Biomedical subjects

T Beyer

Publications and source records attributed to T Beyer.

At least 19 recordsLinked to original sources

PubMed2000

A combined PET/CT scanner for clinical oncology.

UNLABELLED: The availability of accurately aligned, whole-body anatomical (CT) and functional (PET) images could have a significant impact on diagnosing and staging malignant disease and on identifying and localizing metastases. Computer algorithms to align CT and PET images acquired on different scanners are generally successful for the brain, whereas image alignment in other regions of the body is more problematic. METHODS: A combined PET/CT tomograph with the unique capability of acquiring accurately aligned functional and anatomical images for any part of the human body has been designed and built. The PET/CT scanner was developed as a combination of a Siemens Somatom AR.SP spiral CT and a partial-ring, rotating ECAT ART PET scanner. All components are mounted on a common rotational support within a single gantry. The PET and CT components can be operated either separately, or in combined mode. In combined mode, the CT images are used to correct the PET data for scatter and attenuation. Fully quantitative whole-body images are obtained for an axial extent of 100 cm in an imaging time of less than 1 h. When operated in PET mode alone, transmission scans are acquired with dual 137Cs sources. RESULTS: The scanner is fully operational and the combined device has been operated successfully in a clinical environment. Over 110 patients have been imaged, covering a range of different cancers, including lung, esophageal, head and neck, melanoma, lymphoma, pancreas, and renal cell. The aligned PET and CT images are used both for diagnosing and staging disease and for evaluating response to therapy. We report the first performance measurements from the scanner and present some illustrative clinical studies acquired in cancer patients. CONCLUSION: A combined PET and CT scanner is a practical and effective approach to acquiring co-registered anatomical and functional images in a single scanning session.

Adult↗

PubMed1999

Rate and time dependent effects of D-sotalol on the monophasic action potential after sudden increase of the heart rate.

Experimental and clinical data suggests that almost all Class III antiarrhythmic agents diminish their ability to prolong cardiac repolarization at fast heart rates. However, only limited data exists about the time course of efficacy decay of Class III agents after sudden increase of the heart rate. In the present study, we assessed both rate and time dependent changes of the efficacy of d-sotalol in higher stimulation frequencies following an abrupt increase in heart rate. This might imitate the situation seen in the development of paroxysmal tachycardias. Monophasic action potentials were recorded from the right ventricular apex during sinus rhythm and constant stimulation with the paced cycle length (PCL) of 550 ms, 400 ms, and 330 ms in the baseline and 20 minutes after intravenous administration of d-sotalol (2.5 mg/kg) in seven patients with documented life-threatening ventricular tachyarrhythmias. D-sotalol significantly prolonged monophasic action potential duration at different steady-state heart rates (sinus rhythm: 21.1% +/- 3.6%; PCL 550 ms: 16.6% +/- 4.3%, 400 ms: 11.2% +/- 2.7%, 330 ms: 5.8% +/- 2.1%). The prolongation is significantly shorter in higher steady-state pacing, confirming a pronounced reverse-use dependent decrease of the efficacy of d-sotalol at faster stimulation frequencies. After the abrupt increase in heart rate, the beat-to-beat adaptation of the postdrug action potential prolongation exhibits only slight reverse-use dependent shortening. The decrease of the efficacy of d-sotalol is insignificant for the first 20 consecutive beats at the stimulation frequency of the PCL of 400 msec (from 16.6% at PCL of 550 ms to 14.6% at the 20th beat of the PCL of 400 ms), and for the first ten consecutive beats at the stimulation frequency of the PCL of 330 ms (from 16.8% at PCL of 550 ms to 12.3% at the 10th beat of the PCL of 330 ms). This slow decay of action potential prolongation after an abrupt increase in heart rate might contribute to the antiarrhythmic action of d-sotalol in cardiac tachyarrhythmias.

Action Potentials↗

PubMed1998

Adverse events with transvenous implantable cardioverter-defibrillators: a prospective multicenter study. European 7219 Jewel ICD investigators.

