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.

Objectives To assess the probability of left ventricular systolic dysfunction without echocardiography in patients from general practice. Design Cross sectional study using multivariate regression models to examine the relation between clinical variables and left ventricular systolic dysfunction as determined by echocardiography. Setting Three general practices in Copenhagen. Subjects 2158 patients aged > 40 years were screened by questionnaires and case record reviews; 357 patients with past or present signs or symptoms of heart disease were identified, of whom 126 were eligible for and consented to examination. Main outcome measures Clinical variables that were significantly (P < 0.05) related to ejection fraction <0.45 and their predictive value for left ventricular systolic dysfunction. Results 15 patients (12%) had left ventricular systolic dysfunction. The prevalence was significantly related to three questions: does the electrocardiogram have Q waves, left bundle branch block, or ST-T segment changes? (P = 0.012); is resting supine heart rate greater than the simultaneous diastolic blood pressure? (P = 0.002); and is plasma N-terminal atrial natriuretic peptide > 0.8 nmol/l? (P = 0.040)? Only one of 60 patients with a normal electrocardiogram had systolic dysfunction (2%, 95% confidence interval 0% to 9%) regardless of response to the other two questions. The risk of dysfunction was appreciable in patients with a yes answer to two or three questions (50%, 27% to 73%). Conclusions A normal electrocardiogram implies a low risk of left ventricular systolic dysfunction. Patients can be identified for echocardiography on the basis of an abnormal electrocardiogram combined with increased natriuretic peptide concentration or a heart rate greater than diastolic blood pressure, or both.

Abstract. Svendstrup Nielsen L, Svanegaard J, Wiggers P, Egeblad H (Haderslev

The measurement of atrial natriuretic peptide separated the patients into low and high risk groups after acute myocardial infarction.

In the presence of a primary disorder in myocardial contractility and/or extraordinary hemodynamic pressure on the heart, ventricular performance depends on several compensating mechanisms. In the past, studies were mostly focused on the importance of the Frank-Starling mechanism and the hypertrophy and dilation of the heart in maintaining a circulation sufficient for metabolic intake during heart failure. Recently, however, the existence of neurohormonal systems has been demonstrated (the sympathetic nervous system, the renin-angiotensin system, atrial natriuretic peptide and several locally produced vasoactive substances), which change considerably according to the severity of the heart failure. While these compensatory mechanisms support the circulation in patients with acute heart failure, in whole or in part, neurohormonal activation over an extended period of time might be harmful to patients with chronic congestive heart failure since several neurohormonal factors might be inappropriately activated. This article will review the key neurohormonal systems and their importance in heart failure on the basis of the current literature.