[ICD-implantation--for which patients is its value for primary prevention secure?].
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Biomedical subjects
Publications and source records attributed to C Reithmann.
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In patients with drug-refractory atrial fibrillation, left-atrial catheter ablation represents a new curative therapeutic option. Segmental ostial or circumferential pulmonary vein isolation can achieve stable sinus rhythm in some 70% of patients with paroxysmal atrial fibrillation but no severe structural heart disease. In patients with chronic atrial fibrillation, complex left-atrial linear, or substrate-oriented ablation strategies may additionally be applied. In patients with cardiac insufficiency or more severe systolic left-ventricular dysfunction, restoration of a stable sinus rhythm through the use of left-atrial catheter ablation can improve the left-ventricular ejection fraction and reduce the severity of cardiac failure. Potential complications of ablation include, in particular, pulmonary veins stenosis, iatrogenic left-atrial tachycardia, thromboembolic events and fatal atrio-esophageal fistulas.
We report the case of a bundle branch reentrant tachycardia (BBRT) in a 40-yearold patient with a calcified bicuspid aortic valve and normal left ventricular function. The ventricular tachycardia was eliminated by successful radiofrequency ablation of the right bundle branch. As the aortic valve annulus is in close proximity to the specialized conduction system, premature degeneration of a bicuspid aortic valve may involve the bundle of His and the proximal bundle branches by invading calcifications. We speculate that calcifications invading the proximal bundle branches from the bicuspid aortic valve may have created the substrate for the BBRT in this patient.
BACKGROUND: Implantable cardioverter defibrillators represent an effective therapy to prevent sudden cardiac death in patients with ventricular arrhythmias. This implies a change in the spectrum of causes of death. There exist no large studies providing an exact differentiation of these causes of death. METHODS: During a mean observation period of 41+/-29 months (3 d-12 yrs), we analyzed the outcome of 429 ICD patients (CAD n=274, dilative CMP n=97, others n=23, no structural heart disease n=35), mean age 62+/-12 years (23-87 yrs). RESULTS: The overall survival rate was 79.7% whereby 3.5% of these patients underwent successful heart transplantation and 2.1% died suddenly. 60.9% of all deaths showed a non-sudden cardiac cause (heart failure 56.3%, myocardial infarction 4.6%). In 28.7% a non-cardiac fatal event was present (cancer 11.5%, septicemia 6.9%, stroke 4.6%). The deceased showed significantly more often structural heart disease (100 vs 92%, p<0.02) and a lower left ventricular ejection fraction (37+/-14 vs 44+/-18%, p<0.02). Significant higher survival rates were associated with medication with beta blockers (88 vs 75%, p<0.02) and the class III antiarrhythmic agents sotalol und amiodarone (85 vs 77%, p<0.03). CONCLUSIONS: Mortality due to sudden death was reduced to 2.1% in ICD patients associated with a shift of causes of death towards severe heart failure. Therefore, special attention should be paid to the signs of heart failure in these patients to enable early initiation of appropriate therapeutic strategies.
Syncope is one of the most common symptoms leading to hospital admission. Thereby syncope can be induced by several diseases. It is crucial to detect underlying structural heart disease or high grade arrhythmias, as these are associated with an increased mortality. The careful history and physical examination can often give sufficient evidence to evaluate the origin of syncope. Additional examinations should only be applied selectively. In patients with structural heart disease the specific treatment should be initiated, in patients with cardiac arrhythmias the implantation of a pacemaker or ICD might be indicated. The most common neurally-mediated and orthostatic syncopes can often be treated successfully by physical training. Beside syncope epilepsy might be responsible for a transient loss of consciousness. Again careful history taking helps to differentiate between these two entities.
A 71-year-old female, who has been treated with steroids for 3 weeks, developed a severe pneumonia with septic shock and acute respiratory distress syndrome (ARDS). Despite broad antibiosis due to the detection of pseudomonas aeruginosa (blood culture) the inflammatory markers remained high and the respiratory situation went critical. No proof of a malignoma or autoimmune process was found, despite multiple round foci in x-ray and computer tomography. Finally the delayed diagnosis of pulmonary nocardiosis was adjusted, due to the long incubation period of the pathogen Nocardia farcinica. The infectious origin may be assumed in so called "hay packs" used during the patient's residence at a health resort. After adequate change of the antibiotic regimen stabilization was achieved and the patient meanwhile recovered from the disease.