BACKGROUND: A newly developed classification system relates adverse events to the surgical procedure or the function of the implantable defibrillator. METHODS AND RESULTS: Adverse events were monitored during prospective clinical evaluation of the Medtronic model 7219 Jewel ICD and were classified according to the definitions of the ISO 14155 standard for device clinical trials into 3 groups: severe and mild device-related and severe non-device-related adverse events. In addition, events were related to the surgical procedure, treatment with the device, or cardiac function. Seven hundred seventy-eight patients were followed up for an average of 4.0 months after ICD implantation. In total, 356 adverse events were observed in 259 patients. At 1, 3, and 12 months after ICD implantation, 99%, 98%, and 97% of the patients, respectively, survived; 95%, 93%, and 92%, respectively, were free of surgical reintervention; and 79%, 68%, and 51%, respectively, were free of any adverse event. Twenty patients died: 6 deaths were related to the surgical procedure, 12 deaths were considered unrelated to ICD treatment, and 2 patients died of an unknown cause. Of 111 nonlethal severe adverse device effects, 47 required surgical intervention, 19 times for correction of a dislodged lead. Inappropriate delivery of therapy was observed 128 times in 111 patients, and the events were typically resolved by reprogramming or drug adjustment. Nine of these required rehospitalization. CONCLUSIONS: Approximately 50% of patients experience an adverse event within the first year after ICD implantation. The observed adverse event rate depends on the definitions and the prospective monitoring. The incidence of inappropriate therapy emphasizes the need for improved detection algorithms and for quality-of-life evaluations, especially when considering ICD treatment in high-risk but arrhythmia-free patients.

Algorithms↗

PubMed1998

Differential rate and potassium-dependent effects of the class III agents d-sotalol and dofetilide on guinea pig papillary muscle.

The class III agents d-sotalol and dofetilide have been shown to exhibit differential effects in large controlled clinical trials. The aim of this study was to investigate the basic electrophysiological properties of these two antiarrhythmia agents in an in vitro experimental model with regard to potential antiarrhythmic and proarrhythmic action. Using standard microelectrode techniques, we evaluated the electrophysiological effects of d-sotalol and dofetilide on action potential parameters recorded from guinea pig papillary muscle at 2.5 mM, 3.5 mM, and 5.6 mM extracellular potassium concentrations. The following parameters were recorded: resting membrane potential (RMP), action potential amplitude (APA), action potential duration at 90% repolarization (APD 90), and maximum upstroke velocity (Vmax). Under all conditions studied, both d-sotalol and dofetilide exhibited highly selective reverse rate-dependent class III action. In contrast to dofetilide, the class III activity of d-sotalol was markedly influenced by changes in extracellular potassium concentrations, predominantly at low pacing rates. Hypokalemia enhanced the action potential-prolonging effects of d-sotalol, whereas hyperkalemia diminished this effect. In addition, reverse rate dependence associated with dofetilide was significantly more pronounced than reverse rate dependence associated with d-sotalol. Our observations provide a potential electrophysiological basis for differential antiarrhythmic and proarrhythmic mechanisms associated with these two drugs.

Action Potentials↗

PubMed1998

Differential effects of d-sotalol on subendocardial Purkinje myocytes isolated from normal or 10 to 14 days postinfarction canine hearts: role of extracellular potassium concentration.

Electrophysiologic properties of surviving Purkinje cardiomyocytes in the late postmyocardial-infarction phase are not well established. By using standard microelectrode techniques, we evaluated the effects of the class III agent d-sotalol on action potential parameters of single Purkinje cardiomyocytes isolated from normal canine hearts or those 10-14 days after infarction. Measurements were obtained at 2.5, 3.5, and 6 mM extracellular potassium concentrations. Action-potential parameters recorded at baseline did not differ significantly between normal and infarct-surviving Purkinje cardiomyocytes. At 3.5 and 6 mM extracellular potassium concentrations, surviving Purkinje cells appeared to be more sensitive to the effects of d-sotalol than normal Purkinje cells. In contrast, at 2.5 mM extracellular potassium concentration, the differential responses of normal and infarct-surviving Purkinje cells to d-sotalol was abolished. Reverse rate dependence was more prominent in normal than in postinfarction Purkinje cells, independent of the extracellular potassium concentration studied. The previously described enhanced sensitivity of subacutely infarcted tissue to class III agents seems to persist on a cellular level 10-14 days after myocardial infarction, even after full normalization of baseline action-potential parameters. Differential membrane-regulation mechanisms, dependent on the extracellular potassium concentrations, may account for the increased susceptibility to antiarrhythmia agents in the late postinfarction phase.

Action Potentials↗

PubMed1998

Attenuation correction for a combined 3D PET/CT scanner.

