LDL-C is a clinically validated risk factor for atherosclerotic cardiovascular disease (CVD). Atherosclerosis, fatty build up in the arteries supplying blood to the heart, brain and legs, leads to CVD which includes heart attacks, angina, heart failure, stroke and peripheral arterial disease (PAD). CVD is globally still the leading cause of morbidity and mortality and continues to grow due to aging populations, increasing obesity and diabetes. It is no longer just a disease found in westernized, affluent societies but is now a major concern, and the leading cause of death, in rapidly westernizing countries such as India and China. CVD is projected to result in more than 22 million deaths over the next 15 years.
Over the last 30 years, mostly since the introduction of statins, large reductions in all types of CVD events and death have been well established by numerous well-controlled trials. Studies have also shown that further LDL-C reductions in people already on statins and other LDL-C lowering drugs achieve even greater reductions in CVD events with a new class of therapies called PCSK9 inhibitors.
The data generated over the last 30 years strongly supports an accepted mathematical relationship for drugs like statins, ezetimibe and PCSK9 inhibitors which all lower LDL by increasing its removal from the blood stream: for every 40 mg/dL reduction in LDL-C there is a 22% decrease in CVD events in the next 2 to 3 year period. Furthermore, studies show that this reduction in risk increases the longer the LDL-C remains decreased.
Based on cardiovascular outcome trials (CVOTs), stringent LDL-C guidelines are now harmonized between the US, Europe and Asia. For the majority of ASCVD patients who fail to meet LDL-C goals on maximally tolerated statins (or for statin-intolerant patients), the PCSK9 class is recommended / accepted as adjunct therapy.
Proprotein convertase subtilisin/kexin 9 (PCSK9), which is synthesized primarily in the liver, enters the circulation, where it binds to hepatic low-density lipoprotein (LDL) receptors and targets them for degradation. This process reduces the capacity of the liver to bind and remove LDL cholesterol and results in increased LDL cholesterol levels.
Lerodalcibep binds specifically to PCSK9 in the blood stream and blocks it from attaching to the LDL receptors, increasing LDL receptor recycling, increasing LDL-C clearance, and lowering LDL-C.
The rich text element allows you to create and format headings, paragraphs, blockquotes, images, and video all in one place instead of having to add and format them individually. Just double-click and easily create content.
A rich text element can be used with static or dynamic content. For static content, just drop it into any page and begin editing. For dynamic content, add a rich text field to any collection and then connect a rich text element to that field in the settings panel. Voila!
Headings, paragraphs, blockquotes, figures, images, and figure captions can all be styled after a class is added to the rich text element using the "When inside of" nested selector system.