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CLINICAL STUDIES

Enhanced activity of sodium–lithium countertransport in patients with cardiac syndrome X

A potential link between cardiac and metabolic syndrome X

Achille Gaspardone, MD, MPhil, FACC^a, Claudio Ferri, MD^*, Filippo Crea, MD, FACC^a, Francesco Versaci, MD, FACC^a, Fabrizio Tomai, MD, FACC^a, Anna Santucci, MD, Luigi Chiariello, MD, FACC^a and Pier A. Gioffre, MD^a

^a Divisione di Cardiochirurgia, Università Tor Vergata, Rome, Italy
^* Fondazione Andrea Cesalpino, Università La Sapienza, Rome, Italy
Dipartimento di Medicina Interna e Sanità Pubblica, Università de L’Aquila, L’Aquila, Italy

Manuscript received March 6, 1998; revised manuscript received July 13, 1998, accepted August 6, 1998.

Address for correspondence: Dr. Achille Gaspardone, Divisione di Cardiochirurgia, Università Tor Vergata, via Portuense 700, 00149 Rome, Italy
gaspardone{at}tin.it

Objectives. This study was aimed at assessing both stimulated insulinemia and the sodium–lithium countertransport in a 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 a 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 plasma 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 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.

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