Aortic valve rupture after blunt chest trauma.
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Biomedical subjects
Publications and source records attributed to F Beyersdorf.
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AIM: Dural ectasia is a major diagnostic criterion for Marfan syndrome using the Ghent nosology. Our aim was to evaluate the efficacy of three different radiological methods previously proposed for the assessment of dural sac diameter in Marfan syndrome. METHODS: Marfan syndrome was diagnosed in our study using the Ghent criteria, disregarding dural ectasia as a criterion. Three proposed radiological methods were applied to measure dural sac diameter, examined for 41 patients (18 patients with and 23 without Marfan syndrome) by computed tomography or magnetic resonance imaging. RESULTS: Using Oosterhof's method, 94% of the patients with and 44% of the patients without Marfan syndrome fulfilled the criteria of dural ectasia. According to Villeirs, dural ectasia was diagnosed in 18% of the patients with and in none of the patients without Marfan syndrome. With Ahn's method, dural ectasia was found in 72% of the patients with and in 44% of the patients without Marfan syndrome. In only two patients with Marfan syndrome was dural ectasia diagnosed by all three methods. CONCLUSION: Our results reveal overt discrepancy between the three methods of assessing dural ectasia. Considering the key role played by dural ectasia in reinforcing the diagnosis of Marfan syndrome according to the Ghent nosology, a standardized and reliable method should be sought.
UNLABELLED: Left ventricular unloading by mechanical assist devices induces myocardial atrophy. We aimed to systematically identify differentially expressed genes in a model of physiological atrophy (unloading of healthy rat myocardium) and compare these changes to those in a unloaded, failing human heart. METHODS: Atrophy in rat hearts was induced by heterotopic transplantation of a donor heart into the abdomen of an isogenic recipient. After one week, donor and recipient RNA was isolated. Differential gene expression was assessed by subtractive hybridization. Two screens with radioactive probes were performed to verify differentially expressed clones. Positive clones were sequenced and cDNA of genes of known homology were used as probes for hybridization with RNA from separate atrophied rat hearts and human tissue from a normal, failing or failing and unloaded left ventricle. RESULTS: We picked 1880 clones from the subtractive hybridization procedure (940/940: forward/reverse runs assessing up- or down-regulation, respectively). The first screen verified 465/140 and the second screen verified 67/30 clones. 24/23 clones were sequenced and 14/10 homologies to known genes were found. In the atrophied heart, respiratory chain and metabolic genes were down-regulated (NADH-DH, cytochrome c oxidase, acetyl-CoA synthetase, myoglobin) and cellular recognition and stress genes were up-regulated (MHC1 and 2, HSP70). In the human heart, cytochrome c oxidase, acetyl-CoA synthetase, and myoglobin expression was increased in the failing heart and returned to normal with unloading. Unloading also resulted in up-regulation of HSP70. CONCLUSIONS: The genetic responses of failing human and healthy rat myocardium to mechanical unloading show similarities that appear to be independent of species differences and/or underlying disease. Thus, heterotopic heart transplantation is a relevant model for investigating the mechanisms of mechanical unloading.
BACKGROUND: The purpose of this study was to assess the complementary use of different methods of measuring spinal cord perfusion during thoracoabdominal aortic surgery. METHODS: The spinal cords of 28 patients undergoing surgery on the thoracoabdominal aorta were monitored with transcranial electrical stimulation (tcMEP) and somatosensory-evoked potentials (SSEP). Available approaches of spinal cord-protection included: Moderate systemic hypothermia, constant cerebrospinal fluid (CSF) drainage and pressure monitoring, reimplantation of segmental arteries, cardiopulmonary bypass (CPB), and staged clamping. RESULTS: Fourteen of 19 patients (75%) undergoing open surgical treatment (Group I) exhibited loss of tcMEP after proximal aortic clamping. In nine cases (47%), we observed recovery of tcMEP after intraoperative interventions, while two patients subsequently developed paraplegia and three died. Seventeen of 19 patients showed loss of SSEP, with recovery in 12 cases (63%). During stent-graft implantation (Group II), one of nine patients (11%) demonstrated tcMEP loss with intraoperative, intervention-related recovery. The SSEP-recording course remained stable. CONCLUSIONS: tcMEP/SSEP monitoring has proved to be an excellent means of detecting spinal cord ischaemia during surgery on thoracoabdominal aortic aneurysms. The prognostic value of tcMEP monitoring should be considered superior to that of SSEP measurements, because of its direct and rapid response to spinal malperfusion. Through combined neurophysiological monitoring, vital parameter balancing and intraoperative interventions, spinal cord perfusion improves and recovery of tcMEP and SSEP is achievable, reducing the prevalence of postoperative paraplegia.
