Dosing of levosimendan with a 10-min bolus of 6 to 24 microg/kg followed by an infusion of 0.05 to 0.2 microg/kg/min is well tolerated and leads to favorable hemodynamic effects.

One week of creatine supplementation to patients with chronic heart failure did not increase ejection fraction but increased skeletal muscle energy-rich phosphagens and performance as regards both strength and endurance. This new therapeutic approach merits further attention.

(Gln4)-neurotensin was infused i.v. for 5 to 70 min at 3 different infusion rates (6, 12 and 18 pmol X kg-1 X min-1, respectively) in 19 male volunteers, aged 26-47. The plasma concentration of neurotensin-like immunoreactivity (NTLI), the lower esophageal sphincter (LES) pressure, blood pressure, heart rate. ECG and blood glucose concentration were measured. The volunteers did not report any subjective effects during the infusion. Following infusion periods of 30 min or more the volunteers often reported bowel movements starting 5 min or more after cessation of the infusion. Neither blood pressure nor heart rate changed significantly. No changes were noted in the continuous ECG or in the blood glucose concentration. Apparent steady state levels of about 300 pM NTLI were reached at about 40 min during infusion of 12 pmol X kg-1 X min-1 (Gln4)-neurotensin. In all volunteers the LES pressure was significantly reduced within 5 min of starting the infusion. In 6 volunteers 12 pmol X kg-1 X min-1 (Gln4)-neurotensin was infused i.v. for 5 min. The LES pressure decreased significantly (P less than 0.01) from 13.7 +/- 1.3 mmHg to 5.3 +/- 0.8 mmHg. The decrease in the LES pressure occurred at plasma NTLI concentrations of approximately 50 pM, i.e. at levels below those obtained in man after a meal or the ingestion of fat. The present data further support the hypothesis that in man plasma neurotensin, or a neurotensin metabolite is an endocrine hormone involved in the postprandial regulation of the motor functions of the gastrointestinal tract.

Acute myocardial infarction occurred in 11 of 212 consecutive renal transplant recipients. This incidence is more than 10 times greater than that for an age- and sex-matched unselected population. All 11 patients died from infarction. 5 of the first attack and the rest within the nest 12 months from recurrence. The risk of developing myocardial infarction was greatest for older recipients who had been suffering from angina pectoris prior to the transplantation.

. Yue Q‐Y, Beermann B, Lindstrom B, Nyquist 0 (Huddinge University Hospital, Huddinge, and the Medical Product Agency, Uppsala, Sweden). No difference in blood thiamine diphosphate levels between Swedish Caucasian patients with congestive heart failure treated with furosemide and patients without heart failure. Intern Med 1997; 242:49 1‐49 5. Objectives: To determine whether furosemide treatment in congestive heart failure (CHF) patients is associated with thiamine deficiency. Design: Patients without heart failure and without diuretic treatment were included to compare with patients with CHF belonging to New York Heart Association (NYHA) functional class I1 and 111‐IV, respectively, and receiving furosemide therapy. Setting: All patients were recruited from the emergency ward of the cardiology section, Huddinge University Hospital, where they were admitted due to CHF or acute myocardial infarction. Subjects: Ninety‐nine patients were included from whom a blood sample was taken, as well as routine admission blood samples for the analysis of thiamine diphosphate (TPP) concentrations: Patients taking vitamin preparations were excluded. Main outcome measures: Blood TPP concentrations were measured by high performance liquid chromatography (HPLC) and compared between the patient groups by the use of ANOVA. Results: No significant difference was found between the groups in blood TPP concentrations. Conclusions: Thiamine deficiency may not be a complication of furosemide treatment in the studied Swedish patient population.