[Arterial hypertension and cardiac arrhythmias]. / Hochdruck und Herzrhythmusstörungen.

VENTRICULAR ARRHYTHMIAS: Different factors--like hypertrophy, fibrosis, ischemia and apoptosis increase the risk of ventricular arrhythmias and sudden arrhythmic death. ACE inhibitors and Angiotensin receptor antagonists offer a curative therapeutic approach. Beta-blocker are strongly recommended. Amiodarone may be used for symptomatic arrhythmia suppression--but with no proven favourable prognostic effect. The use of class-1 antiarrhythmic drugs is obsolete in the presence of left ventricular hypertrophy and heart failure. Implantable cardioverter/defibrillators (ICD) have been proven to have a positive effect on survival in secondary and primary prevention of sudden cardiac death, and so has cardiac synchronization in severe cardiac dysfunction and widened QRS complex. Atrial fibrillation (AF): Arterial hypertension represents the main risk factor for AF. Patients' age, left ventricular hypertrophy, left atrial dilatation and angiotensin-II activation play an important role in the induction and maintenance of AF. Angiotensin-receptor and beta-blockers seem to be efficacious in AF suppression and also on the regression of hypertrophy. The use of antiarrhythmic agents (AA) is limited because of their relatively low long-term efficacy and pro-arrhythmia properties. Best results may be achieved with class 1C AA drugs in patients with no or minimal structural heart disease. In all other cases amiodarone is suitable but is limited by its side effects. In patients with no or only a few symptoms rate control may be sufficient, but if there are symptoms interventional left atrial ablation of pulmonary veins should be attempted as a real curative strategy.

Myocardial perfusion/metabolism mismatch and ventricular arrhythmias in the chronic post infarction state.

AIM: Ventricular arrhythmias have been shown to originate in the myocardial peri-infarct region due to irregular heterotopic conduction. Hypoperfused but viable myocardium is often localised in those areas and may be involved in the pathogenesis of arrhythmias. We tested the hypothesis that these myocardial perfusion/metabolism mismatches (MM) are significantly associated with ventricular arrhythmias in the chronic post infarction state. PATIENTS, METHODS: 47 post infarction patients were included in the study. 33 suffered from ventricular arrhythmia whereas 14 did not. All patients underwent (99m)Tc tetrofosmin SPECT and (18)F-FDG PET. A region-of-interest(ROI)-analysis was used to assess viable myocardium based on predefined MM-criteria. Univariate analyses as well as a logistic regression model for the multivariate analysis were carried out. RESULTS: 94% of the arrhythmic patients displayed at least one MM-segment as compared to 64% of the non-arrhythmic patients. MM-segments and arrhythmia showed a statistically significant relation (p = 0.018). The logistic regression model predicted the occurrence or absence of arrhythmia in 85% of all cases. Multivariate analysis gave consistent results, after adjusting for symptomatic chronic heart failure (CHF), aneurysms and age. CONCLUSION: Our results support the hypothesis that hypoperfused but viable myocardium represents an arrhythmogenic substrate and is a relevant risk factor for developing ventricular arrhythmias following myocardial infarction. Therefore, the detection of MM-segments allows the identification of patients with a higher risk for future cardiac events.

[Long-term follow-up of right atrial multilinear high-frequency ablation in the treatment of recurrent paroxysmal atrial fibrillation]. / Langzeitverlauf nach rechtsatrialer, multilinearer Hochfrequenzablation zur Behandlung von rezidivierendem paroxysmalem Vorhofflimmern.

