Herwig Antretter

Prognostic markers in patients with severe accidental hypothermia and cardiocirculatory arrest

The aim of this retrospective study was to investigate whether plasma potassium, pH and activated clotting time (ACT), obtained from a central venous blood sample immediately after admission to hospital, could predict outcome in patients with severe accidental hypothermia and cardiocirculatory arrest. Twenty-two patients rewarmed with cardiopulmonary bypass were studied retrospectively (12 patients after avalanche accidents, seven patients after cold water submersion and three patients after prolonged exposure to cold). In 12 patients stable spontaneous circulation could not be restored. In 10 patients stable spontaneous circulation could be restored. Two of these 10 patients survived long-term. Plasma potassium, central venous pH and ACT were clinically useful prognostic markers in hypothermic arrest victims after avalanche accidents: a plasma potassium value exceeding 9 mmol/l, a pH equal to or less than 6.50 or an ACT exceeding 400 s was seen in patients in whom spontaneous circulation could not be restored. Plasma potassium, central venous pH and ACT were of only limited prognostic value in hypothermic arrest victims following cold water submersion or prolonged exposure to cold. In hypothermic arrest victims after cold water submersion a central venous pH as low as 6.51 on admission did not exclude long-term survival. Moderate and severe hyperkalemia in arrest victims after prolonged exposure to cold need not necessarily indicate postmortem autolysis. A decision to continue or terminate resuscitation cannot be based on laboratory parameters. Nevertheless, our data suggest that plasma potassium, central venous pH and ACT on admission can be used to identify hypothermic arrest victims in whom death preceded cooling. If several hypothermic arrest victims are admitted simultaneously after avalanche accidents, these 3 parameters can help not to waste limited cardiopulmonary bypass facilities for patients with no hope of survival.

Mitochondrial respiratory control and early defects of oxidative phosphorylation in the failing human heart.

Heart failure is a consequence of progressive deterioration of cardiac performance. Little is known about the role of impaired oxidative phosphorylation in the progression of the disease, since previous studies of mitochondrial injuries are restricted to end-stage chronic heart failure. The present study aimed at evaluating the involvement of mitochondrial dysfunction in the development of human heart failure. We measured the control of oxidative phosphorylation with high-resolution respirometry in permeabilized myocardial fibres from donor hearts (controls), and patients with no or mild heart failure but presenting with heart disease, or chronic heart failure due to dilated or ischemic cardiomyopathy. The capacity of the phosphorylation system exerted a strong limitation on oxidative phosphorylation in the human heart, estimated at 121 pmol O(2)s(-1)mg(-1) in the healthy left ventricle. In heart disease, a specific defect of the phosphorylation system, Complex I-linked respiration, and mass-specific fatty acid oxidation were identified. These early defects were also significant in chronic heart failure, where the capacities of the oxidative phosphorylation and electron transfer systems per cardiac tissue mass were decreased with all tested substrate combinations, suggesting a decline of mitochondrial density. Oxidative phosphorylation and electron transfer system capacities were higher in ventricles compared to atria, but the impaired mitochondrial quality was identical in the four cardiac chambers of chronic heart failure patients. Coupling was preserved in heart disease and chronic heart failure, in contrast to the mitochondrial dysfunction observed after prolonged cold storage of cardiac tissue. Mitochondrial defects in the phosphorylation system, Complex I respiration and mass-specific fatty acid oxidation occurred early in the development of heart failure. Targeting these mitochondrial injuries with metabolic therapy may offer a promising approach to delay the progression of heart disease.

Transvenous Pacemaker Lead Removal Is Safe and Effective Even in Large Vegetations: An Analysis of 53 Cases of Pacemaker Lead Endocarditis

Background: The aim of this study was to investigate whether transvenous lead removal is safe and effective in patients with lead vegetations greater than 1 cm in size.

