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102. Thrombembolien und pulmonale Hypertonie.

Author

Drömann, D.

Abstract

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Published
2009
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103. Obstruktive Lungenerkrankungen und pulmonale Hypertonie.

Author

Neumann, C., Volk, C., Wewel, A.R., and Braun, J.

Abstract

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Published
2009
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104. Interstitielle Lungenerkrankungen und pulmonale Hypertonie.

Author

Hauber, H.P.

Abstract

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Published
2009
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105. Diagnostik der pulmonalen Hypertonie.

Author

Leschke, M., Wädlich, A., Waldenmaier, S., and Faehling, M.

Abstract

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Published
2009
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106. Pathophysiologie des rechten Ventrikels bei Lungenerkrankungen.

Author

Steiner, S. and Strauer, B.E.

Abstract

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Published
2009
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107. Therapie der pulmonalarteriellen Hypertonie.

Author

Voswinckel, R., Reichenberger, F., Gall, H., Seeger, W., Grimminger, F., and Ghofrani, H.A.

Abstract

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Published
2009
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110. Lungenbeteiligung bei Sklerodermie.

Author

Prasse, A., Germann, M., and Müller-Quernheim, J.

Abstract

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Published
2008
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111. Pulmonale Hypertonie und Rechtsherzversagen auf der Intensivstation.

Author

Meyer, F.J., Katus, H.A., and Borst, M.M.

Abstract

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Published
2008
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112. Bewegungstherapie bei pulmonaler Hypertonie.

Author

Klein, H., Ehlken, N., Isele, A., Wenz, H., Herth, F.J.F., and Grünig, E.

Abstract

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Published
2008
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113. Rechtsherzinsuffizienz und Cor pulmonale.

Author

Leschke, M. and Wädlich, A.

Abstract

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Published
2007
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114. Chronische Lungenembolie – Radiologische Bildmorphologie und Differenzialdiagnose.

Author

Coppenrath, E., Herzog, P., Attenberger, U., and Reiser, M.

Abstract

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Published
2007
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115. Lungenerkrankungen und Herzfunktion.

Author

Rasche, K., Orth, M., Kutscha, A., and Duchna, H. W.

Abstract

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Published
2007
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116. Therapie der chronischen Thromboembolie (CTEPH).

Author

Wilkens, H.

Abstract

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Published
2007
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117. Pathophysiologie der Lungenembolie.

Author

Breuer, H.-W.

Abstract

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Published
2007
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118. Seltene Ursache einer diffusen alveolären Hämorrhagie bei einem 45-Jährigen.

Author

Schreiber, J., Häntze, S., Florschütz, A., Knolle, J., Kachel, R., August, C., and Schück, R.

Abstract

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Published
2006
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119. Vaskulopathien bei pulmonal-arterieller Hypertonie.

Author

Dorfmüller, P., Humbert, M., and Capron, F.

Abstract

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Published
2006
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120. Expression des Angiotensin converting enzyme (ACE) bei pulmonaler Hypertonie.

Author

Müller, A., Maas, M., Kozianka, U., and Franke, F.

Abstract

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Published
2006
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122. Pulmonale Hypertonie.

Author

Eickelberg, O. and Seeger, W.

Abstract

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Published
2005
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130. Pulmonale Hypertonie bei chronischen myeloproliferativen Erkrankungen.

Author

Einsfelder, B. and Müller, K.-M.

Abstract

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Published
2005
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131. Medikamentöse Therapie der pulmonalen Hypertonie.

Author

Olschewski, H., Ghofrani, A., Enke, B., Reichenberger, F., Voswinckel, R., Kreckel, A., Ghofrani, S., Wiedemann, R., Schulz, R., Grimminger, F., and Seeger, W.

Abstract

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Published
2005
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133. Langzeitbehandlung der pulmonalen Hypertonie bei Patienten mit COPD.

Author

Worth, H.

Abstract

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Published
2004
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134. Therapie der pulmonalen Hypertonie.

Author

Olschewski, H.

Abstract

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Published
2004
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135. Diagnostik der pulmonalen Hypertonie.

Author

Meyer, F., Ley, S., and Borst, M.

Abstract

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Published
2004
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136. Klassifikation der pulmonalen Hypertonie.

Author

Golpon, H., Hoeper, M., and Welte, T.

Abstract

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Published
2004
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137. Extrakardiale Ursachen der Rechtsherzinsuffizienz.

Author

Maisch, B. and Christ, M.

