Secondary prevention in diabetic and nondiabetic coronary heart disease patients: Insights from the German subset of the hospital arm of the EUROASPIRE IV and V surveys.

BACKGROUND: Patients with coronary heart disease (CHD) with and without diabetes mellitus have an increased risk of recurrent events requiring multifactorial secondary prevention of cardiovascular risk factors. We compared prevalences of cardiovascular risk factors and its determinants including lifestyle, pharmacotherapy and diabetes mellitus among patients with chronic CHD examined within the fourth and fifth EUROASPIRE surveys (EA-IV, 2012-13; and EA-V, 2016-17) in Germany. METHODS: The EA initiative iteratively conducts European-wide multicenter surveys investigating the quality of secondary prevention in chronic CHD patients aged 18 to 79 years. The data collection in Germany was performed during a comprehensive baseline visit at study centers in Würzburg (EA-IV, EA-V), Halle (EA-V), and Tübingen (EA-V). RESULTS: 384 EA-V participants (median age 69.0 years, 81.3% male) and 536 EA-IV participants (median age 68.7 years, 82.3% male) were examined. Comparing EA-IV and EA-V, no relevant differences in risk factor prevalence and lifestyle changes were observed with the exception of lower LDL cholesterol levels in EA-V. Prevalence of unrecognized diabetes was significantly lower in EA-V as compared to EA-IV (11.8% vs. 19.6%) while the proportion of prediabetes was similarly high in the remaining population (62.1% vs. 61.0%). CONCLUSION: Between 2012 and 2017, a modest decrease in LDL cholesterol levels was observed, while no differences in blood pressure control and body weight were apparent in chronic CHD patients in Germany. Although the prevalence of unrecognized diabetes decreased in the later study period, the proportion of normoglycemic patients was low. As pharmacotherapy appeared fairly well implemented, stronger efforts towards lifestyle interventions, mental health programs and cardiac rehabilitation might help to improve risk factor profiles in chronic CHD patients.

[Short version of the 2nd edition of the German-Austrian S3 guidelines "Cardiogenic shock complicating myocardial infarction-Diagnosis, monitoring and treatment"]. / Kurzversion der 2. Auflage der deutsch-österreichischen S3-Leitlinie "Infarkt-bedingter Kardiogener Schock ­ Diagnose, Monitoring und Therapie".

BACKGROUND: The present guidelines ( http://leitlinien.net ) focus exclusively on cardiogenic shock due to myocardial infarction (infarction-related cardiogenic shock, ICS). The cardiological/cardiac surgical and the intensive care medicine strategies dealt with in these guidelines are essential to the successful treatment and survival of patients with ICS; however, both European and American guidelines on myocardial infarction and heart failure and also position papers on cardiogenic shock focused mainly on cardiological aspects. METHODS: Evidence on the diagnosis, monitoring and treatment of ICS was collected and recommendations compiled in a nominal group process by delegates of the German Cardiac Society (DGK), the German Society for Medical Intensive Care Medicine and Emergency Medicine (DGIIN), the German Society for Thoracic and Cardiovascular Surgery (DGTHG), the German Society for Anaesthesiology and Intensive Care Medicine (DGAI), the Austrian Society for Internal and General Intensive Care Medicine (ÖGIAIM), the Austrian Cardiology Society (ÖKG), the German Society for Prevention and Rehabilitation of Cardiovascular Diseases (DGPR) and the German Interdisciplinary Association for Intensive Care and Emergency Medicine (DIVI), under the auspices of the Working Group of the Association of Medical Scientific Societies in Germany (AWMF). If only poor evidence on ICS was available, general study results on intensive care patients were inspected and presented in order to enable analogue conclusions. RESULTS: A total of 95 recommendations, including 2 statements were compiled and based on these 7 algorithms with defined instructions on the course of treatment.

Transcoronary pacing : Reliability during myocardial ischemia and after implantation of a coronary stent.

