Losses of cd, hg, and Zn during metamorphosis in the beetle Tenebrio molitor (Coleoptera: Tenebrionidae).
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to M Block.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Antihapten antibodies binding to ligand-hapten conjugates are able to mediate complement mediated lysis in vitro. Based on this observation we propose a new in vivo immunotherapy using molecules that combine a low molecular weight hapten binding to antibodies preexisting in serum and a cell specific ligand. The ligand-hapten conjugates are potential cytotoxic drugs which may (1) be specific for a given target cell, (2) be nonimmunogenic, (3) be of low molecular weight, (4) form soluble complexes with preexisting antibodies resulting in prolonged half life of the drug, and (5) induce a potent antibody mediated rejection of target cells. These novel compounds could be useful for the elimination of certain cell subsets involved in allograft rejection, cancers, infectious diseases, etc., without some of the pitfalls of conventional immunotherapies. The feasibility of this approach was demonstrated in an animal model using a compound consisting of one interleukin 2 and one fluorescein molecule (IL-2-FITC). BALB/c mice (H2d) previously immunized and expressing anti-FITC antibodies were transplanted with a fully mismatched C57BL/6 (H2b) heterotopic heart allograft. Untreated controls rejected their graft by day 9 (MSD = 9 +/- 0.7). Mice with preexisting anti-FITC antibodies treated with IL-2-FITC maintained their grafts for 38.7 +/- 7.1 days (P < 0.02). No prolongation of graft survival was observed in immunized animals that were treated with IL-2 alone (MSD = 10 +/- 1.4). Nonimmunized animals treated with IL-2-FITC rejected their grafts on day 9.4 +/- 1.1. This demonstrates that IL-2-FITC therapy specifically prolonged graft survival in animals with circulating anti-FITC antibodies. The data suggest that a ligand/hapten pair can redirect preexisting antihapten antibodies toward target cells in vivo. Such compounds may be developed for human use as alternatives to polyclonal or monoclonal antibody therapy.
Poor left ventricular function is a predictor of sudden death. Both antiarrhythmic drugs and implantable cardioverter-defibrillators (ICDs) promise to reduce the sudden death rate in these patients and consequently improve survival. In patients without spontaneous ventricular tachyarrhythmias, only beta-blocking agents and amiodarone have been shown to reduce sudden death and improve survival in some studies, whereas class I antiarrhythmic drugs increased mortality. For patients with documented ventricular tachyarrhythmias, protection against sudden death by serially tested class I antiarrhythmic drugs is at best moderate. There is some evidence suggesting that therapy with class III antiarrhythmic drugs, either amiodarone or dl-sotalol, may reduce sudden death rates and improve overall mortality in comparison to therapy with class I antiarrhythmic drugs. ICDs have been shown to prevent sudden death reliably. In published patient cohorts in which only patients who were not inducible off antiarrhythmic drugs or still inducible on antiarrhythmic drugs received an ICD, the ICD seemed to improve overall survival in comparison to class I antiarrhythmic drugs. A small prospective randomized study that compared a conventional therapy strategy to primary ICD implantations showed an improved outcome with ICDs as therapy of first choice. However, these studies included many patients treated with class I antiarrhythmic drugs considered to be less effective. In matched control studies comparing the ICD to amiodarone or dl-sotalol, less sudden deaths and an improved overall survival could be shown for the ICD in general without stratification for left ventricular function. Thus, in patients with hemodynamically nontolerated ventricular tachyarrhythmias, the ICD seems to improve survival in comparison to class I antiarrhythmic drugs, dl-sotalol, or amiodarone. However, in patients with poor left ventricular function, therapy with ICDs seems to be less cost-effective than in patients with preserved left ventricular function. In patients with very poor left ventricular function who are evaluated for cardiac transplantation, the ICD seems to change only the mode of death from sudden to a nonsudden cardiac death if transplantation cannot be performed soon.
