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Biomedical subjects

W Jung

Publications and source records attributed to W Jung.

At least 109 records · Page 6Linked to original sources
PubMed1998

Anti-CD16/CD30 bispecific antibodies as possible treatment for refractory Hodgkin's disease.

Fifteen patients with refractory Hodgkin's disease were treated in a phase I/II dose escalation trial with the NK-cell activating bispecific monoclonal antibody HRS-3/A9 which is directed against the Fcgamma-receptor III (CD16 antigen) and the Hodgkin's associated CD30 antigen, respectively. HRS-3/A9 was given four times every 3-4 days starting with 1 mg/m2. The treatment was well tolerated and the maximum tolerated dose was not reached at 64 mg/m2, the highest dose given due to limited amounts of HRS-3/A9 available. Mild to moderate side effects occured in six patients and consisted of fever, pain in involved lymph nodes, and a maculopapulous rash. Median counts of NK-cells and of all lymphocyte subsets were considerably decreased in the patients before therapy and showed no consistent changes under therapy. Eight patients developed human anti-mouse immunoglobulin antibodies, and five patients showed an allergic reaction after attempted retreatment. One complete and one partial remission (lasting 6 and 3 months, respectively), three minor responses (lasting 1 to 15 months), two disease stabilizations (for 2 and 17 months, respectively), and one mixed response were achieved. There was no clearcut dose-side effect or dose-response correlation. Our results encourage further clinical trials with this novel immunotherapeutic approach and emphasize the necessity to reduce the immunogenicity of the murine bispecific antibodies.

Adult↗
PubMed1998

Dose-dependent reduction of myocardial infarct mass in rabbits by the NHE-1 inhibitor cariporide (HOE 642).

The aim of this study was to investigate the dose-dependent effect of pretreatment with the selective sodium-hydrogen exchange NHE-subtype 1 inhibitor cariporide on myocardial infarct mass in a rabbit model of coronary ligation and reperfusion. Furthermore, in a second part of the study, we tested the effect of cariporide in the rabbits when given prior to reperfusion. Rabbits (n=49) were randomized in 7 groups: saline vehicle, cariporide: 0.01, 0.03, 0.1 and 0.3 mg/kg, and subjected to a 30 min occlusion of a branch of the left coronary artery followed by 2 h reperfusion. Cariporide was given as a bolus intravenously 10 min before occlusion or 5 min before reperfusion. After reperfusion, myocardial infarct mass was determined by triphenyl tetrazolium chloride staining and expressed as a percent of area at risk. Cariporide given intravenously 10 min before occlusion in doses of 0.01, 0.03, 0.1, 0.3 mg/kg, led to a dose-dependent reduction in infarct mass from 58+/-6% in controls to 48+/-4% (-17%, NS), 36+/-5% (-38%, p<0.05), 26+/-6% (-55%, p<0.05), 11+/-4% (-81%, p<0.05) respectively, whereas area at risk did not differ in between the groups. The effect of the lowest dose of 0.01 mg/kg did not reach significance. Plasma levels at different doses of cariporide were correlated to the respective infarct mass. After coronary occlusion left ventricular end-diastolic pressure (LVEDP) significantly increased throughout occlusion and reperfusion. Cariporide in the doses of 0.3, 0.1 and 0.03 mg/kg normalized LVEDP when measured after 2 h reperfusion. In controls hemodynamic parameters such as mean arterial blood pressure (MAP), heart rate (HR), left ventricular pressure (LVP) and LV dP/dt(max) were not significantly changed by ischemia/reperfusion with the exception of MAP, LVP and LV dP/dt(max) which were significantly decreased after 120 min reperfusion. Cariporide at doses of 0.1, 0.03 and 0.01 mg/kg did not significantly influence these parameters, whereas the highest dose of 0.3 mg/kg prevented the decrease of MAP and LVP. Cariporide (0.3 mg/kg i.v.) administered 5 min before reperfusion significantly reduced infarct mass by 31%. Under these conditions the increase of LVEDP after coronary occlusion was not influenced by cariporide. As in the pretreatment experiments, the decrease of MAP and LVP was prevented when measured 2 h after reperfusion. The results show that pretreatment with the NHE-subtype 1 inhibitor cariporide is cardioprotective by reducing infarct mass in rabbits in a dose-dependent manner. While the cardioprotective effect of pretreatment could be demonstrated over a broad range of doses, the efficacy of the compound when given only on reperfusion was significant but more limited.