Abstract

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Published
2004
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138. Hämodynamische Wirkung der inhalativen Applikation von Stickstoff-Monoxyd und Iloprost bei Patienten mit geplanter Herztransplantation.

Author

Friedrich, Ivar, Hentschel, Thomas, Czeslick, Elke, and Sablotzki, Armin

Abstract

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Published
2003
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139. Pulmonale Plasmakatecholaminspiegel bei Patienten mit angeborenen Herzfehlern und erhöhtem pulmonalarteriellen Fluss.

Author

Knirsch, Walter, Eiselt, Michele, Nürnberg, Jan, Haas, Nikolaus A., Berger, Felix, Dähnert, Ingo, Uhlemann, Frank, and Lange, Peter E.

Abstract

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Published
2002
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140. The effect of amlodipine on exercise-induced pulmonary hypertension and right heart function in patients with chronic obstructive pulmonary disease.

Author

Franz, I.-W., van der Meyden, Jochen, Schaupp, S., and Tönnesmann, Ulrich

Abstract

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Published
2002
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141. Bedeutung von inhalativem Stickstoffmonoxid (iNO) für die Behandlung der pulmonalen Hypertonie Neugeborener.

Author

Wirbelauer, J. and Speer, C.

Abstract

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Published
2002
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142. Indikation zur Lungen- oder Herz-/Lungen-Transplantation bei pulmonaler Hypertonie.

Author

Behr, Jürgen

Abstract

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Published
2002
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143. Cor pulmonale: Interaktion mit pulmonaler Hypertonie, Schlafapnoe und Lungenerkrankungen.

Author

Richter, P. and Gottwik, M.

Abstract

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Published
2002
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144. Komplexe Pulmonalgefäßveränderungen bei aortopulmonalem Fenster im Erwachsenenalter.

Author

Müller, A. M., Schulz, F., and Müller, K.-M.

Abstract

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Published
2001
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145. Inhalatives Stickstoffmonoxid in der Therapie der schweren bronchopulmonalen Dysplasie.

Author

Bohnhorst, B., Poets, C., and Freihorst, J.

Abstract

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Published
2001
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146. Medikamentöse Therapie bei akuter und chronischer respiratorischer Insuffizienz.

Author

Welte, T.

Abstract

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Published
2001
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147. Rolle des four and-a-half LIM domain 1 (FHL-1) Proteins bei der Entstehung der Rechtsherzhypertrophie im Mausmodell des pulmonalarteriellen bandings

Author

Neghabian, Dariusch and Justus Liebig University Giessen

Subjects
ddc:610, Rechtsherzhypertrophie, pulmonale Hypertonie, pulmonary hypertension, right heart hypertrophy, PAB, pulmonary arterial banding, FHL-1, pulmonalarterielles banding
Abstract