BACKGROUND: Transcoronary pacing is a useful therapeutic option for the treatment of unheralded bradycardias in the setting of percutaneous coronary interventions (PCI). OBJECTIVES: In the present study, we investigated the influence of stent implantation and transient myocardial ischemia on the feasibility of transcoronary pacing in a porcine model. METHODS: 7 adult pigs underwent a percutaneous coronary intervention with implantation of a coronary stent under general anaesthesia in an animal catheterization laboratory. Transcoronary pacing was established by using a standard guidewire isolated with an angioplasty balloon positioned in the periphery of the right coronary artery serving as the cathode. As the indifferent anode, a skin patch electrode at the back of the animal was used. The reliability of transcoronary pacing was assessed by measurement of threshold and impedance data and the magnitude of the epicardial electrogram at baseline, after implantation of a coronary stent and finally during myocardial ischemia. RESULTS: Effective transcoronary pacing could be demonstrated in all cases with the standard unipolar transcoronary pacing setup yielding a low pacing threshold at baseline of 1.3 ± 0.8 V with an impedance of 283 ± 67 Ω. Implantation of a coronary stent did not influence the pacing threshold (1.0 ± 0.4 V) and impedance (262 ± 63 Ω). Acute myocardial ischemia lead to a significant but clinically nonrelevant increase of the pacing threshold to 2.0 ± 0.6 V and a drop in pacing impedance (137 ± 39 Ω). CONCLUSIONS: Transcoronary pacing in the animal model is not affected by implantation of a coronary stent in the same vessel used for pacing. Despite a significant increase in pacing threshold, the transcoronary pacing approach is reliable in acute myocardial ischemia during a percutaneous coronary intervention.

Vasopressors for acute myocardial infarction complicated by cardiogenic shock.

Several international evidence-based guidelines reveal the lack of evidence on the treatment of patients with acute myocardial infarction (AMI) complicated by cardiogenic shock (CS) for all recommended therapies. We included 6 studies with 842 eligible patients and one ongoing study. Three different adrenergic agents (norepinephrine, dopamine, epinephrine), vasopressin and the NOS inhibitor tilarginine were compared in 4 different combinations. On the small basis of all available evidence we can state that there is no evidence to use tilarginene, some evidence to avoid dopamine due to increased rates of arrhythmias, but some evidence, which suggests to prefer norepinephrine in comparison to epinephrine as vasopressor.

[Infarct-related cardiogenic shock : Prognosis and treatment]. / Infarktbedingter kardiogener Schock : Prognose und Behandlung.

Patients with ST segment elevation myocardial infarction (STEMI) and non-ST segment elevation myocardial infarction (NSTEMI) experience cardiogenic shock in about 6-10% of cases during the hospital treatment. In recent years, the incidence seems to be decreasing due to invasive diagnostics and therapy after myocardial infarction. Early diagnosis is important to initiate immediate revascularization using percutaneous coronary intervention (PCI) with stent implantation as part of cardiogenic shock treatment. Thus, a significant improvement in survival can be achieved. Pharmacological and mechanical support is needed to maintain perfusion of the myocardium and organs. Drug therapy for infarct cardiogenic shock relies on dobutamine for inotropic agent and norepinephrine as a vasopressor. For further inotropic support, data on additional levosimendan treatment are available. The pharmacological therapy is supplemented by mechanical support systems such as Impella (ABIOMED, Danvers, MA, USA) or extracorporeal membrane oxygenation (ECMO). The intra-aortic balloon pump (IABP) is hardly used anymore. The majority of cardiogenic shock survivors have little functional cardiac impairment in the long term. This shows the transient damage component (stunning, inflammation), which underlines the need for a fast and effective cardiovascular supportive therapy.

Advanced hemodynamic monitoring in intensive care medicine : A German web-based survey study.

BACKGROUND: Advanced hemodynamic monitoring is recommended in patients with complex circulatory shock. OBJECTIVES: To evaluate the current attitudes and beliefs among German intensivists, regarding advanced hemodynamic monitoring, the actual hemodynamic management in clinical practice, and the barriers to using it. MATERIALS AND METHODS: Web-based survey among members of the German Society of Medical Intensive Care and Emergency Medicine. RESULTS: Of 284 respondents, 249 (87%) agreed that further hemodynamic assessment is needed to determine the type of circulatory shock if no clear clinical diagnosis can be made. In all, 281 (99%) agreed that echocardiography is helpful for this purpose (transpulmonary thermodilution: 225 [79%]; pulmonary artery catheterization: 126 [45%]). More than 70% of respondents agreed that blood flow variables (cardiac output, stroke volume) should be measured in patients with hemodynamic instability. The parameters most respondents agreed should be assessed in a patient with hemodynamic instability were mean arterial pressure, cardiac output, and serum lactate. Echocardiography is available in 99% of ICUs (transpulmonary thermodilution: 91%; pulmonary artery catheter: 63%). The respondents stated that, in clinical practice, invasive arterial pressure measurements and serum lactate measurements are performed in more than 90% of patients with hemodynamic instability (cardiac output monitoring in about 50%; transpulmonary thermodilution in about 40%). The respondents did not feel strong barriers to the use of advanced hemodynamic monitoring in clinical practice. CONCLUSIONS: This survey study shows that German intensivists deem advanced hemodynamic assessment necessary for the differential diagnosis of circulatory shock and to guide therapy with fluids, vasopressors, and inotropes in ICU patients.

