| M. John Chapman National Institute
for Health and Medical Research (INSERM), France
 Atherothrombosis
results from direct interaction between the atherosclerotic plaque
and arterial thrombosis, and underlies most forms of cardiovascular
disease (CVD). The pathophysiology of atherosclerosis is now recognised
to involve endothelial dysfunction and dyslipidemia with cholesterol
accumulation, as well as critical immuno-inflammatory and apoptotic
dimensions. Erosion or rupture of a vulnerable, lipid-rich, inflammatory
atherosclerotic plaque triggers the formation of a platelet-rich
thrombus that may partially or completely occlude the artery,
with resultant clinical scenarios including stable and unstable
angina, acute myocardial infarction (MI) and ischaemic stroke.
Insight into the pathophysiology of atherothrombosis indicates
that an integrated risk factor approach, focusing particularly
on management of dyslipidaemia (with a statin) and thrombosis
(with aspirin), may constitute an optimal therapeutic approach.
Both agents have established roles in secondary prevention. Statin
action on atherogenic lipoproteins mediates plaque stabilisation,
modification of plaque morphology and attenuation of inflammation,
and may lead to plaque regression, while aspirin reduces platelet
activation and aggregation, decreases release of inflammatory
cytokines at sites of vascular injury and attenuates vasoconstriction.
Given these complementary modes of action, this combination would
be a logical choice for reducing atherothrombotic risk in patients
with CVD. Meta-analysis of 5 major clinical studies has demonstrated
that the combination of pravastatin plus aspirin was significantly
more effective than either agent alone in reducing the relative
risk of key cardiovascular endpoints including MI and ischaemic
stroke. This combination may therefore represent an important,
cost-efficient therapeutic approach to reduction of cardiovascular
risk and prevention of recurrent events in stable CVD.
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