Library

feed icon rss

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
  • 1
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Journal of cardiovascular electrophysiology 11 (2000), S. 0 
    ISSN: 1540-8167
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Arrhythmias in Heart Failure. About one half of deaths in patients with heart failure are sudden, mostly due to ventricular tachycardia (VT) degenerating to ventricular fibrillation or immediate ventricular fibrillation. In severe heart failure, sudden cardiac death also may occur due to bradyarrhythmias. Other dysrhythmias complicating heart failure include atrial and ventricular extrasystoles, atrial fibrillation (AF), and sustained and nonsustained ventricular tachyarrhythmias. The exact mechanism of the increased vulnerability to arrhythmias is not known. Depending on the etiology of heart failure, different preconditions, including ischemia or structural alterations such as fibrosis or myocardial scarring, may he prominent. Reentrant mechanisms around scar tissue, afterdepolarizations, and triggered activity due to changes in calcium metabolism significantly contribute to arrhythmogenesis. Furthermore, alterations in potassium currents leading to action potential prolongation and an increase in dispersion of repolarization play a significant role. Treatment of arrhythmias is necessary either because patients are symptomatic or to reduce the risk for sudden cardiac death. The individual history, left ventricular function, electrophysiologic testing, and the signal-averaged ECG give useful information for identifying patients at risk for sudden cardiac death. The implantable cardioverter defibrillator (ICD) has evolved as a promising therapy for life-threatening arrhythmias. A potential role may exist for antiarrhythmic drugs, mainly amiodarone. There is growing evidence that patients with sustained VT or a history of resuscitation have the best outcome with ICD therapy regardless of the degree of heart failure. Many of these patients require additional antiarrhythmic therapy because of AF or nonsustained VTs that may activate the device. Catheter ablation or map-guided endocardial resection are additional options in selected patients but seldom represent the only therapeutic strategy.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 2
    ISSN: 1432-2277
    Keywords: Heart transplantation, selection ; Selection, heart transplantation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The increasing discrepancy between the numbers of patients selected for cardiac transplantation and the available donor organs requires validation of markers of high risk at the time of initial evaluation that may help to determine which patients profit from aggressive therapy. We retrospectively examined the case records of 91 heart transplant caddidates selected out of a total of 140 consecutive patients referred for evaluation. Of these 91 patients, 48 were transplanted during follow-up. Of the remaining 43 patients, 25 died after a mean survival time of 1.6±2.5 months. The causes of death were pump failure in 18 (72%) and sudden cardiac death in 7 (28%). Multivariate analysis identified 4 out of 26 parameters at initial evaluation that distinguished the 25 nonsurvivors from the 18 survivors. These were: mean arterial pressure (P=0.03), pulmonary capillary wedge pressure (P=0.002), mean pulmonary artery pressure (P=0.007). The mode of death could not be predicted. We conclude that there are prognostic markers at initial evaluation that allow more restrictive selection of patients for cardiac transplantation and mechanical bridging.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 3
    ISSN: 1432-2277
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 4
    ISSN: 1615-6692
    Keywords: Key Words Transplant vasculopathy ; Coronary artery disease ; Immunopathogenesis ; Schlüsselwörter Transplantatvaskulopathie ; Koronare Herzkrankheit ; Immunpathogenese
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Obwohl die Transplantatvaskulopathie und die native Atherosklerose klinisch und pathophysiologisch zwei unterschiedliche Entitäten darstellen, weisen ihre Pathomechanismen einige Gemeinsamkeiten auf. Beide können als Antwort auf Schädigungen innerhalb eines erweiterten Konzeptes des Immunsystems aufgefaßt werden. Alloantigene (zum Beispiel auf Spenderendothelzellen) oder Autoantigene (zum Beispiel oxydiertes LDL-Cholesterin) werden durch antigenpräsentierende Zellen den T-Zellen des körpereigenen Immunsystems präsentiert. Mit dem geeigneten kostimulatorischen Signal erzeugt diese Muster eine differenzierte T-Zell-, B-Zell- und inflammatorische Antwort, während ohne dieses Zweitsignal eine Apoptose der Immunzellen erfolgt. Im Falle einer Proliferation und Differenzierung der Immunzellen wird ein koordiniertes Zytokinmuster initiiert. In diesen Prozeß einbezogen sind von Monozyten abstammende Makrophagen. Dieser Prozeß führt zum “Rolling”, “Sticking” und zur Diapedese von Immunzellen durch die koronare Endothelzellmembran. Nachfolgend findet sich ein Phänotypwechsel der mediaständigen glatten Muskelzellen mit Produktion von wachstumsfördernden Zytokinen, die zur Intimahyperplasie führen. Zusammengefaßt stellen in einem erweiterten Konzept der Rolle des Immunsystems sowohl die Transplantatvaskulopathie als auch die native Atherosklerose möglicherweise zwei verschiedene Facetten einer integrierten pathophysiologischen Antwort auf eine Endothelschädigung dar.
    Notes: Abstract Although transplant vasculopathy and native atherosclerosis are clinically and pathologically different entities, the pathogenesis of both diseases exhibits some common mechanisms. Both may be regarded as responses to injury within a broadened concept of the immune system. Alloantigens (e. g. on donor endothelial cells) or autoantigens (e. g. oxydized LDL cholesterol) are presented by antigen presenting cells to the T cells of the body's immune system. With the appropriate costimulatory signal, this signal pattern generates a differentiated T cell, B cell, and inflammatory cell response whereas without the second signal, the immune cells undergo apoptosis. In case of immune cell proliferation and differentiation, a coordinated pattern of cytokine release is initiated. Monocyte-derived macrophages are also involved in this process which culminates in rolling, sticking, and idapedesis through the coronary vascular endothelium and phenotype switch of medial smooth muscle cells mediated by generation off growth-promoting cytokines. Thus, viewed within a broadened paradigm of the immune system's role both disease entities may represent different vignettes of an integrated pathophysiological response to an endothelial injury.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...