In this work we demonstrate the proof of principle of CT-based attenuation correction of 3D positron emission tomography (PET) data by using scans of bone and soft tissue equivalent phantoms and scans of humans. This method of attenuation correction is intended for use in a single scanner that combines volume-imaging (3D) PET with x-ray computed tomography (CT) for the purpose of providing accurately registered anatomical localization of structures seen in the PET image. The goal of this work is to determine if we can perform attenuation correction of the PET emission data using accurately aligned CT attenuation information. We discuss possible methods of calculating the PET attenuation map at 511 keV based on CT transmission information acquired from 40 keV through 140 keV. Data were acquired on separate CT and PET scanners and were aligned using standard image registration procedures. Results are presented on three of the attenuation calculation methods: segmentation, scaling, and our proposed hybrid segmentation/scaling method. The results are compared with those using the standard 3D PET attenuation correction method as a gold standard. We demonstrate the efficacy of our proposed hybrid method for converting the CT attenuation map from an effective CT photon energy of 70 keV to the PET photon energy of 511 keV. We conclude that using CT information is a feasible way to obtain attenuation correction factors for 3D PET.

Biophysical Phenomena↗

PubMed1996

Transesophageal echo phase imaging for localizing accessory pathways during adenosine-induced preexcitation in patients with the Wolff-Parkinson-White syndrome.

Transesophageal phase images and precordial electrocardiography (ECG) were used to localize accessory pathways during adenosine-induced preexcitation in 30 patients (18 men, mean age +/- SD 33 +/- 14 years) undergoing endocardial mapping for suspected Wolff-Parkinson-White syndrome. Digitized 2-dimensional echocardiographic cine loops were mathematically transformed using a first harmonic Fourier algorithm before and after catheter ablation. Endocardial mapping found single accessory pathways with anterograde conduction in 20 patients, concealed pathways in 7, and atrioventricular reentry circuits in 3 patients. At baseline, precordial ECG correctly localized 8 pathways (40%) with anterograde conduction and predicted 5 adjacent locations (25%), but findings were normal in 7 patients (35%). Phase imaging correctly identified only 3 pathway locations (15%), findings were normal in 15 (75%), and could not be obtained in 2 patients (10%). Adenosine augmented manifest but minimal preexcitation in 9 patients and unmasked latent preexcitation in 7. In 4 patients, preexcitation was already maximal at baseline. During adenosine-augmented preexcitation, ECG correctly identified 13 locations (65%), but still predicted 7 adjacent locations (35%). However, phase imaging correctly identified 15 locations (75%) and predicted only 3 adjacent locations (15%). All midseptal (n = 2) and anteroseptal (n = 2) locations were correctly identified by phase imaging, but none by ECG. On follow-up studies in 16 patients, successful catheter ablation (n = 13) was equally well confirmed by ECG and phase imaging. Therefore, transesophageal echocardiographic phase imaging during adenosine-induced preexcitation is a readily available and safe procedure that appears clinically most useful for identifying septal pathways.

Adenosine↗

PubMed1996

[Calcium antagonists in treatment of ventricular tachycardia].

Of the traditional antiarrhythmic agents administered in the treatment of ventricular tachycardias, those belonging to Class III are most commonly used. However, some ventricular tachycardias displaying special clinical, electrocardiographic and/or electrophysiologic characteristics have been successfully treated with calcium antagonists. Otherwise, Class IV antiarrhythmic agents are primarily used in the treatment of supraventricular tachyarrhythmias. It is reasonable to suspect that calcium-dependent phenomena underlie ventricular tachyarrhythmias in a number of patients. Verapamil-sensitive sustained left ventricular tachycardias represent a typical example. Sufficient response to calcium antagonists has also been demonstrated for exercise-induced ventricular tachycardias and repetitive monomorphic ventricular tachycardias. Characteristically, these arrhythmias occur in young patients with no structural heart disease. The long-term prognosis of these patients is in fact very good, but because of intrusive symptoms, pharmacological or nonpharmacological (radiofrequency ablation) treatment is often indicated. Through correct diagnosis and implementation of a short- and long-term therapy with calcium antagonists, and excellent alternative to the potentially harmful therapy with Class I and Class III antiarrhythmic agents can be offered.

Anti-Arrhythmia Agents↗

PubMed1996

[New aspects of defibrillator therapy].