BACKGROUND AND OBJECTIVE: To investigate the long-term follow-up after right atrial compartmentalization using radiofrequency catheter ablation to treat recurrent paroxysmal atrial fibrillation. PATIENTS AND METHODS: 33 patients (eight women / 25 men, mean age 56.1+/-9.9 years) with highly symptomatic recurrent paroxysmal atrial fibrillation and mostly unresponsive to antiarrhythmic drugs were enrolled in this prospective study. All patients underwent radiofrequency catheter ablation, including right atrial compartmentalization and ablation of the right atrial isthmus region. The primary goal during follow-up was documentation of arrhythmia-related symptoms using a SF-36 quality-of-life questionnaire. RESULTS: During a mean follow-up of 2.1 years 21 % of patients were free of a relapse under continued antiarrhythmic medication, 79 % suffered at least from one period of atrial fibrillation. According to the underlying heart disease patients classified as "lone atrial fibrillation" (40 % without a relapse) showed improvement particularly compared to patients with coronary heart disease (10 % without a relapse). In the group of patients with a relapse of atrial fibrillation the mean of duration of an arrhythmic episode decreased significantly from 10.6 to 2.3 hours under continued administration of antiarrhythmic drugs (p = 0.01), as did the number of episodes, from 2.2 to 1.9/week. CONCLUSION: Despite of the high rate of clinical relapse, patients can profit due to an improved responsiveness to antiarrhythmic drugs after ablation. Right atrial compartmentalization should not be understood as a causal therapy but as an approach to a symptomatic form of hybrid therapy.

Adenosine in the noninvasive diagnosis of dual AV nodal conduction: use as a follow-up parameter after slow pathway ablation in AVNRT.

OBJECTIVE: The aim of this study was to evaluate if administration of adenosine during sinus rhythm to patients with PSVT of unknown mechanism is capable to detect dual AV nodal conduction and furthermore to evaluate this diagnostic parameter as a controlling test after slow pathway ablation in AVNRT. METHODS AND RESULTS: Before electrophysiological study 35 consecutive patients with PSVT were given adenosine during sinus rhythm. After radiofrequency ablation the adenosine test was repeated in a subset of 19 patients. The electrophysiological study revealed 19 patients (54%) with typical AVNRT (study group), 10 (29%) with atrioventricular reentry tachycardia (AVRT), 4 (11%) with ectopic atrial tachycardia (EAT) and 2 patients (6%) with inducible atrial flutter (AF) (control group). We observed a sudden increment of the PQ interval of more than 50 msec between two consecutive beats in 15 of 19 patients (79%) in the study group (75+/-35 msec) and in 2 patients (1 with EAT, AF) of the control group (19+/-12 msec) (p<0.001). After slow pathway radiofrequency ablation the sudden increment of PQ interval persisted in 4 of 12 patients (33%) of the study group. Three of these 4 patients had a relapse of AVNRT during a follow-up of 3 months. CONCLUSION: The administration of adenosine during sinus rhythm is an excellent noninvasive diagnostic test for identifying dual AV nodal conduction and additionally for verifying radiofrequency ablation results in patients with AVNRT.

Optimal method to achieve consistently low defibrillation energy requirements.