A 15-year-old girl was admitted with signs of severe cardiac failure. There were no symptoms of cardiac insufficiency 4 weeks before hospital admission. She presented with permanent supraventricular tachycardia with negative P-waves in leads II, III and aVF, the heart rate was 150 beats per minute. The electrophysiological examination showed a permanent junctional reentry tachycardia. A postero-septal accessory pathway could be eliminated successfully by radiofrequency catheter ablation. Immediately after the procedure cardiac function deteriorated with slight decrease of the strongly reduced cardiac output. Intensive care and application of dobutamine led to clinical stability. During a follow-up of two years the young patient showed permanent sinus rhythm and an age related physical strain. This case report documents the rapid and severe manifestation of cardiac failure owing to permanent junctional reentry tachycardia in a 15-year-old girl. She was referred for consideration of heart transplantation. Invasive electrophysiological treatment led to permanent sinus rhythm with improvement of left ventricular function.
AIMS: Catheter ablation of the inferior vena cava-tricuspid annulus isthmus and continuation of antiarrhythmic drug therapy have been shown to be an effective hybrid therapy for atrial flutter which results from antiarrhythmic drug treatment of atrial fibrillation. The aim of this study was to determine the risk factors for recurrence of atrial fibrillation in patients undergoing hybrid therapy for antiarrhythmic drug-induced atrial flutter. METHODS AND RESULTS: 90 patients with paroxysmal (n=46) or persistent atrial fibrillation (n=44) developed atrial flutter due to the administration of amiodarone (n=48), flecainide (n=22), propafenone (n=14) or sotalol (n=6). Recurrence of atrial fibrillation after ablation was assessed during follow-up on continued antiarrhythmic drug therapy and during long-term follow-up, irrespective of the initial antiarrhythmic medication. During the follow-up on continued antiarrhythmic drug therapy (16+/-13 months), recurrence of atrial fibrillation was documented in 24 of 90 patients (27%). The presence of accompanying pre-ablation episodes of atrial fibrillation on antiarrhythmic treatment (Odds ratio 7.1, 95% confidence interval 2.3 to 25, p=0.001) and decreased left ventricular ejection fraction (Odds ratio 3.7, 95% confidence interval 1.01 to 12.5, p=0.048) were significant and independent predictors of post-ablation atrial fibrillation. Antiarrhythmic medication was discontinued during long-term follow-up due to adverse drug effects (amiodarone, n=12; flecainide, n=1) in 13 patients (14%). During the long-term follow-up, irrespective of the initial antiarrhythmic medication (21+/-15 months), stable sinus rhythm was maintained in 60 of 90 patients (67%). CONCLUSION Hybrid therapy can be considered as the first line therapy for patients with antiarrhythmic drug-induced atrial flutter but patients should be carefully evaluated for accompanying pre-ablation episodes of atrial fibrillation and possible adverse drug effects before initiation of hybrid therapy.
Atrial fibrillation is the most relevant arrhythmia in daily clinical practice. The pathophysiology is determined by multiple independent reentrant wavelets in both atria. Repetitive triggers and an underlying substrate may favor the initiation and maintenance of atrial fibrillation. Mapping studies in patients with drug-refractory paroxysmal atrial fibrillation identified potentials from the ostia of pulmonary veins as a main source of triggers that initiate atrial fibrillation. In ongoing clinical trials, catheter ablation of pulmonary vein foci is used to eliminate atrial premature beats and thereby prevent the initiation of atrial fibrillation. The autonomic modulation of the heart rate and the occurrence of other supraventricular tachycardias that degenerate into atrial fibrillation are also considered as triggering mechanisms of atrial fibrillation. Since symptomatic bradycardia is associated with an increased incidence of atrial fibrillation, atrial pacing therapies for prevention of atrial fibrillation are another concept. Ongoing clinical trials evaluating the efficacy of pacing in patients with and without a primary pacemaker indication are currently under investigation. To date, data to which extent anatomical and electrophysiological characteristics of the atria influence the initiation and maintenance of atrial fibrillation are still missing. The myocardial adaptation to atrial fibrillation, the so-called "atrial remodeling", includes shortening of the atrial refractory period, slowing of atrial conduction, shortening of the atrial action potential, a progressive reduction of L-type calcium channel expression and microfibrosis of the myocardial tissue. New drug developments target atrial remodeling by modulating ion channel function and receptors of the angiotensin metabolism.
