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Biomedical subjects

M Borggrefe

Publications and source records attributed to M Borggrefe.

At least 73 records · Page 4Linked to original sources
PubMed2000

Arrhythmias in heart failure: current concepts of mechanisms and therapy.

About one half of deaths in patients with heart failure are sudden, mostly due to ventricular tachycardia (VT) degenerating to ventricular fibrillation or immediate ventricular fibrillation. In severe heart failure, sudden cardiac death also may occur due to bradyarrhythmias. Other dysrhythmias complicating heart failure include atrial and ventricular extrasystoles, atrial fibrillation (AF), and sustained and nonsustained ventricular tachyarrhythmias. The exact mechanism of the increased vulnerability to arrhythmias is not known. Depending on the etiology of heart failure, different preconditions, including ischemia or structural alterations such as fibrosis or myocardial scarring, may be prominent. Reentrant mechanisms around scar tissue, afterdepolarizations, and triggered activity due to changes in calcium metabolism significantly contribute to arrhythmogenesis. Furthermore, alterations in potassium currents leading to action potential prolongation and an increase in dispersion of repolarization play a significant role. Treatment of arrhythmias is necessary either because patients are symptomatic or to reduce the risk for sudden cardiac death. The individual history, left ventricular function, electrophysiologic testing, and the signal-averaged ECG give useful information for identifying patients at risk for sudden cardiac death. The implantable cardioverter defibrillator (ICD) has evolved as a promising therapy for life-threatening arrhythmias. A potential role may exist for antiarrhythmic drugs, mainly amiodarone. There is growing evidence that patients with sustained VT or a history of resuscitation have the best outcome with ICD therapy regardless of the degree of heart failure. Many of these patients require additional antiarrhythmic therapy because of AF or nonsustained VTs that may activate the device. Catheter ablation or map-guided endocardial resection are additional options in selected patients but seldom represent the only therapeutic strategy.

Anti-Arrhythmia Agents↗
PubMed2000

Maintenance of sinus rhythm as a therapy goal.

Despite recent advances in our understanding of the mechanisms and consequences of atrial fibrillation, appropriate management of this common condition presents something of a dilemma. Control of ventricular rate alone is a common strategy, considered by many physicians to be the safest treatment option and a relatively simple approach to preserving left ventricular function. Rhythm control using antiarrhythmic agents, however, offers a number of important advantages, with the potential to correct abnormal physiology, increase exercise tolerance, reduce thromboembolic risk, prevent atrial remodelling and eliminate the risk of tachycardia-induced cardiomyopathy. Selection of an appropriate antiarrhythmic agent for such long-term prophylaxis is however problematic. Class I agents are associated with an unacceptable proarrhythmic risk especially in patients with structural heart disease and long-term therapy with the class III agent amiodarone can result in serious non-cardiac adverse effects. It is apparent, therefore, that there is little consensus on appropriate management strategies for atrial fibrillation and less still on the antiarrhythmic agent to be used. A number of studies are, however, ongoing which attempt to determine the benefits of rhythm versus rate control. These include the PIAF (Pharmacological Intervention in Atrial Fibrillation), AFFIRM (Atrial Fibrillation Follow-up Investigation of Rhythm Management) and RACE (Rate Control versus Electrical Cardioversion) studies, which should provide valuable answers which will help to guide physicians in their therapy choices.

Atrial Fibrillation↗
PubMed1999

Living anatomy of the atrioventricular junctions. A guide to electrophysiologic mapping. A Consensus Statement from the Cardiac Nomenclature Study Group, Working Group of Arrhythmias, European Society of Cardiology, and the Task Force on Cardiac Nomenclature from NASPE.