Reduction of the defibrillation energy requirement offers the opportunity to decrease implantable cardioverter defibrillator (ICD) size and to increase device longevity. Therefore, the purpose of this prospective study was to obtain confirmed defibrillation thresholds (DFTs) of < or = 15 J in each patient with an endocardial dual-coil lead system incorporating an active pectoral pulse generator (TRIAD lead system: RV- --> SVC+ + CAN+). According to our previous clinical and experimental studies, we tried to lower DFTs that were > 15 J by repositioning the distal coil of the endocardial lead system in the right ventricle. A total of 190 consecutive patients requiring ICDs for ventricular fibrillation and/or recurrent ventricular tachycardia were investigated at the time of ICD implantation (42 women, 148 men; mean age 61.9 +/- 12.0 years; mean left ventricular ejection fraction 42.7 +/- 16.6%). Coronary artery disease was present in 139 patients; nonischemic dilated cardiomyopathy in 34 patients; and other etiologies in 17 patients; 47 patients had undergone previous cardiac surgery. Regardless of optimal pacing and sensing parameters, for patients having DFTs > 15, we repositioned the distal coil of the endocardial lead system toward the intraventricular septum to include this part of both ventricles within the electrical defibrillating field. In 177 of 190 patients, induced ventricular fibrillation was successfully terminated with < or = 15 J (group I) using the initial lead position. Repositioning of the endocardial lead was necessary in 13 patients whose DFT(plus) (DFT(plus) = second additional success at lowest energy level) were > 15 J (group II). In all patients, repositioning was successful within a 15 J energy level (100% success). The mean DFT(plus) was 7.3 +/- 3.5 J (group I) and 11.0 +/- 4.5 J (group II; p<0.005). The mean DFT(plus) of all patients enrolled in the study was 7.6 +/- 3.7 J (range: 2 to 15 J). In 87% of all patients, DFT(plus) of < or = 10 J was achieved. Repositioning of the endocardial lead in the right ventricle is a simple and effective method to reduce intraoperative high DFTs. As a result of this procedure, ICDs with a 20 J output should be sufficient for the vast majority (87%) of our patients. Furthermore, we were able to avoid additional subcutaneous or epicardial electrodes in all patients.

T wave alternans as a risk predictor in patients with cardiomyopathy and mild-to-moderate heart failure.

The analysis of t wave alternans (TWA) was introduced to identify patients with an increased risk of ventricular tachyarrhythmias. The inducibility of ventricular tachyarrhythmias and the spontaneous arrhythmic events are correlated with a positive TWA in patients with a reduced left ventricular ejection fraction and survived myocardial infarction. In contrast, this study is the first to investigate the correlation of a survived sudden cardiac death and TWA in patients without coronary heart disease and only slightly decreased left ventricular function. Sixty patients were included in the study. The TWA analysis was performed using the Cambridge Heart system (CH2000). Patients were sitting on a bicycle ergometer and exercised with a gradual increase of workload to maintain a heart rate of at least 105 beats/min. The exercise test was stopped after recording 254 consecutive low noise level heart beats. The electrocardiographic signals were digitally processed using a spectral analysis method. The magnitude of TWA was measured at a frequency of 0.5 cycles/beat. A TWA was defined as positive if the ratio between TWA and noise level was > 3.0 and the amplitude of the TWA was > 1.8 microV. Twelve (20%) of the included 60 patients showed a positive TWA. The sensitivity concerning a previous arrhythmic event amounted to 65%, the specificity up to 98%, respectively. The alternans ratio was significantly higher in patients with a previous event (30.3 +/- 53.2 vs 2.9 +/- 5.9, P < 0.001) and cumulative alternans voltage (4.67 +/- 3.55 vs 1.75 +/- 1.88 microV, P < 0.001). In 19 patients, invasively investigated by an electrophysiological study, a significant correlation between inducibility of tachyarrhythmias and a positive TWA result was found (Spearman R = 0.51, P = 0.01). In conclusion, the TWA analysis seems to identify patients with nonischemic cardiomyopathy who are at an increased risk of ventricular tachyarrhythmias.

Chemoreflexsensitivity in patients with survived sudden cardiac arrest and prior myocardial infarction.

