Calcium Channel Blocker Slows Hardening Of Arteries In Some Key Arteries, But Not Others

November 11, 1998

WINSTON-SALEM, N.C. -- A large clinical trial on whether a major calcium channel blocker could slow hardening of the arteries and thus reduce heart disease and stroke produced mixed results, a research team from the Wake Forest University School of Medicine and the University of Michigan reported today at the American Heart Association meeting.

The research team, headed by Curt D. Furberg, M.D., Ph.D. of Wake Forest and Bertram Pitt, M.D. of the University of Michigan, reported that amlodipine (Norvasc) had no significant effect in preventing new coronary artery atherosclerosis, hardening of the arteries, or on the progression of preexisting coronary artery atherosclerosis. However, it appeared to slow progression of atherosclerosis in the carotid arteries in the neck.

The coronary arteries supply blood to the heart, and a blocked coronary artery can lead to a heart attack. The carotid arteries provide blood to the brain, and a blocked carotid can lead to stroke.

There was no difference in the overall mortality, in rate of heart attack or stroke, or in major vascular "events" between patients on amlodipine and those on an inert placebo, which was consistent with a lack of effect on the coronary arteries, according to Robert P. Byington, Ph.D., associate professor of public health sciences and head of the section on epidemiology at Wake Forest, who headed the study's national data coordinating center.

But, Pitt, a professor of internal medicine, said, "Amlodipine significantly reduced the incidence of angina pectoris," severe chest pain that results from lack of oxygen to heart muscles.

Furberg, professor and chairman of public health sciences at Wake Forest and a national co-chairman of the study, noted, "This reduction in angina is a known symptomatic effect of amlodipine."

This reduction in symptoms led to fewer procedures to relieve angina, such as coronary artery bypass surgery. Because of that finding, amlodipine "may have an important role in the management of symptoms of patients with coronary artery lesions" by deferring the need for bypass surgery or angioplasty, he said.

The study, which was called PREVENT (prospective randomized evaluation of the vascular effects of Norvasc trial) involved 825 patients at 16 clinical centers in the United States and Canada who had coronary artery disease documented through heart catheterization. To be part of the trial, at least one coronary artery had to have less than 30 percent blockage. The patients were randomized to amlodipine or placebo, and followed for three years, with neither investigator nor patient knowing which pill they were taking.

One of the 16 centers was the Wake Forest University Baptist Medical Center, where David M. Herrington M.D. conducted the study.

At the end of the three years, the patients had a second heart catheterization.

The investigators had hoped to show that regular administration of amlodipine over three years would reduce the progress of atherosclerosis in segments of the coronary arteries with less than 30 percent blockage, as measured by heart catheterization (also known as angiography).

However, amlodipine appeared to slow the progression of carotid artery atherosclerosis, as measured by ultrasound. That study involved 376 of the 825 patients. These participants had an ultrasound exam at baseline and then every six months.

The differences between those who got amlodipine and those who got placebo, as measured by ultrasound, were highly significant in the common carotid artery, the major carotid artery.

Byington noted that the heart catheterization and the ultrasonography were really measuring different things. The heart catheterization measures the size of the inside of the artery, which doctors call the lumen, whereas the ultrasound measures thickening of the arterial wall, which may or may not be accompanied by compensating enlargement (dilation) of the artery.

"There was no difference, angiographically, between placebo and amlodipine, but there was a difference in ultrasound," Byington noted.

The investigators found the results somewhat surprising, since two other studies of calcium channel blockers, involving nifedipine and nicardipine, had suggested an effect. Nifedipine was reported to reduce the formation of new atherosclerosis lesions, while nicardipine reduced the progression of atherosclerosis in lesions that already had begun.

There were no major safety concerns linked to use of amlodipine. Ward A. Riley, Ph.D., professor of neurology at Wake Forest, was involved in the ultrasound analysis for the study.
-end-
Media Contact: Robert Conn, Jim Steele or Mark Wright at (336) 716-4587
-end-


Wake Forest Baptist Medical Center

Related Heart Attack Articles from Brightsurf:

Top Science Tip Sheet on heart failure, heart muscle cells, heart attack and atrial fibrillation results
Newly discovered pathway may have potential for treating heart failure - New research model helps predict heart muscle cells' impact on heart function after injury - New mass spectrometry approach generates libraries of glycans in human heart tissue - Understanding heart damage after heart attack and treatment may provide clues for prevention - Understanding atrial fibrillation's effects on heart cells may help find treatments - New research may lead to therapy for heart failure caused by ICI cancer medication

Molecular imaging identifies link between heart and kidney inflammation after heart attack
Whole body positron emission tomography (PET) has, for the first time, illustrated the existence of inter-organ communication between the heart and kidneys via the immune system following acute myocardial infarction.

Muscle protein abundant in the heart plays key role in blood clotting during heart attack
A prevalent heart protein known as cardiac myosin, which is released into the body when a person suffers a heart attack, can cause blood to thicken or clot--worsening damage to heart tissue, a new study shows.

New target identified for repairing the heart after heart attack
An immune cell is shown for the first time to be involved in creating the scar that repairs the heart after damage.

Heart cells respond to heart attack and increase the chance of survival
The heart of humans and mice does not completely recover after a heart attack.

A simple method to improve heart-attack repair using stem cell-derived heart muscle cells
The heart cannot regenerate muscle after a heart attack, and this can lead to lethal heart failure.

Mount Sinai discovers placental stem cells that can regenerate heart after heart attack
Study identifies new stem cell type that can significantly improve cardiac function.

Fixing a broken heart: Exploring new ways to heal damage after a heart attack
The days immediately following a heart attack are critical for survivors' longevity and long-term healing of tissue.

Heart patch could limit muscle damage in heart attack aftermath
Guided by computer simulations, an international team of researchers has developed an adhesive patch that can provide support for damaged heart tissue, potentially reducing the stretching of heart muscle that's common after a heart attack.

How the heart sends an SOS signal to bone marrow cells after a heart attack
Exosomes are key to the SOS signal that the heart muscle sends out after a heart attack.

Read More: Heart Attack News and Heart Attack Current Events
Brightsurf.com is a participant in the Amazon Services LLC Associates Program, an affiliate advertising program designed to provide a means for sites to earn advertising fees by advertising and linking to Amazon.com.