None of these answers are correct. There is no conclusive evidence that any of these surrogate markers should be routinely
measured as part of a cardiovascular risk assessment.
There is no evidence that reducing an elevated level of lipoprotein (a) results in a reduction in the incidence of
first or subsequent cardiovascular events. In addition, lipoprotein (a) levels are hard to alter clinically. Therefore
widespread testing of lipoprotein (a) levels and attempts to reduce levels are neither recommended nor warranted.
Folic acid is known to lower homocysteine levels, however this does not appear to reduce cardiovascular risk. There
is no evidence that homocysteine is a reliable marker of cardiovascular disease.
The evidence is inconclusive whether high sensitivity CRP (HsCRP) has a direct effect on cardiovascular risk prediction.
Elevated HsCRP could indicate atherosclerosis, but levels can also be temporarily raised by inflammation. In addition,
there is significant individual variation in baseline levels.
Observational studies have shown an association between low vitamin D levels and increased risk of cardiovascular
events. There is also a suggestion that vitamin D has a protective effect in terms of cardiovascular risk, for patients
using calcium supplements. However, the evidence is limited and not sufficient to justify widespread vitamin D supplementation
There is mixed evidence as to whether uric acid is an independent marker of cardiovascular risk. Although over one
quarter of respondents selected uric acid as a marker that should be routinely measured as part of cardiovascular risk
assessment, the jury is still out.