For evaluation of patients with an increased risk of sudden cardiac death, the analyses of ventricular late potentials, heart rate variability, and baroreflexsensitivity are helpful. But so far, the prediction of a malignant arrhythmic event is not possible with sufficient accuracy. For a better risk stratification other methods are necessary. In this study the importance of the ChRS for the identification of patients at risk for ventricular tachyarrhythmic events should be investigated. Of 41 patients included in the study, 26 were survivors of sudden cardiac arrest. Fifteen patients were not resuscitated, of whom 6 patients had documented monomorphic ventricular tachycardia and 9 had no ventricular tachyarrhythmias in their prior history. All patients had a history of an old myocardial infarction (> 1 year ago). For determination of the ChRS the ratio between the difference of the RR intervals in the ECG and the venous pO2 before and after a 5-minute oxygen inhalation via a nose mask was measured (ms/mmHg). The 26 patients with survived sudden cardiac death showed a significantly decreased ChRS compared to those patients without a tachyarrhythmic event (1.74 +/- 1.02 vs 6.97 +/- 7.14 ms/mmHg, P < 0.0001). The sensitivity concerning a survived sudden cardiac death amounted to 88% for a ChRS below 3.0 ms/mmHg. During a 12-month follow-up period, the ChRS was significantly different between patients with and without an arrhythmic event (1.64 +/- 1.06 vs 4.82 +/- 5.83 ms/mmHg, P < 0.01). As a further method for evaluation of patients with increased risk of sudden cardiac death after myocardial infarction the analysis of ChRS seems to be suitable and predicts arrhythmias possibly more sensitive than other tests of neurovegetative imbalance. The predictive importance has to be examined by prospective investigations in larger patient populations.

[Inflammation of the myocardium as an arrhythmia trigger]. / Entzündung des Myokards als Arrhythmietrigger.

In patients with acute or chronic myocarditis, arrhythmias are a common and often the only clinical symptom in the natural course of the disease. The potentially malignant tachy- and bradyarrhythmias are of particular significance in the differential diagnosis of sudden cardiac death in myocarditis. Factors responsible for the increased incidence of cardiac arrhythmias are structural changes, parameters of ventricular dynamics and vascular changes. On the one hand, inflammatory processes in the cardiac myocytes and interstitium can lead directly to fluctuations in membrane potential. Fibrosis and scarring of the myocardial tissue and secondary hypertrophy and atrophy of the myocytes favor the development of ectopic pacemakers, late potentials and reentry as a result of inhomogeneous stimulus conduction. Furthermore, parameters of ventricular dynamics such as increased wall tension, increased myocardial oxygen consumption and diminished coronary reserve in the case of disturbed systolic or diastolic left ventricular function also contribute to the increased incidence of arrhythmias. Lastly, vascular factors can further increase the arrhythmogenicity of the inflamed myocardium through the disturbance of micro- and macrovascular perfusion and the resulting myocardial ischemia. Non-invasive rhythmological evaluation by 24 h Holter ECG, measurement of ventricular late potentials and heart rate variability can be used for orienting risk stratification of the at-risk patient with myocarditis. Programmed atrial and ventricular electrophysiological stimulation also has a relatively high predictive value for spontaneous ventricular tachyarrhythmias. It should be emphasized that, at the present time, optimal electrophysiological parameters with a high predictive value do not exist. In a selected patient population, immunosuppressive therapy in addition to conventional antiarrhythmic therapy can lead to the reduction or complete suppression of spontaneous and inducible arrhythmias. Nevertheless, in the interim, further precautionary antiarrhythmic measures such as serial antiarrhythmic treatment, VT ablation and ACID implantation are necessary in patients with malignant cardiac arrhythmias. Right ventricular myocardial biopsy for demonstration or exclusion of myocarditis is an important additional examination which can improve the differential diagnosis and treatment of patients with cardiac arrhythmias of unclear etiology.

[Arrhythmia risk in left ventricular hypertrophy]. / Das Arrhythmierisiko bei linksventrikulärer Hypertrophie.

The incidence of supraventricular and ventricular arrhythmias in patients with arterial hypertension is up to 96% and is about 10 times higher than in normotensives. Predictors for an increased ventricular arrhythmogenic risk are left ventricular hypertrophy (LVH), impaired left ventricular function with enlarged end diastolic and end diastolic volumes as well as late potentials which in case of LVH increase from a 7% to 18% incidence. Especially the Simson criteria fQRS and RMS seem to characterize patients at risk. In addition a longer duration of hypertension in conjunction with a higher muscle mass index and a larger amount of couplets and non-sustained ventricular tachycardias, documented by Holter recording, are determinants of life threatening arrhythmias. In addition, an increased ventricular vulnerability in electrophysiological study significantly depends on left ventricular hypertrophy. Regression of LVH goes along with a decreased rate of ventricular extrasystoles. We therefore hypothesize that by pharmacological regression of hypertrophy the prevalence of complex arrhythmias decreases.

