Heart Disease Without the Symptoms
By Peter Libby, M.D.
25 june 2008--Tim Russert’s fatal heart attack revealed what many cardiologists already knew: Heart disease cannot always be detected. (Reuters)
The death of television commentator Tim Russert at age 58 has raised many questions about how cardiologists assess a patient’s condition, as Denise Grady reports in Science Times. Among other confusions, many are wondering how Mr. Russert could have passed a recent stress test, as well as other evaluations, and still have succumbed to sudden cardiac death.
Unfortunately, this is an all too common scenario. About half of men, and an even greater percentage of women, who die suddenly from coronary artery disease never have a warning symptom.
We used to think that heart attacks occurred due to the gradual and progressive formation of blockages that impede blood flow in the arteries coursing around the surface of the heart. According to this traditional view, the flow of oxygen and nutrients eventually becomes so scanty that the patient will experience chest pains, especially when the heart is stressed by exertion. Physicians also may be alerted to heart trouble by changes in electrocardiogram readings observed as a patient exercises, or by nuclear imaging scans used to visualize areas of poor blood flow.
More recently, however, we have come to understand that the disease plays tricks on us. As fatty plaques form in the wall of an artery, they usually first grow outward, toward the exterior of the vessel, and do not protrude inward where they might block blood flow. These plaques can develop for decades without causing symptoms or showing up on electrocardiograms or nuclear scans, even under maximal exercise effort during a stress test. The non-obstructive plaques may not even show up on conventional angiograms, during which a cardiologist injects a fluid opaque to x-rays directly into the heart’s arteries.
Two types of arterial plaques. The lesion shown at top, a stenotic plaque, usually will cause symptoms in the patient. The type below, a non-stenotic plaque, is more frequent and harder to detect. (Circulation. 2005;111:3481-3488. (c) 2005 American Heart Association, Inc. Used with permission.)
We now know that these outward-bowing plaques cause the lion’s share of fatal heart attacks, outnumbering the inward-growing plaques that produce the familiar warning signs. We probably will never know which sort of rupture caused Mr. Russert’s death, but heart specialists have learned that hidden plaques can prove particularly lethal.
Often an inward-growing plaque will stimulate the growth of extra arterial branches (collateral vessels) that allow the deprived muscle to receive blood redirected from less blocked arteries. But outward-growing plaques do not stimulate formation of these vessels, and so a sudden rupture, leading the formation of an occlusive blood clot, can prove particularly disastrous, as there is no back-up blood supply.
How can we assess the risk of a sudden unheralded heart attack, and how can we prevent them? Here’s an animation that describes the process in fuller detail. I’ll be posting more on this subject in the next couple of weeks. Meanwhile, please submit your questions below and I’ll do my best to offer a few answers on Tuesday.
By Peter Libby, M.D.
25 june 2008--Tim Russert’s fatal heart attack revealed what many cardiologists already knew: Heart disease cannot always be detected. (Reuters)
The death of television commentator Tim Russert at age 58 has raised many questions about how cardiologists assess a patient’s condition, as Denise Grady reports in Science Times. Among other confusions, many are wondering how Mr. Russert could have passed a recent stress test, as well as other evaluations, and still have succumbed to sudden cardiac death.
Unfortunately, this is an all too common scenario. About half of men, and an even greater percentage of women, who die suddenly from coronary artery disease never have a warning symptom.
We used to think that heart attacks occurred due to the gradual and progressive formation of blockages that impede blood flow in the arteries coursing around the surface of the heart. According to this traditional view, the flow of oxygen and nutrients eventually becomes so scanty that the patient will experience chest pains, especially when the heart is stressed by exertion. Physicians also may be alerted to heart trouble by changes in electrocardiogram readings observed as a patient exercises, or by nuclear imaging scans used to visualize areas of poor blood flow.
More recently, however, we have come to understand that the disease plays tricks on us. As fatty plaques form in the wall of an artery, they usually first grow outward, toward the exterior of the vessel, and do not protrude inward where they might block blood flow. These plaques can develop for decades without causing symptoms or showing up on electrocardiograms or nuclear scans, even under maximal exercise effort during a stress test. The non-obstructive plaques may not even show up on conventional angiograms, during which a cardiologist injects a fluid opaque to x-rays directly into the heart’s arteries.
Two types of arterial plaques. The lesion shown at top, a stenotic plaque, usually will cause symptoms in the patient. The type below, a non-stenotic plaque, is more frequent and harder to detect. (Circulation. 2005;111:3481-3488. (c) 2005 American Heart Association, Inc. Used with permission.)
We now know that these outward-bowing plaques cause the lion’s share of fatal heart attacks, outnumbering the inward-growing plaques that produce the familiar warning signs. We probably will never know which sort of rupture caused Mr. Russert’s death, but heart specialists have learned that hidden plaques can prove particularly lethal.
Often an inward-growing plaque will stimulate the growth of extra arterial branches (collateral vessels) that allow the deprived muscle to receive blood redirected from less blocked arteries. But outward-growing plaques do not stimulate formation of these vessels, and so a sudden rupture, leading the formation of an occlusive blood clot, can prove particularly disastrous, as there is no back-up blood supply.
How can we assess the risk of a sudden unheralded heart attack, and how can we prevent them? Here’s an animation that describes the process in fuller detail. I’ll be posting more on this subject in the next couple of weeks. Meanwhile, please submit your questions below and I’ll do my best to offer a few answers on Tuesday.
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