Let's not forget timing

Posters 12. Miscellaneous including statements describing body habitus, cholesterol level, whether the patients was seen by a dietitian and the advice provided if seen. The dietetic database was checked to see how many patients received dietetic advice. None of the 76 discharge summaries mentioned the patients’ weight or body mass index. 4 discharge summaries mentioned that the patient was obese or overweight. Only 1 discharge summary mentioned that the patient was advised to lose weight. Nineteen of the patients were referred to the dietetic service and were provided with advice for lipid lowering (S), diabetes/lipid lowering (6), lipid lowering/weight reduction (4) and diabetes/high protein diet (1) respectively. None of the patients with a cholesterol < 5.0 mmol/L recorded in the discharge summaries was referred for dietary advice. Requests for lipid lowering advice seems to be the main reason for referral to the dietetic service for patients post myocardial infarction. Obesity does not seem to rate highly as a risk factor in the prevention of coronary heart disease despite its prevalence and metabolic effects. Senior House Officers wrote the majority of discharge summaries. An educational programme outlining the risk factors that should be communicated to the primary healthcare team may thus improve the quality of the discharge summaries. Additionally, the dietetic referral procedures may need to be reviewed. IP233

TIMING

IS IMPORTANT

P.J. ‘Rvomey. Department of Clinical Biochemistry, Edinburgh EH3 4EU, UK

Royal Znjrmary

Following the Joint British recommendations on prevention of coronary heart disease in clinical practice a retrospective audit was conducted on 65 patients aged ~75 who were discharged in 1999 post an acute admission for a myocardial infarction. All patients were followed up by a cardiac rehabilitation sister and were actively encouraged by her to have their cholesterol re-measured in the community. The purpose of the audit was to determine the lipid request pattern for these patients after hospital discharge to assess the implementation of the Joint British recommendations. Data was obtained from the laboratory computer system commencing from the admission date recorded in the patients’ case notes.

Number

of cbcdesterol requests between

6-13 weeks post event

Number

0

37 (56)%

I

27 (42)%

2

I (Z)%

of patients

Approximately half of the patients did not meet the Joint British recommendation criteria of having their cholesterol re-measured between 6 and 13 weeks post myocardial infarction. By six months, more than a quarter of patients still needed their cholesterol to be re-measured. One-fifth of patients had a cholesterol re-measurement that was performed during the acute phase response. It is worrying that 56% of these patients who were actively followed up by a cardiac rehabilitation sister did not meet the criteria set down by the Joint British recommendations. The fact that 28% of patients did not have a recorded cholesterol level by 6 months suggests that an alternative strategy may be needed. The prescription of efficacious statin doses before discharge from the hospital setting may help to overcome the under-treatment of these patients. For such a policy to work, the cholesterol level on samples obtained within 24 hours of the onset of chest pain is necessary to establish the degree of cholesterol lowering that is required to attain target values. The 20% of patients who had samples analysed too soon may have an underestimation of the degree of dyslipidaemia. The result may be the absence of treatment or decreased efficacy of treatment for hypercholesterolaemia. Should be we not spread the message to cardiologists and general practitioners that timing is everything if they want to reduce the burden of ischaemic heart disease? IP234

LET’S NOT FORGET

TIMING

P.J. Twomey. Department of Clinical Biochemistry, Edinburgh EH3 4EU, UK

Royal Znjrmaty

Following the Joint British recommendations on prevention of coronary heart disease in clinical practice a retrospective audit was conducted on 65 patients aged ~75 who were discharged in 1999 post an acute admission for a myocardial infarction. The purpose of the audit was to determine the lipid request pattern while these patients were under the care of the cardiologists.

