Molecular forms of brain natriuretic peptide and cardiotrophin-1 in the assessment of left ventricular systolic dysfunction after myocardial infarction and in subjects with chronic heart failure

Heart failure is common, has a poor prognosis and can be treated. The incidence is increasing, partly because of improved survival after myocardial infarction and partly because the population is aging and heart failure is a disease of the elderly. Despite advances in our understanding of the pathophysiology of heart failure, the diagnosis of heart failure remains enigmatic and requires the skills of the physician. Those skills have not yet been superseded by technology. The natriuretic peptide family of hormones have been used extensively to study a range of cardiovascular disorders. Plasma levels of brain natriuretic peptide (BNP-32), are elevated following myocardial infarction and in patients with heart failure with well documented associations of BNP-32 with indices of left ventricular function and prognosis in patients suffering these conditions. Amino-terminal pro brain natriuretic peptide (NT-proBNP) is a recently identified processing fragment of preproBNP (y-BNP) which circulates in plasma in higher concentrations than BNP-32 itself and may represent a more competent marker of underlying left ventricular function. Measurement of plasma NT-proBNP may serve an objective and cost- effective method for investigating ventricular dysfunction in clinical practice. Another candidate peptide for assessing left ventricular systolic dysfunction is Cardiotrophin -1 (CT-1), a member of the growing family lnterleukin-6 (IL-6) related cytokines that function via the glycoprotein 130 signalling pathway. CT-1 was originally identified as a cytokine capable of inducing cardiac hypertrophy. More recent indications from animal work suggest a role for CT-1 in the pathogenesis of left ventricular dysfunction following myocardial infarction and in models of heart failure. There is a clear need to take a broader view of heart failure management and seek to apply improvements in diagnostic methods and treatment more widely in the community for the benefit of all eligible patients. Increased emphasis on the early detection of left ventricular systolic dysfunction and intervention to delay progression and improve long term outcome should be our main priority.