Current nomenclature for the atrioventricular (AV) junctions derives from a surgically distorted view, placing the valvar rings and the triangle of Koch in a single plane with antero-posterior and right-left lateral coordinates. Within this convention, the aorta is considered to occupy an anterior position, although the mouth of the coronary sinus is shown as being posterior. Although this nomenclature has served its purpose for the description and treatment of arrhythmias dependent on accessory pathways and atrioventricular nodal reentry, it is less than satisfactory for the description of atrial and ventricular mapping. To correct these deficiencies, a consensus document has been prepared by experts from the Working Group of Arrhythmias of the European Society of Cardiology and the North American Society of Pacing and Electrophysiology. It proposes a new anatomically sound nomenclature that will be applicable to all chambers of the heart. In this report, we discuss its value for description of the AV junctions, establishing the principles of this new nomenclature.

Atrioventricular Node↗
PubMed1999

A new algorithm to determine complete isthmus conduction block after radiofrequency catheter ablation for typical atrial flutter.

The induction of a complete conduction block of the isthmus between inferior vena cava and tricuspid annulus is considered the best predictor for lack of arrhythmia recurrence if radiofrequency catheter ablation for typical atrial flutter is performed. We evaluated a simplified algorithm to determine complete isthmus block that, in our series, had a predictive accuracy of 100% when compared with the gold standard.

Algorithms↗
PubMed1999

Combining nonpharmacologic therapies for advanced heart failure: the Münster experience with the assist device-defibrillator combination.

Implantable cardioverter defibrillators (ICDs) and ventricular assist devices (VADs) have been used as a bridge to cardiac transplantation. In selected patients, the combined implantation may be required. This study was motivated by a case of a 33-year-old female patient with giant cell myocarditis who died of ventricular tachyarrhythmias after having been placed on a VAD with which she had been treated on an out-of-hospital basis for a prolonged period of time. A subsequent retrospective analysis of our data showed that, of 73 patients who had to be bridged mechanically (54 Novacor, 12 TCI Heartmate, 4 Thoratec, 3 Medos) in our institution between 1993 and 1998, 10 patients had undergone defibrillator implantation either before (n = 8) or after (n = 2) implantation of a VAD. The cases are presented, and the feasibility of the combination therapy discussed.

Adult↗
PubMed1999

The LQT syndromes--current status of molecular mechanisms.

Our knowledge on the molecular genetics of inherited cardiac arrhythmias is very recent in comparison to the advances of genetics achieved in other inherited cardiac disorders. This is related to the high mortality and early disease onset of these arrhythmias resulting in mostly small nucleus families. Thus, traditional genetic linkage studies that are based on the genetic information obtained from large multi-generation families were made difficult. In 1991, the first chromosomal locus for congenital long-QT (LQT) syndrome was identified on chromosome 11p15.5 (LQT1 locus) by linkage analysis. Meanwhile, the disease-causing gene at the LQT1 locus (KCNQ1), a gene encoding a K+ channel subunit of the IKs channel, and three other, major genes, all encoding cardiac ion channel components, have been identified. Taken together, LQT syndrome turned out to be a heterogeneous channelopathy. Moreover, the power of linkage studies to reveal the genetic causes of the LQT syndrome was also important to identify unknown but fundamental channel components that contribute to the ion currents tuning ventricular repolarization. In-vitro expression of the altered ion channel genes demonstrated in each case that the altered ion channel function produces prolongation of the action potential and thus the increasing propensity to ventricular tachyarrhythmias. Since these ion channels are pharmacological targets of many antiarrhythmic (and other) drugs, individual and potentially deleterious drug responses may be related to genetic variation in ion channel genes. Very recently, also in acquired LQT syndrome, which is a frequent clinical disorder in cardiology a genetic basis has been proposed in part since mutations in LQT genes have been specifically found. The discovery of ion channel defects in LQT syndrome represents the major achievement in our understanding and implies potential therapeutic options. The knowledge of the genomic structure of the LQT genes now offers the possibility to detect the underlying genetic defect in 80-90% of all patients. With this specific information, containing the type of ion channel (Na+ versus K+ channel) and electrophysiological alteration by the mutation (loss-of-function versus change-of-function mutation), gene-directed, elective drug therapies have been initiated in genotyped LQT patients. Based on preliminary data, that were supported by in vitro studies, this approach may be useful in recompensating the characteristic phenotypes in some LQT patients. Mutation detection is a new diagnostic tool which may become of more increasing importance in patients with a normal QTc or just a borderline prolongation of the QTc interval at presentation. These patients represent approximately 40% of all familial cases. Moreover, LQT3 syndrome and idiopathic ventricular fibrillation are allelic disorders and genetically overlap. In both mutations in the LQT3 gene SCN5A encoding the Na+ channel alpha-subunit for INa have been reported. Thus, the clinical nosology of inherited arrhythmias may be reconsidered after elucidation of the underlying molecular bases. Meanwhile, genotype-phenotype correlations in large families are on the way to evaluate intergene, interfamilial, and intrafamilial differences in the clinical phenotype reflecting gene specific, gene-site specific, and individual consequences of a given mutation. LQT syndrome is phenotypically heterogeneous due to the reduced penetrance and variable expressivity associated with the mutations. This paper discusses the current data on molecular genetics and genotype-phenotype correlations and the implications for diagnosis and treatment.

