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

• Published in: Journal of the American College of Cardiology Vol. 32; no. 7; pp. 2031 - 2034
• Main Authors: GASPARDONE, A, FERRI, C, CREA, F, VERSACI, F, TOMAI, F, SANTUCCI, A, CHIARIELLO, L, GIOFFRE, P. A
• Format: Journal Article
• Language: English
• Published: New York, NY Elsevier Science 01-12-1998
• Subjects: Biological and medical sciences; Biological Transport, Active; Cardiology. Vascular system; Coronary heart disease; Erythrocytes - metabolism; Female; Heart; Humans; Insulin - blood; Ion Transport; Lithium - metabolism; Male; Medical sciences; Microvascular Angina - blood; Microvascular Angina - physiopathology; Middle Aged; Radioimmunoassay; Sodium - metabolism; Human; Hyperinsulinemia; Countercurrent; Pathogenesis; X Syndrome; Sodium ion; Clinical form; Ion transport; Cardiovascular disease; Coronary heart disease; Lithium ion
• ISSN: 0735-1097; 1558-3597
• DOI: 10.1016/S0735-1097(98)00470-7

This study was aimed at assessing both stimulated insulinemia and the sodium-lithium countertransport in a selected group of patients with cardiac syndrome X.
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.
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 a double-antibody radioimmunoassay.
Maximal velocity of sodium-lithium countertransport was higher in patients with syndrome X compared to controls (635+/-200 vs. 324+/-49 micromol/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 plasma levels of insulin >420 pmol/liter, which corresponds to the mean value +2 SD of controls (p = 0.006).
Both enhanced activity of the sodium-lithium countertransport and stimulated hyperinsulinemia 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 a common cause of the metabolic and vascular alterations frequently found in syndrome X.