Aim: Evaluation of N-terminal pro-brain natriuretic peptide (NT-proBNP) to confirm or disprove heart failure in community patients complaining of dyspnoea. Methods and results: General practitioners referred 345 consecutive patients complaining of dyspnoea to our hospital-based clinic, where a diagnosis was established based on a combined programme for heart and lung diseases including echocardiography. The level of NT-proBNP in plasma was also measured. The mean (S.D.) concentration of NT-proBNP in patients with heart failure was significantly higher, 189 (270) pmolyl in patients with heart failure (ns81), than in patients with non-cardiac dyspnoea (ns264), 17 (38) pmolyl (P-0.001). In patients 050 years NT-proBNP -11 pmolyl for men and -17 pmolyl for women excluded heart failure with a negative predictive value of 97% while the positive predictive value was 53%, the sensitivity 95% and the specificity 68%. Areas under receiver operator characteristic curves for men and women were 0.93 and 0.90, respectively. Conclusion: In a relevant setting of primary care patients complaining of dyspnoea, NTproBNP seems promising for disproval of heart failure, and this test may reduce the need for echocardiographic screening with 50%. However, the discrimination levels of NT-proBNP found in this study may need prospective confirmation, before the test can be generally recommended.
The effects of 4 wk of detraining on maximal O2 uptake (VO2max) and on endurance capacity defined as the maximal time to exhaustion at 75% of VO2max were studied in nine well-trained endurance athletes. Detraining consisted of one short 35-min high-intensity bout per week as opposed to the normal 6-10 h/wk. Detraining had no effect on VO2max (4.57 +/- 0.10 vs. 4.54 +/- 0.08 l/min), but endurance capacity decreased by 21% from 79 +/- 4 to 62 +/- 4 min (P < 0.001). Endurance exercise respiratory exchange ratio was higher in the detrained than in the trained state (0.91 +/- 0.01 vs. 0.89 +/- 0.01; P < 0.01). Muscle [K+] values were unchanged during exercise and were similar in the trained and detrained states. Muscle [Mg2+] values were similar at rest and at minute 40 (30.3 +/- 0.9 vs. 30.8 +/- 0.6 mmol/kg dry wt) but increased significantly at exhaustion to 33.8 +/- 1.0 mmol/kg dry wt in the trained state and to 33.9 +/- 0.9 mmol/kg dry wt in the detrained state. The elevated muscle [Mg2+] at exhaustion could contribute to fatigue in prolonged exercise through an inhibition of Ca2+ release from sarcoplasmic reticulum. It is concluded that the endurance capacity can vary considerably during detraining without changes in VO2max. Altered substrate utilization or changes in electrolyte regulation may account for the reduced endurance capacity.
To explore a possible interaction between digoxin and verapamil, a single‐dose kinetic study of digoxin was performed and then repeated after 10 days of verapamil treatment in eight healthy subjects. Verapamil diminished the apparent central distribution volume of digoxin from 0.83 ± 0.25 to 0.64 ± 0.17 l/kg (P < 0.05) and reduced total body clearance of digoxin from 3.28 ± 0.58 to 2.15 ± 0.66 ml/min/kg (P < 0.001) by impairing both renal and extrarenal clearance. Biological digoxin half‐life rose from 38.6 ± 8.5 to 50.5 ± 8.3 hr (P < 0.005). Reduction of renal clearance of digoxin may be due to inhibition of tubular secretion. The underlying mechanisms of extrarenal interaction are not known, but impaired hepatic degradation of digoxin induced by verapamil should be considered. Clinical Pharmacology and Therapeutics (1981) 30, 311–316; doi:
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