The double guidewire approach for transcoronary pacing in a porcine model.

BACKGROUND: Transcoronary pacing is used for treatment of unheralded bradycardias in the setting of percutaneous coronary interventions (PCI). OBJECTIVES: In the present study we introduced a new concept - the double guidewire approach - for transcoronary pacing in a porcine model. METHODS: Transcoronary pacing was applied in 16 adult pigs under general anaesthesia in an animal catheterization laboratory. A special guidewire with electrical insulation by PTFE coating except for the distal part of the guidewire was positioned in the periphery of a coronary artery serving as the cathode. As the indifferent anode, an additional standard floppy tip guidewire was advanced into the proximal part of the same coronary vessel. The efficacy of double guidewire transcoronary pacing was assessed by measurement of threshold and impedance data and the magnitude of the epicardial electrogram compared with unipolar transcoronary pacing using a standard cutaneous patch electrode as indifferent anode. RESULTS: Transcoronary pacing was effective in all cases. Pacing thresholds obtained with the double guidewire technique (1.5 ± 0.9 V) were similar to those obtained by standard unipolar transcoronary pacing with a cutaneous patch electrode (1.2 ± 0.7 V) and unipolar transvenous pacing against the same cutaneous patch electrode (1.5 ± 1.0 V). Bipolar transvenous pacing yielded the lowest pacing threshold at 0.8 ± 0.4 V. CONCLUSIONS: Transcoronary pacing in the animal model with the novel "double guidewire approach" is a simple and effective pacing technique with comparable pacing thresholds obtained by standard unipolar transcoronary and transvenous pacing.

Predictive value of outcome scores in patients suffering from cardiogenic shock complicating AMI: APACHE II, APACHE III, Elebute-Stoner, SOFA, and SAPS II.

BACKGROUND: Scoring systems in critical care patients are essential for prediction of outcome and for evaluation of therapy. In this study we determined the value of the APACHE II, APACHE III, Elebute-Stoner, SOFA, and SAPS II scoring systems in the prediction of mortality in patients with cardiogenic shock (CS) complicating acute myocardial infarction (AMI). MATERIAL AND METHODS: In this prospective, observational study, patients who were admitted to the ICU with CS complicating AMI were consecutively included. Data for the APACHE II, APACHE III, Elebute-Stoner, SOFA, and SAPS II scores were recorded on admission and during the following 96 h. Receiver operating characteristic curve analyses and the area under the curve (AUC) were used to estimate the predictive ability (mortality) of the scoring systems on admission and the maximum value. RESULTS: Mortality among the 41 patients included in this study was 44 %. On admission, the mean APACHE II (p = 0.035), APACHE III (p = 0.003), SAPS II (p = 0.001), and SOFA (p = 0.042) scores were significantly higher in nonsurvivors than in survivors. At maximum score, APACHE II (p = 0.009), APACHE III (p < 0.001), and SAPS II (p < 0.001) appeared to have higher significance. On admission, the discrimination for APACHE III was 0.786, for SAPS II 0.790, and for APACHE II 0.691. The maximum-score AUC for APACHE II was 0.726, for APACHE III 0.827, and for SAPS II 0.832. Elebute-Stoner and SOFA did not yield valuable results at maximum score or, in the case of Elebute-Stoner, on admission. CONCLUSION: These results suggest that at the time of diagnosis and at maximum value, the SAPS II, APACHE III, and APACHE II scores may be useful in predicting a high probability of survival of patients with CS complicating AMI.

Acute myocardial infarction and cardiogenic shock: prognostic impact of cytokines: INF-γ, TNF-α, MIP-1ß, G-CSF, and MCP-1ß.

