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 Due to limitations in existing studies and ongoing experiments
involving these and other drugs, researchers not involved with the
analysis caution that it’s too early to give up on medications that
increase high-density lipoprotein (HDL) cholesterol, however.
“In the time before statins were available, there were several
pieces of evidence that HDL-raising drugs reduce cardiovascular
events, but since the time statins have been used there is now
evidence that HDL-targeted therapies don’t do anything to decrease
mortality,” said Dr. Darrel Francis, the study’s senior author from
Imperial College London.
Unlike low-density lipoprotein (LDL), which is the so-called “bad”
cholesterol that piles up in blood vessels, HDL is considered good
because it’s thought to chip away LDL cholesterol.
People with low HDL levels and high LDL levels are known to be at an
increased risk of death, the researchers write in the journal The
BMJ.
Drugs known as statins - such as Pfizer’s Lipitor - that lower LDL
have been found to be effective at reducing deaths. Attention has
turned to the development of drugs that increase levels of HDL to
achieve added benefits.
Francis and his colleagues examined the results of 39 randomized
controlled trials - the gold standard in medical research - that
evaluated the use of three drugs known as niacin, fibrates and
cholesterylester transfer protein (CETP) inhibitors.
While the drugs differ in how they work, all three increase the
amount of HDL cholesterol in the body.
Overall, the drugs did not reduce the number of deaths from any
cause or deaths from heart disease before or after statins became
common.
Before statins, fibrates reduced heart attacks and niacin reduced
heart attacks and strokes. After statins, the benefit from the two
HDL-increasing drugs disappeared.
The researchers write that the simple idea that a drug that raises
HDL levels should also decrease the number of heart attacks and
strokes may not be correct.
“Even if HDL is carrying cholesterol away from the coronary
arteries, that doesn't mean that any therapy that raises HDL is
automatically protective,” Francis said. “After all, the therapy
could just be blocking cholesterol traveling on HDL from exiting.”
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But a closer look should be given to specific groups of patients
before researchers abandon work on drugs targeting HDL cholesterol
levels, cautioned Dr. Leonard Kritharides in an editorial
accompanying the new study.
Kritharides, the head of cardiology at Concord Repatriation General
Hospital in Sydney, Australia, said other research has suggested
there may be a benefit among people with low HDL cholesterol and
high triglycerides, which is another type of fat in blood.
“The possibility of important benefits for some patients should not
be dismissed too lightly,” he wrote.
Dr. Steven Nissen, the chair of cardiovascular medicine at the
Cleveland Clinic in Ohio, also said the studies included in the
analysis had limitations and there are more studies on HDL-increasing
drugs underway.
“I think the science here hasn’t been fully worked out and the only
way to answer it is with randomized controlled trials and that’s
what a number of people are doing,” said Nissen, who wasn’t involved
with the new study. He is the head of a trial for a CETP inhibitor
from Eli Lilly.
“If every study underway fails, we’ll have to give up on HDL at some
point,” he said, adding that researchers aren’t there yet.
“What we don’t need here is to prejudge ongoing research,” Nissen
said.
SOURCE: http://bit.ly/1o0aGXw
and http://bit.ly/1zcpif4 The
BMJ, July 18, 2014.
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