Bei der pulmonalen Hypertonie ist die Kompensationsfähigkeit des rechten Ventrikels der lebenslimitierende Faktor. Daher ist dieser und die in ihm ablaufenden Anpassungsvorgänge bei erhöhter Druckbelastung Gegenstand intensiver Forschung. Insbesondere die Wahrnehmung der erhöhten Druckbelastung im rechten Ventrikel und die daraus resultierenden Umbauprozesse sind wichtige Aspekte, um die Pathophysiologie genauer zu verstehen und neue spezifische Therapieansätze zu entwickeln.Das zytoskelettale Signalprotein FHL-1 könnte eine wichtige Rolle in diesem Zusammenhang spielen. Untersuchungen am linken Ventrikel konnten nachweisen, dass FHL-1-Knockout-Mäuse eine abgeschwächte Reaktion auf eine chronische Druckbelastung zeigten und somit gegenüber einer Linksherzhypertrophie geschützt waren.Über die Rolle von FHL-1 im rechten Ventrikel ist bisher nur sehr wenig bekannt. Ziel der vorliegenden Arbeit war es daher zu untersuchen, ob ein FHL-1-Knockout auch im rechten Ventrikel einen protektiven Faktor bei chronischer Druckbelastung darstellt. Dazu wurde mittels pulmonalarteriellem banding (PAB) eine chronische Druckbelastung in den rechten Ventrikeln generiert und zu unterschiedlichen Zeitpunkten echokardiographische und hämodynamische Funktionsparameter sowie histologische und biomolekulare Veränderungen zwischen Wildtyp- und FHL-1-Knockout-Mäusen verglichen. In den Ergebnissen zeigten sich keine signifikanten Unterschiede zwischen den FHL-1-Knockout- und den Wildtyp-Mäusen. Das PAB führte zu einem erhöhten rechtsventrikulären Druck, einer vergrößerten rechtsventrikulären Wandstärke und einer Kammerdilatation sowie zu einer verschlechterten rechtsventrikulären Funktion. Auch in den histologischen Untersuchungen zeigte sich eine Rechtsherzhypertrophie infolge des PAB in Form von vergrößerten Kardiomyozyten. Des Weiteren fielen eine verstärkte Fibrosierung und eine erhöhte Kapillarenanzahl auf. Auf biomolekularer Ebene kam es zu einem Anstieg in der Expression von Hypertrophie- und Kollagen-Genen. Die Expression von Genen der Kalzium-Homöostase blieb durch das PAB unverändert. Insgesamt zeigte sich in keinem der erfassten Parameter einen Einfluss durch den FHL-1-Knockout. Somit wurde deutlich, dass sich die pathophysiologischen Signalwege im Rahmen einer chronischen Druckbelastung im linken und rechten Ventrikel unterscheiden., The ability of the right ventricle to compensate the pressure overload is the life-limiting factor in pulmonary hypertension. Therefore the right ventricle and its adaptation processes to pressure overload are subjects of intensive research. Especially the perception of elevated pressure and the following remodeling processes are important to understand the underlying pathophysiology and to develop new specific therapies.The cytoskeletal signalling protein FHL-1 could play an important role in these processes. Studies on the left ventricle revealed that FHL-1 knockout mice possessed an attenuated reaction to chronic pressure overload and seem to be protected against left heart hypertrophy.So far, the role of FHL-1 in right heart hypertrophy has not been addressed. The aim of the present study was to examine whether a FHL-1 knockout is also a protective factor in the right ventricle in case of chronic pressure overload. For this purpose a chronic right ventricle pressure overload was generated by pulmonary arterial banding (PAB). Echocardiographic and haemodynamic parameters as well as potential histological and biomolecular alterations were assessed at different time point post banding experiments and compared between FHL-1 knockout and wildtype mice. The results demonstrated no significant differences between the FHL-1 knockout and wildtype mice. PAB induced an increase in right ventricular pressure, increased right ventricular wall thickness and chamber dilation and impaired right ventricular function. Histological examinations revealed an increase in cardiomyocyte size and thus confirmed right heart hypertrophy following PAB. Furthermore an enhanced fibrosis and increased number of capillaries could be found. Biomolecular examinations showed an increase in the expression of hypertrophic and collagen genes. The expressions of genes of the calcium homeostasis were not changed after PAB. Finally, none of the parameters assessed was influenced by FHL-1 knockout. In conclusion, the present study shows that pathophysiological pathways activated following chronic pressure overload might differ in left and right heart.

Published
2019
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148. Analysis of atriums in patients with pulmonary hypertension

