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CLINICAL STUDIES

Enhanced exercise-induced hyperkalemia in patients with syndrome X

Hans Erik Bøtker, MD, PhD^*, Helle Sauer Sonne, MD^*, Ole Frøbert, MD, PhD^* and Frederik Andreasen, MD, PhD

^* Department of Cardiology, Skejby Hospital, University Hospital Aarhus, Aarhus, Denmark
Department of Clinical Pharmacology, Institute of Pharmacology, University of Aarhus, Aarhus, Denmark

Manuscript received April 27, 1998; revised manuscript received October 26, 1998, accepted December 17, 1998.

Reprint requests and correspondence: Hans Erik Bøtker, MD, PhD, Department of Cardiology, Skejby Hospital/University Hospital Aarhus, Brendstrupgaardsvej, DK-8200 Aarhus N, Denmark

OBJECTIVES

The purpose of this study was to determine whether patients with syndrome X have altered potassium metabolism.

BACKGROUND

Patients with syndrome X have angina pectoris and exercise induced ST segment depression on the electrocardiogram despite normal coronary angiograms. Increasing evidence suggests that myocardial ischemia 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 hyperkalemia 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 a bicycle test at a 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, plasma catecholamines and plasma 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, plasma norepinephrine and lactate concentrations during exercise. The rate of serum potassium increment correlated with the rate of plasma 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, plasma catecholamines and lactate.

CONCLUSIONS

Patients with syndrome X have enhanced exercise induced hyperkalemia 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.

Abbreviations and Acronyms   ATPase = adenosine triphosphatase   ECG = electrocardiogram   EGTA = ethylene glycol tetraacetic acid   VO2 peak = peak oxygen uptake

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