Heart surgery has been performed in an increasing number of elderly patients in the recent years. Currently about 20 % of all patients in cardiac surgery are older than 75 years, however their number is increasing constantly. Valve replacement (mainly aortic valve replacement, AVR), coronary artery bypass grafting (CABG) or combined procedures (AVR and CABG) are the most common procedures in the elderly. However, surgical therapy of heart failure, implantation of assist devices or cardiac transplantation have been performed only in a limited number of elderly patients. Surgical pathways in the therapy of coronary artery disease or valve disease are described. Furthermore, age related morbidity and mortality and related surgical options to improve the outcome are discussed.
OBJECTIVES: The article describes a procedure for the intraoperative neurophysiological placement of electrodes to control the spinal cord function during thoracoabdominal aortic aneurysm repair. MATERIAL AND METHODS: Intraoperative monitoring is performed by motor-evoked myogenic potentials after transcranial electric stimulation (tcMEP) and somatosensory-evoked potentials (SSEP). In tcMEP, the stimulating percutaneous needle electrodes are placed at C3 and C4 according to the 10 - 20 system for EEG recordings. TcMEP are recorded from the anterior tibial and gastrocnemius muscles on both sides. The SSEP electrodes are placed laterally and caudally onto the malleolus medialis in order to stimulate the tibial nerve. The stimulus is documented via electrodes attached to the scalp within the sensory cortex region. RESULTS: The application of the electrodes is both easy to learn and can be performed without further difficulties. Once attached, the electrodes provide a quick assessment and interpretation of spinal cord function. The identification of external sources of disturbance during the monitoring (e. g. insufficient impedance, unfavourable electrode positioning, and technical interference caused by medical equipment) enables the supervisor to differentiate between normal and abnormal neurological responses. CONCLUSIONS: TcMEP and SSEP allow an adequate, direct, and reliable intraoperative assessment of spinal cord function, enabling the surgeon to diagnose an impending ischaemia and act accordingly. This measurement technique provides the surgical team with a means of integrating neurological aspects during thoracoabdominal aneurysm repair.
OBJECTIVES: The study's aim is to evaluate whether intraoperative neurophysiological monitoring with transcranial motor-evoked potentials (tcMEP) permits early recognition of neuronal lesions, thus making interventions to prevent irreversible spinal cord damage possible. MATERIAL AND METHODS: TcMEP monitoring was carried out in twelve patients (mean age 60 years) during open surgical thoracoabdominal aortic replacement. Current approaches for corrective, spinal cord-protecting interventions consist of: raising distal perfusion by increasing cardiopulmonary bypass (CPB) flow, catecholamine application, reducing central venous pressure, reimplantation of segmental arteries, and cerebrospinal fluid (CSF) drainage. RESULTS: Nine patients exhibited loss of tcMEP after segmental aorta clamping. In five patients we observed a recovery of tcMEP through counteractive measures. Three patients died intraoperatively, one patient presented with postoperative paraplegia and loss of tcMEP. CONCLUSION: TcMEP loss is associated with spinal cord ischaemia, causing postoperative paraplegia. TcMEP monitoring is an excellent method to detect spinal cord ischaemia at an early stage.