BACKGROUND: Implantable cardioverter-defibrillators (ICDs) and d,l-sotalol are widely used to treat ventricular tachyarrhythmia and ventricular fibrillation (VT/VF). The purpose of this study was to compare the long-term efficacy of d,l-sotalol and ICDs in patients with coronary artery disease. METHODS AND RESULTS: In a case-control study, 50 patients treated with oral d,l-sotalol were matched to 50 patients treated with ICDs. Both groups were matched for sex (82 men), age (58 +/- 10 years), ejection fraction (40 +/- 12%), extent of coronary artery disease, presenting arrhythmia, and year that treatment began. In all patients in the sotalol group, VT/VF was inducible in the drug-free electrophysiological study. Induction of sustained VT/VF was suppressed by d,l-sotalol (438 +/- 95 mg/d). In the ICD group, either VT/VF was not inducible (n = 5) or inducible sustained VT/VF was refractory to antiarrhythmic drug treatment (n = 45). Sotalol treatment led to a marked reduction in arrhythmic events. Whereas 83% of the patients in the sotalol group were free of sudden death and nonfatal VT at 3 years, only 33% of the ICD patients did not receive appropriate ICD therapies (P < .005). Actuarial rates for absence of sudden death at 3 years were 85% in the sotalol group and 100% in the ICD group (P < .005). Actuarial rates for overall survival at 3 years were 75% in the sotalol group and 85% in the ICD group (P = .02). CONCLUSIONS: In this case-control study, ICD therapy was more effective tha electrophysiologically guided antiar-rhythmic treatment with d,l-sotalol in prevention of sudden death and reduction of total morality in patients with coronary artery disease. Prospective studies are needed to confirm these results.
BACKGROUND: Algorithms to reject irregular tachyarrhythmias are available in implantable cardioverter-defibrillator devices to discriminate ventricular tachycardia (VT) from atrial fibrillation (AF). The hazard of underdetection of irregular monomorphic VTs using these algorithms has not yet been fully evaluated. The purpose of this study was to determine the ability of a commonly used stability algorithm to reject AF and to correctly detect VT with a high RR interval variability. METHODS AND RESULTS: The electrophysiological studies from 232 patients with induced monomorphic VT (cycle length > 250 ms) and 21 with AF were reviewed. A preliminary analysis was performed to classify the VT episodes in irregular (successive RR differences > 20 ms after 4 seconds from onset) or regular (otherwise). Three study groups were defined: group 1 (27 patients with irregular VT), group 2 (22 randomly selected patients with regular VT), and group 3 (21 patients with AF). A computer program analyzed the first 50 RR intervals of the induced VT (AF), resetting a VT counter if the interval was greater than a tachycardia detection interval (TDI) or if its absolute difference with the preceding three beats exceeded a programmed stability value (STAB). The VT was detected when the VT counter reached a preset number of intervals (NIDs). Different combinations of TDI, STAB, and NID were analyzed. All VTs in group 2 were correctly detected. In contrast, up to 10 VTs from group 1 were not detected when high NIDs and low STAB parameters were programmed. With usual values (10 to 16 beats and 50 to 60 ms, respectively), only 1 to 2 VTs remained undetected, but 20% to 50% had a detection delay > 8 seconds. Undetected VTs were significantly slower than early detected VTs for most STAB and NID combinations. With usual stability and NID values, 10% to 20% of episodes of AF were inappropriately detected. Changes in TDI had a small impact on sensitivity and specificity when currently used values for stability were programmed. CONCLUSIONS: Animplantable cardioverter-defibrillator tachycardia detection algorithm with a stability criterion of 50 to 60 ms and 12 to 14 RR intervals is able to detect over 90% of monomorphic irregular VTs. Nevertheless, significant VT detection delays may arise, and inappropriate detection of AF cannot be totally prevented.