Animals↗
PubMed1998

Left atrial appendage function after internal atrial defibrillation.

To determine the value of echocardiographic parameters for predicting maintenance of sinus rhythm after internal atrial defibrillation (IAD), transthoracic and transesophageal echocardiography were performed in 38 patients with atrial fibrillation (AF) before IAD. In addition, serial echocardiographic examinations were performed at 1, 7, and 28 days after IAD in 20 patients to assess the effect of IAD on echocardiographic markers of thromboembolic risk. AF had recurred in 49% of patients within 6 months following IAD. Left atrial chamber and appendage size and ejection fraction were not predictive of recurrence of atrial fibrillation. However, peak emptying velocities of the left atrial appendage were significantly lower in patients with recurrence of atrial fibrillation as compared with patients who had maintained sinus rhythm (0.26 +/- 0.1 m/sec vs 0.49 +/- 0.17 m/sec; P = 0.001). A peak emptying velocity < 0.36 m/sec had a sensitivity of 82% and specificity of 83% for predicting the recurrence of AF. Peak A wave velocities increased gradually after cardioversion from 0.47 +/- 0.16 m/sec at 24 hours to 0.61 +/- 0.13 m/sec after 7 days (P < 0.05). One patient developed a new thrombus in the left atrial appendage and another patient suffered a thromboembolic event after IAD. Assessment of left atrial appendage function adds information regarding the probability of maintaining sinus rhythm after the procedure and the need for anticoagulation therapy with IAD.

Anticoagulants↗
PubMed1998

Radiofrequency ablation of atrial flutter.

Atrial flutter can be understood as atrial tachycardia due to a single intra-atrial macroreentrant circuit that is determined by fixed or functional boundaries. In various types of atrial flutter, radiofrequency ablation has become an established curative therapy. During the course of an ablation procedure, five steps can be distinguished: (1) determination of the reentrant circuit; (2) identification of the boundaries; (3) proof of the participation of an isthmus between the boundaries in the reentrant circuit; (4) connection of the barriers by a linear lesion; and (5) proof that the line of block is complete. After establishing these five steps, the acute and long-term results of atrial flutter ablation are comparable to those of other supraventricular tachycardias. In this review, we discuss these principles of atrial flutter ablation with an emphasis on typical atrial flutter.

Atrial Flutter↗
PubMed1998

Quality of life in patients with atrial fibrillation.

INTRODUCTION: The efficacy of a treatment is based primarily on objective criteria such as mortality and morbidity. Besides these criteria, the interest in measuring quality of life in relation to health care has increased in recent years. METHODS AND RESULTS: Although the concept of quality of life inherently is subjective and definitions vary, it generally is agreed that quality of life is a multidimensional construct. The impact of atrial fibrillation (AF) on quality of life has not been evaluated widely using validated methods. Therefore, an international prospective study was designed to assess quality of life over time in patients with AF using validated generic measures and specific conducted disease scales. In addition to a standard demographic questionnaire, patients will complete two predictive scales at baseline and four outcome scales at baseline, and 3-, 6-, and 12-month follow-up. An AF severity score based on subjective and physician-recorded assessments will be used to classify the patient's burden of AF as mild, moderate, or severe. CONCLUSION: Rigorous yet practical approaches are needed to allow for a comprehensive understanding of quality of life in patients with AF. The international study design outlined in this review article represents an attempt to systematically address quality of life in patients with AF and may serve as an example of the types of measures that may be useful in assessing quality of life in patients with AF.

Animals↗
PubMed1998

Specific considerations with the automatic implantable atrial defibrillator.

