Key result
Patients with syndrome X had a significantly enhanced rate of exercise-induced serum potassium increment compared to matched healthy controls (70 vs. 30 micromol/liter/min, p < 0.001).
Why the study?
Do patients with syndrome X have enhanced exercise-induced hyperkalemia compared to healthy controls?
Case-Control (n=31)
Do patients with syndrome X have enhanced exercise-induced hyperkalemia compared to healthy controls?
Absolute Event Rate: 70% vs 30%
p-value: p=< 0.001
Patients with syndrome X exhibit enhanced exercise-induced hyperkalemia, suggesting altered potassium metabolism as a potential mechanism for their symptoms and ECG changes.
May implicate potassium dysregulation in syndrome X symptoms; hypothesis-generating and requires prospective validation before clinical consideration.
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 micromol/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.
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Bøtker et al. (1999) conducted a case-control in Syndrome X (n=31). Syndrome X vs. Matched healthy control subjects was evaluated on Rate of exercise-induced increment of serum potassium (micromol/liter/min) (p=< 0.001). Patients with syndrome X had a significantly enhanced rate of exercise-induced serum potassium increment compared to matched healthy controls (70 vs. 30 micromol/liter/min, p < 0.001).
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