The implantable cardioverter defibrillator is currently a therapy of first choice in patients with malignant therapy refractory ventricular arrhythmias. The occurrence of malignant ventricular tachycardia cannot be suppressed by the defibrillator but is treated using antitachycardia pacing, cardioversion or defibrillation. During recent years, electrodes, defibrillation shockforms and device size were continuously optimized. The development of transvenous lead systems resulted in significant reduction of perioperative mortality and morbidity. With the availability of biphasic shockforms and single-lead unipolar devices marked reduction of defibrillation thresholds were achieved and transvenous lead systems without subcutaneous could be implanted. Improvements in device technology lead to smaller devices which can be implanted subpectorally even using local anaesthesia. But there is still enormous potential to develop an ideal antiarrhythmic device. One of the most significant problems of the defibrillator therapy represents the delivery of inappropriate shocks due to supraventricular tachyarrhythmias and sinustachycardia. To solve this problem different approaches are currently developed. Extension in memory allows to store several data logs and intracardiac electrograms for individual adapted adjustment of the therapy. Intracardiac electrogram width measurement for discrimination between ventricular and supraventricular arrhythmias is currently evaluated. Dual-chamber arrhythmia discrimination algorithms of an integrated dual-chamber pacemaker and defibrillator are clinically studied. Hemodynamic sensors for determining the severity of the arrhythmia are currently under experimental evaluation. The combination of latissimus dorsi dynamic cardiomyoplasty and ICD therapy may improve survival in patients with severely depressed left ventricular function and malignant ventricular arrhythmias. Several randomized prospective trials are currently in progress potentially expanding the use of the ICD in patients at risk for sudden cardiac death. The high costs of defibrillator therapy is still a limitation for its use, but higher production figures and advancing technology could reduce the system prize.

Anti-Arrhythmia Agents↗

PubMed1995

Nematode development is inhibited by methyl viologen and high oxygen concentrations at a rate inversely proportional to life span.

Eight strains of C. elegans, including seven recombinant inbred (RI) strains with mean life spans ranging from 10.9 to 28.8 days, were reared under two conditions (95% oxygen or methyl viologen) known to elevate the concentration of free radicals. Both agents inhibited development, as ascertained by measuring the lengths of animals at regular intervals. The degree of inhibition correlated inversely with mean life span with both agents; that is, development of short-lived strains was inhibited more profoundly than was development of long-lived strains. Thus, at least some of the polygenes which prominently influence aging are the same as those which control resistance to free radicals. These genes likely influence aging and response to oxidative stress in many ways, both direct and indirect.

Animals↗

PubMed1995

Impaired function of inhibitory G proteins during acute myocardial ischemia of canine hearts and its reversal during reperfusion and a second period of ischemia. Possible implications for the protective mechanism of ischemic preconditioning.

A brief antecedent period of myocardial ischemia and reperfusion can delay cellular injury during a subsequent ischemic condition. Recent observations suggest that this protective mechanism depends on the continued activation of adenosine A1 receptors and Gi proteins. During acute myocardial ischemia, sufficient amounts of adenosine for maximal activation of adenosine A1 receptors are released, independent of a preconditioning ischemia. Hence, the protective mechanism of ischemic preconditioning may not exclusively be explained by activation of adenosine A1 receptors. As a working hypothesis, an increased responsiveness of Gi proteins toward receptor-mediated activation, leading to an increased response of Gi-regulated effectors, was tested in this study. In 47 anesthetized dogs, ischemia was induced by proximal ligation of the left anterior descending coronary artery. Animals underwent either a single period of 5 minutes of ischemia (n = 9), a single period of 15 minutes of ischemia (n = 10), 5 minutes of ischemia followed by 15 minutes of reperfusion (n = 8), 15 minutes of ischemia followed by 60 minutes of reperfusion (n = 5), or 5 minutes of ischemia followed by 15 minutes of reperfusion and a second period of 5 minutes of ischemia (n = 15). Sarcolemmal membranes were prepared from the central ischemic area and from the posterior left ventricular wall, which served as the control. During ischemia, carbochol-stimulated GTPase decreased by 38% (control, 33.5 +/- 17.7; ischemia, 24.2 +/- 15 pmol.min-1.mg protein-1; n = 9; P < .001). The decrease in carbachol-stimulated GTPase activity was associated with a 45% decrease in carbachol-mediated inhibition of adenylyl cyclase (control, 28.9 +/- 2.4% maximal inhibition; ischemia, 15.1 +/- 2.6% maximal inhibition; n = 5; P < .001). Prolongation of the ischemic period to 15 minutes did not lead to a further reduction of the Gi-mediated signal transduction. The binding properties of muscarinic receptors were not affected by ischemia. Furthermore, as demonstrated by carbachol-stimulated binding of [gamma-35S]GTP to sarcolemmal membranes, high- and low-affinity binding sites for the muscarinic antagonist carbachol, the EC50 for carbachol-stimulated GTPase activity and the substrate dependency of the high-affinity GTPase, the interaction between muscarinic receptors and inhibitory G proteins, and GTP binding to G proteins were not altered (n = 14). Immunoblotting with alpha 1- and alpha 2-specific antibodies did not indicate a loss of Gi proteins during ischemia that could explain the reduced GTPase activity.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1994