These results suggest that analysis of heart rate variability recorded even very early after acute myocardial infarction (1 to 2 days after onset of pain) is feasible in clinical routine and strongly related to subsequent arrhythmic events and cardiac mortality. Decreased HRV is considered not only a marker of impaired vagal activity of the heart but complete autonomic impairment, strongly associated with the degree of myocardial damage. HRV represents the integrated response of the cardiovascular system to a variety of different influences: the plasma level of catecholamines, the baroreflex activation and the direct sympathetic and vagal activity. The HRV profile is dynamic-HRV reduction caused by myocardial damage changes over time presenting a progressive increase up to normality over a 2-month follow-up. The observed early differences between anterior and inferior myocardial infarction disappear later in the healing phase. However, group analysis results of different HRV indices are stabile over time and highly reproducible, but presenting large individual variations. HRV parameters which are adjusted to heart rate (e. g. CV) seemed to be more stabile. The role of HRV analysis in risk stratification of patients after myocardial infarction is strongly related to the actual model of the genesis of ventricular arrhythmias. Multiple experimental and clinical studies described the development of life threatening ventricular arrhythmias as a multifactorial event which can not be described adequately using just one risk parameter for stratification. The arrhythmogenic substrate representing the underlying inhomogeneity of electrical behaviour of adjacent myocardial areas might be detectable by the analysis of ventricular late potentials or frequency disturbances from the signal averaged ECG. The autonomic modulation of this substrate is represented by an altered heart rate variability. Possible trigger factors to initiate arrhythmias in a modulated arrhythmogenic substrate like ventricular premature beats or transient myocardial ischemia can be detected by conventional arrhythmia and ST segment analysis from Holter tapes. The optimized combination of these non-invasive risk predictors together with well known evident clinical risk parameters, like left ventricular ejection fraction, may lead to a valid set of screening parameters for individual risk estimation after myocardial infarction.
The volume of current implantable cardioverter defibrillators (ICD) is not convenient for pectoral implantation. One way to reduce the size of the pulse generator is to find a more effective defibrillation pulse waveform generated from smaller volume capacitors. In a prospective randomized crossover study we compared the step-down defibrillation threshold (DFT) of a standard biphasic waveform (STD), delivered by two 250-microF capacitors connected in series with an 80% tilt, to an experimental biphasic waveform delivered by a single 450-microF capacitor with a 60% tilt. The experimental waveform delivered the same energy with a lower peak voltage and a longer duration (LVLD). Intraoperatively, in 25 patients receiving endocardial (n = 12) or endocardial-subcutaneous array (n = 13) defibrillation leads, the DFT was determined for both waveforms. Energy requirements did not differ at DFT for the STD and LVLD waveforms with the low impedance (32 +/- 4 omega) endocardial-subcutaneous array defibrillation lead system (6.4 +/- 4.4 J and 5.9 +/- 4.2 J, respectively) or increased slightly (P = 0.06) with the higher impedance (42 +/- 4 omega) endocardial lead system (10.4 +/- 4.6 J and 12.7 +/- 5.7 J, respectively). However, the voltage needed at DFT was one-third lower with the LVLD waveform than with the STD waveform for both lead systems (256 +/- 85 V vs 154 +/- 51 V and 348 +/- 76 V vs 232 +/- 54 V, respectively). Thus, a single capacitor with a large capacitance can generate a defibrillation pulse with a substantial lower peak voltage requirement without significantly increasing the energy requirements. The volume reduction in using a single capacitor can decrease ICD device size.
Adequate sensing is a basic requirement for appropriate therapy with ICDs. Integrated sense pace defibrillation leads, which facilitate ICD implantation, show a close proximity of sensing and defibrillation electrodes that might affect the sensing signal amplitude by the high currents of internal defibrillation. In 99 patients, we retrospectively examined two integrated sense pace defibrillation leads, either both with a distance of 6 mm between the tip of the lead (sensing cathode) and the right ventricular defibrillation electrode (sensing anode) or one with a distance of 12 mm. Three seconds after a shock of 20 J, mean sensing signal amplitude during sinus rhythm (SR) decreased from 10.5 +/- 4.3 mV to 5.1 +/- 3.7 mV (P < 0.001) for the 6-mm lead, but showed no significant decrease for the 12-mm lead. The degree of signal reduction was inversely related to the time passed since defibrillation. Significant differences in reduction of sensing signal amplitude concerning monophasic and biphasic shocks could not be observed. Mean sensing signal amplitude of VF after shocks that failed to terminate it decreased in the same order as during SR (from 8.3 +/- 4.1 mV to 4.1 +/- 3.2 mV), but resulted in no failure of redetection during ongoing VF. DFTs did not differ for the 6-mm and the 12-mm lead. In conclusion, close proximity of the right ventricular defibrillation coil to the sensing tip of an integrated sense pace defibrillation lead causes energy and time related reduction in sensing signal amplitude after defibrillation, and might cause undersensing in the postshock period. A new lead design with a more proximal position of the right ventricular defibrillation coil avoids these problems without impairing DFTs.
