Enhanced exercise-induced hyperkalemi in patients with syndrome X

OBJECTIVES The purpose of this study was to determine whether patients with syndrome X have altered potassium metabolism. BACKGROUND Patients with syndrome X have angin pectoris and exercise induced ST segment depression on the electrocardiogram despite normal coronary angiograms. Increasing evidence suggests that myocardial ischemi is uncommon in these patients. Altered potassium metabolism causing interstitial potassium accumulation in the myocardium may be an alternative mechanism for chest pain and ST segment depression in syndrome X. METHODS We compared the magnitude of exercise-induced hyperkalemi in 16 patients with syndrome X (12 female and four male, mean ± SD age 53 ± 6 years) and 15 matched healthy control subjects. The participants underwent bicycle test at fixed load of 75 W for 10 min, and blood samples were taken for analysis of potassium, catecholamines and lactate before, during and in the recovery period after exercise. In five patients with syndrome X, the test was repeated during alpha1 adrenoceptor blockade. RESULTS Baseline concentrations of serum potassium, plasm catecholamines and plasm lactate were similar in patients and control subjects. The rate of exercise-induced increment of serum potassium was increased in the patients (70 ± 29 vs. 30 ± 21 μmol/liter/min in control subjects, p < 0.001). Six patients, who stopped before 10 min of exercise, showed very rapid increments in serum potassium concentration. Compared to the control subjects, patients also demonstrated larger increments in rate–pressure product, plasm norepinephrine and lactate concentrations during exercise. The rate of serum potassium increment correlated with the rate of plasm norepinephrine increment in the patients (r = 0.63, p < 0.02), but not in the control subjects (r = 0.01, p = 0.97). Blockade of alpha1 adrenoceptors decreased systolic blood pressure at baseline, but did not influence the increment of serum potassium, plasm catecholamines and lactate. CONCLUSIONS Patients with syndrome X have enhanced exercise induced hyperkalemi in parallel with augmented increases of circulating norepinephrine and lactate. The prevailing mechanisms behind the abnormal potassium handling comprise sources distinct from alpha1-adrenoceptor activation.