UNLABELLED: Early reinitiation of atrial fibrillation (ERAF) following external or internal electrical cardioversion is one of the factors determining unsuccessful electrical cardioversion. Prevention of ERAF has not been studied systematically in patients on amiodarone therapy. METHODS AND RESULTS: 22 patients had ERAF within 1 min after external electrical cardioversion of atrial fibrillation. 11 patients were on amiodarone therapy and 11 patients had no antiarrhythmic medication. The effect of atropine, post-shock atrial pacing and intravenous ajmaline on ERAF was consecutively tested in these patients. Administration of atropine before repeated defibrillation or post-shock atrial pacing prevented ERAF in 9 of the 11 patients (82%) on amiodarone therapy but in only 3 of 11 patients (27%) without amiodarone (p<0.05). In the remaining patients, intravenous ajmaline was effective in the suppression of ERAF in 5 patients without amiodarone and in 1 patient with amiodarone. The PP interval preceding the atrial premature beat reinitiating atrial fibrillation was nonsignificantly longer in amiodarone-treated patients (1127+/-419 ms) in comparison to patients without amiodarone (896+/-271ms). 27% of patients without amiodarone at the time of electrical cardioversion and 55% of patients with amiodarone remained in sinus rhythm during the follow-up of 29+/-14 and 30+/-14 months, respectively. CONCLUSIONS: ERAF in patients on amiodarone can be treated by atropine or atrial pacing to prevent bradycardia-dependent ERAF. ERAF in amiodarone-treated patients does not apparently predict late recurrence of atrial fibrillation on continued amiodarone therapy.
AIMS: Incisional atrial tachycardias in patients following surgery for congenital heart disease are based on complex structural abnormalities in these hearts. The aim of this study was to evaluate the use of the electroanatomical mapping system, CARTO, in consecutive patients with different forms of incisional atrial tachycardia. METHODS AND RESULTS: The electroanatomical mapping system combines electrophysiological and spatial information and allows visualization of atrial activation in a three-dimensional anatomical reconstruction of the atria. Electroanatomical mapping of right atrial activation was performed in 10 patients after surgery for congenital heart disease, surgery for Wolff-Parkinson-White syndrome, or heart transplantation presenting with 13 incisional atrial tachycardias. The three-dimensional mapping allowed a rapid distinction between focal (n=3) and reentrant mechanisms (n=10) and visualization of the activation wavefronts along anatomical and surgically created barriers. Electroanatomical activation maps (mean right atrial activation time 213+/-107 ms) were constructed with 89+/-60 catheter positions during an average mapping time of 48+/-33 min. Reentrant tachycardias propagating through the tricuspid annulus-vena cava inferior isthmus (n=6) or along periatriotomy loops (n=4) were identified in eight patients. Ectopic atrial foci near surgical scars could be localized in three patients. Catheter ablation by creation of a lesion in a critical isthmus of conduction or by targeting the arrhythmogenic focus eliminated 11 of 13 incisional atrial tachycardias. CONCLUSION: Visualization of atrial activation in a three-dimensional reconstruction of the right atrium using the electroanatomical mapping system CARTO facilitates understanding of the mechanism and defines the reentrant circuits of incisional atrial tachycardias. This new method may improve the success rate of electrophysiologically guided and anatomically guided catheter ablation of incisional atrial tachycardias.
UNLABELLED: Prerequisite for succesful radiofrequency catheter ablation of tachycardias is the exact mapping during the electrophysiological study. The new mapping system CARTO allows a three-dimensional color-coded electroanatomic map of impulse propagation using electromagnetic technology. The aim of this study was to determine the feasibility and safety of the new electromagnetic mapping technology CARTO for atrial tachycardias. RESULTS: Electrophysiologic study and CARTO mapping was performed in 38 atrial tachycardias. The mapping procedure took 26 +/- 23 min. We created 33 maps within the right atrium and 5 maps within the left atrium with a mean of 74 +/- 38 different catheter positions. The mechanism was determined as reentrant in 9, junctional in 1 and focal in 28 tachycardias. In focal tachycardias the tachycardia cycle length (CL) and the total atrial activation time (AT) were clearly different (352 +/- 98 ms vs 99 +/- 25 ms). Reentrant tachycardias had a comparable CL and AT (236 +/- 44 ms vs 240 +/- 56 ms). In 83% of the focal tachycardias and in 67% of the reentrant tachycardias, ablation was performed successfully. No complications occured. CONCLUSION: The electroanatomic mapping system allows high resolution visualization of electrical activity and may therefore improve precision and simplify the determination of the arrhythmogenic substrate during tachycardias for successful catheter ablation.