Coronary endothelial injury after local occlusion on the human beating heart

BACKGROUND Occlusion of coronary arteries during beating heart surgery bears the potential for mechanical trauma to the arterial wall with consequent endothelial injury. The aim of this study was to elucidate the effects of local occlusion on the beating heart in human coronary arteries. METHODS Coronary arteries of patients with dilated cardiomyopathy (n = 7) or ischemic heart disease (n = 10) undergoing heart transplantation were locally occluded after starting cardiopulmonary bypass. Immediately after excision of the diseased heart, the vessels were fixed. Unoccluded segments served as controls. Integrity of endothelial lining was observed with scanning electron microscopy. RESULTS Scanning electron microscopy revealed significantly more severe endothelial injury in the area of occlusion than in the adjacent, not manipulated control segments. In the region of local occlusion, plaque rupture was noted in three of 34 atherosclerotic vessel specimens, injury to side branches was evident in two of 44, and local microthrombus formation was evident in six of 44 samples. CONCLUSIONS Local occlusion of human coronary arteries during beating heart coronary surgery may cause focal endothelial denudation, local microthrombosis, atherosclerotic plaque rupture, and injury to target vessel side branches.

Cardiac hepatopathy before and after heart transplantation

Chronic cardiac hepatopathy is a common entity in patients evaluated for heart transplantation (HTX). Hepatic injury is caused by severe heart failure resulting from prolonged recurrent congestion and/or impaired arterial perfusion. No data are available on the reversibility of cardiac hepatopathy in patients undergoing HTX. Data of 56 consecutive adult patients undergoing HTX during 2000–02 at the University Hospital of Innsbruck were analysed retrospectively. The following parameters were evaluated at the time of listing and 3, 6 and 12 months after HTX. Plasma levels of gamma‐glutamyl transferase (γ‐GT), alkaline phosphatase (AP), bilirubin, aspartate aminotransferase (AST), alanine aminotransferase (ALT), lactate dehydrogenase (LDH) and total plasma protein. When listed for HTX, only 12% of all patients analysed had physiological values throughout the seven laboratory parameters assessed. Elevated levels of γ‐GT, AP, bilirubin, AST, ALT, LDH and total plasma protein were detected in 66.6%, 29%, 50%, 16.7%, 10%, 40% and 18% of all patients respectively. Accordingly, median plasma levels of γ‐GT, bilirubin and LDH were elevated, whereas the mean plasma level of AP was at the upper normal range. In contrast, median plasma level of AST and mean plasma levels of ALT and total plasma protein were within the normal range: γ‐GT (median, 109.0; range, 634.0 U/l; n = 36), AP (mean, 120.2 ± 78.9 U/l; n = 29), bilirubin (median, 1.3; range, 16.1 mg/dl; n = 32), LDH (median, 226.0; range, 2355.0 U/l; n = 33), AST (median, 29.0; range, 145.0 U/l; n = 36), ALT (mean, 28.3 ± 20.8 U/l; n = 36) and total plasma protein (mean, 7.2 ± 1.1 g/dl; n = 25). Within 3 months after HTX, elevated parameters except LDH significantly ameliorated: γ‐GT (median, 59.0; range, 1160.0 U/l; P = 0.011), AP (92.2 ± 75.2 U/l; P = 0.016), bilirubin (median, 0.9; range, 8.1 mg/dl; P = 0.004), LDH slightly increased (median, 281.0; range, 543.0 U/l; P = 0.039), but there was a delayed improvement of this parameter after 6 and 12 months post‐HTX. End‐stage heart failure is characterized by a cholestatic liver enzyme profile with elevated plasma levels of γ‐GT and bilirubin. These parameters significantly improve within 3 months after HTX. Therefore, chronic cardiac hepatopathy seems to be a benign, potentially reversible disease.

