The human heart beats 100,000 times a day, propelling six
quarts of blood through 60,000 miles of vessels–20 times the distance across
the US from coast to coast. The blood flows briskly, surging out of a ten-ounce
heart so forcefully that large arteries, when severed can send a jet of blood
several feet into the air. Normally the relentless current helps keep blood
vessels clean. But when an artery bends, tiny eddies form, as in a bend in a
river. This is where bits of sticky, waxy cholesterol and fat can seep into the
artery wall and oxidize, like butter going rancid. Other matter piles up too.
Eventually, the whole mass calcifies into a kind of arterial stucco or plaque.
Until recently, Cardiologists approached heart disease as a
plumbing problem. Just as mineral deposits restrict the flow of water through a
pipe, an accretion of plaque impedes the flow of water through a pipe; an
accretion of plaque reduces the flow of blood through an arterial channel. The
more crud in the system, the greater the likelihood that a clogged artery will
trigger a heart attack. Doctors now dismiss this "clogged-pipes model" as an
idea whose time has passed. It’s just not that simple.
Most heart attacks are caused by plaque embedded within the
artery wall that ruptures, cracking the wall and triggering the formation of a
blood clot. The clot blocks the flow of blood to the heart muscle, which can
die from lack of oxygen and nutrients. Suddenly, the pump stops pumping.
Today, heart specialists agree that heart attacks generally
occur in arteries that have minimal or moderate blockage and their occurrence
depends more on the kind of plaque than on the quantity. Scientists have been
struggling to figure out what type is most responsible. Findings suggest,
softer plaques rich in cholesterol are more likely to rupture than the hard,
calcified, dense plaques that extensively narrow the artery channel. But
understanding the root cause of the disease will require much more research.
For one thing, human hearts–unlike plumbing fixtures–are not stamped from a
mold. Like the rest of our body parts, they are products of our genes.
Heart disease is not a one-or two-gene problem. Most
cardiac researchers suspect that dozens of genes contribute to a disposition:
some affect arterial integrity, others inflammation. Both can cause and
exacerbate arterial cracks. Additional genes affect the processing of lipids
that turn into plaque. Many Cardiologists believe any person’s heart attack risk
is “50 percent genetic and 50 percent cheeseburger.”
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