Is it time to measure Lp(a) as part of coronary heart disease risk assessment?

Is Lp(a) culpable in atherosclerosis? This is a question for scientists. Lp(a) fulfills two of Koch's four criteria for causation for CHD. However, the actual mechanism by which Lp(a) promotes atherosclerosis remains unproven. Should we investigate Lp(a) as part of assessment of CHD risk? There are some reasons that favour measuring plasma Lp(a) in selected patients. First, a high Lp(a) can exist without physical or historical evidence. Second, the measurement of Lp(a) might affect diagnosis, treatment and/or prognosis. However, presently there is no standard assay for Lp(a) and there is no evidence for benefit of treatment elevated Lp(a). Furthermore, there is no current evidence that knowledge of a patient's Lp(a) status would affect management of other aspects of a patient's CHD risk. Lp(a) can be considered to be a non-modifiable potential CHD risk factor, as are family history and gender. If Lp(a) is to be measured, it must be done so using a validated, reliable and commonly used assay. Measuring Lp(a) could be reserved for subjects in whom there is equivocation over how aggressively to treat the traditional CHD risk factors, such as elevated plasma LDL cholesterol. If Lp(a) were found to be high in such a subject, the modifiable CHD risk factors should be addressed more aggressively. However, the medical community awaits the results of prospective studies addressing this particular issue.