Transferral of extrathoracic donor neoplasm by the cardiac allograft.

The transference of neoplasm from the donor to the recipient is a rare but recognized complication of organ transplantation. It has been reported after kidney transplantation from cadaver donors. We report a case in which an extrathoracic tumor was transmitted by the donor heart. The donor heart was harvested from a 46-year-old local donor and immediately transplanted to a 62-year-old female recipient. While implantation was performed, a hypernephroma was detected in the multiorgan donor. The ongoing heart transplantation could not be stopped. Four weeks after operation, the patient was discharged from the hospital. During the first year after transplantation, the clinical course was uneventful. One year after operation, the patient was admitted to the hospital with symptoms of weakness and fever. A right facial hemiparesis occurred, and a soft tumor was palpable subcutaneously in the right supraorbital region. Histologic examination revealed a malignant tumor with characteristics identical to the donor hypernephroma. In spite of chemotherapy and radiation therapy, dramatic tumor progression occurred with multiorgan metastases, which led to the death of the patient 2 months after admission.

Pectoral implantation of single-lead implantable cardioverter-defibrillators in patients without transvenous access.

With the introduction of the single-lead "Active-Can" implantable cardioverter-defibrillators, the implantation of the internal defibrillators has become a technically easy procedure. With these systems lowest defibrillation thresholds are achieved with a very low complication rate. For patients with thrombosis of both subclavian veins, however, a transvenous implantation technique is not possible. These patients are still equipped with epicardial patch electrodes. This article describes an alternative technique for implantation of this system in such patients, eliminating the need for epicardial patches and related complications.

Temporary atrial electrode for the treatment of supraventricular tachycardia after cardiac operations.

BACKGROUND: Supraventricular tachycardia is a common postoperative complication early after cardiac operations. A temporary atrial patch electrode for low-energy atrial defibrillation was developed in 1992 and subsequently tested. METHODS: The electrode first was tested and removed intraoperatively during open heart operations in 10 patients (phase I). After the intraoperative testing, the temporary atrial patch electrode was implanted in 20 patients for postoperative termination of spontaneous episodes of supraventricular tachycardia (phase II). When supraventricular tachycardia occurred, biphasic shocks (1.2 to 5 J) were applied and the atrial defibrillation thresholds were measured. RESULTS: In phase I, the mean intraoperative atrial defibrillation threshold was 1.6 +/- 1.4 J, with a mean shock impedance of 64 +/- 7.3 omega. In phase II, 6 of 20 patients (30%) had 7 episodes of atrial fibrillation (n = 6) and atrial flutter (n = 1) after operation. In 5 patients, the supraventricular tachycardia could be converted to a sinus (n = 5) or normofrequent atrioventricular rhythm (n = 1). The mean postoperative defibrillation threshold was 2.7 +/- 2.1 J, with a mean shock impedance of 50.2 +/- 6.8 omega. CONCLUSIONS: The temporary atrial patch electrode allows low-energy defibrillation of episodes of atrial fibrillation. It may serve as an alternative therapeutic option for the treatment of supraventricular tachycardia.

Atrioventricular valve insufficiency and atrial geometry after orthotopic heart transplantation.

BACKGROUND: The etiology of tricuspid and mitral valve regurgitation (TR and MR) after heart transplantation is still controversial. METHODS: We studied 25 patients undergoing transplantation and intraoperative transesophageal echocardiography to evaluate the incidence, the degree, and the cause of TR and MR. The degree of valve regurgitation was assessed by color Doppler echocardiography. Cross-sectional areas of the recipient (R) and donor (D) portions of the atria and their ratio (R/D) were measured to assess the distortion of atrial geometry. Tricuspid and mitral valve annuli, their systolic shortening, and hemodynamic indices were measured preoperatively and perioperatively. RESULTS: Tricuspid valve regurgitation was found in 21 of 25 patients (84%) and MR in 12 of 25 (48%). The degree of MR was mild, whereas TR was mild to moderate. Mitral valve regurgitation did not show any correlation with the studied indices; TR showed no correlation with the hemodynamic indices but a significant correlation with R/D ratio (r = 0.90; standard error of the estimate = 0.2). An inverse correlation was found between the degree of TR and systolic shortening of tricuspid annulus (r = -0.88; standard error of the estimate = 0.03) and between R/D ratio and systolic shortening of tricuspid annulus (r = -0.85; standard error of the estimate = 0.04). CONCLUSIONS: Tricuspid valve regurgitation has a higher incidence than MR and occurs immediately after transplantation; MR is mild and correlates with neither hemodynamic indices nor atrial distortion. An increased R/D ratio, and hence distortion of right atrial geometry, may lead to a reduction in systolic annulus shortening, which in turn causes TR. Surgical attempts to reduce the R/D ratio may decrease the incidence and the degree of TR after heart transplantation.

