Stroke is the third leading cause of death in the US. Fortunately, diagnostic imaging for stroke risk and stroke-prevention strategies have advanced greatly in recent years. It is now possible to reduce the artery-clogging plaque that leads to stroke, offering hope that this debilitating condition can be prevented.
If you have ever witnessed a stroke victim, you understand the humbling nature of this disease, which can reduce the mightiest human being to an immobile, helpless creature. Stroke can destroy or impair crucial functions such as speech, swallowing, walking, and bowel and bladder control. Even the perpetually youthful television personality Dick Clark was struck down by stroke at the age of 75, despite his outward appearance of perfect health. Clark’s stroke resulted in a six-week hospital stay and, judging from fragmentary reports, significant disability.
The disease process that underlies stroke requires decades—30 or 40 years—to develop. With that much lead time, why are we not better able to detect or stop this crippling disease? The truth is that we are able to predict many, if not most, strokes. Advances in imaging technology allow detection of the atherosclerotic plaque that causes stroke years before it becomes a threat. Similar progress has been made in deciphering the causes of stroke.
Unfortunately, most physicians still focus on diagnosing the crisis rather than averting it. With stroke as with heart disease, most physicians prefer to deal with catastrophe once it occurs and are only minimally interested in prevention. The medical community focuses on procedures such as carotid surgery or stents instead of preventive diagnostics and care. Even when a person is forewarned by a “mini-stroke,” or transient ischemic attack, little is done once it has been determined that surgery is not immediately necessary—even though this person has a high risk for future stroke. For someone recovering from a transient ischemic attack, the risk for recurrent stroke, heart attack, or death approaches 50% over 10 years.1
A more powerful approach to stroke prevention would use screening and diagnostic procedures to assess risk, and would implement nutritional strategies and lifestyle changes to reverse plaques. Surgical procedures such as carotid endarterectomy (to remove a buildup of plaque from the carotid artery) would be used only after exhausting preventive care options. The need for invasive procedures represents a failure of preventive medicine.
How Stroke Occurs
Stroke develops when some portion of the brain is deprived of blood and thus oxygen. This usually results when a tiny bit of debris dislodges from an atherosclerotic plaque within an artery wall and blocks a blood vessel to the brain. The same sort of plaque accumulates in coronary arteries to cause heart attack. The sources of debris have been a subject of controversy for decades, but new imaging technologies have settled the question: essentially, any blood vessel that leads from the heart to the brain can be a source of the debris that causes stroke. The two carotid arteries that lie on both sides of your neck are a frequent source, as these arteries are very prone to develop plaque.
In the last decade, medical researchers have recognized the aorta as another source of stroke. The aorta is the body’s main artery, with branches that emerge from the heart and lead to the head, arms, and legs. New imaging devices such as transesophageal echocardiography (ultrasound performed with a probe in the esophagus) allow imaging of the aorta, an eight-inch vessel that is a common site for plaque.2
Atherosclerotic plaque is a live tissue that, given a chance through poor diet, inactivity, high cholesterol, or excess weight, can grow and become progressively unstable. At some point, the plaque can fragment. Little bits and pieces break away, traveling to the brain. Fractured plaque also exposes its deeper structures to flowing blood, triggering blood-clot formation, which in turn can also fragment and travel to the brain. Atherosclerotic plaque is thus a prerequisite of risk for the most common causes of stroke.
If most strokes are caused by plaque, why not measure plaque to determine whether you are at risk for stroke? How can we easily, safely, and accurately quantify plaque in the areas that present stroke risk, such as the carotid arteries and aorta? And if plaque can be measured, can it be shrunk or inactivated to reduce or eliminate the risk of stroke? These compelling questions will form the basis of this article.
How Can Plaque Be Measured?
New imaging technologies are becoming more accurate and accessible. Just 20 years ago, the only practical way to identify plaque in the carotids or aorta was by angiography, which requires the insertion of catheters into the body to inject x-ray dye. Angiography was not practical as a broad screening measure and was not a good test of the health of the arterial wall.
Computed tomography (CT) scanning and magnetic resonance imaging (MRI) are emerging as exciting methods of imaging both the carotid arteries and the aorta. Unfortunately, most imaging centers and physicians are much more focused on the diagnostic use of these technologies for people who have already suffered a stroke or other catastrophe. The application of these devices for preventive uses is still evolving. One exception is when aortic calcification or aortic enlargement is incidentally noted on the increasingly popular CT heart scans; this is an important finding that can signal the presence of aortic plaque that increases stroke risk.