Chromosome Mapping↗
PubMed1999

[Brugada-Brugada syndrome. An atypical case].

The Brugada-Brugada syndrome is a rhythmologic disorder which can be diagnosed because of typical ECG criteria. A high-take off descending ST segment localized to the right chest leads, associated with right bundle branch block and ventricular fibrillation or syncopes are characteristic of the syndrome. ECG alterations in the right precordial leads were recorded in a 47 year old female patient who was admitted to hospital because of enteritis and associated syncope. The ECG alterations were initially not realized as Brugada-Brugada syndrome. Because of "recognizing" comparable ECG alterations during a congress lecture, the diagnosis was made. The patient was treated with an ICD.

Ajmaline↗
PubMed1999

Extracardiac contributions to chest pain perception in patients 6 months after acute myocardial infarction.

OBJECTIVES: The amount of perceived anginal pain in patients after infarction deserves the attention of the physician. This study sought to identify the modulating influence of extracardiac factors on persistent angina pectoris after myocardial infarction. METHODS AND RESULTS: A total of 552 male survivors of acute myocardial infarction (age 29 to 65 years, median 54 years) were followed for a period of 6 months; the affective state was assessed immediately after the acute event. The prognostic importance of postinfarction depression on chest pain perception was evaluated 6 months after the cardiac event in 376 patients. After the 6-month follow-up period, 199 (53%) of the patients with myocardial infarction had angina pectoris. Somatic risk factors and electrocardiographic data at initial testing did not contribute to the risk of having chest pain. However, patients with high levels of depression at initial testing had an almost 3-fold risk of having angina pectoris 6 months after the index event. Older age, lower social class status, and preinfarction angina were also significantly related to angina pectoris at the end of the study. Patients who were pain free before the index infarction reported significantly more symptoms of chest pain at the study end point (P </=.02), when they had moderate to high degrees of postinfarction depression. In the logistic regression model, depression, then followed by preinfarction angina pectoris and low social class index, contributed significantly to the prediction of follow-up angina pectoris. CONCLUSIONS: The results of this study add evidence to the hypothesis that the perception of chest pain may be triggered not only by the nociceptive stimulation of the ischemic heart but also by extracardiac sources. Depressive mood state, when concomitant with cardiac disease, is shown to intensify perceived chest pain.

Adult↗
PubMed1999

Living anatomy of the atrioventricular junctions. A guide to electrophysiological mapping. A Consensus Statement from the Cardiac Nomenclature Study Group, Working Group of Arrythmias, European Society of Cardiology, and the Task Force on Cardiac Nomenclature from NASPE. North American Society of Pacing and Electrophysiology.