[Sotalol].

Explore the source record for details and available documents.

Arrhythmias, Cardiac↗

PubMed1994

Advances in follow-up techniques for implantable defibrillators.

The complexity of newer implantable defibrillators has made device follow-up increasingly more intricate. Extensive data-logging capacity provides specific information on recorded events, which facilitates more accurate determination of patient arrhythmias. This helps the clinician judge whether the device is detecting and treating arrhythmias appropriately, or whether false sensing of external signals or supraventricular rhythms is occurring. There is also a record of the efficacy of delivered therapy from the device that helps in optimizing subsequent programming. Programming itself has become much more complicated, with multiple independently programmable therapy zones, each with numerous available therapeutic modalities. In addition, defibrillator status information has been improved. Accurate battery voltage measurements give a reasonable estimate of remaining device life, and pace/sense and shock lead impedances can be measured to provide information on total system integrity. Together, these advances allow more specific programming of the device to the individual patient's condition but require increasing experience and expertise of the physician.

Defibrillators, Implantable↗

PubMed1994

Differential effects of the new class III agent dofetilide on potassium currents in guinea pig cardiomyocytes.

The electrophysiologic effects of dofetilide (UK 68,798), a new class III antiarrhythmic drug were investigated on the following currents in guinea pig left ventricular cardiomyocytes by whole-cell patch-clamp technique: (a) delayed rectifier potassium current with its fast component (IKr) and its slow component (IKs), (b) inward rectifier potassium current (IK1), (c) fast sodium current (INa), and (d) L-type calcium current (ICa). Dofetilide in 10(-6) M reduced the amplitude of IKr to 61% of control currents, as measured by 200-ms test pulses and analysis of the deactivating tail currents of IKr. On the deactivating tail currents of IKs, dofetilide caused no significant amplitude change, but time constants of deactivation became 2.3 times slower, as measured by 2,000-ms test pulses and analysis of the deactivating tail currents of IKs. When the concentration of dofetilide was increased, these effects were more pronounced. Rapid application of the substance to the cells showed that IKr was reduced in the first minute to 60% of control currents. For complete current suppression, at least 3 min were necessary. The suppression effect remained unchanged during a 10-min washout phase. Dofetilide had no effect on IK1. Neither were amplitudes and Hodgkin-Huxley parameters of sodium current influenced by dofetilide. Calcium currents were not blocked by dofetilide. Dofetilide is not only a highly selective blocker of IKr, but also delays deactivation of IKs.

Animals↗

PubMed1994

Acute efficacy and chronic follow-up of patients with non-thoracotomy third generation implantable defibrillators.

Non-thoracotomy implantation of implantable cardioverter defibrillators (ICDs) has simplified the process of device insertion, promising to decrease associated procedural complications while providing sudden death protection at least equal to epicardial systems. This study presents the acute and chronic results of 110 patients who underwent attempted non-thoracotomy ICD implantation with the Medtronic Transvene lead system and PCD model 7217 or 7219. Of the 110 patients attempted, 100 (91%) had the system successfully implanted without the need for an epicardial patch. One patient died 1 week postoperatively of septic shock related to the implantation (0.9% perioperative mortality). During follow-up of 16 +/- 11 months, 45% of the patients had an event detected as ventricular tachycardia; 26% of these detections were felt clinically to be due to supraventricular rhythms. Of the remainder, 87% were successfully treated with the first VT therapy, and 98% were terminated by the final therapy; 66% of the patients had at least one episode of ventricular fibrillation, of which 5% were felt to be inappropriate detections; 85% of the appropriate episodes were successfully treated with the first VF therapy, and all were converted by the final therapy. Total mortality at 6, 12, and 24 months was 3%, 11%, and 19% respectively. Only one patient had sudden cardiac death, occurring at 13 months postimplant. Overall, the non-thoracotomy lead system for this ICD displayed infrequent implant complications and proved to be reliable at terminating arrhythmias and maintaining a low rate of sudden cardiac death in this high risk population.