Analysing ventricular fibrillation ECG-signals and predicting defibrillation success during cardiopulmonary resuscitation employing N(α)-histograms

Mean fibrillation frequency may predict defibrillation success during cardiopulmonary resuscitation (CPR). N(alpha)-histogram analysis should be investigated as an alternative. After 4 min of cardiac arrest, and 3 versus 8 min of CPR, 25 pigs received either vasopressin or epinephrine (0.4, 0.4, and 0.8 U/kg vasopressin versus 45, 45, and 200 microg/kg epinephrine) every 5 min with defibrillation at 22 min. Before defibrillation, the N(alpha)-parameter histogramstart/histogramwidth and the mean fibrillation frequency in resuscitated versus non-resuscitated pigs were 2.9+/-0.4 versus 1.7+/-0.5 (P=0.0000005); and 9.5+/-1.7 versus 6.9+/-0.7 (P=0.0003). During the last minute prior to defibrillation, histogramstart/histogramwidth of > or =2.3 versus mean fibrillation frequency > or =8 Hz predicted successful defibrillation with subsequent return of a spontaneous circulation for more than 60 min with sensitivity, specificity, positive predictive value and negative predictive value of 94 versus 82%, 96 versus 89%, 98 versus 93% and 90 versus 74%, respectively. We conclude, that N(alpha)-analysis was superior to mean fibrillation frequency analysis during CPR in predicting defibrillation success, and distinction between vasopressin versus epinephrine effects.

Temporary extracorporeal membrane oxygenation in the treatment of acute traumatic lung injury

PurposeTo report two cases of acute life-threatening traumatic lung injury, who required temporary extracorporeal veno-venous membrane oxygenation (ECMO), and airlifting to a level l trauma centre.Clinical featuresThe first patient suffered a severe motor vehicle accident with prolonged entrapment in the wreckage. After extrication, tracheal intubation, and fluid resuscitation, respiratory therapy failed to result in sufficient ventilation and oxygenation within the first hours after trauma due to severe lung contusion and intraparenychmal bleeding.The second patient was hit by a falling tree and suffered isolated blunt chest trauma. Due to pulmonary contusions and tracheal rupture, subsequent ventilation management was limited by extensive mediastinal emphysema. Both patients were airlifted to a University Hospital and placed on ECMO for four and six days without complications, respectively. After emergency surgery and 21 and 26 days intensive care treatment, both patients were transferred to a general ward, and discharged from the hospital with full recovery.ConclusionThese cases demonstrate the role of ECMO in the treatment of traumatic respiratory failure. If ventilatory support strategies fail due to severe lung or airway injury, ECMO may be an option for the temporary management of gas exchange in trauma patients.RésuméObjectifRapporter deux cas d’atteinte pulmonaire traumatique, mettant la vie en danger, qui ont nécessité une oxygénation extracorporelle (OEC) veino-veineuse et un transport aérien vers un centre de traumatologie de premier niveau.Aspects cliniquesLe premier patient a été victime d’un sévère accident d’automobile où il est resté coincé pendant une longue période. Après avoir été dégagé, on a procédé à une intubation endotrachéale et à une réanimation volémique, mais la thérapie respiratoire n’a pu fournir une ventilation et une oxygénation suffisantes pendant les premières heures qui ont suivi le traumatisme à cause des contusions pulmonaires sévères et du saignement intraparenchymateux. Le second patient a été blessé par la chute d’un arbre et a subi un traumatisme thoracique isolé. La présence de contusions pulmonaires et d’une rupture de la trachée a limité le traitement subséquent par ventilation en causant un emphysème médiastinal important. Les deux patients ont été transportés par avion vers un hôpital universitaire et placés sous OEC pendant quatre et six jours respectivement et ce, sans complication. Suivant une chirurgie d’urgence et 21 et 26 jours de traitement à l’unité des soins intensifs, les deux patients ont été déplacés à l’unité des soins généraux et ils ont quitté l’hôpital complètement rétablis.ConclusionCes cas démontrent le rôle de l’OEC dans le traitement d’une défaillance respiratoire traumatique. Si les stratégies de soutien respiratoire ne réussissent pas à cause de lésion sévère des poumons ou des voies aériennes, l’OEC peut se présenter comme un choix de traitement temporaire des échanges gazeux chez les patients victime d’un traumatisme.