Author

Römmelt, Maximilian

Subjects
ddc:616, Pulmonale Hypertonie
Abstract

Die Diagnostik der pulmonalen Hypertonie bei älteren Patienten über 65 Jahre stellt auf Grund zahlreicher Begleiterkrankungen eine besondere Herausforderung dar. Wegen der Möglichkeit der spezifischen Therapie für Patienten mit PAH und CTEPH ist es von besonderer Bedeutung, diese Patienten von den Fällen der PH bei Linksherzerkrankung zu differenzieren. Eine entscheidende Bedeutung kommt hierbei der Echokardiographie als primärem diagnostischen Schritt zu. Die Daten der vorliegenden retrospektiven Analyse von Patienten der PH-Ambulanz der Missionsärztlichen Klinik in Würzburg zeigen, dass vergrößerte linke Vorhöfe bei Patienten mit PAH und CTEPH keine Seltenheit sind. Ebenso bestätigen unsere Ergebnisse, dass pulmonale Hypertonie in allen Untergruppen mit einem signifikant erhöhten Auftreten von Vorhofflimmern im Vergleich zur Normalbevölkerung vergesellschaftet ist. Diese Rhythmusstörung geht unabhängig von der Ätiologie der PH mit einer Vergrößerung sowohl des rechten, als auch des linken Vorhofs einher. Der Quotient aus rechts- und linksatrialen Flächenmaßen (RA/LA-Quotient) setzt die beiden Vorhöfe in Relation zueinander und erlaubt eine Differenzierung von Patienten mit und ohne PH. Außerdem ist der RA/LA-Quotient bei vaskulopathischer PH (PAH oder CTEPH) signifikant höher und signifikant häufiger > 1 als bei PH in Folge von Linksherzerkrankungen. Eine signifikante Unterscheidung von PAH und PH 2 gelang auf Grund mangelnder Fallzahlen knapp nicht. Darüberhinaus zeigt sich der RA/LA-Quotient vom Herzrhythmus unabhängig und behält im Gegensatz zur Einzelbetrachtung der Vorhöfe bei der Differenzierung der Gruppen seine Gültigkeit. Ein RA/LA-Quotient > 1 kann somit bei Unsicherheiten in der Zuordnung, die durch den Nachweis einer linksatrialen Vergrößerung entstehen, auf eine vaskulopathische PH hinweisen. Im Rahmen einer gezielten Diagnostik von Patienten mit pulmonaler Hypertonie sollten somit ein vergrößerter linker Vorhof und Vorhofflimmern nicht vorschnell zur Diagnose einer PH in Folge von Linksherzerkrankungen und dem Verzicht auf eine weitere Abklärung mittels Rechtsherzkatheter führen. Vielmehr sollte auch in diesen Fällen an eine präkapilläre PH gedacht werden und die Diagnostik konsequent weitergeführt werden. Der RA/LA-Quotient kann in diesem Zusammenhang ein hilfreiches diagnostisches Werkzeug darstellen. Weitere Analysen mit höheren Fallzahlen müssen nun diese Ergebnisse und insbesondere den RA/LA-Quotienten als möglichen Parameter zur Unterscheidung zwischen PAH und PH 2 bestätigen., Due to multiple co-diseases diagnostics of pulmonary hypertension (PH) in elderly patients requires special attention. Echocardiography is one of the main tools of the diagnostic algorithm. Data of this retrospective anlaysis of patients with PH show that left atrial enlargement is no a rare finding in PAH and CTEPH. Furthermore PAH/CTEPH is associated with a significant higher ratio of right and left atrial sizes (RA/LA-Ratio) than the control group and also than PH due to left heart diesease. Thus RA/LA-Ratio may help to identify patients with PH and to distinguish the individual subgroups, especially pre- from post-capillary PH. This is important because of the special treatment options available for patients with PAH and CTEPH in comparison to PH due to left heart disease. Further prospective studies with larger sample sizes are neccasary to confirm these results.

Published
2019

149. Vergleichende histologische und molekularbiologische Untersuchungen eines Hypoxie-bedingten vaskulären Remodelings in der Lunge und der Dura mater von Mäusen (Mus musculus)

Author

Mecheri, Badreddine (M. Sc.)

Subjects
ddc:570, 570 Biowissenschaften, Biologie, Biochemie, Lunge, Migräne, Blutgefäß, Remodeling, Pulmonale Hypertonie
Abstract

Unter hypoxischen Bedingungen entwickeln Mäuse Symptome einer pulmonalen Hypertonie (vaskuläres Remodeling (vR)). Zudem entwickeln sie eine erhöhte Sensitivität gegen den 5-HT2B/2C-Rezeptoragonisten meta-Chlorphenylpiperazin, der bei Migränikern Migräne-Attacken auslösen kann. Primär wurden histologische und molekularbiologische Untersuchungen von Hypoxie-induzierten Blutgefäßveränderungen in der Dura mater durchgeführt; Untersuchungen des vR in der Lunge wurden zu Vergleichszwecken durchgeführt (anatomische Positivkontrolle fürs vR). Die anatomischen und molekularbiologischen Ergebnisse zeigten, dass in der Dura mater kein vR im Sinne einer zunehmenden Muskularisierung stattfindet, das mit jenem in der Lunge vergleichbar wäre. Die Untersuchungen auf Protein-Ebene deuten auf andere Mechanismen für ein vR in der Dura mater hin. Hier kommt es anscheinend eher zu einer leichten Reduktion der Muskulatur, bei eventuell gleichzeitigen Veränderungen im Durchmesser arterieller Gefäßabschnitte.

