Which one of the following is not correct regarding the SCORE risk charts?
Diabetes is not part of the SCORE scoring system as these patients have already identified themselves as high risk and require intensive risk factor modification. Diabetic patients are defined as very high risk if there is evidence of end-organ damage or an additional CV risk factor.
A type 2 diabetic patient has proven microalbuminaemia. The fasting lipid profile is:
What do you recommend regarding lipid control?
This diabetic patient already has evidence of end-organ damage reflected by microalbuminaemia. This identifies very high risk irrespective of other factors. Immediate drug therapy is indicated for LDL >1.8 (and should be considered even with very low LDL) with aggressive risk factor modification. Other very high risk factors are chronic kidney disease (GFR < 30), established atherosclerotic disease (including carotid plaque), and a SCORE risk ≥10%. The treatment target LDL-C is <1.8 (or at least 50% reduction) in these very high risk patients.
A patient who has recently had a myocardial infarction asks you about their target cholesterol.
What do you recommend?
Total cholesterol and LDL-C constitute the primary targets for treatment (as opposed to the protective HDL-C) primarily because of the large volume of compelling data and the fact that they can be modified with lifestyle changes and pharmacotherapy. The ESC recommends LDL-C targets which are graded to risk (<1.8 for very high risk, <2.5 for high risk, and <3.0 for moderate risk). JBS2 and NICE currently recommend TC <4.0 (LDL-C < 2.0). Therefore answer D can also be correct! The ESC uses the SCORE chart to calculate CV death risk. Diabetes is not included in the risk charts and these individuals are assumed to be high risk (very high risk if evidence of end-organ damage). JBS2 charts calculate CV disease development risk, but JBS3 will include lifetime risk. JBS2 (2005) and NICE (2008) regard a 20% risk of developing CV disease over 10 years as high risk and the threshold for statin therapy for primary prevention.
A patient 12 months post myocardial infarction is complaining of muscle aches. The GP highlights that this may be due to simvastatin 80 mg and is concerned about myopathy. They have performed a CK test which is normal and recent fasting lipid profile reveals TC 4.5, LDL-C 2.2. There is no muscle weakness and the patient feels that the symptoms are currently tolerable.
This patient is experiencing myalgia (occurs in 5–10% patients), but not myopathy, secondary to high-dose simvastatin. However, the patient has not achieved target cholesterol post MI. Atorvastatin is a more potent statin and may be better tolerated without requiring maximal titration. If the target is still not reached, combination therapy is appropriate.
A 73-year-old woman has been given a fasting lipid test by her GP (TC 6.2, LDL 3.8). She feels that she has put on weight recently as a result of a general lack of energy and activity. The GP started simvastatin 40 mg nocte but the patient stopped it because she felt that it caused constipation.
This patient has features of hypothyroidism which is associated with cholesterol elevation and is solved by thyroid correction. Secondary causes of hypercholesterolaemia should be considered prior to pharmacological intervention. These include:
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