Cardiovascular prevention screening beyond risk markers and contributors

The traditional approach to reduction of risk for cardiovascular disease events has been to screen the healthy population for “risk factors” and intervene with nonpharmacologic or pharmacologic approaches in those whose measurements are above a level defined as “normal”, the so-called primary prevention It also meant for aggressive intervention in those individuals, who have suffered from a cardiovascular event with therapy aimed at secondary prevention.

The Framingham Heart Study, initiated over 50 years ago, introduced the concept of risk factors for coronary heart disease (CHD) and has served as the standard for risk assessment over the years. Major risk factors identified by the Framingham Heart Study, including age, sex, total cholesterol, high-density lipoprotein (HDL) cholesterol, smoking, and systolic blood pressure, have been incorporated into a scoring system that identifies subjects at high (>20%), intermediate (10%–20%), and low (<10%) risk for developing CHD over the next 10 years. (1,2)

Risk factor modification in asymptomatic individuals is aimed at slowing the progression of atherosclerotic disease that is at the root of most cardiovascular morbid events. These risk markers, such as elevated levels of blood pressure, cholesterol, blood sugar, homocysteine and c-reactive protein, are statistically related to the risk of an event, but they may be viewed as risk contributors, not as direct markers for the atherosclerotic disease. Many individuals who harbor these markers are free of disease and many individuals with atherosclerotic disease manifest none of the risk markers.

Studies have demonstrated that plaque rupture, in many cases, occurs from plaques that are not severe enough to limit blood flow or cause symptoms or abnormal functional test. The atherosclerotic process is thus present and actively progressing many years before symptoms, acute cardiac events, and exercise or stress-inducible ischemia. It is also apparent that measurements of the presence and activity of the preclinical atherosclerotic process, representing the vascular expression of multiple interacting risk factors, is essential to not only enhance risk assessment, but may also provide new targets for risk reduction therapy. Endothelial dysfunction, a potential measure of disease activity, is present very early in the atherosclerotic process, even in arteries that do not demonstrate significant plaque development. A variety of new technologies are now available to assess preclinical vascular disease, atherosclerotic plaque burdens, and endothelial function before the onset of symptoms. (3)

Therefore there is a need to develop a comprehensive and cost effective risk stratification model, which incorporates predisposing and emerging risk factors and noninvasive assessment of preclinical atherosclerosis in order to detect early asymptomatic cardiovascular disease.(4) This risk score is to be validated prospectively in a large group of subjects and relating the measurements to subsequent disease outcomes.

The content of this article reflects the personal opinion of the author/s and is not necessarily the official position of the European Society of Cardiology.