INSULIN SENSITIVITY IN CARDIOLOGICAL SYNDROME-X

Objectives. To test whether cardiological syndrome X is an insulin-res istant state. Setting, design and subjects. The coronary care unit of a referral centre for angina pectoris in Pisa, Italy. A case-control s tudy, involving 10 patients with unequivocal (angiographycally proven) cardiological syndrome X, but normal glucose tolerance, blood pressur e and lipid levels, and 13 matched healthy subjects. Main outcome meas ures. Insulin sensitivity and pattern of substrate oxidation (assessed by the euglycaemic insulin clamp technique in combination with indire ct calorimetry). Results. Fasting plasma glucose and insulin levels we re 5.05 +/- 0.11 versus 4.88 +/- 0.11 mmol l(-1) and 68 +/- 10 versus 56 +/- 6 pmol l(-1), respectively (controls versus patients, ns). Duri ng the insulin clamp, was nearly identical in (25.9 +/- 1.8 and 27.2 /- 1.8 mu mol kg(-1) min(-1), respectively, P = 0.88). Non-oxidative g lucose disposal accounted for similar proportions of total glucose upt ake (59 versus 53%, patients versus controls, ns). Resting energy expe nditure (13.7 +/- 0.6 versus 13.8 +/- 0.8 cal kg(-1) min(-1), ns) and insulin-induced thermogenesis were similar in the two groups. Fasting plasma NEFA concentrations (0.64 +/- 0.09 and 0.64 +/- 0.06 mmol l(-1) , patients and controls, ns) fell in a similar time-course and to virt ually identical nadirs (0.13 +/- 0.02 and 0.14 +/- 0.02 mmol l(-1)) af ter insulin infusion. Fasting plasma potassium was similar in patients and controls (3.99 +/- 0.10 and 4.16 +/- 0.04 mmol l(-1), ns), and in sulin induced equivalent hypokalaemia (-14 versus -19%). Conclusions. None of the in vivo actions of insulin were impaired in patients with 'pure' syndrome X when compared to matched controls. Therefore, we con clude that cardiological syndrome X is not an insulin resistant state per se, and that any decrease in insulin sensitivity found in this con dition is likely to be secondary.