BACKGROUND: We evaluated patient outcomes and complications associated with the microaxial Impella Recover left ventricular assist device (Impella Cardiosystems AG, Aachen, Germany) for postcardiotomy low-output syndrome. This low-cost device is inserted across the aortic valve through a 10-mm vascular graft sewn to the ascending aorta. METHODS: Impella patients were compared with 198 patients treated with an intraoperative intra-aortic balloon pump between January 2000 and December 2002. Three risk scores were used: the Hausmann score, the Texas Heart Institute score, and the Cleveland intensive care unit score. Between September 2001 and March 2003, 24 patients were treated with the Impella Recover for low-output syndrome. Before device insertion, 21 could not be separated from cardiopulmonary bypass, and 3 had postoperative hemodynamic instability despite high-dose catecholamines. Sixteen were treated with the Impella and intra-aortic balloon pump and 8 with the Impella alone (no intra-aortic balloon pump because of peripheral vascular disease or because deemed unnecessary). RESULTS: No technical problems with device insertion occurred. Pump flow was 3.3 +/- 0.7 L/min at 28,000 +/- 4500 RPM. Support time was 61 +/- 56 hours (range, 7-228 hours). Four devices required repositioning. One device failed (leaking purge line) and was removed. Hemolysis was minimal (lactate dehydrogenase levels of 540 +/- 260 U/dL for Impella survivors). Mortality for Impella patients was 54% (13/24), similar to that for high-risk intra-aortic balloon pump patients (Hausmann score > or =2 [57%], intensive care unit score > or =2 [51%], Texas Heart Institute score > or =0.75 [55%], and cardiac index < or =2.3 [45%]). Cardiac output data were available in 19 Impella patients. Impella patients able to increase their cardiac output to 1 L/min or more above the pump flow of the Impella Recover had a 10% (1/10) mortality, versus 88% (8/9) in patients with a residual cardiac function of 1 L/min or less (P =.001). Comparison of high-risk intra-aortic balloon pump patients with Impella patients with residual cardiac function of 1 L/min or more showed a significant reduction in mortality, regardless of the high-risk definition used. Residual cardiac function was the strongest predictor of survival in Impella patients. CONCLUSIONS: The Impella Recover device provides 3 to 4 L/min flow. It improves survival in patients with low-output syndrome if the heart is able to pump 1 L/min or more above device flow.
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OBJECTIVES: Device-related infections remain a considerable problem of left-ventricular support. We compared the device-related-infections between the HeartMate left ventricular assist device (LVAD) and the Jarvik 2000 permanent LVAD, a device with a novel retroauricular power-supply. METHODS: Between December 2000 and September 2002 we implanted the HeartMate-vented, electrical-system in 11 patients and the permanent Jarvik 2000 in six patients. Total support time was 1626 patient-days (HeartMate, 26-271 days) versus 1246 patient-days (Jarvik 2000, 8-411 days). As potential risk factors for infection we analyzed age, preoperative hospital-days, total protein, cardiac index, maximal oxygen uptake, use of inotropes, LVAD risk-score-index and Aaronson-Mancini-score, intubation time, and intensive care unit stay. We used the Center of Disease Control definitions for surgical site infections. RESULTS: HeartMate-patients were younger than Jarvik 2000 patients (46+/-13 versus 58+/-6 years, P=0.056), there were no other differences in the risk factors. Four HeartMate-patients needed late (>or=48 h) surgical revisions for bleeding/hematomas versus no revisions in the Jarvik 2000 patients. In the HeartMate-patients, there were seven (64%) driveline-infections, five (45%) device-pocket infections, and three (27%) bloodstream-infections, or 0.43 device-related infections/100 patient-days. Infections occurred early (34+/-31 days). Three patients required urgent transplantation due to bloodstream infection. There were no adverse outcomes in the HeartMate-group due to infection. In the Jarvik 2000 patients, there was one driveline-infection (16%) after 270 days of support (0.08 device-related infections/100 patient-days), significantly less than in the HeartMate-group (P=0.044). Driveline infections resolved with antibiotics and local wound care in the Jarvik 2000 patient, but only in one of seven HeartMate-patients. CONCLUSIONS: Implantation of the Jarvik 2000 is associated with less device-related infections than the HeartMate-LVAD. The power-supply of the permanent Jarvik 2000 is suitable for long-term mechanical support.
