Because of her treatment, Gloria’s quality of life will likely improve. She’ll breathe easier and maybe live longer. But she is hardly cured. Her coronary atherosclerosis—a hardening and narrowing of the arteries that supply the heart with oxygen-rich blood—still leaves her vulnerable to future blockages and coronary heart disease.

Although hearts suffer many maladies—valves leak, membranes become inflamed—coronary heart disease, which can lead to heart attack and ultimately to heart failure, is the number one killer of both men and women in the United States, where 500,000 die annually. Worldwide, it kills 7.2 million people every year. Exacerbated by the export of Western lifestyle—motorized transport, abundant meat and cheese, workdays conducted from the comfort of a well-padded chair—incidence of the disease is soaring.

To help stem this lethal tide, cardiologists can prescribe such cholesterol-lowering drugs as statins to help keep arteries clear. They can advise patients to change their habits, or they can operate to fix an immediate problem. Angioplasty is one procedure, and surgery to bypass the diseased arteries is another—each year more than 400,000 bypasses are performed in the U.S. Transplants can replace severely damaged hearts, and artificial ones can keep people alive while they wait for a donor heart. But in the face of an impending global epidemic, none of these stopgap measures addresses the essential question: Who gets heart attacks and why?

The human heart beats 100,000 times a day, propelling six quarts of blood through 60,000 miles (97,000 kilometers) of vessels—20 times the distance across the U.S. from coast to coast. The blood flows briskly, surging out of a ten-ounce (0.3 kilograms) 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 where 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 blood through an arterial channel. The more crud in the system, the greater likelihood that a dammed 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.