INTRODUCTION: Perioperative mortality of patients undergoing implantation of automatic implantable cardioverter defibrillators (ICDs) has been reduced dramatically following the availability of transvenous-subcutaneous defibrillation leads. However, patients with severely reduced left ventricular function show a substantial rate of nonsudden cardiac mortality within the first year. Whether repeated intraoperative inductions of ventricular tachycardia/fibrillation (VT/VF) during implantation lead to hemodynamic deterioration and thus might contribute to development of end-stage heart failure in these patients is unknown. The purpose of the present study was to determine cardiac output and hemodynamic performance during transvenous-subcutaneous ICD implantation in patients with severe left ventricular dysfunction. METHODS AND RESULTS: In 11 patients with a left ventricular ejection fraction (EF) < or = 0.35, cardiac output was measured automatically with a combined continuous cardiac output/mixed venous oxygen saturation pulmonary artery catheter system. ICD implantation was performed during standardized general anesthesia. In the 11 patients (EF = 27 +/- 2% [mean +/- SEM]) a total of 95 episodes of VT/VF followed by defibrillation were induced (episodes per patient = 9 +/- 1; range 6 to 11). Cardiac index was 2.2 +/- 0.2 L.min-1.m-2 after induction of anesthesia (before start of surgery), and 1.9 +/- 0.1 L.min-1.m-2 immediately before first induction of VT/VF. After the last episode of VT/VF, cardiac index was 2.1 +/- 0.2 L.min-1.m-2. Cardiac index measured 1, 2, and 3 minutes after induction of VT/VF was not significantly different when compared to the preinduction value during any episode of VT/VF induction. Similarly, stroke volume index was 39 +/- 5 mL.m-2 immediately before first induction of VT/VF and 36 +/- 3 mL.m-2 after the last episode of VT/VF (NS). At the end of surgery, hemodynamic parameters did not exhibit any significant difference when compared to the data obtained before start of ICD implantation and testing. CONCLUSION: Extensive defibrillation tests during transvenous-subcutaneous ICD implantation in patients with severe left ventricular dysfunction are not associated with acute deterioration of cardiac performance.
Indications for of automatic cardioverter-defibrillators of automatic in patients with ventricular tachyarrhythmias have changed since the publications of first guidelines in 1991. Less invasive surgical approaches reduced the perioperative mortality. Tiered therapy devices improved the quality of life by reducing appropriate and inappropriate shocks. A low annual incidence of sudden death with implantable cardioverter defibrillators and frustrating results with antiarrhythmic drugs caused an extension of implantable cardioverter-defibrillator indications. Despite the absence of prospective studies implantable cardioverter-defibrillators have become a first line treatment for patients with ventricular tachyarrhythmias which are not due to acute myocardial infarction. In cardiac arrest survivors implantable cardioverter-defibrillator therapy has become the gold standard due to the low annual incidence of sudden death seen in implantable cardioverter-defibrillator patients. The results of ongoing prospective studies comparing implantable cardioverter-defibrillator therapy to antiarrhythmic drugs have to be awaited and will influence tomorrow's indications for implantable cardioverter-defibrillator therapy in patients with documented ventricular tachyarrhythmias. Additionally, studies evaluating prophylactic implantable cardioverter-defibrillator implantations in patients at high risk for ventricular tachyarrhythmias might expand indications for implantable cardioverter-defibrillator therapy.