BACKGROUND: Orthotopic heart transplantation following ischemic times beyond four hours is associated with increased risk of early graft failure. The use of modern myocardial preservation strategies could enable safe transplantation after long-term conservation. In this study, we tested a new myocardial protection regime in an experimental model of 24 h storage. METHODS: Orthotopic heart transplantations (n=15) were performed in a pig model. Donor hearts were flushed with Bretschneider solution, excised, and stored for 24 hours at 4 degrees C. During implantation, controlled reperfusions with substrate-enriched leukocyte-depleted blood cardioplegia were performed after each anastomosis. Blood cardioplegia contained 1 mmol/l of the Na(+)-H(+)-exchange inhibitor HOE 642 and 100 mg/l of adenosine. Controlled reperfusion was continued with leukocyte-depleted blood for 20 min. A microaxial pump was inserted after heart transplantation and circulatory assistance was maintained for five hours to prevent right heart failure. RESULTS: No initial graft failure could be observed. Thirteen hearts could be weaned from extracorporeal circulation. Due to bleeding problems, kidney and lung failure only five hearts could be included in the final analysis. Hemodynamics of these hearts remained stable with epinephrine at 0.1 micro g/kg/min. Myocardial oxygen consumption 20 min after start of reperfusion (5.3+/-2.0 ml/100 g/min) did not differ significantly versus baseline (6.8+/-2.0 ml/100 g/min). Oxygen extraction six hours after heart transplantation was also well preserved compared to baseline (58.0+/-10.2 versus 49.2+/-8.8 %). Histological examination six hours after transplantation using luxol fast blue staining revealed that only 1.0 % of the myocytes were irreversibly damaged. CONCLUSIONS: The data indicate full viability of the myocardium after 24 h conservation. The preservation technique described could contribute to the extension of conservation times in heart transplantation and enable transplantation of marginal donor hearts.
BACKGROUND: Clinical heart failure is generally preceded by hypertrophy. Many animal models (e. g. toxic heart failure models) do not consider this hypertrophy. We set out to develop a heart failure model in rats by inducing pressure-overload hypertrophy. METHODS: We induced coarctation of the aortic arch with a tantalum clip (0.35 mm internal diameter) In 3-week-old rats (n=17). Starting at seven weeks postoperatively, we measured ejection fraction (EF), fractional shortening (FS), end-systolic (LVESD) and end-diastolic (LVEDD) left ventricular dimensions by echocardiography each week. Heart, lung, and liver specimens were analyzed histopathologically at least eleven weeks after the operation. RESULTS: Contractile function was significantly decreased in hearts from animals with aortic banding (EF: 45+/-5% vs. 73+/-5%, p<0.01; FS: 20+/-3% vs. 35+/-5%, p<0.01). At the same time, left ventricles were dilated (LVEDD: 9.1+/-0.6 mm vs. 7.4+/-0.5 mm; LVESD: 7.3+/-0.6 mm vs. 4.8+/-0.4 mm, p<0.01). These observations were associated with clinical and histopathological changes characteristic for chronic left heart failure. CONCLUSION: Placing a tantalum clip around the aortic arch in 3-week-old rats consistently induces left ventricular decrease in contractile function and dilatation after eleven weeks.
The clinical use of mechanical circulatory assist devices as bridge to transplantation has been proved as life-saving therapy in a large population of patients. Learning from the clinical experience the construction of the blood pumps has been markedly improved over the last years. The better outcome of the patients has enabled a broader use of ventricular assist devices. The novel axial pumps are designed for long-term circulatory support. After further reduction of device related complications (first of all thromboembolic events) these systems may provide a future alternative to heart transplantation.
The Jarvik-2000 is an axial-flow left-ventricular-assist-device (LVAD) designed for permanent use. The power supply is provided by a cable plugged into a skull-pedestal mounted in the retro-auricular area. We describe the surgical technique and discuss potential and encountered problems.
BACKGROUND: An imbalance of sympathetic and parasympathetic drive to the heart is an important risk factor for cardiac death in patients with coronary heart disease, diabetes, and renal insufficiency. The amount of neurotransmitter released from peripheral autonomic nerves is modulated by presynaptic receptor systems. In analogy to alpha-autoreceptors on sympathetic nerves, muscarinic autoreceptors activated by endogenous acetylcholine may exist on parasympathetic nerves in the human heart. METHODS AND RESULTS: We developed a technique to study acetylcholine release from human atria and investigated muscarinic autoreceptor function. A pharmacological and molecular approach was used to characterize the subtype involved. Of the 5 muscarinic receptor subtypes cloned, only mRNA encoding for M(2)- and M(3)-receptors were detected. Potencies of several muscarinic antagonists against the release-inhibiting effect of the nonselective muscarinic agonist carbachol at the cardiac autoreceptor were correlated with published data for human cloned M(1)- through M(5)-receptors. CONCLUSIONS: This analysis clearly indicates that acetylcholine release in human atria is controlled by muscarinic M(2)-receptors. Blockade of these receptors by atropine doubles the amount of acetylcholine released at a stimulation frequency of 5 Hz. In atria of patients >70 years of age and patients with late diabetic complications, acetylcholine release is reduced. Locally impaired cardiac acetylcholine release may therefore represent a pathophysiological link to sudden cardiac death in elderly and diabetic patients.