INTRODUCTION: Internal atrial defibrillation has been evaluated as an alternative approach to the external technique for more than two decades. Previous studies in animals and humans have shown that internal atrial defibrillation is feasible with relatively low energies. The promising results achieved with internal atrial defibrillation have facilitated the development of an implantable atrial defibrillator (IAD). METHODS AND RESULTS: For any new therapy, it is imperative to demonstrate safety, efficacy, tolerability with improvement in quality of life, and cost-effectiveness compared with therapeutic options already available. Maintenance of sinus rhythm or prolonged duration in arrhythmia-free intervals should be demonstrated clearly with an IAD. Initial clinical experience with the Metrix system indicates stable atrial defibrillation thresholds, appropriate R wave synchronization markers, no shock-induced ventricular proarrhythmia, and excellent detection of atrial fibrillation (AF) with a specificity of 100%. Ventricular proarrhythmia has not been reported for correctly R wave synchronized low-energy shocks when closely coupled to RR intervals, and long-short cycles are avoided. CONCLUSION: Preliminary experience with the Metrix system suggests that the IAD may offer a therapeutic alternative for a subgroup of patients with drug-refractory, symptomatic, long-lasting, and infrequent episodes of AF. Further efforts must be undertaken to reduce the patient discomfort associated with internal atrial defibrillation in an attempt to make this new therapy acceptable to a larger patient population with AF.

Algorithms↗
PubMed1997

Neoexpression of the c-met/hepatocyte growth factor-scatter factor receptor gene in activated monocytes.

Hepatocyte growth factor-scatter factor (HGF-SF ) mediates mito-, moto-, and morphogenic effects through the MET receptor, a membrane bound tyrosine kinase. HGF-SF/MET signaling is mitogenic for a large number of epithelial and endothelial cells and activates organ regeneration. HGF-SF transcripts have been detected in various myeloid cell lines. Therefore, the potential role of HGF-SF/MET signaling for circulating cells of the immune system, especially under conditions of inflammation, was evaluated. Several B-lymphoid and myeloid cell lines were found to express HGF-SF or c-met transcripts, while activity of both genes was mutually exclusive with the exception of low level coexpression in two B-cell lines. HGF-SF transcripts were present in low quantities in freshly isolated peripheral blood mononuclear cells (PBMNCs). In contrast, c-met expression was not detected in freshly isolated cells from peripheral blood, but was induced in monocytes by activation of monocytic or T-cell function. HGF-SF incubation led to an increased c-fos steady state transcript level in myeloblastic K562 cells and moderately promoted cell viability of freshly isolated preactivated monocytes. c-met expression is thus established in activated monocytes, in particular under conditions resembling inflammation, making these cells accessible to functional effects of HGF-SF.

Gene Expression Regulation↗
PubMed1997

[The effect of a lower stimulation frequency on the AV synchronicity of VDD pacemakers].

BACKGROUND AND OBJECTIVE: Implantation of a VDD pacemaker (ventricular pacing; dual sensing [atrial and ventricular]; dual response [triggered + inhibited]) together with a single VDD electrode catheter restores synchronous AV ventricular stimulation in patients with higher-grade AV block and intact sinus function. If higher-frequency stimulation occurs it may be a sign of pacemaker malfunction or of inadequate pacemaker programming. This study was undertaken to determine, at first follow-up examination, in how many patients with a VDD pacemaker VVI stimulation occurred more than 5% of the time; how such patients differed from those with 5% or fewer VVI stimulations; and whether a changed program reduced the proportion of VVI stimulations. PATIENTS AND METHODS: 67 consecutive patients were tested 1 to 3 months after implantation of the Unity VDD pacemaker (Sulzer Intermedics). The frequency of VVI stimulations was determined via a diagnostic pacemaker memory store. After intermediate analysis, programming was optimized and the patients then re-tested 12 months after the initial implantation. RESULTS: At the first follow-up examination 54 patients had VVI stimulations of < or = 5% (0.5 +/- 0.9%) and 13 had > 5% of the time (19.8 +/- 10.7%). The two groups differed significantly from one another in their lower intervention frequency (< or = 5% VVI stimulations: 47 +/- 6/min; > 5% VVI stimulations: 58 +/- 5/min). In particular, the pacemakers in patients with > 5% VVI stimulations had been significantly more often programmed to values of > 50/min. As a result, the pacemakers of these patients were reprogrammed to a lower frequency. A year after implantation there was no longer any difference in the lower intervention frequency, 44 +/- 4/min, between patients with initially > 5% VVI stimulations and those with initially < or = 5% stimulations. At the same time, the proportion of VVI stimulations fell to 4 +/- 6%, with 67% of patients having AV synchronicity of > 95%. INTERPRETATION: At first follow-up, patients with > 5% VVI stimulations differed from those with < or = 5% stimulations with regard to an increased lower intervention frequency. In most of these patients the proportion of AV stimulations was increased to > 95% by reducing the lower intervention frequency to < or = 50/min.

