Eduardo J. Balbona, M.D.
Cardiovascular disease remains the leading cause of death and disability in the United States. It is the product of atherosclerosis and ultimately leads to the complications of heart attack and stroke. Cardiovascular disease includes coronary heart disease, the cause of over a million heart attacks annually in the United States. Tragically, for up to a third of heart attacks victims, the first symptom will be sudden death. By the age of 40, the lifetime risk of developing coronary heart disease is one in two for American men and one in three for American women. (1).
“A common pathway to the expression of coronary heart disease is the presence of sub-clinical (pre-symptomatic) atherosclerotic disease. . .. Sub-clinical atherosclerosis may (now) be detected non-invasively by both physiologic and anatomic methods.” Daniel Rader, M.D., The American Journal of Medicine. (2).
Medical research supports the concept of the identification of presymptomatic individuals to allow for prevention of cardiovascular events. Numerous medical studies have found that the development of atherosclerotic plaques begins in childhood or adolescence and then gradually progresses over several decades. Individuals will eventually become symptomatic with the development of a high-grade obstructing lesion (plaque), typically when the artery is over 70% blocked. The time course of cardiovascular disease allows ample opportunity for intervention in the disease process.
Common methods of cardiovascular disease detection and screening are based on the demonstration of symptoms or of significant blood flow obstructing lesions. Both of these findings occur late in the natural history of cardiovascular disease and are thus inadequate for the purposes of prevention . Almost 70% of deaths from heart attacks have culprit lesions associated with less than a 50% obstruction of the coronary artery. (3). These fatal lesions are considered “normal” or “insignificant” on heart catherization and coronary angiography. Instead of focusing on the “lesion” of interest, enlightened physicians should set out to find the “individual” of interest that would benefit most from medical intervention.
Secondary prevention studies, such as the Scandinavian Simvastatin Survival Study (4S) have proven the cost effectiveness of medical therapies such as cholesterol lowering in individuals with known atherosclerosis. (4) The 4S study demonstrated a 42% reduction in coronary deaths and a 37% reduction in the need for angioplasty or bypass surgery. Based on this study, in order to prevent one cardiovascular event (over 5.5 years) only 12 patients would need treatment as opposed to almost 120 patients that would require intervention (over 4.8 years) for the same result in the case of primary prevention (individuals with no atherosclerosis documented). (5).
Non-invasive screening provides clinically pertinent information. Consider the fact that current national cholesterol education program (NCEP) guidelines will accept an LDL cholesterol of 220 mg/dL in a young adult. However, the same NCEP guidelines mandate medical intervention to maintain the LDL below 100 mg/dL once atherosclerosis is demonstrated. Furthermore, the earlier the intervention occurs, the greater the benefit. For example, a 10% reduction in cholesterol by age 40 yields over a 50% decline in the lifetime coronary heart disease risk, while only a 40% benefit if done at age 50 and only 27% if at age 60. (6)
Non-invasive documentation of atherosclerotic lesions is now possible and the case for screening for sub-clinical cardiovascular disease is compelling. Carotid ultra-sonography identifies the presence of atherosclerosis in the carotid arteries. The extent of carotid atherosclerosis has been shown to correlate with coronary plaque burden and is an independent risk factor for major cardiovascular events. (7).
The ankle-brachial index (ABI) is also a useful means of detecting peripheral atherosclerosis. Clinical studies have shown an abnormal ABI to be a predictor of coronary heart disease that justifies the institution of secondary prevention guidelines. (8). Similarly, prospective studies have demonstrated that cardiac calcification scores in asymptomatic individuals (via EBCT) are highly predictive of subsequent symptomatic coronary disease. (9).
“The key to reducing the risk of heart disease is to have a system in place to identify and treat patients that are at high risk. Currently, many people are not identified or are inadequately treated …” Harlan Krumholz M.D., cardiologist, Yale School of Medicine. ( 10)
The non-invasive identification of pre-symptomatic atherosclerosis transforms the physician’s role from one of reaction to a sudden cardiovascular crisis, to that of prudent pro-active prevention via medical management. Proven preventative measures include: anti-hyperlipidemic, anti-thrombotic, anti-inflammatory and anti-oxidant interventions as well as smoking cessation, strict blood pressure control and diabetes management.
Early identification of pre-symptomatic individuals with atherosclerotic lesions benefits not only the patient, but also the community, health system and employers that are no longer burdened with the consequences, complications and costs of advanced cardiovascular disease.
References
I . Loyd-Jones DM, Larson M, Beiser A, Levy D. Lifetime risk of developing coronary heart disease. (The Framingham Heart Study) Lancet. 1999; 353: 89-92.
2. Rader DJ. Noninvasive Procedures for Subclinical Atherosclerosis Risk Assessment. Proceedings of Symposium . The American Journal of Medicine. 1999; I 07: 25S-27S.
3. Rumberger JA, Brundage BH, Rader DJ, Kondos G. Electron Bean Computed Tomographic Coronary Calcium Scanning : A Review and Guidelines for Use in Asymptomatic Persons. Mayo Clinic Proceedings. 1999; 74: 243-252 .
4. Pederson , et al. Randomized Trial of Cholesterol Lowering in 4,444 Patients with Coronary Heart Disease: the Scandinavian Simvastatin Survival Study (4S). Lancet. 1994; 344: 1383-1389.
5. Brown BG. Assessment for Subclinical Ischemia: Bridging the Gap Between Primary and Secondary Prevention . Proceedings of Symposium. The American Journal of Medicine. 1999; 107: 28S-30S.
6. Kwiterovich PO. Young Adults with Hypercholesterolemia . Proceedings of Symposium. The American Journal of Medicine. 1999; I 07: 40S-42S.
7. O’Leary DH, Polak JF, Kronmal RA, Manolio TA, Burke GL, Wolfson SK, Carotid Artery intima and medial thickness as a Risk Factor for Myocardial Infarction and Stroke in older Adults: Cardiovascular Health Study Collaborative Research Group. The New England Journal of Medicine. 1999; 340: 14-22.
8. Grundy SM. Primary Prevention of Coronary Heart Disease: Selection of Patients for Aggressive Cholesterol Management. Proceedings of Symposium. The American Journal of Medicine. 1999; I 07: 2S-6S.
9. Arad Y, Spadaro LA, Goodman K, Lledo-Perez A, Sherman S, Lerner G, Guerci AD. Predictive Value of Electron Beam Computed Tomography of the Coronary Arteries: a 19-month study of 1173 asymptomatic subjects. Circulation. 1996; 93: 1951-1953.
10. Peterson C. Aggressive Cholesterol Management bests Heart Disease. Identifying and Treating Patients at High Risk and Suppressing LDL Might Stave Off Surgery. Managed Healthcare . 2000 : 41-42.
