Norepinephrine, at plasma levels easily attained during exercise, enhances platelet aggregability and platelet secretion in vivo in healthy humans. Aspirin may be less effective as an antithrombotic drug during sympathoadrenal activation in humans.

1. The effects of mental stress induced by a colour word conflict test (CWT; n = 9) or 3 h infusions of placebo or adrenaline (0.4 nmol min-1 kg-1; n = 9) on platelet function in vivo were studied in 16 healthy male volunteers. 2. Platelet function was assessed by a filtragometry technique, which reflects aggregability in vivo, and by measurements of the plasma levels of beta-thromboglobulin (beta-TG) and platelet factor 4 (PF4). 3. Adrenaline and CWT induced marked cardiovascular responses as expected. Venous plasma adrenaline increased from 0.1-0.2 nmol/l at rest to 4.87 +/- 0.42 nmol/l during adrenaline infusion and to 0.46 +/- 0.10 nmol/l during CWT. 4. Filtragometry measurements were reproducible within individuals with coefficients of variation of 7.9% during placebo infusion and 5.4% for resting measurements between days. 5. Platelet aggregability, as measured by filtragometry, was similarly increased during both adrenaline infusion (P less than 0.05) and CWT (P less than 0.01). 6. The coefficients of variation for beta-TG and PF4 levels were 17.3% for log beta-TG and 27.9% for log PF4 between days, but could not be calculated for within-day variability. Both beta-TG (P less than 0.05) and PF4 (P less than 0.01) levels decreased time-dependently during placebo infusion, indicating that long resting periods (hours) are needed to attain basal levels. Artefactual results could not be identified by evaluating beta TG/PF4 ratios. 7. beta-TG and PF4 levels did not decrease time-dependently during adrenaline infusion. There were no significant changes of beta-TG or PF4 during CWT.(ABSTRACT TRUNCATED AT 250 WORDS)

Swenne I, Larsson PT. Heart risk associated with weight loss in anorexia nervosa and eating disorders: risk factors for QTc interval prolongation and dispersion. Acta Paediatr 1999; 88: 304-9. Stockholm. ISSN 0803-5253Risk factors for QT c interval prolongation and dispersion, indicators of an increased risk for cardiac arrhythmia and sudden death, have been investigated in patients with eating disorders (ED) and ongoing weight loss. Patients were characterized with regard to weight, body mass index (BMI; weight/length 2 ), duration of weight loss, rate of weight loss and rate of weight loss immediately preceding examination. At examination, a 12-lead electrocardiographic (ECG) registration and blood samples for analysis of serum electrolytes were obtained. In total, 92 examinations in 58 female patients aged 15.5 AE 1.7 (mean AE SD) y were analysed. Control ECG recordings were obtained from 38 normal-weight teenage girls with no known heart disease. Patients with ED weighed 40.7 AE 7.8 kg, corresponding to BMI 15.2 AE 2.4 kg/m 2 following a weight loss of 11.8 AE 6.5 kg. In ED patients, the ECG showed bradycardia, a shift to the right of the QRS axis, diminished amplitudes of the QRS complex and T wave, and prolongation and increased dispersion of the QT c interval. In multiple regression analyses low weight, low BMI and rapid weight loss immediately preceding the examination were the most important independent predictors of QT c interval prolongation and dispersion. It is concluded that an ECG examination is an important part of the assessment of patients with ED and ongoing weight loss, even in the absence of electrolyte disturbances, and especially if the patient is severely underweight or weight loss is rapid.

Risk factors for QTc interval prolongation and dispersion, indicators of an increased risk for cardiac arrhythmia and sudden death, have been investigated in patients with eating disorders (ED) and ongoing weight loss. Patients were characterized with regard to weight, body mass index (BMI; weight/length2), duration of weight loss, rate of weight loss and rate of weight loss immediately preceding examination. At examination, a 12-lead electrocardiographic (ECG) registration and blood samples for analysis of serum electrolytes were obtained. In total, 92 examinations in 58 female patients aged 15.5+/-1.7 (mean +/- SD) y were analysed. Control ECG recordings were obtained from 38 normal-weight teenage girls with no known heart disease. Patients with ED weighed 40.7+/-7.8 kg, corresponding to BMI 15.2+/-2.4 kg/m2 following a weight loss of 11.8+/-6.5 kg. In ED patients, the ECG showed bradycardia, a shift to the right of the QRS axis, diminished amplitudes of the QRS complex and T wave, and prolongation and increased dispersion of the QTc interval. In multiple regression analyses low weight, low BMI and rapid weight loss immediately preceding the examination were the most important independent predictors of QTc interval prolongation and dispersion. It is concluded that an ECG examination is an important part of the assessment of patients with ED and ongoing weight loss, even in the absence of electrolyte disturbances, and especially if the patient is severely underweight or weight loss is rapid.

1. The effects of phentolamine (500 micrograms/min) on platelet aggregability in vivo at rest and during adrenaline infusion were assessed by ex vivo filtragometry and measurements of plasma beta-thromboglobulin levels in 10 healthy male subjects. Plasma levels of von Willebrand factor antigen and free fatty acids were also measured. 2. Adrenaline induced marked and expected increases in heart rate and systolic blood pressure and decreased diastolic blood pressure when venous plasma adrenaline levels were elevated from 0.12 +/- 0.02 to 2.9 +/- 0.3 nmol/l (P less than 0.01). 3. Adrenaline caused platelet activation in vivo. Ex vivo filtragometry readings were shortened by 58 +/- 9% (P less than 0.01), plasma beta-thromboglobulin levels increased by 99 +/- 44% (P less than 0.01) and platelet counts increased by 26 +/- 6% (P less than 0.01). Plasma levels of von Willebrand factor antigen and free fatty acids increased by 53 +/- 5% and 475 +/- 113% (both P less than 0.01), respectively. 4. Phentolamine enhanced the beta-adrenergic vasodilator responses to adrenaline, as both the decrease in diastolic blood pressure and the reflexogenic increase in heart rate were enhanced (both P less than 0.01). Marked elevations in plasma noradrenaline levels were found during infusions of phentolamine and adrenaline (P less than 0.001). 5. Phentolamine did not alter platelet indices at rest, but abolished adrenaline-induced platelet activation, as filtragometry readings, plasma beta-thromboglobulin levels and platelet counts remained at, or below, resting levels. Responses of plasma levels of von Willebrand factor antigen and free fatty acids to adrenaline were not influenced by phentolamine and did not seem to influence platelet responses.(ABSTRACT TRUNCATED AT 250 WORDS)