Presented by: Euan Ashley, MD, PhD
Assistant Professor, Cardiovascular Medicine
Stanford University Medical Center
- Heart disease comes in many forms and variations; blood vessel plaque also has variations
- The body’s immune system appears to play a role in the buildup of arterial plaque
- No test yet exists to image the kind of vulnerable plaque buildup that might lead to a heart attack
- Most of the risk factors for heart disease can be modified with changes to diet, exercise, stress reduction and other lifestyle behaviors
Patient A is in his 40s, overweight and sedentary, and thinks a fast-food burger with the works is a good dinner. Determined to get back into shape, he challenges a junior executive to a game of racquetball. Halfway through, he clutches his chest and is rushed to the hospital with a heart attack.
Patient B is 75, retired, eats well and walks a lot. Heading up a hill, however, she needs to stop for the pain in her chest to abate.
Patient C is fit, eats well, has low blood pressure and exercises regularly. Warming up for his routine one morning, he is rushed to the hospital with a heart attack and a stent is inserted into his blocked artery.
While most people understand the circumstances of the first two patients, the third is the one most people-and physicians-find the most confusing. How can you be perfectly healthy one day and have a heart attack the next? What, if anything, can you do to avert the same fate?
While certain measures can be taken to reduce heart disease risk, medicine is still working to understand the many factors that lead to heart attack and cannot yet perfectly predict who is most susceptible, according to Euan Ashley, MD, PhD, an assistant professor of cardiovascular medicine and director of Stanford Hospital’s Hypertrophic Cardiomyopathy Center.
“Ten years ago, we would refer to the heart and blood vessels as plumbing, and we cardiologists thought of ourselves as plumbers,” said Ashley, who gave a presentation sponsored by the Stanford Health Library on assessing heart attack risk. “The idea was that there were two stages of heart disease: angina, where there is not enough blood circulating to the heart, and heart attack, which is a complete blockage. This turned out to be too simplistic, because, among other reasons, it doesn’t help us explain why seemingly perfectly healthy people die of sudden heart attack.”
Simple plumbing does not fit the evidence, he continued. Angina, the chest pain that occurs when an area of your heart muscle doesn’t get enough blood, does not necessarily lead to heart attack, and many people who have heart attacks do not show symptoms of angina.
“The logic didn’t add up, so we needed a new paradigm,” he said.
Inflammation in the Arteries
Cholesterol is one key factor. Since the fat we eat doesn’t dissolve in the blood, the body must find ways to package and store it using lipoproteins of different sizes. When high levels of cholesterol occur in the bloodstream, excess low-density lipoprotein (LDL, or “bad”) cholesterol seeps into the inner wall of the artery, triggering an inflammatory response. White blood cells are attracted from the bloodstream and smooth muscle cells from the vessel wall migrate and start to form a fibrous cap.
As long as the cap doesn’t rupture, it remains a flow problem: an area of the heart needs more blood than the artery can deliver and chest pain develops, a condition known as stable angina.
With unstable angina, a thin-capped “vulnerable plaque” gets disrupted and the contents of the plaque are exposed to blood. These contents are among the most powerful clot-producing substances known. Many people who have heart attacks do not have thick buildups of plaque caused by high cholesterol but instead have vulnerable plaque that sometimes does not even block the blood flow through the artery.
“Inflammation is key, and cholesterol is part of the trigger,” said Ashley. “The plaque builds up, the fibrous cap ruptures and a clot blocks the artery, causing a heart attack. It’s not so much the size that matters-it’s the stability of the plaque. Often it’s the smaller lesions that open up.”
While there is still no way to predict exactly who will have a heart attack, there are still many ways to reduce its risk. Certain factors, like age, gender and genetic makeup, can’t be changed, but most risk factors can be modified for improved cardiovascular health.
Ashley referred to a large-scale, international study that showed that the key factors involved in 90 percent of all heart attacks could be controlled, leading to an 84 percent decrease in cardiovascular risk for study participants. These controllable lifestyle factors include cholesterol, blood pressure, stress, smoking, diet, obesity, alcohol use and exercise.
Ashley also explained the various medications available that work in different ways to reduce heart attack risk. These therapeutics include statins, which lower cholesterol and stabilize the plaques; aspirin or other agents which inhibit the ability of platelet cells to cause clotting; and diuretics, ACE inhibitors and calcium channel blockers, which cause the muscles in the blood vessels to relax and control high blood pressure.
As far as diet goes, Ashley said to use common sense and keep everything-including alcohol-in moderation.
“Every day you hear about a different fad diet,” he said. “But a guinea pig has the right idea. Your diet should be low in saturated fat, have lots of whole grains, be high in fiber with lots of fruits and vegetables, and rich in omega-3 fatty acids. Of all the supplements out there, fish oil absolutely does have benefits.”
He also emphasized the importance of reducing stress, and cited a 1998 study that found that heart attack rates in France dropped drastically the day of the World Cup soccer match, illustrating the effect of societal stress on heart health.
As for exercise, Ashley listed more than 25 benefits of a regular regimen, from reduced risk of stroke to increased bone density.
“The heart is a glorious organ- a remarkable muscle that beats more than 3 billion times over a lifetime,” said Ashley. “Overall the message is positive: 90 percent of the risk for heart attack can be explained. I’m a huge fan of lifestyle change, and exercise and diet are clearly part of that.”
At the end of his presentation, Ashley introduced a patient who described his sudden and unexpected heart attack two years ago.
About the Speaker
Euan Ashley, MD, PhD, is an assistant professor of cardiovascular medicine and director of the Stanford Hypertrophic Cardiomyopathy Center, a multidisciplinary program that coordinates care for people with heart muscle disease. He has a particular interest in the care of athletes with cardiovascular disease and works closely with the Stanford Sports Medicine program. He also oversees a research laboratory that is looking at the molecular and genetic causes of heart failure and the fundamental biology of the heart’s signaling pathways. A graduate of the University of Glasgow, Ashley received his DPhil in molecular cardiology from the University of Oxford and his MRCP in medicine from the Royal College of Physicians. He joined the Stanford faculty in 2003.
For More Information:
Ashley’s Research Laboratory
Stanford Human Performance Lab
Hypertrophic Cardiomyopathy Association
American Heart Association