BACKGROUND: The IABP SHOCK trial was designed as a morbidity-based randomized controlled trial to determine the effect of intraaortic balloon pulsation (IABP) in patients with infarct-related cardiogenic shock (CS). The primary endpoint was the change in the APACHE II score over a 4-day period. The prospective hypothesis was that adding IABP therapy to "standard care" would reduce CS-triggered multiorgan dysfunction syndrome (MODS). The primary endpoint showed no difference between conventionally managed cardiogenic shock patients and those with additional IABP support. In an inflammatory marker substudy, we analyzed the prognostic value of the cytokines interferon-γ (INF-γ), tumor necrosis factor-α (TNF-α), macrophage inflammatory protein-1ß (MIP-1ß), granulocyte-colony stimulating factor (G-CSF), and monocyte chemoattractant protein-1ß (MCP-1ß). We also investigated the influence of IABP support, age, and gender on cytokine levels. DESIGN: The inflammatory marker substudy of the prospective, randomized, controlled, open label IABP SHOCK Trial (ClinicalTrials.gov ID NCT00469248). MATERIALS AND METHODS: A prospective, randomized, single-center study in a 12-bed intensive care unit at a university hospital was performed. A total of 40 consecutive patients were enrolled. The observational period was 96 h. RESULTS: The investigated cytokines showed a significant contribution in the prediction of mortality. Initial (on admission) and maximal cytokine levels during the observational period showed a similar predictive power. Patients with elevated levels of pro- and antiinflammatory cytokines had a higher risk of dying. The maximal level measured over the observation period in the hospital was also suited to identify the survivors. Close correlations between maximal cytokine levels resulted in the choice of only one independent marker (MIP-1ß) into the multivariate model (OR 1.024, 95% CI 1.005-1.043). Initial cytokine levels were also suitable to predict the survivors; the risk of death significantly increases with increasing IFN-γ level (OR 1.119, 95% CI 1.005-1.246). Cytokine levels were not affected by the presence of IABP support. Age (< 75 or > 75 years) and gender did not have a clinically relevant effect on INF-γ, TNF-α, MIP-1ß, G-CSF, and MCP-1 in CS patients. CONCLUSION: The inflammatory response in patients with myocardial infarction complicated by CS, as reflected by the inflammatory markers INF-γ, TNF-α, MIP-1ß, G-CSF, and MCP-1ß, have been shown to be of prognostic value in estimating clinical outcome.

[Thrombocytopenia in a patient with coronary artery disease after percutaneous coronary intervention]. / Thrombozytopenie bei einem Patienten nach perkutaner Koronarintervention.

Thrombocytopenia in patients with percutanous coronary intervention is a known complication of glycoprotein IIb/IIIa inhibitors. This can limit the application of these agents. Platelet count monitoring 2, 6, 12 and 24 hours after starting the treatment reveals most cases of acute thrombocytopenia. Side effects can be avoided by the early discontinuation of the glycoprotein IIb/IIIa antagonist treatment. A selective diagnostic approach by laboratory measures should exclude any confusion with heparin-induced thrombocytopenia and pseudo thrombocytopenia.

Sodium/hydrogen exchange inhibition with cariporide reduces leukocyte adhesion via P-selectin suppression during inflammation.

BACKGROUND AND PURPOSE: The Na(+)/H(+) exchange (NHE) inhibitor cariporide is known to ameliorate ischaemia/reperfusion (I/R) injury by reduction of cytosolic Ca(2+) overload. Leukocyte activation and infiltration also mediates I/R injury but whether cariporide reduces I/R injury by affecting leukocyte activation is unknown. We studied the effect of cariporide on thrombin and I/R induced leukocyte activation and infiltration models and examined P-selectin expression as a potential mechanism for any identified effects. EXPERIMENTAL APPROACH: An in vivo rat mesenteric microcirculation microscopy model was used with stimulation by thrombin (0.5 micro ml(-1)) superfusion or ischaemia (by haemorrhagic shock for 60 min) and reperfusion (90 min). KEY RESULTS: Treatment with cariporide (10 mg kg(-1) i.v.) significantly reduced leukocyte rolling, adhesion and extravasation after thrombin exposure. Similarly, cariporide reduced leukocyte rolling (54+/-6.2 to 2.4+/-1.0 cells min(-1), P<0.01), adherence (6.3+/-1.9 to 1.2+/-0.4 cells 100 microm(-1), P<0.01) and extravasation (9.1+/-2.1 to 2.4+/-1.1 cells per 20 x 100 microm perivascular space, P<0.05), following haemorrhagic shock induced systemic ischaemia and reperfusion. The cell adhesion molecule P-selectin showed a profound decrease in endothelial expression following cariporide administration in both thrombin and I/R stimulated groups (35.4+/-3.2 vs 14.2+/-4.1% P-selectin positive cells per tissue section, P<0.01). CONCLUSIONS AND IMPLICATIONS: The NHE inhibitor cariporide is known to limit reperfusion injury by controlling Ca(2+) overload but these data are novel evidence for a vasculoprotective effect of NHE inhibition at all levels of leukocyte activation, an effect which is likely to be mediated at least in part by a reduction of P-selectin expression.