Hypothalamic LH-RH release after acute and chronic treatment with morphine studied in a combined in vivo/in vitro model.

Rats were treated with the opiate agonist, morphine, and the release of luteinizing hormone-releasing hormone (LH-RH) from their hypothalami was studied in vitro. Within 16-24 h after morphine treatment, basal LH-RH release rates were observed to be higher compared to those from hypothalami derived from opiate-naive rats, suggesting that dependence had occurred in the neural mechanisms underlying LH-RH release. Maintenance of tissues exposed to morphine in vivo in medium containing morphine in vitro did not alter the increased basal release of LH-RH, but because this was significantly greater than control rates, tolerance is not believed to have occurred. Addition of the opioid antagonist naloxone in vitro resulted in a 220% increase in the release of LH-RH by hypothalami exposed to morphine for 48 h in vivo, whereas it caused a 50% reduction in LH-RH release from tissues exposed to morphine for 96 h in vivo. This latter result shows parallels with our previous finding that naloxone paradoxically decreases serum LH levels of chronically morphine-treated rats. In view of recent evidence for presynaptic feedback inhibitory effects operating on opioid neurons, it is suggested that, following chronic exposure to morphine, the opioid neurons which normally inhibit LH-RH neurons are inhibited; upon treatment with naloxone, they are disinhibited and release more opioid peptides which then act to switch off LH-RH neuronal activity.

[A new concept for treatment of supraventricular tachycardia after heart operations: low energy internal cardioversion using a temporary atrial electrode]. / Ein neues Konzept zur Behandlung von supraventrikulären Tachykardien nach Herzoperationen: Niederenergetische interne Kardioversion über eine temporäre atriale Elektrode.

Supraventricular tachycardia (SVT) is a common complication early after cardiac surgery. A novel temporary atrial patch electrode (TAPE) for low energy atrial defibrillation was first implanted for intraoperative testing and subsequently removed during open heart surgery in 10 patients (Phase I). After the intraoperative testing period, the TAPE was implanted in 20 patients for postoperative termination of spontaneous episodes of supraventricular tachycardia (Phase II). In case of supraventricular tachycardia (SVT), biphasic shocks (1.2-5.0 J) were applied, measuring the atrial defibrillation thresholds. Phase I: The mean intraoperative atrial defibrillation threshold was 1.6 +/- 1.4 J with a mean shock-impedance of 64.0 +/- 7.3 Ohms. Phase II: Postoperatively, 6 out of 20 patients (30%) developed 7 episodes of atrial fibrillation (n = 6) and atrial flutter (n = 1). In 5 patients, SVT could be converted to sinus rhythm (n = 5) or junctional rhythm (n = 1). The mean postoperative defibrillation threshold (DFT) was 2.7 +/- 2.1 J with a mean shock-impedance of 50.2 +/- 6.8 Ohms. In conclusion, the TAPE allows low-energy defibrillation of atrial fibrillation. It seems to be a useful alternative in the treatment of supraventricular tachycardia.

Adjustable atrial and ventricular temporary electrode for low-energy termination of tachyarrhythmias early after cardiac surgery.