Adult↗

PubMed1994

[Arrhythmogenic right ventricular disease].

In patients with arrhythmogenic right ventricular disease (ARVD), life threatening ventricular tachyarrhythmias and sudden cardiac death mostly occur in adolescence, or in young adults before the age of 40. In the right ventricle, progressive fibrolipomatous replacement of the ventricular myocardium is pathognomonic. In severe cases progressive congestive right heart failure can develop although mild forms are extremely difficult to recognized. In most cases the disease can be diagnosed only by elaborate investigation. Right ventricular cineangiography, myocardial biopsy, MRI, and electrophysiological investigation are the most important diagnostic procedures. If the disease is diagnosed in an early stage the risk of life-threatening arrhythmias can be reduced by carefully selected antiarrhythmic therapy.

Adolescent↗

PubMed1994

[Electrophysiological effects of antiarrhythmic drug UK-68798 on different AV nodal cells in rabbit heart].

By means of microelectrode techniques the electrophysiological effects of a new class III antiarrhythmic agent, UK-68798 (Dofetilide), were investigated on atrionodal (AN), nodal (N), nodal-His (NH) and His (H) cells in the AVN area of rabbit heart. UK-68798 (5 x 10(-9) to 5 x 10(-6) mol/L) had no effect on APA and RP of the 4 kinds of cells but caused a dose-dependent decrease in AVN spontaneous rhythm without changing the A-H conduction time. APD50 and APD90 were prolonged markedly by the drug in a dose-dependent manner. Among the 4 kinds of cells, N cell had the highest percentage increment in APD, indicating a prominent sensitivity to the drug. For example, at 5 x 10(-6) mol/L, the prolongation percentages of APD90 are: 95 +/- 26% (N), 75 +/- 22% (AN), 63 +/- 26% (H), 46 +/- 26% (NH). The effective refractory periods (ERP) of the 4 kinds of cells were lengthened also in a dose-dependent manner, while the ERP increment percentages (delta ERP%) of the 4 kinds of cells did not show significant difference. However, ERP corresponding repolarization membrane potentials (ERP-RMP) of the 4 kinds of cells were not affected by the drug. The above results suggested that though ERP increased in parallel with APD prolongation, the homogeneous delta ERP% and unchanged ERP-RMP values of the 4 kinds of cells would prevent the AVN area from becoming a source of reentry arrhythmias under the action of UK-68798.

Action Potentials↗

PubMed1994

[The implantable cardioverter/defibrillator (ICD). Developments up to the present time and future perspectives].

The implantable cardioverter/defibrillator is gaining increasing significance in the therapy of life-threatening ventricular arrhythmias. Independently, the team of Mirowski and the team of Schuder started to develop experimental automatic implantable defibrillators in the seventies. In 1980, the first human implant of an automatic defibrillator was done by Levi Watkins together with the team of Mirowski in Baltimore, USA. Since 1989 implantable cardioverter/defibrillators exhibit multiple functions among which are high energy defibrillation therapy, low energy cardioversion, antitachycardia pacing, permanent and post therapy antibradycardia pacing, diagnostic counters, and device status parameters. This offers a markedly improved technical device to the patients. Evaluation of the patient's diagnostic counters provide a detailed overview about the patient's arrhythmia history and information for optimizing antitachycardia pacing therapy and additional antiarrhythmic drug therapy. The availability of non-thoractomy transvenous lead systems and biphasic shock forms allows the insertion of the device without open chest surgery and even without subcutaneous leads resulting in low mortality rates and an exclusively transvenous system. Single-lead unipolar devices are currently investigated in clinical trials. Future development of atrial sensing lead systems may further reduce inappropriate shock therapy triggered by sinus tachycardia or atrial tachyarrhythmias, e.g. atrial fibrillation, and may be used for dual chamber stimulation. Hemodynamic sensors for determining the severity of the arrhythmia are currently under experimental evaluation. Possible prognostic indications of ICD therapy in patients without a history of malignant arrhythmias are currently studied in several prospective trials. All new directions hold promise to expand and improve the use of ICDs in patients at risk for sudden cardiac death.

Death, Sudden, Cardiac↗