[Heart rate variability and chemoreflex sensitivity. Proved and new methods in risk prediction of malignant arrhythmias]. / Herzfrequenzvariabilität und Chemoreflexsensitivität. Bewährtes und Neues in der Risikoprädiktion maligner Herzrhythmusstörungen.

For the analysis of a disturbed autonomic function as a risk predictor for ventricular tachyarrhythmias, tonic and phasic procedures are available. The heart rate variability as a tonic procedure shows significant differences between patients with an increased risk of malignant arrhythmias and patients without increased risk. This can be demonstrated in patients with survived myocardial infarction, dilated cardiomyopathy and congestive heart failure. But the positive predictive value amounts only to about 50%. The chemoreflex sensitivity as a new phasic method represents a new possibility for the evaluation of a dysfunction of autonomic reflex arches. It is reduced due to a decreased left ventricular function and increasing age. Furthermore, it shows significant differences between patients with ventricular arrhythmias and patients without. The predictive accuracy concerning malignant ventricular arrhythmias in a population of 60 patients in the chronic postinfarction stadium amounts to 55%, the relative risk to 7.6. Thus, this method shows a high predictive power, but more investigations in larger patient cohorts are necessary to corroborate these results.

[14-year experience with implantable cardioverter/defibrillators: determination of prognosis and discharge behavior]. / 14 Jahre Erfahrung mit implantierbaren Cardioverter/Defibrillatoren: Determinanten der Prognose und des Auslöseverhaltens.

BACKGROUND: The treatment of life threatening ventricular arrhythmias with implantable cardioverter/defibrillators (ICD) has become the therapy of choice; the survival benefit of ICD treatment compared to drug therapy in patients with aborted sudden cardiac death (SCD) and hemodynamically unstable ventricular tachycardia has been proven. In addition for the primary prevention of SCD in high risk patients, ICD therapy is gaining growing acceptance. PATIENTS AND METHODS: We analyzed the long-term follow-up of 274 consecutive patients (211 male, 63 female, age 59 +/- 12 years, left ventricular ejection fraction 39 +/- 15%) provided with an ICD between 1984 and 1998. The aim of the study was to ascertain the survival rate in different subgroups and to discover determining factors of ICD discharge and prognosis. RESULTS: Long-term survival probability at 10 resp. 14 years was 84 resp. 65% for the total collective, and the freedom of event probability (neither shocks nor antitachycardiac pacing from the ICD) to 28% each. The risk to die from SCD was below 3% over time. The most pronounced differences regarding prognosis ensued from dividing the collective into heart insufficiency stages. Thus in NYHA class I and II versus III and IV, the cumulative event rate was 61% vs 82% at 5 years, and survival rate amounted to 94 vs 63% at 5 years and 87% vs 30% at 14 years (p < 0.001). Calculating the relative benefit of ICD therapy survival benefit provided by the ICD was shown to decrease significantly after 5 years for patients in NYHA class III/IV, while it increased progressively for patients in NYHA class I/II up to 10 years. Additional determinants of prognosis and ICD discharge rate were identified left ventricular ejection fraction, age and tendency for the basic cardiac disease, however neither the result of electrophysiological testing nor the results of non-invasive risk stratification. In patients with ischemic heart disease, revascularization procedures improved prognosis only in tendency, while the effect of ICD therapy was significant. In patients with the non-obstructive form of hypertrophic cardiomyopathy ICD, discharges occurred in about 50% of patients; in contrast patients with surgical myectomy for obstructive cardiomyopathy showed no events during follow-up. In patients with chronic inflammatory heart disease and normal left ventricular function (LVF), a very low event rate was expected if patients were treated by immunosuppressive drugs. Patients with dilated cardiomyopathy did not differ from patients with ischemic heart disease with respect to prognosis and ICD discharge rate. CONCLUSION: Significant determinants of prognosis and ICD discharge rate are left ventricular function, age and with limitations the basic cardiac disease. In contrast to patients with better LVF relative survival benefit decreases significantly after 5 years in patients with a worse LVF. Patients with aborted SCD and preserved LVF experience half the ICD discharges compared to patients with poor LVF and gain at the same time a normalization of life expectancy. Causative treatment of the basic disease has an impact on the overall prognosis and event rate, but should in general not influence the decision for IDC implantation in high risk patients.