Aged↗
PubMed1997

All-trans-retinoic acid blocks cell cycle progression of human ovarian adenocarcinoma cells at late G1.

We prepared single cell clones from two ovarian carcinoma cell lines, CA-OV3 and SK-OV3, and analyzed the effect of all-trans-RA treatment on cell division, DNA synthesis, and cell cycle stage distribution of these single cell clones. Our results show that despite the well-known heterogeneous nature of these cell lines, all single cell clones of SK-OV3 cells are resistant to the growth inhibitory effects of all-trans-RA. In contrast, all single cell clones of CA-OV3 cells were growth inhibited by all-trans-RA. However, the extent of growth inhibition did vary somewhat from clone to clone. Additional studies employing flow cytometry showed that all-trans-RA blocked CA-OV3 cell cycle progression in the G1 stage. Finally, all-trans-RA was able to inhibit G1 progression in growth-arrested CA-OV3 cells following stimulation with fetal bovine serum, insulin, IGF-1, or estrogen. Since each of these growth factors is known to act via distinct signal transduction pathways, our results suggest that all-trans-RA blocks G1 progression by targeting a downstream process or event which occurs at a point after the insulin/IGF-1, estrogen, and serum signal transduction pathways converge.

Adenocarcinoma↗
PubMed1997

[Catheter ablation and implantable atrial defibrillators in supraventricular cardiac arrhythmias].

Non-pharmacological tools for treatment of supraventricular tachycardias include radiofrequency catheter ablation, antiarrhythmic surgery, and electrical therapies. Radiofrequency catheter ablation is the first choice in the treatment of symptomatic patients with AV nodal reentrant tachycardias and atrioventricular reentrant tachycardias because of its high success rate and its low complication rate. Furthermore, transvenous radiofrequency catheter ablation may be considered as a curative approach in patients with atrial flutter and in patients with ectopic atrial tachycardias. Whereas the application of radiofrequency catheter ablation for the curative treatment of atrial fibrillation is still experimental, palliative therapy modalities such as AV nodal modification or AV nodal ablation may be performed in patients with drug refractory atrial fibrillation with rapid ventricular response. The recurrence rate of atrial fibrillation is in the range of 40 to 60% within a year despite antiarrhythmic drug treatment. Internal atrial fibrillation is a safe and effective method for acute termination of atrial fibrillation, especially after unsuccessful external cardioversion. The electrotherapy with the implantable atrial defibrillator should be considered as an alternative approach in patients with symptomatic, long lasting, and drug refractory episodes of atrial fibrillation. This innovative electrotherapeutic tool is currently under clinical evaluation. For the selection of the most appropriate therapy, the risk-benefit-ratio has to be taken into account in each individual patient.

Catheter Ablation↗
PubMed1997

Treatment of refractory Hodgkin's disease with an anti-CD16/CD30 bispecific antibody.