Glycoprotein IIb/IIIa inhibitor-induced thrombocytopenia: diagnosis and treatment.

Thrombocyte glycoprotein IIb/IIIa inhibitors prevent fibrinogen binding and thereby thrombocyte aggregation. The inhibition of thrombocyte activation at the damaged coronary plaque is the target of the new therapeutic strategies in treating acute coronary syndrome. This reduces the ischemic complications associated with the non-STelevation myocardial infarction (NSTEMI) and percutaneous coronary intervention (PCI). Thrombocytopenia is a known complication of glycoprotein (GP) IIb/IIIa inhibitors. Although, in general, GP IIb/IIIa inhibitor-induced thrombocytopenia is a harmless side effect which responds readily to thrombocyte transfusion, it can occasionally be a very serious complication associated with serious bleeding. In addition patients developing thrombocytopenia have unfavorable outcome (e.g., death, myocardial infarction, bypass surgery or additional PCI) in comparison to patients without thrombocytopenia. Advanced age (> 65 years), low BMI and a low initial thrombocyte count (<180,000/microl) are independent risk factors of thrombocytopenia. The risk of bleeding is higher with this form of thrombocytopenia not only due to the low thrombocyte count but also to the impaired function of the remaining thrombocytes. It is important to closely monitor platelet count during GP IIb/IIIa antagonist treatment. Platelet count monitoring two, six, twelve and 24 hour after starting the treatment reveals most cases of acute thrombocytopenia. Side effects can be avoided by the early discontinuation of the GP IIb/IIIa antagonist treatment. This article reviews the diagnosis and treatment of glycoprotein IIb/IIIa inhibitor-induced thrombocytopenia and summarizes the differential diagnosis from heparin-induced thrombocytopenia and laboratory-related pseudothrombocytopenia.

Thromboembolic cerebral ischaemic attack complicating cardiac catheterization. Successful local thrombolytic therapy with reduced dose rt-PA.

Cerebral ischaemia caused by thromboembolism is a possible complication of diagnostic and interventional cardiac catheterization. In this case report we describe the diagnostic steps and successful treatment strategy in the management of a patient who suffered from cerebral ischaemia during cardiac catheterization. Initial CT scanning to exclude cerebral haemorrhage was followed by angiography through the cardiac catheterization sheath in the right femoral artery. Occlusion just before the intracranial bifurcation of the right internal carotid artery was found and local thrombolysis given with a reduced dose of 34 mg rt-PA. The subsequent angiogram showed restored perfusion in the affected vessel after completion of thrombolytic therapy and resolution of neurological symptoms.

[Catecholamine therapy in cardiogenic shock: helpful, useless or dangerous?]. / Katecholamine im kardiogenen Schock: hilfreich, nutzlos oder gefährlich?

Cardiogenic shock is characterized by inadequate organ and tissue perfusion, due to cardiac dysfunction, predominantly following acute myocardial infarction. Mortality rates for patients with cardiogenic shock remain high, ranging from 50-70 % despite effective therapy. Rapid diagnostics, aggressive therapeutic approach (invasive or surgical revascularisation) and pharmacological support are currently used to improve the clinical outcome and survival. In the first line commonly sympathomimetics like dopamine, dobutamine, epinephrine and norepinephrine are used for the pharmacological treatment. They have a high affinity for alpha- and beta adrenergic receptors, leading to a positive inotropic cardiac function, an increase in heart rate, oxygen enhanced demand, and an increase in vasoconstriction. However, there are also some disadvantages in the use of sympathomimetics in patients with cardiogenic shock. Clearly, metabolic acidosis due to the increased oxygen demand can be observed. Vasoconstriction induced by sympathomimetics can lead to perfusion mismatch or even deficit within the microcirculation. Additionally, in some studies which give evidence that the use of sympathomimetics can directly lead to enhanced systemic inflammatory response due to an increased IL-6 expression. However, sympathomimetics are still first line therapeutics for treatment of cardiogenic shock -- with respect to dosage and duration of treatment.

[Cardiogenic shock: pathophysiology, clinics, therapeutical options and perspectives]. / Kardiogener Schock. Pathomechanismen, klinischer Verlauf, therapeutische Ansätze und Perspektiven.

