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The last supper?

Okay, so you splurged on a fatty meal. Maybe it was a special occasion, maybe it was your favorite food, maybe it was just too good to stop.

So what? You can always make up for it by eating rice and beans tomorrow. Or can you?

New research suggests that if your arteries are partially clogged with plaques--and if one of those plaques happens to rupture several hours later, that fatty meal could be your last.

"Hours after a fat-rich meal, an individual is at a higher risk of a fatal heart attack than at other times," says researcher George Miller of the Medical College of St. Bartholomew's Hospital in London.

Grease-filled food raises blood levels of a protein called factor VII, he explains. The higher your factor VII, the more massive a clot you'll form to stop the bleeding from a ruptured plaque...and the slimmer your chances of surviving.

Even Miller calls his evidence preliminary. But one thing is clear: Blood clots are enormously more important than researchers used to think.

"The actual heart attack is caused by a blood clot more than 95 percent of the time," explains Scott Goodnight, a cardiovascular disease expert at the Oregon Health Sciences Center in Portland.

The question is: How do you stop a clot?


"In the last two or three years, we've seen a substantial shift in our thinking about coronary heart disease," says Basil Rifkind of the National Heart, Lung and Blood Institute (NHLBI) in Bethesda, Maryland.

Researchers now have a clearer grasp of what leads to heart attacks. It's not just atherosclerosis--the clogging of arteries by "plaques" (deposits of fats, calcium, blood-clotting material, and cellular debris). The tendency for blood to clot--a process called thrombosis--is also critical.

Contrary to what scientists used to think, it's rare for a plaque, or lesion, to grow so large that it completely cuts off the flow of blood to the heart.

"The dangerous lesions aren't so much the large, advanced ones," says Rifkind, "but smaller, unstable lesions covered by a small fibrous cap."

When that cap ruptures, the plaque bleeds, the bleeding triggers a clot...and that means trouble.

Let's say the blood vessel were already half-narrowed by plaque. One good-sized clot could be enough to block it off entirely.

"If the plaque ruptures into the bloodstream and not the artery wall," says Rifkind, "the clot can provoke a heart attack or sudden death."


Over the last thirty years, researchers have identified "risk factors" that distinguish people who are more or less likely to get heart attacks.

But the well-established risk factors--like high blood cholesterol, smoking, and high blood pressure--predict only about a third of all heart attacks, notes Paul Ridker, a cardiologist at Harvard Medical School.

"Despite the tremendous advances of widespread cholesterol screening, we're left with the problem that most heart attacks occur in low-risk patients," he points out. "We need to look for the markers of risk that are more directly related to clot formation and dissolving."

Among the "markers" under scrutiny are:

* Fibrinogen. The protein that gets converted to fibrin--the elastic filaments that form the lattice of a clot (see photo, p. 7).

* Activated factor VII. One of the dozen or so "factors" that convert fibrinogen to fibrin.

* Platelets. The circulating plate-shaped disks that fit into the lattice of fibrin to form a clot.

People with high levels of fibrinogen and activated factor VII have a higher risk of heart attacks.[1,2] Scientists are trying to figure out what alters those levels.

"Smoking is far and away the biggest offender," says Ridker. "It greatly increases fibrinogen. And if you stop smoking, fibrinogen levels will head back down."

Anything that slows platelets from sticking together also tips the balance towards less clotting. "That's why aspirin is so effective in preventing heart attacks," says Oregon's Scott Goodnight.

Alcohol also seems to prevent clots by making platelets less "sticky" and by boosting the body's clot-dissolving agents. But alcohol causes society too much pain and suffering for physicians to recommend that non-drinkers take up drinking.

Instead, says Ridker, "we have to find out what in alcohol does this and figure out a way to deliver it in drug form."

Smoking, aspirin, and alcohol aside, researchers are far less certain about how to curb clots.


"One factor that determines the propensity to form clots is the amount of fat circulating in the blood at the time," says British researcher George Miller.

That's because fat raises factor VII activity within a couple of hours after a meal, he says. If you're unlucky enough to rupture a plaque at that time, the factor VII recognizes damage on the artery wall and triggers a clot.

"The higher the factor VII, the more likely the clot is a serious one," contends Miller, who adds that factor VII determines "not whether you're going to develop a heart attack, but how severe it will be."

But so far, the evidence for fat's role as a clot-promoter is still sketchy.

For one thing, most studies haven't been carefully designed. One of the better ones was conducted by Peter Marckmann of the Royal Veterinary and Agricultural University in Frederiksberg, Denmark.[3]

"If you eat a high-fat meal, it seems to activate the coagulation system," says Marckmann.

He found that men who ate diets that got a hefty 50 percent of calories from fat had higher factor VII levels than men who ate 20 percent of calories from fat. The greatest difference was at 9:30 p.m. (dinner was served at 6 p.m.). But he only studied six men for two days on each diet.

A more recent study, by Miller's team, measured factor VII in five men who ate special diets for four weeks. Miller also found more factor VII activity on a high-fat diet, especially one rich in saturated fat. But that diet got 62 percent of its calories from fat.[4]

What's more, so far all of the studies have examined only activated factor VII levels in blood samples. That's just one clue as to what's happening in the body, where a slew of clotting factors interact.

"These studies measure some change in blood," says Scott Goodnight. "But that doesn't tell you if you're going to have an increased rate of thrombosis."

Miller agrees. "To show that the rate of heart attack is raised after a fat-rich meal would be very nice."


Scientists are pursuing other links between diet and blood clots. For example, dozens of studies suggest that fish oils may help prevent clots (see "A Fish Tale," p. 8).

Meanwhile, experts are pleased that their advice for avoiding plaque caused by atherosclerosis should also help people avoid blood clots: Don't smoke, avoid obesity, and eat less fat.

One key difference: Stearic acid, a saturated fat that doesn't cause plaque, may still promote clots (see "A Bum Stear," p. 5).

Of course, clots don't happen if you have no plaques to rupture in the first place. Says Miller: "If your blood vessels are perfectly pristine and healthy, you'll never get into trouble."

[1] Arteriosclerosis and Thrombosis 14: 54, 1994.

[2] Lancet 2: 533, 1986.

[3] Atherosclerosis 101: 225, 1993.

[4] Arteriosclerosis and Thrombosis 14: 214, 1994.
COPYRIGHT 1994 Center for Science in the Public Interest
No portion of this article can be reproduced without the express written permission from the copyright holder.
Copyright 1994, Gale Group. All rights reserved. Gale Group is a Thomson Corporation Company.

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Title Annotation:includes related information; high-fat meal can increase risk of heart attack
Author:Liebman, Bonnie
Publication:Nutrition Action Healthletter
Date:May 1, 1994
Previous Article:A bum stear.
Next Article:A fish tale.

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