30 patients (mean age 51.4 +/- 11.6 years; female n = 6) were studied early after orthotopic heart transplantation (11.6 +/- 5.5 weeks). Twelve recipients had undergone specific treatment for biopsy proven rejection. Using a mechanical intravascular ultrasound device (3.5-F catheter), 153 coronary artery segments (16 left coronary main stem, 122 left anterior descending artery, 15 left circumflex artery) were studied. Intimal index and circumferential extension of a three-layer appearance of the vessel wall were assessed. In all segments, systolic-diastolic changes in area (delta A) with respect to vessel area and pressure (delta P) were used to study normalized compliance (normalized compliance = [delta A/A]/delta P [mm Hg-1 x 10(3)]). Intravascular ultrasound findings were correlated to perioperative ischemia time, LDL/HDL-ratio, Lp(a) and donor age. In a subgroup of 13 recipients, intravascular ultrasound investigation was repeated after an interval of 67.4 +/- 10.2 weeks. At first investigation, mean intimal index of all coronary segments was 0.07 +/- 0.10. Mean circumferential extension of a three-layer appearance of the vessel wall was 84 +/- 112 degrees. Normalized compliance was 2.43 +/- 1.90 mm Hg-1 in the left main stem 2.45 +/- 1.47 mm Hg-1 within the left anterior descending artery, and 2.66 +/- 1.72 mm Hg-1 within the circumflex artery (differences n.s.). No correlation was found between intimal index and normalized compliance (r = -0.322), nor between circumferential extension of intimal thickening and normalized compliance (r = -0.362). Furthermore, there was no correlation between normalized compliance and donor age. Normalized compliance was significantly lower in recipients with proven rejection than in those without (1.76 +/- 0.81 versus 2.95 +/- 1.22 mm Hg-1, p = 0.005). Both, intimal index and circumferential extension of intimal thickening, were significantly higher in recipients following rejection periods (p < 0.05). The extent of coronary vessel wall alterations on ultrasound correlated to donor age but not to perioperative ischemia time, LDL/HDL-ratio and Lp(a). Re-investigation of a subgroup of 13 recipients 67.4 +/- 10.2 weeks after the first study showed an insignificant increase of the intimal index (from 0.03 to 0.09) and of the circumferential extension of intimal thickening (from 40 to 111 degrees). Normalized compliance changed from 2.53 +/- 1.48 to 2.87 +/- 1.33 mm Hg-1 (differences n.s.). Early after orthotopic heart transplantation, a significant correlation between atherosclerotic coronary vessel wall alterations assessed by intravascular ultrasound and donor age can be confirmed. Heart recipients following rejection periods present with significantly more atherosclerotic vessel wall alterations and a severely reduced compliance of the coronary vessels.
BACKGROUND: The feasibility of radiofrequency (RF) catheter ablation for the treatment of sustained ventricular tachycardia (VT) in patients with coronary artery disease and remote myocardial infarction has recently been demonstrated. At present, therapeutic options for VT in patients with idiopathic dilated cardiomyopathy (DCM) include antiarrhythmic drugs and implantable cardioverter/defibrillators (ICD). The purpose of the present study was to investigate the feasibility of RF catheter ablation in patients with idiopathic DCM who could not be adequately treated by conventional treatment modalities because of incessant or frequent, recurrent VT. METHODS AND RESULTS: RF current application for ablation of 9 VTs (mean cycle length, 402 +/- 78 ms) was attempted in 8 patients with idiopathic DCM (4 men, 4 women; mean age, 54 +/- 6 years; mean left ventricular ejection fraction, 30 +/- 9%). Inclusion criteria for ablation were incessant VT (n = 4) or frequent, recurrent VT reproducibly inducible with programmed electrical stimulation (n = 5). Three patients had suffered aborted sudden cardiac death, and 2 had experienced syncope. Two patients were artificially ventilated and catecholamine dependent for hemodynamic reasons at the time of attempted ablation. Potential target sites for RF current application were identified by detailed endocardial mapping during sinus rhythm, activation and entrainment mapping during VT, and pace mapping. After 7 +/- 5 RF pulses (range, 2 to 18 pulses; median, 6 pulses) applied with 32 +/- 7 W for 39 +/- 9 seconds, 6 of the 9 target VTs (67%) were rendered noninducible (4 of 4 incessant VTs and 2 of 5 chronic recurrent VTs). In 6 patients, VTs with ECG morphologies other than the target VTs were inducible after RF catheter ablation. Seven patients were on antiarrhythmic drugs during the ablation procedure and during the