BACKGROUND: Although the concept of reducing wall tension as a treatment for advanced heart failure is convincing, clinical data from the Batista operation are conflicting. Despite a number of publications, it is not clear whether left ventricular reduction surgery is truly of benefit for patients with idiopathic, dilated cardiomyopathy (DCM). Surgery may reduce wall tension but the reason for dilation and contractile dysfunction remains. Thus, the potential benefit of the operation may be overshadowed by the natural course of the underlying disease. CASES: We report a series of five cases where left ventricular reduction was performed and physiological geometry was restored in patients with DCM by a modification of Dor's endoventricular patch plasty. All patients demonstrated an improvement in cardiac function immediately after the operation. This improvement was sustained in one of the patients at 18 months follow-up. Another patient developed severe heart failure due to therapy resistant ventricular arrhythmia (Lown IVb), and underwent successful transplantation 4 months after ventricular reduction surgery. Left ventricular dilation reoccurred in two patients 9 and 12 months after reduction surgery, and they were listed for transplant. One patient died after 9 weeks due to sepsis and respiratory dysfunction. CONCLUSIONS: Although the endoventricular patch plasty as used in this study is well tolerated by most patients with dilated cardiomyopathy and results in immediate improvement of contractile function, the long-term benefits of this technique for DCM are uncertain. Thus, the technique is currently not an alternative for heart transplantation. However, the procedure may be an option in patients with contraindications for transplantation.
Myocardial contractility depends on temperature. We investigated the influence of mild hypothermia (37-31 degrees C) on isometric twitch force, sarcoplasmic reticulum (SR) Ca2+-content and intracellular Ca2+-transients in ventricular muscle strips from human and porcine myocardium, and on in vivo hemodynamic parameters in pigs. In vitro experiments: muscle strips from 5 nonfailing human and 8 pig hearts. Electrical stimulation (1 Hz), simultaneous recording of isometric force and rapid cooling contractures (RCCs) as an indicator of SR Ca2+-content, or intracellular Ca2+-transients (aequorin method). In vivo experiments: 8 pigs were monitored with Millar-Tip (left ventricle) and Swan-Ganz catheter (pulmonary artery). Hemodynamic parameters were assessed at baseline conditions (37 degrees C), and after stepwise cooling on cardiopulmonary bypass to 35, 33 and 31 degrees C. Hypothermia increased isometric twitch force significantly by 91 +/- 16 % in human and by 50 +/- 9 % in pig myocardium (31 vs. 37 degrees C; p < 0.05, respectively). RCCs or aequorin light emission did not change significantly. In anesthetized pigs, mild hypothermia resulted in an increase in hemodynamic parameters of myocardial contractility. While heart rate decreased from 111 +/- 3 to 73 +/- 1 min(-1), cardiac output increased from 2.4 +/- 0.1 to 3.1 +/- 0.31/min, and stroke volume increased from 21 +/- 1 to 41 +/- 3 ml. +dP/dtmax increased by 25 +/- 8% (37 vs. 31 degrees C; p < 0.05 for all values). Systemic and pulmonary vascular resistance did not change significantly during cooling. Mild hypothermia exerts significant positive inotropic effects in human and porcine myocardium without increasing intracellular Ca2+-transients or SR Ca2+-content. These effects translate into improved hemodynamic parameters of left ventricular function.
Among the treatment options for congestive heart failure, ventricular assist devices (VADs) are an emerging new technology, which may serve as a realistic therapeutic option once the complication rate is reduced. Whereas these devices were used in the past almost exclusively as a bridge to transplant, today permanent VAD and full-implantable VAD are considered for destination therapy. It is therefore necessary to compare this treatment modality with other current strategies with regard to not only current survival, quality of life, and complication metrics but also relative costs between treatments. Comparable studies evaluating treatment costs are rare and future research must focus on theses issues because of the demands of permanent cost containment.