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Arterielle Gefäßsteifigkeit – Ursachen und Konsequenzen

Empfehlungen der Deutschen Hochdruckliga e. V. DHL® – Deutsche Gesellschaft für Hypertonie und Prävention

Arterial stiffness – Causes and consequences

Recommendations of the German Hypertension League (DHL®) – German Society of Hypertension and Prevention

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Der Kardiologe Aims and scope

Zusammenfassung

Die Messung der aortalen Pulswellengeschwindigkeit (aPWV) ist ein direktes Maß für die arterielle Steifigkeit der Aorta und beträgt bei normotensiven Gesunden altersabhängig 4–9 m/s. Die aPWV besitzt über klassische kardiovaskuläre Risikofaktoren hinaus eine additive prädiktive Wertigkeit für kardiovaskuläre Ereignisse. Eine Erhöhung der aPWV um 1 m/s ist mit einer Steigerung des kardiovaskulären Risikos bis zu 15 % verbunden. Die Unterscheidung zwischen kalzifizierender Arteriosklerose und nicht kalzifizierender Atherosklerose ist klinisch wichtig. Aus dem Befund einer erhöhten Gefäßsteifigkeit kann nicht direkt auf das Vorliegen einer Atherosklerose, wie z. B. koronare Herzerkrankung, geschlossen werden. Als Goldstandard für die Messung der aortalen Steifigkeit wird die Pulswellengeschwindigkeit zwischen Karotis und Femoralarterie angesehen. Bis weitere Studiendaten vorliegen, sollte bei Normotonie eine aPWV über 10 m/s als pathologisch betrachtet werden. Viele der bereits auf dem Markt angebotenen Geräte zur Messung der Gefäßsteifigkeit zeigen eine noch unzureichende Standardisierung bezüglich Messmethode und Messgenauigkeit. Es sollte eine herstellerunabhängige, standardisierte Validierung gegen invasiven oder nichtinvasiven Goldstandard vorliegen sowie eine in epidemiologischen und prognostischen Studien belegte additive prädiktive Wertigkeit. Das wichtigste Therapieziel bei der Behandlung der arteriellen Gefäßsteifigkeit ist eine Normalisierung der Blutdruckwerte gemäß aktueller ESH (European Society of Hypertension)-Leitlinien. Aufgrund längerfristiger Einflüsse auf das vaskuläre Remodeling sind nach heutigem Stand vermutlich Blocker des Renin-Angiotensin-Aldosteron-Systems am ehesten geeignet, eine über reine Blutdruckeffekte hinausgehende Wirkung auf die Gefäßsteifigkeit zu erzielen. Inwieweit eine antihypertensive Therapie mit dem Zielparameter „Gefäßsteifigkeit“ sich darüber hinaus positiv auf harte kardiovaskuläre Endpunkte auswirkt, ist Gegenstand zurzeit laufender Studien.

Abstract

Measurement of the aortic pulse wave velocity (aPWV) is a direct measure for the arterial stiffness of the aorta and is 4–9 m/s in normotensive healthy individuals, depending on age. In comparison to classical cardiovascular parameters, the aPWV has an additive predictive value for cardiovascular events. An increase in the aPWV of 1 m/s is associated with an increase in cardiovascular risk of up to 15 %. The differentiation between calcified arteriosclerosis and non-calcified atherosclerosis is clinically important. The presence of atherosclerosis, such as coronary heart disease, cannot be directly deduced from a finding of increased vascular stiffness. The gold standard for measurement of aortic stiffness is considered to be the PWV between the carotid and femoral arteries. Until the results of further studies are available, an aPWV above 10 m/s should be considered as pathological in normotensive individuals. Many of the instruments available on the market for measurement of vascular stiffness still show an insufficient standardization with respect to the measurement method and measurement accuracy. A standardized validation against invasive or non-invasive gold standards should be available, independent of the manufacturer and an additive predictive value confirmed by epidemiological and prognostic studies. The most important therapeutic aim of the treatment of arterial vascular stiffness is a normalization of blood pressure values according to the current European Society of Hypertension (ESH) guidelines. Based on long-term influences on vascular remodeling, according to the current state of the art blockers of the renin-angiotensin-aldosterone system are assumed to be more suitable to achieve extended effects on vascular stiffness other than pure blood pressure effects. Whether antihypertensive therapy with the target parameter of vascular stiffness also has a positive influence on concrete cardiovascular endpoints, is the subject of currently running studies.

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Author information

Authors and Affiliations

  1. Excellence Centre European Society of Hypertension, Kerckhoff-Klinik, Ludwigstraße 41, 61231, Bad Nauheim, Deutschland

    T. Mengden

  2. Med. Klinik I, Allgemeine, Innere Medizin, Nephrologie, Rheumatologie, Pneumologie, Städtisches Klinikum Karlsruhe, Karlsruhe, Deutschland

    M. Hausberg

  3. Sektion Angiologie, Klinik für Kardiologie, Pneumologie und Angiologie, Univ.-Klinikum Düsseldorf, Düsseldorf, Deutschland

    C. Heiss

  4. Med. Klinik I, Allg. Innere Medizin/Nephrologie, Marienhospital Herne, Univ.-Klinikum der Ruhr‑Universität Bochum, Herne, Deutschland

    A. Mitchell

  5. European Prevention Center – EPC Düsseldorf und Kardiologische Privatpraxis, Medical Center Düsseldorf („Grand Arc“), Düsseldorf, Deutschland

    U. Nixdorff

  6. Nephrologie und Hypertensiologie, Univ.-Klinikum Erlangen, Erlangen, Deutschland

    C. Ott

  7. Bereich Sport- und Bewegungsmedizin, Institut für Sport- und Sportwissenschaft, Universität Basel, Basel, Schweiz

    A. Schmidt-Trucksäss

  8. Health & Environment Department, Biomedical Systems, AIT Austrian Institute of Technology GmbH, Wien, Österreich

    S. Wassertheurer

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  1. T. Mengden
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Correspondence to T. Mengden.

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Interessenkonflikt

T. Mengden, M. Hausberg, C. Heiss, A. Mitchell, C. Ott und A. Schmidt-Trucksäss geben an, dass kein Interessenkonflikt besteht. S. Wassertheurer ist Erfinder eines Patentes, welches teilweise in den AIT ARCSolver Algorithmen verwendet wird. U. Nixdorff: honorierte Vortragsaktivitäten bei den Firmen Hitachi/Aloka; Itamar, Sanofi und Diadexus.

Dieser Beitrag beinhaltet keine Studien an Menschen oder Tieren.

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Mengden, T., Hausberg, M., Heiss, C. et al. Arterielle Gefäßsteifigkeit – Ursachen und Konsequenzen. Kardiologe 10, 38–46 (2016). https://doi.org/10.1007/s12181-015-0041-5

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