Known as non-obstructive coronary artery disease, this condition can trigger heart attacks down the road.
You just had a cardiac stress test and you passed with flying colors. Does that mean you are free of heart attack risk? Not necessarily, says Dr. Ron Blankstein, assistant professor of medicine at Harvard Medical School and preventive cardiologist at Brigham and Women’s Hospital.
“Stress tests are designed to pick up so-called obstructive lesions that block blood flow through the coronary artery. These are the lesions that typically cause a narrowing of at least 50% and are the ones that may cause chest discomfort during exercise or stress,” he explains. But when imaging techniques such as invasive coronary angiography or CT angiography are used to view the coronary artery vessel wall, areas of plaque that are too small to impede blood flow will show up in approximately 30% of people referred for testing who haven’t been diagnosed with heart disease. This finding is termed non-obstructive coronary artery disease, and until recently, it was not considered to be important to overall heart attack risk.
Danger from small plaques
“Traditionally, the emphasis has been on people with obstructive disease, or what we call stenosis, because these are the individuals who are deemed at higher risk for heart attack and are possible candidates for angioplasty and stenting,” says Dr. Blankstein. However, new research is pointing to a more subtle threat.
Heart attacks aren’t always the result of the progressive accumulation of fatty plaque that narrows the channel for blood flow. More frequently, inflammation stemming from damage to the inner lining of an artery accelerates the atherosclerotic plaque to a point where it suddenly ruptures. The resulting blood clot cuts off blood flow to part of the heart, causing a heart attack. Furthermore, the majority of ruptures originate from non-obstructive plaques that do not cross the 50% threshold, so the more of these small plaques you have, the greater your risk.
The new understanding of the risks involved in non-obstructive coronary artery disease is key to how people with the condition need to be counseled and treated, says Dr. Blankstein. “Once I identify someone who has plaque in multiple segments of the heart or multiple arteries, there are several important steps I take. I look at all the individual’s risk factors and how they can be reduced. Most often, this requires paying attention to both medications and lifestyle therapies, such as diet and exercise. Most of these people can benefit from statin therapy to reduce LDL cholesterol. Some, but not all, could also benefit from taking aspirin to reduce blood clotting risk.” Most importantly, individuals and their doctors need to understand that coronary artery disease exists on a spectrum, and a negative stress test may not signal a clean bill of health.
From healthy artery to heart attack
Stage 1 Excess LDL passes through the artery
Cholesterol travels in the bloodstream in particles called lipoproteins. About two-thirds of blood cholesterol is in the form of low-density lipoprotein (LDL), or “bad” cholesterol. Excess LDL leaves the blood and lodges in the artery walls.
Stage 2 Plaque builds up and the artery narrows
Any injury to the inner layer of cells lining the artery (caused by high blood pressure, smoking, or diabetes, for example) hastens the buildup of arterial deposits. White blood cells arrive on the scene and engulf LDL cholesterol. These cells then enlarge and transform into fat-laden foam cells.
Stage 3 A fibrous cap tops the plaque
As foam cells die, they release soft, fatty gruel that provokes further inflammation. Smooth muscle cells in the artery wall form a cap over the interior buildup and add to the bulk of the plaque. The bigger the plaque, the more blood flow is restricted.
Stage 4 The plaque ruptures
Large plaques tend to be covered by thick, fibrous caps that may resist breaking apart. Smaller plaques may be too small to block blood flow and usually do not show up during a cardiac stress test. However, they may have thin, underdeveloped caps that rupture easily. At least half of all heart attacks occur because of plaque rupture.
Stage 5 A clot blocks the artery
Once a plaque ruptures, platelets congregate at the site, starting the clotting process. The result is a thrombus—a clot of red blood cells, platelets, and other material—that completes the blockage and prevents blood from reaching the heart. Deprived of blood and oxygen, a portion of the heart muscle dies.