Current nomenclature for atrioventricular junctions derives from a surgically distorted view, placing the valvar rings and the triangle of Koch in a single plane with antero-posterior and right-left lateral coordinates. Within this convention, the aorta is considered to occupy an anterior position, while the mouth of the coronary sinus is shown as being posterior. While this nomenclature has served its purpose for the description and treatment of arrhythmias dependent on accessory pathways and atrioventricular nodal re-entry, it is less than satisfactory for the description of atrial and ventricular mapping. To correct these deficiencies, a consensus document has been prepared by experts from the Working Group of Arrhythmias of the European Society of Cardiology, and the North American Society of Pacing and Electrophysiology. It proposes a new, anatomically sound, nomenclature that will be applicable to all chambers of the heart. In this report, we discuss its value as regards the description of the atrioventricular junctions, establishing the principles of this new nomenclature.

Atrioventricular Node↗
PubMed1999

Radiofrequency catheter ablation of accessory pathways. Outcome and use of antiarrhythmic drugs during follow-up.

AIMS: The purpose of this study was to assess the acute and long-term success of accessory pathway ablation in a single large-volume centre, concentrating on long-term recurrences and the clinical use of antiarrhythmic drugs. METHODS AND RESULTS: A total of 519 consecutive patients (mean age 40+/-14 years) underwent radiofrequency ablation of manifest or concealed accessory pathways. The patients were seen in the hospital or by the referring physician at 6 and 12 months. Long-term follow-up information was obtained by questionnaire. Pathway conduction was abolished in 476 cases (91.7%). 'Redo' procedures, due to recurrence, were performed in 38 patients (7.3%) and were successful in 30 (78.9%). Follow-up data were obtained from 454 patients (87.5%) with a follow-up duration of 22. 6+/-12.4 months. Among the 398 patients with successful ablations who responded to the questionnaire, 340 (85.4%) were asymptomatic with only 10.6% taking antiarrhythmic drugs. An additional 20 patients (5.0%) had symptoms suspicious of recurrence. In total, 66 out of 398 successfully treated patients (16.6%) were taking antiarrhythmic drugs. Twenty-three out of 56 (41.1%) patients with failed ablations were asymptomatic, 12 of whom (21.4% of patients with failed ablations) had not been administered antiarrhythmic drugs. In the total group of 454 patients with ablation attempts and available follow-up data, 99 (21.8%) were still taking antiarrhythmic drugs during follow-up. CONCLUSIONS: Patients with successful ablation of accessory pathways show excellent long-term results. However, 17% of successfully treated patients were still taking antiarrhythmic drugs during the period of long-term follow-up. On the other hand, 21% of patients with failed ablations were symptom-free without antiarrhythmic drugs. On an intention-to-treat basis, 22% of the patients with ablation attempts were still taking antiarrhythmic drugs during follow-up.

Adolescent↗
PubMed1999

Intraoperative radiofrequency ablation of chronic atrial fibrillation: a left atrial curative approach by elimination of anatomic "anchor" reentrant circuits.

INTRODUCTION: The percutaneous approach to radiofrequency (RF) catheter ablation for curative treatment of atrial fibrillation (AF) is an investigational technique, and the optimal composition of lesion lines is unknown. We tested an intraoperative RF ablation concept with elimination of left atrial anatomic "anchor" reentrant circuits. METHODS AND RESULTS: In 12 patients with an indication for valve surgery and chronic AF, a right atrial-transseptal approach was chosen for access to the left atrium. AF had been present for 4.3 +/- 3.9 years; the left atria measured 56 +/- 7 mm. Under direct vision, contiguous lesion lines were placed endocardially with temperature-guided RF energy applications for treatment of AF with a specially designed probe. The lesion lines were placed between the mitral annulus and the left lower pulmonary vein, further to the left upper pulmonary vein, from there to the right upper pulmonary vein, and finally to the right lower pulmonary vein. The antiarrhythmic ablation procedure lasted 19 +/- 4 minutes. One patient died postoperatively of low cardiac output. During follow-up of 11 +/- 6 months, chronic AF was ablated successfully in 9 of 11 patients (82%). Six patients were in stable sinus rhythm or intermittent pacemaker rhythm, and three patients were in sinus rhythm with intermittent atypical atrial flutter. CONCLUSIONS: Intraoperative RF energy application for induction of contiguous lesion lines is feasible. Elimination of anatomically defined "anchor" reentrant circuits within the left atrium prevented chronic AF in > 80% of the patients treated. Intraoperative validation of lesion line concepts for curative treatment of AF may be transferred to percutaneous ablation techniques.

