PCSK9 inhibitor therapy - The cure for atherosclerosis?
EAS Academy. Raal F. 03/24/17; 175476 Topic: Therapy
Disclosure(s): Professor Raal has received research grants, honoraria, or consulting fees for professional input and/or delivered lectures from AstraZeneca , Pfizer Pharmaceuticals, Merck, Sanofi, Regeneron and Amgen.
Prof. Frederick Raal
Prof. Frederick Raal

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To understand the role of PCSK9-inhibitor therapy in the treatment of hypercholesterolaemia
PCSK9 INHIBITOR THERAPY –THE CURE FOR ATHEROSCLEROSIS?

At one time atherosclerosis was thought to be an irreversible degenerative disease that was an inevitable consequence of ageing. Research in the past decade has shown that atherosclerosis is neither a degenerative disease nor inevitable. The long-term clinical benefits of reducing LDL-cholesterol, and its impact on decreasing coronary artery disease (CAD) morbidity and mortality, have been conclusively demonstrated. Major statin trials involving over 70 000 subjects have yielded reductions of about 30% in the rate of CAD death or non fatal myocardial infarction in both primary (WOSCOPS, AFCAPS-TexCAPS, HPS) as well as secondary (4S, CARE, LIPID) prevention, and in patients with mild to moderate as well as severe LDL-cholesterol elevation. However despite the use of high intensity statin therapy often in combination with other available lipid-lowering drugs such as ezetimibe, residual cardiovascular risk remains. In addition many patients with heterozygous familial hypercholesterolaemia (FH) and nearly all those with homozygous FH are unable to achieve acceptable LDL-cholesterol levels. The discovery of PCSK9 and its role in LDL metabolism has allowed for the rapid development of PCSK9 inhibitors. Monoclonal antibodies (mAbs) against PCSK9 have been shown to be remarkable effective in reducing LDL-cholesterol levels by an additional 50-60% in non-FH and heterozygous FH patients and by 30% in those homozygous FH patients with residual LDL receptor activity. For the first time PCSK9 mAbs have allowed a substantial proportion of FH patients to achieve LDL-cholesterol levels below 1.8 mmol/L (70 mg/dL). While long term safety and cardiovascular outcomes data are still pending, PCSK9 mAbs are the most promising therapeutic class of drugs since statins and are able to fill the unmet need of residual CAD risk. More aggressive lipid modifying treatment and lower LDL-cholesterol targets which can be achieved with PCSK9-inhibitor therapy will very likely reduce the cardiovascular event rate and prolong life even further.
PCSK9 INHIBITOR THERAPY –THE CURE FOR ATHEROSCLEROSIS?

At one time atherosclerosis was thought to be an irreversible degenerative disease that was an inevitable consequence of ageing. Research in the past decade has shown that atherosclerosis is neither a degenerative disease nor inevitable. The long-term clinical benefits of reducing LDL-cholesterol, and its impact on decreasing coronary artery disease (CAD) morbidity and mortality, have been conclusively demonstrated. Major statin trials involving over 70 000 subjects have yielded reductions of about 30% in the rate of CAD death or non fatal myocardial infarction in both primary (WOSCOPS, AFCAPS-TexCAPS, HPS) as well as secondary (4S, CARE, LIPID) prevention, and in patients with mild to moderate as well as severe LDL-cholesterol elevation. However despite the use of high intensity statin therapy often in combination with other available lipid-lowering drugs such as ezetimibe, residual cardiovascular risk remains. In addition many patients with heterozygous familial hypercholesterolaemia (FH) and nearly all those with homozygous FH are unable to achieve acceptable LDL-cholesterol levels. The discovery of PCSK9 and its role in LDL metabolism has allowed for the rapid development of PCSK9 inhibitors. Monoclonal antibodies (mAbs) against PCSK9 have been shown to be remarkable effective in reducing LDL-cholesterol levels by an additional 50-60% in non-FH and heterozygous FH patients and by 30% in those homozygous FH patients with residual LDL receptor activity. For the first time PCSK9 mAbs have allowed a substantial proportion of FH patients to achieve LDL-cholesterol levels below 1.8 mmol/L (70 mg/dL). While long term safety and cardiovascular outcomes data are still pending, PCSK9 mAbs are the most promising therapeutic class of drugs since statins and are able to fill the unmet need of residual CAD risk. More aggressive lipid modifying treatment and lower LDL-cholesterol targets which can be achieved with PCSK9-inhibitor therapy will very likely reduce the cardiovascular event rate and prolong life even further.
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