Fifteen patients with refractory Hodgkin's disease were treated in a phase I/II trial with the natural killer (NK)-cell-activating bispecific monoclonal antibody HRS-3/A9, which is directed against the Fc(gamma)-receptor III (CD16 antigen) and the Hodgkin's-associated CD30 antigen, respectively. Median counts of NK cells and of all lymphocyte subsets were considerably decreased in the patients before therapy. HRS-3/A9 was administered 4 times every 3 to 4 days, starting with 1 mg/m2. The treatment was well tolerated, and the maximum tolerated dose was not reached at 64 mg/m2, the highest dose administered because of the limited amounts of HRS-3/A9 available. Side effects were rare and consisted of fever, pain in involved lymph nodes, and a maculopapulous rash. A total of 9 patients developed human antimouse Ig antibodies, and 4 patients developed an allergic reaction after attempted retreatment. A total of 1 complete and 1 partial remission (lasting 6 and 3 months, respectively) [corrected], 3 minor responses (1 to 11+ months), and 1 mixed response were achieved. There was no clear-cut dose-side effect or dose-response correlation. Our results encourage further clinical trials with this novel immunotherapeutic approach and emphasize the necessity to reduce the immunogenicity of the murine bispecific antibodies.

Adolescent↗
PubMed1997

[Septic myocardial aneurysm in mitral valve endocarditis. Clinical and pathological-anatomical findings].

HISTORY AND CLINICAL FINDINGS: A 68-year-old woman was hospitalized because of fever and tiredness for 3 months. Her general condition was clearly impaired. She had a mild fever of 38.5 degrees C and on auscultation a 3/6 systolic murmur, maximal parasternally in the 3rd intercostal space, transmitted to the apex. There were distant râles over both lungs, the neck veins were distended and there was ankle oedema. INVESTIGATIONS: C-reactive protein was raised to 17.3 mg/dl (normal up to 0.9 mg/dl), WBC count 19,300/microliter. beta-haemolysing streptococcus (S. agalactiae) was grown in the blood culture. The ECG showed sinus tachycardia (rate of 98/min) and transthoracic echocardiography demonstrated a small pericardial, enlarged ventricles, marked mitral regurgitation and a large vegetation on the posterior mitral leaflet, as well as a 3 x 4 cm mass in the posterior wall of the ventricle, originating from the posterior mitral valve ring and communicating with the vegetation on the mitral valve. The posterior mitral leaflet was perforated. TREATMENT AND COURSE: As endocarditis of the mitral valve with a complicated course was suspected-abscess of the posterior mitral valve ring and septic myocardial aneurysm with associated pericarditis and haemodynamically insignificant effusion-she was transferred to the intensive care unit where she died suddenly of circulatory arrest only 30 min after transfer. Autopsy confirmed the echocardiographic findings. CONCLUSION: Paravalvular abscess in the course of mitral valve endocarditis is rare, but should be looked for at transthoracic echocardiography so that any necessary surgical intervention can be undertaken early.

Aged↗
PubMed1997

N-acetylcysteine attenuates nitroglycerin tolerance in patients with angina pectoris and normal left ventricular function.

The aim of this study was to assess whether N-acetylcysteine (NAC) is able to prevent tolerance to a 48-hour infusion of nitroglycerin (NTG) in the setting of normal left ventricular function. In 16 patients, the hemodynamic response to 0.8 mg sublingual (s.l.) NTG was assessed by measuring mean arterial, pulmonary artery, pulmonary capillary wedge and right atrial pressures, cardiac output, and calculation of the systemic and pulmonary vascular resistances. The parameters were obtained at baseline and 1 to 10 minutes after the s.l. NTG application (day 1). NTG was started at 1.5 microg/kg/min; concomitantly, a bolus of 2,000 mg of NAC was administered, followed by an infusion of 5 mg/kg/hour. Both infusions were continued for 48 hours, and the hemodynamic study was repeated (day 3). The same measurements were obtained in a matched control group of 15 patients with NTG infusion alone. Plasma renin activity, aldosterone, and norepinephrine were measured before and after the infusion period. The first s.l. NTG infusion (day 1) caused a significant decrease in mean arterial (p <0.01), pulmonary artery (p <0.001), and right atrial pressures (p <0.001), and in systemic (p <0.01) and pulmonary vascular resistances (p <0.001) in both groups. After the 48-hour infusion (day 3), there was a total loss of nitrate-mediated vasodilation (pressure values and vascular resistances day 3 > day 1) in 5 of 16 patients (NAC nonresponders), whereas in the other 11 of 16 patients (NAC responders), there was significant vasodilation throughout the infusion period. Tolerance had developed in 14 of 15 patients with NTG infusion alone. The same difference (responder vs nonresponder vs NTG alone) held true regarding the response to the second s.l. NTG infusion after 48 hours. The neurohormonal counter-regulation and intravascular volume expansion (increase in plasma renin activity, p <0.001, and norepinephrine, p <0.05; decrease in aldosterone, p <0.01) did not differ between responders and nonresponders. We conclude that NAC attenuates tolerance development to a continuous NTG infusion in a specific patient subgroup and that this occurs despite the same amount of neurohormonal counter-regulation and intravascular volume expansion compared with patients with tolerance development.