Supraventricular and ventricular tachycardias are common and serious postoperative complications early after cardiac surgery. We introduce a completely removable temporary adjustable defibrillation electrode (TADE) for low energy cardioversion/defibrillation of postoperative atrial and ventricular tachyarrhythmias. The electrode consists of three loops of steel wires connected to one steel wire, which are movable within an isolation sheet for adjusting the active surface to the individual size of the heart chambers. Evaluation of the electrode was performed in 10 open-chest beagles with a mean weight of 25.5 kg. The electrodes were first positioned on the left and right atrium. Atrial fibrillation (AF) was induced via a bipolar temporary heart wire. Atrial defibrillation thresholds (DFTs) were measured according to a step-down shock protocol (5-0.4 J). Thereafter, the electrodes were adjusted and positioned on the right and left ventricle. Ventricular fibrillation (VF) was induced and DFTs were recorded the same way. Aortic flow and pressure and left ventricular pressure were continuously monitored throughout the experiment. For termination of AF, mean DFTs were 0.4 +/- 0 J (lowest possible shock level) with a mean shock impedance of 70 +/- 7.6 ohms. VF was terminated with a mean DFT of 3 +/- 1.1 J with a mean impedance 56.1 +/- 7.9 ohms. Complete transcutaneous removal of the electrodes was possible in all animals without any complications. In conclusion, successful low energy termination of AF and VF is possible with the tested temporary adjustable electrode. A clinical study is planned for further evaluation.

[Atrioventricular valve insufficiency and atrial geometry in orthotopic heart transplantation]. / Studio dell'insufficienza valvolare atrioventricolare e della geometria atriale nel trapianto cardiaco ortotopico.

Tricuspid and mitral valve regurgitation are commonly observed in patients after orthotopic cardiac transplantation (HTX). The etiology is still controversial. Aim of the present study was to assess the degree of regurgitation and its etiology. Twenty-five patients (mean age 47.9 +/- 11.8 years) undergoing HTX were studied intraoperatively by transesophageal echocardiography. The degree of tricuspid and mitral valve regurgitation was assessed by planimetry of maximum systolic area of the regurgitant jet (JA). The cross-sectional area of right and left atrium and the recipient (R) and the donor (D) cross-sectional area of the atria, and their ratio (R/D) were assessed by two-dimensional echocardiography. The following preoperative and perioperative hemodynamic parameters were measured: systemic arterial pressure, cardiac index, pulmonary artery pressure, and pulmonary vascular resistance. Tricuspid regurgitation was found in 21/25 (84%) patients, mitral regurgitation in 12/25 (48%). The degree of mitral regurgitation showed no correlation to any of the studied parameters. Tricuspid regurgitation showed no correlation to the hemodynamic parameters, but showed significant correlation to R/D ratio (JA versus R/D: r = 0.90; SEE = 0.2) and to the dimensions of the recipient atrium (JA versus R: r = 0.89; SEE = 1.9). Three patients who underwent bicaval anastomoses did not show tricuspid regurgitation. In conclusion, tricuspid regurgitation has a higher prevalence than mitral regurgitation and occurs in most patients immediately after HTX; mitral regurgitation was less frequent than tricuspid regurgitation and was not correlated to the hemodynamic parameters or to the distortion of atrial geometry; tricuspid regurgitation was significantly correlated to the ratio of recipient/donor right atrium; surgical techniques reducing the recipient atrium may decrease the occurrence and the degree of tricuspid regurgitation.

[Temporary adjustable defibrillator electrodes: an alternative method for the treatment of postoperative arrhythmias after heart surgery]. / Temporäre anpassbare Defibrillationselektrode: Ein alternatives Verfahren zur Behandlung von postoperativen Rhythmusstörungen nach Herzoperationen.

INTRODUCTION: Supraventricular and ventricular tachycardias are common and serious postoperative complications early after cardiac surgery. We introduce a new temporary adjustable defibrillation electrode (TADE) for internal low-energy cardioversion/defibrillation of postoperative atrial and ventricular tachyarrhythmias. METHODS: Evaluation of the new electrode was performed in ten open-chest beagles with a mean weight of 25.5 kg. The electrodes were first positioned on the left and right atrium. Atrial fibrillation (AU) was induced via a bipolar temporary heart wire. Atrial defibrillation thresholds (DFT's) were measured according to a step-down shock protocol (5 J-0.4 J). Thereafter, the electrodes were adjusted and positioned on the right and left ventricle. Ventricular fibrillation (VF) was induced and DFT's were recorded the same way. RESULTS: For termination of AF, mean DFT's were 0.4 +/- 0 J (lowest possible shock level) with a mean shock impedance of 70 +/- 7.6 omega. VF was terminated with a mean DFT of 3 +/- 1.1 J with a mean impedance 56.1 +/- 7.9 omega. Complete transcutaneous removal of the electrodes was possible in all animals without any complications. CONCLUSION: Successful low-energy termination of AF and VF is possible with the tested temporary adjustable electrode. A clinical study is planned for further evaluation.