follow-up period of 8 +/- 5 months (range, 2 to 17 months). One patient received an ICD before RF ablation, 4 patients after RF ablation, and 1 patient after ablation of an incessant VT and before attempted ablation of frequent, recurrent VTs. One patient underwent heart transplantation 5 months after ablation in end-stage heart failure. There were no acute complications during the mapping and ablation procedure. During the follow-up period, 1 patient had been resuscitated from ventricular fibrillation 6 weeks after ablation and finally died of congestive heart failure 2 weeks later. No further episodes of incessant VT occurred in the patients who had undergone RF current application for ablation of incessant VT. A complete prevention of VT could be achieved in 2 of 8 patients, whereas in 5 patients, VT episodes were stored in the ICD devices during follow-up. CONCLUSIONS: The results of the present study indicate that RF current application for ablation of VT in a select group of patients with idiopathic DCM is feasible. The efficacy of RF ablation may be high in patients presenting with incessant VT, whereas the success rate seems to be only moderate in patients with chronic recurrent VT. In all patients, additional treatment options, including antiarrhythmic drugs, ICDs, and/or heart transplantation, were applied after RF ablation, indicating that RF ablation for this indication may be an adjunctive and not a curative treatment option.
Defibrillation of the heart is achieved if an electrical current depolarizes the majority of the unsynchronized fibrillating myocardial cells. The applied current or the corresponding voltage described as a function of time is called the waveform. In pacing, to stimulate myocardial cells close to the electrode, a relatively low voltage is needed for a relatively brief duration. However, in defibrillation, approximately a 100-fold higher voltage is needed and achieved by the use of capacitors. The exponential voltage decay of a capacitor during its discharge determines the basic waveform for defibrillation. In an attempt to lower the energy needed for defibrillation, the steepness of the decay (different capacitances), the duration (fixed duration waveforms) or tilt (fixed tilt waveforms), or the initial polarity can be changed. Additionally, the polarity of the electrodes can be reversed during the discharge of the capacitor once (biphasic waveform) or twice (triphasic waveform). If two capacitors and defibrillation pathways are available, bidirectional defibrillation pulses can be delivered sequentially. In humans, the original standard waveform used with endocardial leads was a single monophasic pulse delivered by a 125-microF capacitor using the endocardial right ventricular electrode as cathode. It is now known that a reversal of the initial polarity and a reversal of polarity during capacitor discharge may significantly lower the energy needed for defibrillation, thereby preventing formerly frequent failures of defibrillation with endocardial lead systems. The use of sequential pulses showed no or only slight reductions of energy requirements and was abandoned due to the additional electrode needed. The use of a smaller capacitance (60-90 microF reduced maximum energy output but generally did not reduce energy requirements for defibrillation. However, with more efficient electrodes, smaller capacitances that will help to reduce the size of the defibrillator might be used. Thus, today defibrillation is optimized with respect to energy, capacitor size, and ease of implantation if an approximately 90-microF capacitor is used to deliver a biphasic pulse via a bipolar lead system using the right ventricular electrode as anode.
For most nonthoracotomy defibrillation lead systems, the transvenous anode can positioned independently of the right ventricular (RV) cathode. Usually a vertical position in the superior vena cava (SVC) is chosen. However, it is unknown if this position yields the optimal defibrillation threshold (DFT). Therefore, in 15 patients undergoing defibrillator implantation the SVC position was compared in a crossover study design with a horizontal position in the left brachiocephalic vein (BCV). Mean DFT was not different for SVC and BCV (19.2 +/- 9.6 J vs 18.5 +/- 9.1 J) but DFT of individual patients differed by up to 12 joules. A positive correlation between impedance and DFT in the BCV position (r = 0.6; P < or = 0.05) indicated that the improved geometry of the defibrillation field with the BCV position is opposed by a higher impedance found for this position (63 +/- 15 omega vs 52 +/- 7 omega). Thus, defibrillation is not improved in general although individual patients might benefit.