Intracoronary dipyridamole reduces the incidence of abrupt vessel closure following PTCA: a prospective randomised trial.

OBJECTIVES: To investigate the effect of intracoronary dipyridamole on the incidence of abrupt vessel closure, myocardial infarction, necessity for bypass grafting, and death following percutaneous transluminal coronary angioplasty (PTCA). PATIENTS: Patients were randomly allocated to receive either conventional pretreatment (heparin 15 000 IU and aspirin 500 mg intravenously) or additional intracoronary dipyridamole (0.5 mg/kg bodyweight). Dipyridamole was administered in 550 PTCA procedures (455 interventions in men, mean (SD) age 59.2 (8.4) years; 74 acute coronary syndromes), while conventional pretreatment was administered in 544 interventions (444 interventions in men 58.3 (7.9) years old; 81 acute coronary syndromes). In 53 interventions bail out stenting was performed for threatened abrupt vessel closure. RESULTS: Intracoronary dipyridamole significantly reduced the incidence of abrupt vessel closure (odds ratio 0.42. 95% confidence interval (CI) 0.22 to 0.79). While abrupt vessel closure occurred in 6.1% of interventions following conventional pretreatment, dipyridamole reduced the incidence to 2.5%. Restricting the analysis to balloon angioplasty, this reduction was observed in patients with stable angina (odds ratio 0.49, 95% CI 0.23 to 0.96) as well as in those with acute coronary syndromes (odds ratio 0.29, 95% CI 0.09 to 0.87). Reduction of secondary end points in the dipyridamole treated patients failed to reach significance in the PTCA group. CONCLUSIONS: Intracoronary dipyridamole before PTCA reduces the incidence of abrupt vessel closure following PTCA for stable angina and acute coronary syndromes.

Hemodynamic effects of celiprolol in patients with ischemic and non-ischemic cardiomyopathy.

In this study, the effect of celiprolol (beta-1-antagonist with beta-2-agonistic activity) on hemodynamic and electrocardiographic parameters of patients with congestive heart failure due to ischemic (iCMP) and non-ischemic (niCMP) origin should be evaluated. Sixteen patients were included into the study, nine with iCMP, seven with niCMP. All patients were investigated by radionuclide ventriculography (99mTc), right heart floating catheterization, and late potential analysis and measurement of heart rate variability. All patients received 200 mg celiprolol after a 3-day period of 100 mg celiprolol/day. All patients showed, after a follow-up period of 3 months, a significant improvement of the left ventricular ejection fraction. The changes of hemodynamic parameters were more pronounced in patients with niCMP. Heart rate did not decrease in patients with niCMP. A 3-month therapy with celiprolol as an additional therapy to a preexisting heart failure therapy leads to a significant improvement of the ejection fraction in patients with congestive heart failure. Patients with niCMP seemed to profit more from this additional beta-blocking therapy.

[Is ICD-programming for double intraoperative defibrillation threshold energy safe and effective during long-time follow-up? Results of a prospective randomized multicenter study (Low-Energy Endotak Trial--LEET)]. / Ist eine ICD-Programmierung auf eine Schockenergie der doppelten intraoperativen Defibrillationsschwelle im Langzeitverlauf sicher effektiv? Ergebnisse einer prospektiven randomisierten Multizenterstudie (Low Energy Endotak Trial-LEET).

