Abstract
Since the early 1990 s, both experimental and clinical data have clearly demonstrated
that inflammatory processes accompany atherosclerotic disease from its initiation
to the development of clinical complications. Numerous biomarkers involved at various
levels of the inflammation cascade have been shown to be associated with adverse cardiovascular
outcomes. Among them, the classical acute phase reactant C-reactive protein (CRP)
has been most intensively investigated. Recent research in this field has been driven
by the observation that despite low LDL-cholesterol levels, a remarkably high number
of patients are still at increased risk for recurrent cardiovascular events. This
is argued to be attributable to the presence of a prolonged inflammatory response
(reflected by a persistently elevated hsCRP), a concept, which is currently known
as “residual inflammatory risk”. The unequivocal proof that the inflammatory process
is not only a simple bystander but is also causally involved in atherogenesis, came
from the recent CANTOS trial, showing a 15 % reduction of primary MACE outcomes despite
aggressive statin therapy and lower LDL-cholesterol levels. Thus, an anti-inflammatory
treatment strategy might represent a promising tool to improve the outcome of this
still deadly disease.
Inflammatorische Vorgänge spielen eine entscheidende Rolle in allen Phasen des atherosklerotischen
Prozesses. Die vorliegende Übersicht beschäftigt sich mit dem Stellenwert einer subklinischen
Entzündung, diskutiert die klinische Relevanz der inflammatorischen Marker für die
Risikostratifizierung und belegt die potenzielle Bedeutung einer anti-inflammatorischen
Therapie für die Reduktion kardiovaskulärer Ereignisse bei Hochrisikopatienten.
Schlüsselwörter
Entzündung - Atherosklerose - C-reaktives Protein - residuales kardiovaskuläres Risiko
Key words
inflammation - atherosclerosis - C-reactive protein - residual cardiovascular risk
