It is perhaps worth noting that we have demonstrated that cholesterol
concentrations fall following stroke too. Although it may not be generally
accepted that cholesterol lowering is of value in the secondary prevention
of stroke, many stroke patients who survive the acute event die a
cardiovascular death.
WM
At 12:01 PM 8/31/01 +0100, Bernie Croal wrote:
>We recently did some work in this area – which we presented at the 1999 Eur
>Soc of Cardiology meeting in Barcelona (Croal BL, Simpson WG, Duff P,
>Walton S, Ross IS. The acute coronary syndrome and cholesterol dynamics: An
>association with peak troponin I levels. XXI European Society of Cardiology
>1999:115-119) The paper is within an extra supplement of European Heart
>Journal, and difficult to get, but I can send those interested an
>electronic copy.
>Essentially we found an overall fall in cholesterol in most of the main
>diagnostic categories within the chest pain patients – but those with MIs
>showed the largest fall (mean 0.5mmol/L, but huge range of up to 2.6mmol/L
>fall). We also found that the degree of fall and the rate was strongly
>related to peak Troponin I and Troponin T (? Hence infarct size) and also
>to cardiac mortality at 1 year. Cholesterol appeared to fall immediately
>from presentation, and probably from the moment of coronary instability.
>This would make sense since it is likely to be the inflammatory mediators
>released within the infarct area that are responsible for such a response.
>We concluded to recommend that blood samples for lipoprotein analysis are
>taken only on admission so as to minimise any potential error. Use of
>results from subsequent samples may lead to clinically significant
>misclassification, or misinterpretation of an apparent lack of response to
>subsequent lipid lowering drug therapy. Such potential misclassification
>would appear to be maximised in those patients with the larger infarcts or
>the poorest outcome.
>At the end of the day, as has been pointed out, the evidence suggests that
>most if not all of these patients would benefit from lipid lowering drug
>treatment, and so the important cholesterol level to measure would be the
>one measured at 6 months and 1 year to assess treatment success or
>compliance. The time for cholesterol to normalise is also very variable
>following an MI, and so there is no “safe” period. It will depend upon
>intercurrent illness and subsequent periods of coronary instability – so
>again this makes cholesterol measurement less critical. One patient I
>treated, who had FH and a Chol around 10 mmol/L, developed appendicitis,
>following which her Chol dropped to 3 mmol/L and stayed there for one year
>before returning to 10. – so the effect can be dramatic and prolonged. Hope
>this adds to the confusion !
>Bernie Croal – Aberdeen – UK.
>
|