The aim of this prospective and randomized study was to evaluate the safety and efficacy of a reduced shock strength in transvenous implantable defibrillator therapy. So far clinical data concerning the safety margin of the shock energy in ICD therapy do not exist. The shock energy tested during long-term follow-up in this study was twice the intraoperatively measured defibrillation threshold (DFT). A total number of 176 consecutive patients representing a typical cohort of ICD patients were evaluated. All patients received a non-thoracotomy lead system (CPI, Endotak 0070, 0090) and a biphasic cardioverter-defibrillator with the ability to store episodes (Cardiac Pacemakers Inc., Ventac TM PRx II, PRx III). The intraoperative defibrillation threshold (DFT) was evaluated in a step-down protocol (15, 10, 8, 5 J) and had to be < or = 15 J for inclusion into the study. The lowest effective energy terminating induced ventricular fibrillation had to be confirmed and was defined as DFT+ augmented defibrillation threshold. The DFT+ value was tested immediately after successful implantation, at discharge, and after a follow-up period of one year. Prior to implantation the patients were randomized into two groups. The energy of the first shock in the study group was programmed at twice DFT+ and in the control group at the maximum energy output (34 J). The efficacy of the first shock and its reproducibility in DFT testings and in spontaneous episodes during long-term follow-up of the study group were compared to those in the control group. A DFT+ value was found to be < or = 15 J in 166 of 176 patients (94%). The DFT+ in the study group was 9.6 +/- 3.2; in control group 10.1 +/- 3.5 J. The prohability of successful defibrillation at DFT+ level after one year was 84%. The success rate of the first shock meant to terminate induced ventricular fibrillation (VF) was 99.5% in the study group (217 of 218 episodes) and 99% in the control group (201 of 203 episodes). During follow-up of 24 +/- 9 months spontaneous episodes in the study group, 83/86 (96.5%) monomorphic ventricular tachycardias (MVT) and 38/40 (95%) VF-episodes were converted successfully by the 2x DFT+ shock. In the control group the first shock was successful in 151/156 (96.8%) spontaneous MVTs and in 30/33 (91%) VF episodes. The efficacy of the first shock was not influenced by clinical data such as the underlying cardiac disease, left ventricular function, ongoing antiarrhythmic therapy with amiodarone, or the number of spontaneous episodes per day or by the DFT itself. At a mean follow-up of two years there was no significant difference between the two groups concerning the incidence of sudden cardiac death (2.4% in the study group vs. 3.8% in the control group). In conclusion programming the first shock with the ICD lead system used in this study at 2x DFT+ is as efficient as a shock energy of 34 J in order to terminate induced and spontaneous episodes of VT/VF. Thus, the safety of ICD-therapy is not impaired when programming the shock energy at the 2x DFT+ value.

Safety and efficacy of implantable defibrillator therapy with programmed shock energy at twice the augmented step-down defibrillation threshold: results of the prospective, randomized, multicenter Low-Energy Endotak Trial.

Whether the safety and efficacy of implantable cardioverter defibrillator (ICD) therapy can be assured with lower output devices is an important question. The purpose of this study was to evaluate whether programming the device output at twice the augmented defibrillation threshold was as safe and effective as using the maximum energy. Patients indicated for ICD therapy, but without slow monomorphic ventricular tachycardia (MVT), who achieved an augmented defibrillation threshold (DFT plus) < or = 15 joules (J) with a single endocardial lead system and a biphasic defibrillator were included in the study. Prior to ICD implantation, patients were randomized into 2 groups. The shock energies in test group patient were set as follows: first shock at twice DFT plus, the second to fifth shocks at maximum output (34 J). In control group patients, all shocks were programmed at 34 J. The study population consisted of 166 consecutive patients (mean age 57.4 +/- 12.1 years, mean left ventricular ejection fraction 36.8 +/- 13.8%). Mean DFT plus was 9.6 +/- 3.2 J in test group patients and 10.1 +/- 3.5 J in control group patients (p = 0.36). During a mean follow-up of 24.2 +/- 9.6 months, 736 arrhythmia episodes were analyzed. The first shock efficacy was 98.3% in the test group patients versus 97.4% in the control group (p = 0.45). Total mortality was 6%, equally distributed in both study groups. The results of this study prove that the method of doubling the defibrillation energy at the DFT plus level provides an adequate safety margin in defibrillator therapy.