Acetylcysteine↗
PubMed1997

Association between hemodynamic parameters and the degeneration of sustained ventricular tachycardias into ventricular fibrillation in rats.

UNLABELLED: Sustained ventricular tachycardias (VT) often degenerate into ventricular fibrillation (VF). In the present study, the impact of VT on mean arterial blood pressure (MAP), myocardial blood flow (MBF), and myocardial oxygen consumption (MVCO2) was assessed. In addition, the degeneration of sustained VT into VF was analysed with respect to MAP. MBF was measured in 48 anesthetized rats with colored microspheres; arterial catecholamine levels were measured by HPLC in 16 additional rats during control conditions and VT. MBF (4. 66+/-1.29 ml/g/min; mean+/-s.d.) did not change with the onset of VT (5.37+/-1.92 ml/g/min, n.s.). Epinephrine (0.22+/-0.13 ng/ml) and norepinephrine (0.37+/-0.12 ng/ml) increased during VT (3.55+/-2.68 ng/ml, P<0.01; 0.88+/-0.44 ng/ml, P<0.05), respectively. VF was more frequent when MAP remained normal (MAP>80 mmHg: 26%) than with hypotension (MAP<80 mmHg: 2%, P<0.05). Mechanical failure was observed in 10% of rats with severe hypotension (MAP<60 mmHg), and 2% with moderate hypotension (MAP 60-80 mmHg). The endo-epicardial MBF ratio in the VF group was significantly lower than that in the non-VF group (0.94+/-0.17 v 1.11+/-0.24, P<0.05). CONCLUSIONS: severe hypotension predisposes to the occurrence of acute mechanical failure during VT; moderate hypotension during VT, however, serves as a protective mechanism against VF in structurally normal hearts. Subendocardial hypoperfusion in the presence of an increased energy demand during VT is suggested to be responsible for the initiation of VF.

Animals↗
PubMed1997

[Effect of magnesium on sustained ventricular tachycardia].

Intravenous application of magnesium was suggested for the management of persistent ventricular tachycardia. In patients with torsade de pointes tachycardia the injection of magnesium controlled the life threatening arrhythmias reliably, thus magnesium became the treatment of choice in this setting. The results in patients with persistent monomorphic ventricular tachycardia are controversial. In one study, ventricular tachycardias could be controlled in 8 of 10 patients by 2,000 mg magnesium sulfate. In a randomized trial with 43 patients, termination of the ventricular tachycardia could be accomplished in 6 of 20 patients under the influence of 4,000 mg magnesium sulfate, whereas 3 of 24 patients exhibited termination of the tachycardia following placebo; the difference did not reach statistical significance. In our study 4 patients with torsade de pointes tachycardia could be controlled by the application of magnesium glutamate (2 x 1,000 mg intravenously). Of 25 patients with persistent monomorphic ventricular tachycardia, the arrhythmia ended in 8 patients under the influence of magnesium. No significant change of the RR intervals and the QRS duration during ventricular tachycardia could be demonstrated following magnesium injection. Cardiac index during ventricular tachycardia increased from 2.0 +/- 0.6 l/min x m2 to 2.5 +/- 0.1 l/min x m2 (p < 0.05). In a further investigation the dose of magnesium was increased to 2 x 9 mmol. To detect possible interactions with antiarrhythmic agent, 10 patients under chronic antiarrhythmic therapy with class-III-agents were compared with 10 patients without such treatment. Plasma levels of magnesium increased from 0.79 +/- 0.1 mmol/l to 1.87 +/- 0.5 mmol/l. In 5 of the 20 patients ventricular tachycardia ended under the influence of magnesium: 2 patients were on chronic antiarrhythmic agents, whereas 3 had no chronic therapy. There were no significant differences in the RR intervals and the duration of the monophasic action potentials during the ventricular tachycardia under the influence of magnesium. These data indicate that the bolus therapy of magnesium controls persistent monomorphic ventricular tachycardia in a minority of patients only. Therefore, magnesium injection cannot be recommended for treatment of monomorphic ventricular tachycardia in the emergency setting. On the other hand, magnesium application can be considered the therapy of choice for patients with torsade de pointes tachycardia.

