Enhanced activity of sodium–lithium countertransport in patients with cardiac syndrome X: potential link between cardiac and metabolic syndrome X

Objectives. This study was aimed at assessing both stimulated insulinemi and the sodium–lithium countertransport in selected group of patients with cardiac syndrome X. Background. Hyperinsulinemia, which is frequently present in patients with cardiac syndrome X, is often associated with an enhanced activity of the sodium–lithium countertransport, an in vitro marker of sodium–hydrogen exchange. Methods. Fifteen patients with syndrome X and 14 matched controls were studied. After pharmacological washout, sodium–lithium countertransport was assessed from lithium-loaded red blood cells. Postload insulin levels were evaluated by double-antibody radioimmunoassay. Results. Maximal velocity of sodium–lithium countertransport was higher in patients with syndrome X compared to controls (635 ± 200 vs. 324 ± 49 μmol/liter/h, p = 0.001). Fourteen of the 15 patients with syndrome X (93%) presented sodium–lithium countertransport values higher than the mean +2 SD of the control group. At 120 min, 12 patients with syndrome X (80%) had plasm levels of insulin >420 pmol/liter, which corresponds to the mean value +2 SD of controls (p = 0.006). Conclusions. Both enhanced activity of the sodium–lithium countertransport and stimulated hyperinsulinemi are present in the vast majority of patients with cardiac syndrome X. As enhanced activity of the sodium–lithium countertransport has the potential to cause both glucose intolerance and smooth muscle hyperreactivity, it might represent common cause of the metabolic and vascular alterations frequently found in syndrome X.