Etiology and pathogenetic mechanisms of optic disc swelling with visual loss. An interdisciplinary prospective pilot study of 102 cases.

A nonrandomized, prospective, interdisciplinary pilot study of 102 patients with noncompressive optic disc swelling with visual loss (ODSWVL) was performed in order to investigate etiologic and pathogenetic mechanisms. Forty-six patients suffered from underlying inflammatory disease. Seventeen patients suffered from highly probable cardiogenic embolization, 16 patients from multiple vascular risk factors. The remaining patients of the noninflammatory disease group suffered from leukemia, previously unknown or severely decompensated diabetes mellitus, acute arterial hypertension, different kinds of coagulopathies and others. Ninety-six of the 102 patients required medical treatment according to general medical standards. Inhomogeneity of the underlying disease processes explains the ineffectiveness of different monotherapies in previous studies. Interdisciplinary search for the underlying causes allows causative treatment. ODSWVL and anterior ischemic optic neuropathy in particular seem to be a common final pathway of various pathogenetic mechanisms due to different etiologies rather than a disease entity by itself.

[Myocardial ischemia and ventricular arrhythmia]. / Myokardischämie und ventrikuläre Arrhythmien.

A relation between myocardial ischemia and induction of ventricular arrhythmias can be demonstrated in patients with coronary heart disease--in contrast to patients with primary non ischemic cardiac diseases--using a combined metabolic-electrophysiological investigation protocol consisting of programmed atrial and ventricular stimulation with simultaneous measurement of the arterio/coronary venous difference for lactate, pyruvate, free fatty acids and amino acids. There are significant metabolic distinctions between both ischemic and non ischemic heart disease under pacing stress conditions as well as at rest. Areas of "hibernating myocardium" resp. "mismatch" zones in the myocardium showing reduced or abolished perfusion and preserved metabolism during scintographic SPECT/PET studies, may be found more often in patients with ventricular tachycardias (VT) or ventricular fibrillation (VF) in the chronic post myocardial infarction state than in patients without VT/VF. The proof of such zones may be considered a possible risk factor for arrhythmic events and sudden cardiac death after myocardial infarction. Hereby the concept of an interaction between acute and chronic ischemia triggering the onset of polymorphic VT or VF gaines increasing acceptance. In contrast, monomorphic reentrant VT are usually generated in the border zone of scarred areas where islands of vital fibers are surrounded by fibrotic tissue. These arrhythmogenic origin regions are characterized by a "match" pattern presenting a comparably severe reduction of perfusion and metabolism. Under those circumstances a control resp. suppression of the VT focus can only be provided by interventional techniques like catheter ablation, antitachycardiac surgery or implantation of a cardioverter/defibrillator beyond antiarrhythmic drug therapy. An antiischemic causal treatment (bypass surgery or angioplasty) represents for maximal 40% of patients with ischemically induced ventricular arrhythmias an adequate and sufficient therapeutic option. This pure antiischemic procedure seems to be justified especially in patients with preserved left ventricular function, proof of reversible ischemia and non inducibility of VT/VF following revascularization or non inducibility pre- and post intervention. In all other instances an additional treatment by antiarrhythmic drugs or preferably the implantable defibrillator is required.