Hamostaseologie 2006; 26(02): 99-103
DOI: 10.1055/s-0037-1616892
Original article
Schattauer GmbH

Pathogenetische Mechanismen des akuten Koronarsyndroms

Pathophysiology of acute coronary syndrome
H. Hölschermann
1   Innere Medizin I – Kardiologie / Angiologie, Hochtaunus-Kliniken, Krankenhaus Bad Homburg
,
H. Tillmanns
2   Medizinische Klinik I, Abteilung Kardiologie und Angiologie, Zentrum für Innere Medizin, Universitätsklinikum Gießen und Marburg, Standort Gießen
,
C. Bode
3   Abteilung für Innere Medizin III, Kardiologie und Angiologie, Medizinische Universitätsklinik Freiburg im Breisgau
› Author Affiliations
Further Information

Publication History

Publication Date:
27 December 2017 (online)

Zusammenfassung

Unter dem Begriff akutes Koronarsyndrom werden die Akutmanifestationen der koronaren Herzkrankheit, d. h. die instabile Angina pectoris (iAP), der Nicht-ST-Hebungs- Myokardinfarkt (non-ST-elevation myocardial infarction, NSTEMI) und der ST-Hebungs-Myokardinfarkt (ST-elevation myocardial infarction, STEMI) zusammengefasst. Die Übergänge zwischen den Syndromen sind fließend. Die Differenzialdiagnose des akuten Koronarsyndroms beruht auf Anamnese, Schmerzsymptomatik, 12-Kanal-EKG-Befund und laborchemischem Nachweis myokardialer Nekrosemarker (CK, CK-MB, Troponin).

In aller Regel liegt allen drei klinischen Erscheinungsformen des akuten Koronarsydnroms ein gemeinsames pathophysiologisches Substrat zugrunde: Die Erosion bzw. Ruptur einer atherosklerotischen Plaque, die zur Thromboyztenadhäsion und -aggregation mit Thrombusbildung in der Koronararterie führt. Diese Arbeit gibt eine Übersicht über Faktoren, die zur Plaqueruptur mit anschließender Thrombosierung beitragen.

Summary

This article reviews the current understanding of the pathophysiology of acute coronary syndrome and how these concepts have altered our clinical approach to the acute phase of coronary heart disease. Thrombosis due to erosion or, in most cases, rupture of a vulnerable atherosclerotic plaque underlies most acute coronary syndromes. The protective fibrous cap undergoes degradative processes controlled by inflammatory mediators that break down the interstitial collagen within the fibrous cap. Thrombus formation depends on factors in the solid-phase of the ruptured plaque as well as on fluid-phase determinants in blood. Depending on the degree of thrombus formation the subsequent obstruction of the coronary artery is followed clinically by unstable angina, non-ST- and ST-segment elevation myocardial infarction.

 
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