Objectives: B-type natriuretic peptide (BNP) is a strong diagnostic predictor of left-ventricular (LV)-dysfunction. Recently, the aminoterminal portion of pro-BNP (NT-proBNP) has been introduced, which could be even more sensitive because of its longer half-life. The aim of this study was to evaluate the new marker NT-proBNP within a large, heterogeneous population of patients with suspected cardiovascular disease at risk of cardiovascular dysfunction and to compare it with the established diagnostic parameter BNP. Subjects and methods: NT-proBNP and BNP were measured in 339 hospitalised patients undergoing diagnostic angiography (median age 66 years, 244 male vs. 95 female). Results: Median values of NT-proBNP increased with worsening LV-dysfunction and higher NYHA class. The area under the receiver operator characteristics curve (AUC) of NT-proBNP for detecting severe systolic dysfunction or for detecting any systolic LV-dysfunction was 0.83 and 0.77, respectively. The latter improved (AUCs0.81) when patients with clinically relevant heart disease like valvular dysfunction were included, independent of the haemodynamic values. Compared to BNP, NT-proBNP tended to be more accurate in identifying lesser degrees of LVdysfunction. Conclusions: Even after optimisation of target criteria, there was still a substantial overlap of NT-proBNP values between patients with and without relevant heart disease. Therefore, NT-proBNP is not suitable as a screening test for LVdysfunction in the community. Nevertheless, because of its good negative predictive value, NT-proBNP could be an easy and effective tool to rule out severe systolic LV-dysfunction in high risk patients. No clinically significant advantage of BNP testing could be found.

To assess the effects of fasting on recovery of function and exogenous glucose metabolism after 15 minutes of total ischemia, we perfused isolated working rat hearts from fed and fasted animals. Hearts were perfused in a recirculating system with bicarbonate buffer containing glucose (10 mM). Mechanical performance, release of marker proteins for ischemic membrane damage (lactate dehydrogenase, myoglobin, citrate synthase), and the concentrations of lactate and glucose in the perfusion medium were measured serially. Tissue metabolites were also measured. Fasting raised the myocardial glycogen content by 25%. Cardiac performance of perfused hearts from fed and fasted animals was the same during the preischemic and the post-ischemic period. The time of return of function to preischemic values was significantly less in hearts from fasted rats (2.3 versus 7.8 minutes, p less than 0.025). The release of cytosolic and mitochondrial marker proteins was significantly lower in hearts from fasted rats than in hearts from fed rats. Glucose metabolic rates during control and reperfusion were unchanged for hearts from fasted rats, but decreased for hearts from fed rats during reperfusion. The adenine nucleotide content at the end of ischemia was higher in hearts from fasted animals than in hearts from fed animals. We conclude that increasing glycogen levels prior to ischemia improves recovery of function, lessens membrane damage, and prevents loss of adenine nucleotides.

No abstract

To assess the effects of endogenous substrate on glucose utilization after 15 min of ischemia, we perfused isolated working rat hearts from fed and fasted (16 h) animals with glucose and the positron-emitting glucose analogue 2-[18F]fluoro-2-deoxy-D-glucose (2-FDG). Hearts were perfused in a recirculating system with bicarbonate buffer containing glucose (10 mM) and 2-FDG (0.5 microCi/ml). Mechanical performance and 2-FDG uptake were measured on-line, and glucose and lactate metabolic rates were calculated. Fasting raised the glycogen content by 25% and the triglyceride content by 38%. Hearts in both groups recovered preischemic function. Rates of 2-FDG uptake during the preischemic period were the same in both groups. In contrast, during the postischemic period rates of 2-FDG uptake were significantly depressed in hearts of fed animals but were unchanged in hearts of fasted animals. Thus hearts of fasted animals took up more 2-FDG during the postischemic period than hearts of fed animals (P less than 0.005). The lumped constant (range, 0.38-0.40) was the same in both groups before and after ischemia. Glucose utilization was suppressed during the postischemic period in hearts of fed animals, whereas at the same time lactate utilization was significantly increased. We conclude that 1) 2-FDG accurately traces glucose utilization independent of the nutritional state or ischemic insult; 2) reversibly ischemic, viable myocardium exhibits vastly different rates of glucose utilization depending on the nutritional state of the animal before ischemia; 3) lactate derived from glycolysis suppresses utilization of exogenously supplied glucose in the early reperfusion period without affecting postischemic performance.

Background: Levosimendan, a calcium sensitizer, increases the sensitivity of the heart to calcium, thus increasing myocardial contractility without a rise in intracellular calcium. It was recently shown that levosimendan is beneficial in improving renal function. However, it remains to be established that the beneficial effect is differentially related to renal status during index event.