Aortic input impedance and ventriculoarterial coupling following cardioversion/defibrillation.

Defibrillation shocks are commonly used after cardiac surgery or during defibrillator implantation. The hemodynamic consequences of countershocks on circulatory dynamics are not completely understood, and there is a lack of information concerning the effects on ventriculoarterial interaction. The study presented here was performed to assess the influence of defibrillation shocks on arterial hemodynamics and ventriculoarterial coupling. Eight mongrel dogs (weight 15-18 kg) were anesthetized and median thoracotomy was performed. Pressure in the ascending aorta and the left ventricle and flow in the ascending aorta were continuously monitored. After induction of atrial or ventricular fibrillation, termination was achieved by epicardial low energy shocks (atrium, 3J; ventricle, 51). In an additional attempt ventricular fibrillation was terminated by a high energy shock (34J). Aortic input impedance was calculated by fast-Fourier-transformation of aortic flow and pressure signals, while ventriculoarterial coupling was expressed by the ratio of aortic and ventricular end systolic elastance (Ea/Ees). Defibrillation by low energy shocks of atrial or ventricular fibrillation did not result in changes of the aortic impedance spectrum, and ventriculoarterial coupling remained unaltered compared to control conditions. High energy defibrillation, however, resulted in a marked rise in total peripheral resistance (P < 0.03). The ratio of Ea/Ees increased significantly (P < 0.005). These effects were reversible within 15 minutes. Low energy defibrillation does not alter arterial hemodynamics and ventriculoarterial coupling in this experimental setup. High energy defibrillation, however, results in a temporary increase of ventricular load. This finding may be of particular interest in patients with poor left ventricular function.

Mathematical modelling of extracorporeal circulation: simulation of different perfusion regimens.

Computer- and sensor-aided control of the heart-lung machine is considered a major goal for perfusion sciences for the next few years. At present, control of perfusion is achieved by surgeons, anaesthesiologists and perfusionists making short-term decisions, which leads to variations of the perfusion regimens between different centres and even between different teams in the operating theatre. As the basis for an integrated control of extracorporeal circulation (ECC), we proposed a mathematical model for simulating haemodynamics during pulsatile perfusion. This model was then modified to allow it to simulate the effects of different perfusion regimens on arterial haemodynamics and whole body oxygen consumption. The model was constructed on a PC using MATLAB/SIMULINK. The human arterial tree was divided into a multibranch structure consisting of 128 segments characterized by their particular physical properties. Peripheral branches were terminated by a resistance term representing smaller vessels like arterioles and capillaries. Flow and pressure were expressed by the intensity of current and voltage in an electrotechnical analogon; inductivity, resistance and capacitance were implemented according to the physical properties of the arterial tree and the rheology of blood. The effects of different perfusion regimens (pulsatility, flow amount, acid-base regulation) were studied. After introducing an input signal to the model, flow and pressure waves established themselves throughout the simulated arterial tree. During the simulation experiments, marked differences among different perfusion regimens were displayed by the model. Variations in acid-base management mainly influenced the distribution of perfusion: during simulation of low-flow perfusion (1.2 l/min/m2), cerebral blood flow was 6.2 ml/s using an alpha-stat regimen, while it was increased to 9.4 ml/s during pH-stat, caused by an implementation of reduced cerebral resistance. Whole body oxygen consumption was predominantly regulated by the perfusion rate. While central venous oxygen saturation was calculated to be 84.7% during simulation of high-flow perfusion (2.4 l/min/m2), it dropped to 70% during simulation of low-flow perfusion regimens. The model proved to be useful for a realistic simulation of different perfusion regimens. Therefore it can be considered a continuing step for the derivation of a 'state' observer leading to the realization of an automatically controlled heart-lung machine.

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.