We report an unusual case of the erroneous discharge of a third-generation multiprogrammable implantable cardioverter defibrillator in a 64-year-old patient with a history of recurrent ventricular tachycardias caused by electromagnetic interference while shaving with an electric razor. Electromagnetic interference was related to a defect in the electrode's insulation and could not be provoked in an intact electrode.
INTRODUCTION: The size of current implantable cardioverter defibrillators (ICD) is still large in comparison to pacemakers and thus not convenient for pectoral implantation. One way to reduce ICD size is to defibrillate with smaller capacitors. A trade-off exists, however, since smaller capacitors may generate a lower maximum energy output. METHODS AND RESULTS: In a prospective randomized cross-over study, the step-down defibrillation threshold (DFT) of an experimental 90-microF biphasic waveform was compared to a standard 125-microF biphasic waveform. The 90-microF capacitor delivered the same energy faster and with a higher peak voltage but provided only a maximum energy output of 20 instead of 34 J. DFTs were determined intraoperatively in 30 patients randomized to receive either an endocardial (n = 15) or an endocardial-subcutaneous array (n = 15) defibrillation lead system. Independent of the lead system used, energy requirements did not differ at DFT for the experimental and the standard waveforms (10.3 +/- 4.1 and 9.5 +/- 4.9 J, respectively), but peak voltages were higher for the experimental waveform than for the standard waveform (411 +/- 80 and 325 +/- 81 V, respectively). For the experimental waveform the DFT w as 10 J or less using an endocardial lead-alone system in 10 (67%) of 15 patients and in 12 (80%) of 15 patients using an endocardial-subcutaneous array lead system. CONCLUSIONS: A shorter duration waveform delivered by smaller capacitors does not increase defibrillation energy requirements and might reduce device size. However, the smaller capacitance reduces the maximum energy output. If a 10-J safety margin between DFT and maximum energy output of the ICD is required, only a subgroup of patients will benefit from 90-microF ICDs with DFTs feasible using current defibrillation lead systems.
BACKGROUND: The availability of implantable cardioverter-defibrillators (ICD) that are capable of antitachycardia pacing may lead to an increased use of ICDs in patients with haemodynamically tolerated ventricular tachycardia without a history of cardiac arrest. The frequency of potentially life-threatening fast ventricular tachycardias (cycle length < 250 ms) was investigated in patients who had a third generation ICD with endocardial leads implanted because they had haemodynamically tolerated ventricular tachycardia without a history of cardiac arrest. METHODS: Between January 1990 and October 1993, 50 patients (age (mean (SD)) 60 (11); ejection fraction 39 (16)%; 82% with coronary artery disease and 8% with dilated cardiomyopathy) with haemodynamically tolerated ventricular tachycardia (cycle length (mean (SD)) 348 (60) ms; range 250-500 ms) and without a history of cardiac arrest were treated with third generation ICDs that were capable of antitachycardia pacing. Fast ventricular tachycardia had been induced in 14 (28%) during baseline electrophysiological study. The benefit of ICD treatment was estimated as the difference between total mortality and the occurrence of fast ventricular tachycardia that would have been fatal if it had not been terminated. RESULTS: During follow up of 17 (12) months, 33 patients (66%) had a total of 3861 episodes of ventricular tachycardia. 91% of these episodes were terminated by antitachycardia pacing. 11 patients (22%) had episodes of potentially life-threatening fast ventricular tachycardia and 3 of these also had inducible fast ventricular tachycardia. One patient died suddenly 27 months after implantation. The difference between survival without fast ventricular tachycardia and total mortality was 9%, 12%, 27%, and 27% at 6, 12, 18, and 24 months, respectively. CONCLUSIONS: About a fifth of patients who had been given an ICD to treat haemodynamically tolerated ventricular tachycardia and who had no history of cardiac arrest experienced fast ventricular tachycardia during follow up requiring immediate cardioversion. Prospective studies are needed to investigate whether the prognosis of patients with a history of haemodynamically tolerated ventricular tachycardia without cardiac arrest is improved by ICD therapy.