with eccentric aneurysms.

Cardiac Volume↗
PubMedDate not supplied

The influence of guiding equipment and stents on the beta dose distribution in the brachytherapy of in-stent restenosis.

BACKGROUND: Intracoronary devices such as stents or guide wires may disturb the dose distribution of beta sources in cardiovascular brachytherapy. As clinical observations indicate that underdosage increases the risk of restenosis, accurate measurements are mandatory to investigate these effects. METHODS AND RESULTS: Dose perturbation effects of different interventional equipment were systematically determined. Dose distributions of 90Sr-beta line sources were measured by means of a special set-up employing plastic scintillator dosimeters in a water phantom. Shielding effects were found to be 2-5% for single stents and 5-10% for graft stents, stent-in-stent geometries, and guiding catheters. Guide wires close to the source reduced the dose by 25-30%. CONCLUSIONS: Beta dose perturbation effects of typical stent types are almost negligible and can be corrected by an increased source dwell time if necessary. Guide wires produce effects which are clinically much more important and should therefore be retracted from the irradiation area.

Brachytherapy↗
PubMedDate not supplied

Coronary microembolization.

Atherosclerotic plaque rupture is a key event in the pathogenesis of acute coronary syndromes and during coronary interventions. Atherosclerotic plaque rupture does not always result in complete thrombotic occlusion of the entire epicardial coronary artery with subsequent acute myocardial infarction; however, in milder forms it may result in the embolization of atherosclerotic and thrombotic debris into the coronary microcirculation. The present report summarizes the available morphologic evidence for coronary microembolization in patients who died of coronary artery disease, especially sudden death. The report then goes on to address the experimental pathophysiology of coronary microembolization in animal models of acute coronary syndromes and heart failure. Finally, the report presents the available clinical evidence for coronary microembolization, highlights its key features--arrhythmias, contractile dysfunction, infarctlets and reduced coronary reserve--and addresses prevention by mechanical protection devices and glycoprotein IIb/IIIa antagonism.

Animals↗