#Low density lipoprotein trial
#Low density lipoprotein series

The trial follows studies that identified why some unique people simply don’t get high cholesterol. Now, with an injection, medical science may radically address the danger at a genetic level. The narrowing blocks blood flow to and from the heart and other organs. This buildup is called “plaque.” As your blood vessels build up plaque over time, the insides of the vessels narrow. When your body has too much LDL, cholesterol can build up on the walls of your blood vessels. High-density lipoprotein (HDL), or “good” cholesterol, absorbs cholesterol and carries it back to the liver. High levels of LDL raise your risk for heart disease and stroke. Low-density lipoprotein (LDL), or “bad” cholesterol, makes up most of your body’s cholesterol. Two types of lipoproteins carry cholesterol throughout the body: Dr Ralph Stuart, The Heart Group and Auckland City Hospital cardiologist, tells Jesse Mulligan it is an exciting development, potentially offering a life-long protection from high cholesterol.Ĭholesterol travels through the blood on proteins called lipoproteins. The trial is being hailed as revolutionary. The experiment, part of a clinical trial by the US biotechnology company Verve Therapeutics, involved injecting a version of the gene-editing tool CRISPR in order to modify a single letter of DNA in the patient’s liver cells. In New Zealand just a few weeks ago, a person was injected with new gene-editing material designed to modify the DNA which produces bad cholesterol – a world first in medicine. But there is new hope with recent medical advances. If you're > 60 mg/dL (1.55 mmol/L), then you may see stabilization or you may even see progression, but you're not likely to see regression.High cholesterol causes heart disease, the leading cause of premature death in New Zealand today.įor those battling with high cholesterol, many have been prescribed life-long, daily medication, which still doesn’t guarantee low-enough cholesterol levels to avoid the disease. You go much below that, and you see less plaque at the end of 18-24 months. It showed that the LDL-C level showing regression crosses zero at about 60 mg/dL (1.55 mmol/L). Steve Nicholls was the first author, and it was published in JAMA. We did do a meta-analysis of all of the trials. Our position has been that lower is better. Then, amazingly, with a powerful agent like evolocumab, we got down to an LDL-C of 36 mg/dL (0.93 mmol/L) and there was even more regression. That was the first of our studies to show unequivocal regression. The ASTEROID trial, which came around 2005, achieved an LDL-C of 60 mg/dL (1.55 mmol/L).

#Low density lipoprotein series

What then happened is a series of trials that marched us to a lower and lower level. We knew that at least over that range, lower LDL-C was better. There was neither regression nor progression with the high-dose atorvastatin, but there was clear cut, unequivocal progression with the LDL-C at 110 mg/dL (2.84 mmol/L) with pravastatin.

We achieved an LDL-C of 110 mg/dL (2.84 mmol/L) with a dose of 40 mg of pravastatin and 79 mg/dL (2.04 mmol/L) with 80 mg of atorvastatin. We felt differently, and so we designed the REVERSAL trial. That was based upon a post hoc analysis of the CARE trial. The argument had been made by a number of people, particularly in Boston, that lowering LDL-C below 125 mg/dL had no incremental benefit. When we started this work in the late 1990s, there was a raging debate.