The one test that is widely available and can be performed in just about any center is carotid ultrasound. Simple, painless, and precise, this procedure is useful for assessing two indicators of stroke risk:
1. Plaque detection.
Atherosclerotic plaque that has potential for fragmentation and thus for stroke risk can be clearly visualized. If plaque blocks more than 70% of the diameter of the vessel, or if there are “soft” (unstable) elements in the plaque, then stroke risk may be high enough to justify surgery or stents. Even if there are plaques that are less severe, substantial risk for stroke may still exist, which can be reduced with preventive measures.3
2. Carotid intima-media thickness.
This is a measure of the carotid artery lining in areas that do not yet contain plaque but that often precede the development of more mature plaque. Carotid intima-media thickness also provides an index of body-wide potential for atherosclerotic plaque that can place you at risk for stroke. The aorta, for instance, cannot be imaged by surface ultrasound but can still be a source for stroke. Increased carotid intima-media thickness and carotid plaque are closely associated with the likelihood of aortic plaque. The Rotterdam Study of 4,000 participants demonstrated that if carotid intima-media thickness is greater than normal (1.0 mm), then you can be at risk for stroke (and heart attack), even if no plaques are detected.4
Carotid ultrasound is the one test you should consider that provides the most information with the least effort. Ultrasound is virtually harmless, painless, and can be obtained just about anywhere. Even if your doctor disagrees with your request for a carotid ultrasound, an increasing number of mobile services nationwide make this test available for around $100. One important caveat: many scanners and interpreters will report only whether plaque is present or not. While this is important information, you should request that your carotid intima-media thickness be measured as well. Not all centers can perform this simple measure, but it does not hurt to ask. Any amount of carotid plaque is cause for concern about stroke risk and reason to follow a preventive program, even if the plaque is insufficient to justify surgery.
Can Plaque Be Reduced?
Can we shrink plaque in the carotid arteries and aorta, thereby reducing or perhaps eliminating these sources of stroke?
Study after study has documented that plaque and stroke risk can be reduced. A 10–20% reduction in plaque size is possible within a year or two. The following important influences on carotid and aortic plaque growth need to be considered in any plaque-reduction program. (If you smoke, you need to concentrate on quitting, as the adverse influences of smoking will overwhelm any treatment you follow.)
• Hypertension. Considerable re-search documents the power of lowering elevated blood pressure in helping to prevent stroke.6 The most recently updated guideline for blood pressure, released by the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure, recommends a blood pressure no higher than 140/90, and defines normal as 120/80. The commission also emphasizes that the risks of stroke and heart attack begin to escalate at a blood pressure of 115/75.7
Just how low should your blood pressure be? The best evidence comes from the recent CAMELOT trial, conducted by the Cleveland Clinic’s Steven Nissen, MD. Nearly 2,000 participants with coronary artery disease with starting blood pressure in the normal range of 129/78 had blood pressure further reduced to 124/76 using the drugs amlodipine (Norvasc®) or lisinopril (Prinivil®). In just two years, this blood-pressure reduction produced a modest but significant reduction in future risk of heart attack and stroke.8 This bolsters the argument that the previously acceptable blood pressure of 140/90 may not protect you from stroke and that further reduction is needed.
• Diabetes, Metabolic Syndrome, and Hyperinsulinemia. Just being overweight substantially increases risk of future stroke. A Swedish study of 7,400 men with body mass indexes above 30 (considered “obese”) had double the risk of stroke compared to non-obese men.9 Increased body weight frequently leads to diabetes and its closely related conditions of metabolic syndrome and hyperinsulinemia (increased insulin levels), which play an overwhelmingly important role in increasing stroke risk in the US. Of people who suffer strokes, a shocking 70% will have one of these diagnoses. When diabetes is present, risk for stroke can be as much as sixfold greater.10
Metabolic syndrome and insulin resistance, which are predecessors of diabetes, are far more common than full-blown diabetes and can accompany even modest quantities of excess weight. Metabolic syndrome consists of excessive abdominal fat, high blood pressure, low HDL (high-density lipoprotein), high triglycerides, and resistance to insulin, which results in increased blood insulin levels. Metabolic syndrome is rampant in the US, afflicting as many as one in three adults as a result of sedentary lifestyles, processed foods, and other factors that lead to being overweight or obese.11 High insulin levels and resistance to insulin are powerful drivers of plaque accumulation, causing carotid plaque to grow at a faster rate.12,13 The rapidly escalating prevalence of metabolic syndrome and diabetes in the US population virtually guarantees a future epidemic of stroke.