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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.

Insulin resistance has been demonstrated in patients with angina pectoris irrespective of detectable atherosclerosis at coronary angiograms. We compared insulin sensitivity, lipid profiles, and exercise capacity in 20 patients with syndrome X, 15 patients with variant angina, and 20 healthy controls to investigate whether the presentation of the insulin resistance syndrome differs between the two patient groups with disparate vascular abnormalities. All patients had angiographically normal coronary arteries. Maximal oxygen uptake (VO2 max) was determined at bicycle exercise testing. Insulin sensitivity (SI) was assessed by the minimal model analysis of the intravenous glucose tolerance test. Patients with variant angina had significantly lower VO2 max than controls (mean +/- SE, 25.6 +/- 1.5 vs 30.6 +/- 1.4 ml x kg-1 x min-1, p < 0.05), whereas VO2 max in patients with syndrome X was intermediate (27.1 +/- 1.3 ml x kg-1 x min-1). Compared with controls, patients with syndrome X and variant angina had reduced insulin sensitivity (controls, 1.47 +/- 0.16 10(-4) x min-1/per pmol/L vs syndrome X, 0.86 +/- 0.11 10(-4) x min-1 per pmol/L and variant angina, 0.96 +/- 0.15 x 10(-4) x min-1 per pmol/L; analysis of variance, p < 0.05). Only patients with syndrome X exhibited fasting hyperinsulinemia. Patients with syndrome X also had higher fasting concentrations of triglycerides and total cholesterol and lower concentrations of high-density lipoprotein cholesterol than controls. When adjusting SI for variances of VO2 max, differences in SI vanished between controls and patients with variant angina but not between controls and patients with syndrome X. Thus syndrome X and variant angina are both associated with insulin resistance, but lipid abnormalities are only prominent in patients with syndrome X. A variable expression in terms of concomitant disturbances of lipid profiles and disparate influences of physical capacity suggests different underlying mechanisms.

The clinical value of oesophago-gastro-duodenoscopy and distal oesophageal biopsies was investigated in 49 patients with angina pectoris and normal coronary angiograms. The results were compared to 24 hour oesophageal pH-monitoring of the patients and of a control group of 22 healthy sons. Macroscopic esophagitis--mainly grade I was found in 31% of the patients and microscopic oesophagitis in 25%. The only major abnormalities were the identification of three peptic ulcers (6%). Median (range) reflux index was 1.3 (0.0-13.4) in the patient group and 2.1 (0.0-9.9) in the controls (p = 0.49). There were no differences with respect to endoscopical findings or reflux index between patients with a positive and patients with a normal exercise electrocardiogram. At a median 36 months post study 38% of the patients had undergone acid secretion inhibitor treatment with an effect on symptoms in only 4%. The study provides evidence that routine oesophago-gastro-duodenoscopy is of limited value in this patient group.

Objective: To evaluate the role of nociception in patients with angina despite normal coronary angiograms and to investigate whether any abnormality is confined to visceral or somatosensory perception., Methods: Perception, pain threshold, and brain evoked potentials to nociceptive electrical stimuli of the oesophageal mucosa and the sternal skin were investigated in 10 patients who had angina but normal coronary angiograms, no other signs of cardiac disease, and normal upper endoscopy. Controls were 10 healthy volunteers. The peaks of the evoked potential signal were designated N for negative deflections and P for positive. Numbers were given to the peaks in order of appearance after the stimulus. The peak to peak amplitudes (P1/N1, N1/P2) were measured in microV., Results: (1) Angina pectoris was provoked in seven patients following continuous oesophageal stimulation. (2) Distant projection of pain occurred after continuous electrical stimulation of the oesophagus in four patients and in no controls. (3) Patients had higher oesophageal pain thresholds (median 16.3 mA v 7.3 mA, P = 0.02) to repeated stimuli than controls, whereas the values did not differ with respect to the skin. There were no intergroup differences in thresholds to single stimuli. (4) Patients had substantially reduced brain evoked potential amplitudes after both single oesophageal (P1/N1, median values: 7.2 microV, controls: 29.0 microV; N1/P2: 16.5 microV, controls: 66.0 microV; P < 0.001 for both) and skin (N1/P2: 13.5 microV; controls: 76.0 microV; P < 0.001) stimuli despite the similar pain thresholds., Conclusion: Central nervous system responses to visceral and somatosensory nociceptive input are altered in patients who have angina despite normal coronary angiograms.

The pathophysiology of angina pectoris in patients with a normal coronary angiogram is not clear. Furthermore, the pathophysiological impact of ST changes in syndrome X is controversial. The purpose of this study was to investigate cardiac autonomic function, by measuring 24 h heart rate variability, in patients with and without electrocardiographic evidence of ischaemia during exercise. Thirty-two patients with angina pectoris, a normal coronary angiogram, echocardiogram, hyperventilation test and gastro-oesophageal investigation were studied. Fourteen healthy subjects served as controls. Fifteen patients had significant ST segment depression during stress testing, whereas 17 had no electrocardiographic signs of ischaemia. Heart rate variability was calculated as (1) mean RR = mean of all normal RR intervals, (2) the difference in mean RR level between when awake and when asleep (mean RR wake-sleep)-a tentative index of sympathetic activation, (3) the standard deviation (SD)-a broad band measure of autonomic balance, and (4) a percentage of successive RR interval differences > or = 6% (pNN6%)-an index of vagal modulation. The coronary vascular resistance was measured at rest and during pacing. Mean RR and autonomic indexes did not differ between patients with a positive exercise test and controls (831/884 ms; 24 h SD 125/134 ms; pNN6% 6.715.4%, respectively). Patients with a normal exercise test had shorter mean RR (758 ms vs 844 ms; P < 0.05) and significantly reduced 24-h SD (103 ms vs 134 ms; P < 0.05) than controls, whereas values for vagal index (6.5% vs 5.4%) did not differ from healthy controls. Mean RR wake-sleep also tended to be lower in patients with a normal exercise test (-125 ms vs -173 ms) compared to controls (P < 0.1). Patients with a positive exercise test had a significantly attenuated reduction in coronary vascular resistance during pacing in comparison to patients with a normal exercise test (-0.131 -0.26 mmHg x min. ml-1; P < 0.05). The findings suggest the occurrence of general elevated sympathetic activation in angina patients with a normal exercise test. Patients with a positive exercise test exhibited no signs of autonomic dysfunction although these patients had altered coronary vascular resistance indicating microvascular angina. This supports the suggestion that patients with a normal exercise test constitute an independent pathophysiological entity.