AIMS: Antiarrhythmic drug treatment for atrial fibrillation can cause atrial flutter-like arrhythmias. The aim of this study was to clarify the effect of catheter ablation of the tricuspid annulus-vena cava inferior isthmus on amiodarone-induced atrial flutter and to determine the incidence of atrial fibrillation after catheter ablation of amiodarone-induced atrial flutter in comparison to regular typical flutter. METHODS AND RESULTS: Among 92 consecutive patients with typical atrial flutter who underwent isthmus ablation 28 patients had atrial flutter without a history of previous atrial fibrillation (group I), 10 patients had atrial flutter following the initiation of amiodarone therapy for paroxysmal atrial fibrillation (group II) and 54 patients had atrial flutter and atrial fibrillation (group III). Atrial cycle length during atrial flutter in amiodarone-treated patients (group II) (277+/-24 ms) was significantly longer as compared to the cycle length of atrial flutter in group I (247+/-33 ms) and group III patients (235+/-28 ms). The rate of successful transient entrainment and overdrive stimulation to sinus rhythm was not different between patients with (60%) or without amiodarone therapy (group I: 71%, group III: 53%). Successful isthmus ablation with bidirectional conduction block eliminating right atrial flutter was achieved in 90% of amiodarone-treated patients and 93% of patients without amiodarone therapy. In the amiodarone-treated patient group atrial conduction times during pacing in sinus rhythm were significantly prolonged by 20-30% before and after ablation in all regions of the reentrant circuit. During a mean follow-up of 8+/-3 months post-ablation, atrial fibrillation recurred in two of 10 patients on continued amiodarone therapy after successful isthmus ablation. Thus, successful catheter ablation of atrial flutter due to amiodarone therapy was associated with a markedly lower recurrence rate of paroxysmal atrial fibrillation (20%) as compared to patients with atrial flutter plus preexisting paroxysmal atrial fibrillation (76%) and was similar to the outcome of patients with successful atrial flutter ablation without preexisting atrial fibrillation (25%). CONCLUSION: These data suggest that isthmus ablation with bidirectional block and continuation of amiodarone therapy is an effective therapy for the treatment of atrial flutter due to amiodarone therapy for paroxysmal atrial fibrillation.
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A 72-year-old woman with complete situs inversus underwent successful slow pathway ablation of typical AV nodal reentrant tachycardia. Catheter ablation of AV nodal reentrant tachycardia in dextrocardia required a lengthy procedure but was safe and without complications.
Radiofrequency catheter ablation is now considered as a curative approach in patients with typical atrial flutter. Typical atrial flutter is due to a macrore-entrant circuit within the right atrium and it can be eliminated by a linear lesion in the isthmus between the tricuspid annulus and the vena cava inferior. The electrophysiological criterion of a bidirectional isthmus block has been shown to reduce the recurrence rate of atrial flutter after catheter ablation, thus achieving long-term cure of typical atrial flutter. Acute success rates of 85 to 90% and recurrence rates of 10 to 15% have been reported. The risk of paroxysmal atrial fibrillation continues to be clinically relevant in patients who underwent successful ablation of atrial flutter, in particular in patients with previously documented atrial fibrillation. The incidence of a new onset of atrial fibrillation after ablation of atrial flutter seems to be approximately 20%. Isthmus ablation has also been shown to be beneficial for the majority of patients with typical atrial flutter and atrial fibrillation: In addition to an elimination of typical atrial flutter the isthmus ablation apparently reduces the incidence of paroxysmal atrial fibrillation. At present, atrial fibrillation can only be treated by catheter ablation as a curative approach in the rare cases where an accessory pathway, an AV nodal re-entrant tachycardia, typical atrial flutter or an ectopic atrial tachycardia is the induction mechanism of the atrial fibrillation. The majority of patients with atrial fibrillation is apparently not amenable to a curative local ablation. While AV junction ablation and AV node modification can palliate some of the symptoms of atrial fibrillation by a control of ventricular rate, the arrhythmia persists with the loss of AV synchrony and continued risk of thromboembolism. The surgical MAZE procedure implies a compartimentation of the atria by surgical incisions resulting in areas to small to sustain the arrhythmia. Based on this procedure experimental and clinical studies are currently performed in order to develop catheter ablation cure of atrial fibrillation.
Prerequisite for successful radiofrequency catheter ablation on tachycardias is the exact mapping during the electrophysiologic study. The new mapping system CARTO allows a three-dimensional color-coded electroanatomic map of impulse propagation using electromagnetic technology. Mapping of sinuatrial activation in the right atrium of 11 patients represents the first clinical experience with this new system. The physiological activation sequence could be determined in all patients three-dimensionally, and the sinus node could be localized as a physiological activation focus with interindividual variability only in the sagital plane without complications. The nonfluoroscopic mapping system allows high resolution visualization of electrical activity and may therefore improve precision and simplify the determination of the arrhythmogenic substrate during tachycardias for successful catheter ablation.