Documented mortality from myocardial infarction (MI) has significantly decreased from around 30% in the 1960s to 6-7% currently, following the introduction of intensive care treatment, thrombolysis, effective antithrombotic therapy and coronary angioplasty. However, the approximate mortality of 70-80% of patients with cardiogenic shock following acute MI has hardly improved despite the introduction of modern treatment strategies. The major cause of in-hospital MI mortality remains myocardial failure with consecutive cardiogenic shock and multi-organ failure. Prompt coronary revascularisation by "facilitated" or "adjunctive" percutaneous coronary intervention (PCI), is currently considered the best method to reduce the high mortality in these patients. Facilitated PCI includes administration of glycoproteine receptor antagonists, mechanical circulation support strategies, such as, intraaortic balloon counterpulsation and potentially prehospital thrombolysis.

[Acute beta 1-selective beta-receptor blocker nebivolol poisoning in attempted suicide]. / Akute Intoxikation mit dem beta 1-selektiven beta-Rezeptorenblocker Nebivolol in suizidaler Absicht.

HISTORY AND ADMISSION FINDINGS: A 17-year-old girl had swallowed 80-100 tablets of Nebivolol, 5 mg each, with suicidal intent. She was referred to hospital 8 hours later by an emergency duty physician. On admission she was sweaty and pale, but there were no other obvious abnormalities. Neurological examination revealed decreased responsiveness and slowed movements. She was known to have type 1 diabetes mellitus. INVESTIGATIONS: Blood pressure was 105/55 mmHg, the ECG showed sinus bradycardia of 55 beats/min. Biochemical tests revealed hypoglycaemia (2.1 mmol/l), hypokalaemia (3.4 mmol/l) and respiratory failure (pO2 6.16 kPa, O2 saturation 82%, pCO2 6.55 kPA). Heart and lung were unremarkable on physical examination as were chest radiogram and echocardiogram. Plasma level of nebivolol was 480 ng/ml on admission (therapeutic range 88-195 ng/ml). TREATMENT AND COURSE: After gastric lavage and administration of charcoal and sodium sulphate a temporary pacemaker was connected and glucagon infused intravenously as an antidote. The cardiovascular state stabilized with falling plasma level of nebivolol. Glucose was administered initially, but transient intravenous insulin infusion became necessary to counteract hyperglycaemia. The patient was transferred from the intensive care unit in a stable cardiovascular state after 2 days. CONCLUSION: This case demonstrates that swallowing 400-500 mg nebivolol, resulting in a plasma level of 480 ng/ml, need not be fatal. But the outcome in this patient should not be taken as necessarily applying to similar cases. It depends on the individual patient's metabolic state whether higher plasma levels might be reached with the same amount of ingested nebivolol.

[Significance of the heart-lung machine for the concept of minimal invasive heart surgery]. / Bedeutung der Herz-Lungen-Maschine für das Konzept der minimal-invasiven Herzchirurgie.

Proinflammatory cytokines have been implicated in mediating myocardial dysfunction in a systemic inflammatory reaction following open heart surgery with extracorporeal circulation (ECC). The present study aimed to distinguish the surgical impact on cytokine release from the influence of ECC in a model of supported angioplasty. The extracorporeal circulation and not surgical trauma was found to be the main trigger of the systemic inflammatory response.

[Systemic inflammatory reactions to extracorporeal therapy measures (II): Cardiopulmonary bypass]. / Systemische Entzündungsreaktionen extrakorporaler Therapieverfahren (II): Der kardiopulmonale Bypass.

About 65,000 cardiac patients undergo surgery annually in Germany with the assistance of cardiopulmonary bypass. The "post pump inflammatory response" (the systemic and myocardial inflammatory response syndrome post cardiac surgery), triggered at least in part by the cardiopulmonary bypass, contributes substantially towards morbidity (e.g., myocardial depression) and mortality in these patients. The main mechanisms underlying this inflammatory response are the complement cascade, the activation of blood cells, the release of cytokines and the induction to nitric oxide synthesis. The relative importance of each individual factor, however, is still a matter of debate. Scoring systems and measurements of tumor necrosis factor-alpha, as well as soluble tumor necrosis factor receptors, allow the early detection of an "escalating inflammatory response" in 2-10% of all patients, which is associated with a worse prognosis. Therapeutic attempts to suppress these systemic and myocardial inflammatory reactions focus on blockade of the complement system, coating of CPB membranes with heparin, leucocyte depletion and attenuation of leucocyte function, elimination of toxins and mediators by means of hemofiltration, as well as on the administration of antiproteases, antioxidants, oxygen radical scavengers and also of immune globulins.