ApoA-I
Please mouse over the interactive image to learn about the ApoA-I/HDL Particle.
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ApoA-I is the key cardioprotective protein in high-density lipoprotein (HDL or the “good cholesterol"). ApoA-I production is a highly differentiated approach in rasing HDL. In landmark clinical studies, the beneficial role of ApoA-I prouction has been well established by demonstrating both the reversal of arterial plaque and reduction of CVD risk. Thereby ApoA-I has secured the moniker, the cardioprotective protein.
Epidemiological and interventional studies validated the clinical relevance of a marker (ApoA-I) and also facilitate the rapid clinical and market adoption of a program. Furthermore, interventional studies demonstrated an effectual relationship between a marker and a disease.
Epidemiological evidence
The AMORIS study, with 175,000 patients, concluded that ApoA-I is the key predictive factor for myocardial infarcts and other CVD events including stroke1.
The INTERHEART study, a case-control comparison between 15,000 patients with a first myocardial infarction and their age and gender matched controls, concluded that the ApoA-I/ApoB ratio is the strongest modifiable risk factor for acute myocardial infarction.
Interventional evidence
Two studies where recombinant ApoA-I (rApoA-I) was administered intravenously to patients provided strong support to the concept that ApoA-I is responsible for plaque reduction. In a study led by Dr. Eriksson, a single infusion of rpro-ApoA-I increased neutral sterol excretion by 33% – that is the elimination of 5-7% of cholesterol from the body3. In a similar study utilizing ApoA-IMilano, the removal of 4.2% of coronary atherosclerosis was observed in patients with acute coronary syndromes4. These two monumental studies confirmed the relationship between increasing ApoA-I and the regression of atherosclerotic plaque.
1. Walldius, G. et al; 2001; Lancet; 358(9298):2026-33.
2.Yusuf, S. et al; 2004; Lancet; 364(9438):937-52.
3.Eriksson, M. et al; 1999; Circulation; 100; 594-598.
4.Nissen, S.E. et al; 2003 Nov. 5; JAMA; 290(17):2292-300.
