David Levy, MD, FRCP
Increased cardiac risk in type 2 diabetes, and a re-evaluation of the ‘coronary equivalent’ concept
These subtle differences together may account for some of the increased cardiovascular risk in type 2 diabetes. The level of increased risk is the subject of much academic discussion. In large diabetic populations studied in the past, coronary risks were often found to be approximately doubled compared with non-diabetic groups, and the concept of diabetes as a coronary risk equivalent is almost embedded – type 2 patients who have not yet suffered a coronary event have a similar coronary risk as non- diabetic patients who have already had an event. The therapeutic corollary of this view is that all patients require equally intensive secondary prevention treatment.
More recent studies find a much lower coronary event rate in type 2 patients, and meta-analysis estimates the risk not as twofold increased but about half that of the non-diabetic population with a previous event. This may reflect the gradual but cumulatively important improvements in multimodal management resulting in better cardiovascular outcomes in type 2 diabetes. However, the statistic that is invariant across old and recent studies alike is the extremely high risk of type 2 patients who have had an event (e.g. 10% annual risk, compared with about 2% in those without an event) . Guidelines do not yet reflect this revised view that implies we should individualize risk management with a strong emphasis on the highest risk patients.
Lipid profiles in poorly controlled diabetes and effects of intensive glycemic treatment
In poorly controlled type 1 and 2 diabetes, insulin deficiency increases hepatic VLDL secretion leading to elevated serum triglycerides, sometimes massively so, resulting in lipemic serum, difficulties in measuring many other serum components (including amylase), and an increased risk of acute pancreatitis. In large clinical studies improvement in glycemic control from moderately poor levels primarily reduces triglycerides, with lesser falls in total and HDL cholesterol, but these would not usually be detectable in the individual patient (Table 12.1). Intensified glycemic control in type 1 diabetes often causes weight gain, and intensively treated patients in the DCCT with the greatest weight gain (BMI 34 vs. 24) also showed a global deterioration in lipid profiles, with increased total and LDL cholesterol, increased triglycerides and lower HDL levels . Systolic and diastolic blood pressure and high-sensitivity CRP all increased as well. There must be concern that worsening cardiovascular risk profiles in intensively treated type 2 diabetes may outweigh the limited advantages of tight glycemic control as shown in the recent trials.
There is little point in requesting lipid profiles in severely hyperglycemic newly diagnosed or very poorly controlled patients; leave until control has been stabilized for at least a month (Box 12.1).
Familial hypercholesterolemia may coexist with diabetes; suspect where there is high cholesterol (> 8.0 mmol/L, 310 mg/dL) and normal triglycerides. Clinical characteristics include:
- premature arcus senilis (in the 30–40 year age group);
- tendon xanthomata, xanthelasmata;
- family history of premature coronary artery disease (< 50 years of age) in non-diabetic first-degree relatives.
Familial combined hyperlipidemia is an important, common (1 in 250) but complex polygenic disorder that shares many of the features of the insulin resistance syndrome, and is the most common familial form of hyperlipidemia in young survivors of myocardial infarction. Definitions are not standardized but a typical lipid profile would show total cholesterol 7.0 mmol/L, HDL-cholesterol 0.9 mmol/L and triglycerides 3.0 mmol/L.
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David Levy, MD, FRCP, Consultant Physician, Gillian Hanson Centre, Whipps Cross University Hospital; Honorary Senior Lecturer
Queen Mary University of London London, UK
This edition first published 2011, © 2011 by David Levy. 1st edition 1998 (Greenwich Medical Media/Cambridge University Press) 2nd edition 2006 (Altman Publications)