Coagulation monitoring and management of anticoagulation during cardiac assist device support.

BACKGROUND The incidence of clinically significant thromboembolic events due to the use of cardiac assist device systems remains high. Despite the considerable advances in cardiac assist device technology, the monitoring and management of the hypercoagulable coagulation status, resulting from foreign surfaces of the assist device system, altered rheologic conditions, and blood stasis in the recipient heart remain a challenge. Moreover septic complications and insufficient anticoagulation are responsible for thromboembolic events. METHODS In addition to standard coagulation analysis, functional coagulation tests were performed including the use of a thrombelastographic monitoring system (ROTEG) and a platelet function analyzer (PFA-100). RESULTS Severe biventricular ischemic heart failure developed in a 58-year-old man with acute myocardial infarction and he needed a biventricular assist device for a bridge to cardiac transplantation. Although the patient received acenocoumarol (Sintrom; Novartis Pharma, Vienna, Austria) and acetylsalicylic acid (Aspisol; Bayer AG, Leverkusen, Germany) as usual, ROTEG and the PFA-100 detected hypercoagulability while routine coagulation screening tests showed hypocoagulability. Moreover thrombus formation surrounding the canula of the left ventricular assist device was detected. Antithrombotic therapy with clopidogrel (Plavix) was initiated. Coagulation was closely monitored with modified thrombelastography and the PFA-100 to achieve sufficient but not overwhelming anticoagulation therapy. Three months after biventricular assist device implantation the patient underwent successful transplantation with no major blood loss. CONCLUSIONS Thrombelastography should be the standard form of monitoring in such patients to decrease the risk of thromboembolic events and prevent bleeding complications.

Zygomycosis and other rare filamentous fungal infections in solid organ transplant recipients

Fungi cause severe infections in solid organ transplant (SOT) recipients. Recently, a shift towards non‐Aspergillus filamentous fungal infections (nAFFI) was noticed. In a series of 2878 SOTs (kidney, pancreas, islets, liver, heart, lung, and bowel) performed between January 1995 and December 2006 at the Innsbruck medical university, eleven cases of nAFFI were diagnosed. The encountered species included Zygomyzetes (n = 8), and Alternaria alternate, Pseudallescheria boydii, Trichoderma spp. (one each); there were three liver and three heart, one intestinal, pancreas, lung, bilateral forearm and renal recipient each. Five patients died from nAFFI (zygomycosis: 4, Pseudallerichia boydii: 1); four were diagnosed postmortem. In five cases infection was surgically treated in combination with antifungals. Risk factors for nAFFI were renal failure (73%) and intensified immunosuppression (73%); two cases were associated with post‐transplant lymphoproliferative disorder, one with graft versus host disease. An increase in the incidence of nAFFI was observed parallel to introduction of caspofungin and voriconazole (three cases until 12/2003, seven cases thereafter). NAFFI are increasingly found in SOT recipients. If diagnosed in time, the outcome seems acceptable. Intensified immunosuppression and exposure to antifungals not active against zygomycetes may be risk factors. Surgical therapy may play an important role in these infections.

Capillary deposition of the complement fragment C4d in cardiac allograft biopsies is associated with allograft vasculopathy

Cardiac allograft vasculopathy (CAV) is a long‐term threat in heart transplant recipients and its exact pathogenesis remains to be established. As complement activation contributes to early and late allograft dysfunction, we hypothesized that deposition of the complement fragment, C4d, in capillaries of cardiac allograft biopsies may be associated with CAV. A polyclonal anti‐C4d antibody was used for immunohistochemistry on endomyocardial biopsies obtained from heart transplant recipients during the first year post‐transplantation. CAV was assessed by intracoronary ultrasound performed at 1‐year post‐transplantation. We were able to show that CAV is highly associated with C4d deposition in capillaries of cardiac allografts and that serial C4d studies may predict development of CAV at 1‐year post‐transplantation.