These results suggest that plasma BNP determination provides important, independent prognostic information after AMI. Although plasma ANP appears to be a better predictor of left ventricular dysfunction, plasma BNP may have greater potential to complement standard prognostic indicators used in risk stratification after AMI because of its strong, independent association with long-term survival, enhanced in vitro stability, and simplicity of analysis.

Plasma endothelin concentrations are strongly related to outcome after myocardial infarction and provide prognostic information independent of clinical and biochemical variables previously associated with a poor prognosis.

Results-Logistic regression analysis showed that plasma brain natriuretic peptide was the best predictor of increased left ventricular end diastolic pressure (,i 15 mm Hg) (P < 0.001), decreased left ventricular ejection fraction ( < 45%) (P < 0.001), and the combination of left ventricular ejection fraction < 45% and left ventricular end diastolic pressure > 15 mm Hg (P < 0.001). The areas under the ROC function for the detection of left ventricular dysfunction were 0-789 for brain natriuretic peptide, 0 665 for atrial natriuretic factor, and 0'610 for N-terminal pro-atrial natriuretic factor. Conclusions-Plasma brain natriuretic peptide seemed to be a better indicator of left ventricular function than plasma atrial natriuretic factor or N-terminal pro-atrial natriuretic factor. However, the overall diagnostic accuracy of circulating atrial natriuretic factor, N-terminal proatrial natriuretic factor, and brain natriuretic peptide as indicators of normal and impaired ventricular function in an unselected group of patients with coronary heart disease and a high frequency of previous myocardial infarction was relatively modest. (Heart 1996;76:232-237)

No abstract

The endocrine response to severe physical strain including lack of sleep has been investigated in army personnel during a combat course of 5 days' duration. The thyroxine (T4) concentration in serum increased during the first 24 h, and then declined at a rate corresponding to a halflife of 7.6 days and on day 6 had reached the lowest level, 55 ng/ml. Triiodothyronine (T3) displayed a similar pattern, although an increase during the first 24 h could not be demonstrated. Within 48 h after the course T4 had returned to normal, whereas the serum level of T3 was significantly below the level before the course (p less than 0.05). The serum level of TSH was suppressed during the course. The serum level of prolactin was significantly suppressed and growth hormone was markedly elevated during the course with a significant negative correlation (r=-0.6) between the two. In agreement with a previous report, there was a rapid and sustained suppression of the serum level of testosterone to a mean level of 1.1 ng/ml on day 5. Short periods of sleep (3--6 h) were shown to be effective in reversing the changes described in this paper, especially for growth hormone, prolactin, and testosterone.

No abstract

The effect of prolonged physical and psychological stress on the testicular function was studied in 8 students (age 22–25 years) of the Norwegian Academy of War during a combat course of 5 days' duration. The average urinary excretion of free cortisol and 17‐ketogenic steroids was 81 and 129% higher than the respective control values one week after the course. Plasma cortisol levels increased from 21.7 μg/100 ml at 8 a. m. before the course to 24.6 (P < 0.05), and serum HGH rose from undetectable levels, < 0.08 ng/ml, to an average value of 12.9 ng/ml ± 3.7 (SD) at 8 a. m. during the course. A marked suppressive effect on plasma testosterone levels from 5.6 ng/ml ± 1.4 to 0.9 ± 0.5, and no adjustment to stress was observed over a 5 day period. TeBG increased gradually from 26.9 nmol/l ± 9.9 to 52.7 ± 17.7 on day 6, followed by a slow decrease without reaching control values on day 12, suggesting that the decreased plasma testosterone levels probably reflect reduced production and not increased metabolism of testosterone. LH fluctuated during the course, but was significantly higher in the morning immediately following the end of the course than at the start (P < 0.02). It is postulated that the effect of stress on the plasma testosterone levels is mediated via an action both on the hypothalamus‐pituitary level and on the testis.

Thyroid function was evaluation in 26 postmenopausal women with breast cancer before and at various time intervals during treatment with tamoxifen. Tamoxifen treatment suppressed plasma levels of FT3 and FT4 (p < 0.005 for both) and elevated plasma concentrations of TBG (p < 0.005 and TG (p < 0.025). In general, these changes became significant after 6 months of treatment. Plasma TSH increased significantly after 1 y of treatment (p < 0.025). A fall in FT4 and FT3 combined with increase in TSH suggests a reduced bioavailability of T4 and T3 during tamoxifen treatment. The increase in TG may reflect a reduced synthesis or liberation of T4 resulting in a reduced plasma level of FT4. Our findings suggest that tamoxifen influences the thyroid hormone levels, not only by modulating plasma TBG, but also by interfering with hormone synthesis or secretion in the thyroid gland.