Published
2019
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150. Role of the four and-a-half LIM domain 1 (FHL-1) protein in right heart hypertrophie in mice after pulmonary arterial banding

Author

Neghabian, Dariusch and Excellence Cluster Cardio-Pulmonary System (ECCPS) Gießen

Subjects
Rechtsherzhypertrophie, pulmonale Hypertonie, pulmonary hypertension, right heart hypertrophy, ddc:610, PAB, pulmonary arterial banding, Medical sciences Medicine, FHL-1, pulmonalarterielles banding
Abstract

Bei der pulmonalen Hypertonie ist die Kompensationsfähigkeit des rechten Ventrikels der lebenslimitierende Faktor. Daher ist dieser und die in ihm ablaufenden Anpassungsvorgänge bei erhöhter Druckbelastung Gegenstand intensiver Forschung. Insbesondere die Wahrnehmung der erhöhten Druckbelastung im rechten Ventrikel und die daraus resultierenden Umbauprozesse sind wichtige Aspekte, um die Pathophysiologie genauer zu verstehen und neue spezifische Therapieansätze zu entwickeln. Das zytoskelettale Signalprotein FHL-1 könnte eine wichtige Rolle in diesem Zusammenhang spielen. Untersuchungen am linken Ventrikel konnten nachweisen, dass FHL-1-Knockout-Mäuse eine abgeschwächte Reaktion auf eine chronische Druckbelastung zeigten und somit gegenüber einer Linksherzhypertrophie geschützt waren. Über die Rolle von FHL-1 im rechten Ventrikel ist bisher nur sehr wenig bekannt. Ziel der vorliegenden Arbeit war es daher zu untersuchen, ob ein FHL-1-Knockout auch im rechten Ventrikel einen protektiven Faktor bei chronischer Druckbelastung darstellt. Dazu wurde mittels pulmonalarteriellem banding (PAB) eine chronische Druckbelastung in den rechten Ventrikeln generiert und zu unterschiedlichen Zeitpunkten echokardiographische und hämodynamische Funktionsparameter sowie histologische und biomolekulare Veränderungen zwischen Wildtyp- und FHL-1-Knockout-Mäusen verglichen. In den Ergebnissen zeigten sich keine signifikanten Unterschiede zwischen den FHL-1-Knockout- und den Wildtyp-Mäusen. Das PAB führte zu einem erhöhten rechtsventrikulären Druck, einer vergrößerten rechtsventrikulären Wandstärke und einer Kammerdilatation sowie zu einer verschlechterten rechtsventrikulären Funktion. Auch in den histologischen Untersuchungen zeigte sich eine Rechtsherzhypertrophie infolge des PAB in Form von vergrößerten Kardiomyozyten. Des Weiteren fielen eine verstärkte Fibrosierung und eine erhöhte Kapillarenanzahl auf. Auf biomolekularer Ebene kam es zu einem Anstieg in der Expression von Hypertrophie- und Kollagen-Genen. Die Expression von Genen der Kalzium-Homöostase blieb durch das PAB unverändert. Insgesamt zeigte sich in keinem der erfassten Parameter einen Einfluss durch den FHL-1-Knockout. Somit wurde deutlich, dass sich die pathophysiologischen Signalwege im Rahmen einer chronischen Druckbelastung im linken und rechten Ventrikel unterscheiden. The ability of the right ventricle to compensate the pressure overload is the life-limiting factor in pulmonary hypertension. Therefore the right ventricle and its adaptation processes to pressure overload are subjects of intensive research. Especially the perception of elevated pressure and the following remodeling processes are important to understand the underlying pathophysiology and to develop new specific therapies. The cytoskeletal signalling protein FHL-1 could play an important role in these processes. Studies on the left ventricle revealed that FHL-1 knockout mice possessed an attenuated reaction to chronic pressure overload and seem to be protected against left heart hypertrophy. So far, the role of FHL-1 in right heart hypertrophy has not been addressed. The aim of the present study was to examine whether a FHL-1 knockout is also a protective factor in the right ventricle in case of chronic pressure overload. For this purpose a chronic right ventricle pressure overload was generated by pulmonary arterial banding (PAB). Echocardiographic and haemodynamic parameters as well as potential histological and biomolecular alterations were assessed at different time point post banding experiments and compared between FHL-1 knockout and wildtype mice. The results demonstrated no significant differences between the FHL-1 knockout and wildtype mice. PAB induced an increase in right ventricular pressure, increased right ventricular wall thickness and chamber dilation and impaired right ventricular function. Histological examinations revealed an increase in cardiomyocyte size and thus confirmed right heart hypertrophy following PAB. Furthermore an enhanced fibrosis and increased number of capillaries could be found. Biomolecular examinations showed an increase in the expression of hypertrophic and collagen genes. The expressions of genes of the calcium homeostasis were not changed after PAB. Finally, none of the parameters assessed was influenced by FHL-1 knockout. In conclusion, the present study shows that pathophysiological pathways activated following chronic pressure overload might differ in left and right heart.

Published
2019

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