Dose-Response Relationship, Drug↗
PubMed1997

[Radiofrequency ablation in ventricular extrasystole of the right ventricular outflow tract].

The series of five patients with symptomatic isolated right ventricular outflow tract ectopy and no structural heart disease which were successfully treated with radiofrequency ablation of the ectopic focus are reported in order to discuss radio-frequency ablation as an alternative treatment in patients with right ventricular outflow tract ectopy without ventricular tachycardia.

Cardiac Complexes, Premature↗
PubMed1997

Left atrial chamber and appendage function after internal atrial defibrillation: a prospective and serial transesophageal echocardiographic study.

OBJECTIVES: The purpose of this prospective study was to assess left atrial chamber and appendage function after internal atrial defibrillation of atrial fibrillation and to evaluate the time course of recovery. BACKGROUND: External cardioversion of atrial fibrillation may result in left atrial appendage dysfunction ("stunning") and may promote thrombus formation. In contrast to external cardioversion, internal atrial defibrillation utilizes lower energies; however, it is unknown whether the use of lower energies may avoid stunning of the left atrial appendage. METHODS: Transesophageal and transthoracic echocardiography were performed in 20 patients 24 h before and 1 and 7 days after internal atrial defibrillation to assess both left atrial chamber and appendage function. Transthoracic echocardiography was again performed 28 days after internal atrial defibrillation to assess left atrial function. The incidence and degree of spontaneous echo contrast accumulation (range 1+ to 4+) was noted, and peak emptying velocities of the left atrial appendage were measured before and after internal atrial defibrillation. To determine left atrial mechanical function, peak A wave velocities were obtained from transmitral flow velocity profiles. RESULTS: Sinus rhythm was restored in all patients. The mean +/- SD peak A wave velocities increased gradually after cardioversion, from 0.47 +/- 0.16 m/s at 24 h to 0.61 +/- 0.13 m/s after 7 days (p < 0.05) and 0.63 +/- 0.13 m/s after 4 weeks. Peak emptying velocities of the left atrial appendage were 0.37 +/- 0.16 m/s before internal atrial defibrillation, decreased significantly after internal atrial defibrillation to 0.23 +/- 0.1 m/s at 24 h (p < 0.01) and then recovered to 0.49 +/- 0.23 m/s (p < 0.01) after 7 days. The corresponding values for the degree of spontaneous echo contrast were 1.2 +/- 1.2 before internal atrial defibrillation versus 2.0 +/- 1.0 (p < 0.01) and 1.1 +/- 1.3 (p < 0.01) 1 and 7 days after cardioversion, respectively. One patient developed a new thrombus in the left atrial appendage, and another had a thromboembolic event after internal atrial defibrillation. CONCLUSIONS: Internal atrial defibrillation causes depressed left atrial chamber and appendage function and may result in the subacute accumulation of spontaneous echo contrast and development of new thrombi after cardioversion. These findings have important clinical implications for anticoagulation therapy before and after low energy internal atrial defibrillation in patients with atrial fibrillation.

Anticoagulants↗