Did grandma give you heart disease? The new battle against coronary artery disease.

Atherosclerosis/coronary artery disease (CAD) is largely a result of genetically linked dyslipidemias that can often be identified in clinical practice. Expression of these genetic traits is highly individual and can be affected by environmental factors such as diet and exercise. By understanding the heterogeneity of CAD, it becomes clear that all patients cannot be optimally managed with the same therapeutic regimen. Whereas elevated low-density lipoprotein (LDL) cholesterol is strongly correlated with CAD risk, reduction of LDL cholesterol alone is not an adequate strategy in many cases. Patients with the small, dense LDL of the atherogenic lipoprotein profile (pattern B) experience a 3-fold increased risk of CAD, and pattern B is also correlated with the development of type 2 diabetes. Likewise, elevated lipoprotein(a) increases atherosclerotic risk, particularly in the presence of other risk factors, and is predictive of CAD risk in both women and men. Recent data show that the routine lipid profile--total cholesterol, triglycerides, LDL cholesterol, and high-density lipoprotein (HDL) cholesterol--does not detect the most common inherited dyslipidemias. Newer, more sophisticated tests, such as gradient gel electrophoresis, can detect disease-relevant lipidemic details, e.g., LDL subclass pattern, LDL particle diameter, and LDL subregions. Although these testing procedures are more expensive, their cost must be weighed against the potential lifelong cost of sometimes expensive drug treatment that may be avoided based on the results of such tests. Thus, by attending to the implications of family history, the interactions of genetic, metabolic, and environmental factors, and utilizing more targeted testing procedures, physicians can match the patient's disorder with specifically effective therapy while maintaining a cost-effective approach to disease management.