Aged↗
PubMed1999

ESCWGA/NASPE/P experts consensus statement: living anatomy of the atrioventricular junctions. A guide to electrophysiologic mapping. Working Group of Arrhythmias of the European Society of Cardiology. North American Society of Pacing and Electrophysiology.

Current nomenclature for the AV junctions derives from a surgically distorted view, placing the valvar rings and the triangle of Koch in a single plane with anteroposterior and right-left lateral coordinates. Within this convention, the aorta is considered to occupy an anterior position, whereas the mouth of the coronary sinus is shown as being posterior. Although this nomenclature has served its purpose for the description and treatment of arrhythmias dependent on accessory pathways and AV nodal reentry, it is less than satisfactory for the description of atrial and ventricular mapping. To correct these deficiencies, a consensus document has been prepared by experts from the Working Group of Arrhythmias of the European Society of Cardiology and from the North American Society of Pacing and Electrophysiology. It proposes a new, anatomically sound, nomenclature that will be applicable to all chambers of the heart. In this report, we discuss its value for description of the AV junctions and establish the principles of this new nomenclature.

Atrioventricular Node↗
PubMed1999

Transient local changes in right ventricular monophasic action potentials due to ajmaline in a patient with Brugada Syndrome.

A 48-year-old patient with recurrent episodes of palpitations and syncope presented with transient ST segment elevation in the right precordial ECG leads. Structural heart disease was excluded. No arrhythmias were inducible by programmed ventricular stimulation. Parallel to ST elevation after intravenous ajmaline, a gradual and reversible delay in the upstroke of right ventricular (RV) monophasic action potentials (MAPs) occurred that was most marked in the RV outflow tract and nearly absent at right free-wall recordings. Ajmaline led to a cycle length-dependent increase in RV dispersion of repolarization. Thus, right endocardial MAPs may demonstrate regionally different action potential changes that may contribute to the ECG changes in Brugada syndrome.

Action Potentials↗
PubMed1999

Cardiac 123I-MIBG uptake in idiopathic ventricular tachycardia and fibrillation.

UNLABELLED: Patients with idiopathic ventricular tachycardia or fibrillation have no additional structural or functional myocardial abnormalities. However, the inducibility of typical tachyarrhythmias by physical or mental stress or by catecholamine infusion suggests the involvement of the adrenergic system in the pathogenesis of these potentially life-threatening diseases. METHODS: 45 patients with idiopathic right ventricular outflow tract tachycardia (RVO-VT), 25 patients with idiopathic left ventricular tachycardia (ILVT), 15 patients with idiopathic ventricular fibrillation (IVF) and 10 age-matched control patients were investigated in this study. Diagnoses were made on the basis of detailed evaluation of the results of two-dimensional echocardiography, left and right ventricular angiography, coronary angiography and endomyocardial biopsy. Local presynaptic norepinephrine re-uptake was assessed using the norepinephrine analog 1231-metaiodobenzylguanidine (MIBG), SPECT and semiquantitative 33-segment bull's-eye analysis. RESULTS: Locally reduced 123I-MIBG uptake was found in 27 of 45 RVO-VT patients (60%), 5 of 15 ILVT patients (33%) and 17 of 25 IVF patients (68%). Unlike ILVT patients, RVO-VT and IVF patients had significantly reduced segmental 123I-MIBG uptake of the posterior wall compared with control patients. CONCLUSION: Patients with idiopathic tachycardia and fibrillation show abnormal 1231-MIBG uptake, which indicates presynaptic sympathetic dysfunction. RVO-VT and IVF patients exhibit significantly reduced 123I-MIBG uptake in the posterior left ventricular wall, whereas ILVT patients do not.

3-Iodobenzylguanidine↗