105

Data was obtained from the laboratory computer system commencing from the time of onset of chest pain or admission time recorded in the patients’ case notes. Aaalyte

No. of samples

Sampler collected < 24 houn

Samples

colkcted

> 24 hours

Cholestenul

89

44 (49%)

45 (51%)

Trt@yceride

75

34 (45%)

41 (55%)

HDL-C LDGC

37 35

14(38%) 13(37%)

23 (62%) 22(63%)

The majorityof lipids analysed were on samples that were collected after 24 hours Approximately half of the patients had a sample collected within 24 hours analysed for cholesterol and random triglycerides with about one-fifth having HDL-cholesterol measured within 24 hours. Serum HDL-cholesterol and total cholesterol continue to be risk factors for recurrent ischaemic heart disease events after a myocardial infarction. In patients acutely post myocardial infarction, serum total cholesterol and LDL-cholesterol as well as serum HDL cholesterol decrease. Thus, lipid measurements on a sample that is collected within 24 hours of the onset of chest pain may give some reflection of the concentration of total cholesterol and HDL cholesterol before the acute event. However, samples collected after this period will lead to an underestimation of the dyslipidaemia. It may be in the laboratory’s and patient’s interest to have a mechanism in place such that patients with a myocardial infarction have one full lipid profile requested automatically on a sample that has been collected within the first 24 hours of the onset of a chest pain. Ideally, further lipid requests would be ignored to avoid artefacts due to the acute phase response. My data suggests that such a mechanism may be more cost effective from the laboratory point of view and would also help to identify risk factors such as low HDL-cholesterol that some cardiologists seem to overlook despite the available evidence.

IP235

BINDING OF NATIYE AND NATURALLY OCCURRED MULTIPLE-MODIFIED LDL WITH ELASTIN OF UNINVOLVED AND ATHEROSCLEROTIC HUMAN AORTA

VV Tertov I.\! Suprun, T.A. Scalbe, L.A. Medvedeva, AN. Orekhov. _> Institute of Experimental Cardiology; Institute for Athewxclemsis Research, Moscow, Russia Several years ago we have found and isolated a subfraction of naturally occurred multiple-modified LDL (nomLDL) which produced lipid accumulation in human aortic intimal smooth muscle cells and macrophages. In present study we studied the comparative binding of native LDL and nomLDL with elastin and proteoglycans from early and developed atherosclerotic lesions to evaluate the possible role of nomLDL in extracellular lipid deposition. Native LDL and nomLDL were isolated by lectin chromatography and iodinated using ICl-procedure. Elastin, collagen and proteoglycans were isolated from proteoglycan-rich and muscle elastic sublayers of intima and media of uninvolved and atherosclerotic human aorta. The binding of nomLDL with elastin from proteoglycan-rich sublayer of normal intima was 2-fold higher as compare to native LDL. NomLDL was bound to elastin from proteoglycan-rich sublayer of initial lesions and fatty streaks 2- and 5 fold efKectively than with normal elastin. The association of nomLDL with elastin from proteoglycan-rich sublayer of fibroatheroma was 2-fold lower than to elastin from fatty streaks. The closed changes in lipoprotein binding was observed for the elastin from muscle etastic sublayer of human aorta. The binding of native and nomLDL with elastin from media of normal and atherosclerotic areas was similar. Retention time for nomLDL in preformed lipoprotein-elastin complexes was longer than for native LDL. Binding of nomLDL was correpondent to positive charged amino acid level in aortic elastin. The binding of nornLDL to proteoglycans from proteoglycan-rich and muscle elastic sublayers of normal intima was 2and 3-fold, correspondently, higher than of native LDL. The binding of native LDL and nomLDL to proteoglycans of both intimal sublayers decreased in order: norma > initial lesions > fatty streaks > fibroatheroma. The similar changes in lipoprotein binding was observed for the proteoglycans from media layer of human aorta. The binding of native LDL and nomLDL correlated possitively with proteoglycan level of chondroitin sulphate A and C, and negatively with derrnathan sulphate content. Binding of nomLDL with collagen from proteoglycan-rich and muscle elastic sublayers of fibroatheroma v+as 2-fold higher than to collagen from normal intima. Complexes of nomLDL with collagen, elastin and proteoglycans stimulated cholesterol accumulation

72nd EAS Congress