Experimental drugs that aim at other risk factors for heart disease and stroke might exert useful anti-inflammatory effects as well. Agents that raise levels of HDL or limit the action of angiotensin II come to mind. But treatment with antioxidant vitamins has proved disappointing.
No matter how good a drug is, it will be of no value if it sits unused on pharmacy shelves. Doctors need better ways of detecting dangerous atherosclerosis in the large fraction of people whose lipid levels look too good to justify treatment. Recent findings suggest that blood tests combining lipid testing with monitoring of a substance called C-reactive protein might improve detection.
Toward Early Detection
THE PRESENCE of C-reactive protein in the blood signifies that inflammation is occurring somewhere in the body; highly elevated levels, even in the presence of LDL values too low to prompt treatment under current guidelines, indicate an increased risk of heart attack or stroke. What is more, in at least one study, delivery of statins to people with below-average LDL concentrations but high C-reactive protein levels reduced the incidence of heart attack relative to the rate in a matched group of patients who received no treatment. Such results need to be confirmed in a much larger trial before doctors can confidently treat patients on the basis of the combined test, although some physicians already incorporate tests of Creactive protein in their practices.
Noninvasive methods for specifically identifying vulnerable plaques might also help pinpoint individuals who lack strong warning signs of risk for heart attack or stroke but who nonetheless are destined for disaster. Ideas include measuring the heat of blood vessels (because heat should accompany inflammation) and altering existing imaging technologies, such as MRI or CT scans, to improve their ability to visualize material inside vessel walls. Geneticists, meanwhile, hunt for gene variants that render some people more vulnerable to chronic inflammation and to atherosclerosis and its complications, so that individuals most prone to these disorders can seek more aggressive monitoring and treatment.
For most of human history, inflammation’s ability to ward off infection outweighed its drawbacks. Today, as we live longer, exercise less, eat too much and smoke, many of us suffer from inflammation’s dark side—including its ability to contribute to atherosclerosis and other chronic disorders. Scientists continue to pursue a deeper understanding of inflammation’s role in atherosclerosis and to decipher the devilishly intricate interactions that ignite and drive the inflammatory processes in the arteries. These insights should enable us to make further inroads against a disease of growing worldwide importance that causes extensive disability and takes far too many lives.