Those with Known Cardiovascular Risk

factors or disease or those found to have hypertension, renal dysfunction, or echocardiographic abnormalities. This we feel would leave very few, if any, subjects with important silent CAD. Furthermore, whether such subjects, if present, would have had raised NTpBNP levels is unclear, with no prior study analysing NTpBNP levels in subjects with asymptomatic CAD. Indeed, the paper by Kragelund et al. from which they quote found that in subjects with symptoms or signs of CAD, NTpBNP levels were raised themost in those with left ventricular systolic dysfunction, prior heart attack, diabetes mellitus, clinically significant CAD and renal dysfunction, conditions all excluded in our normal range assessment, and increased age, something stratified for in our study. Furthermore, there was virtually no difference in NTpBNP levels between those with or without CAD on angiography if left ventricular ejection fractionwas normal, despite a higher risk profile in thosewith CAD. Thus, themerits and indeed the ethics of performing coronary angiography on asymptomatic subjects, unlikely to gain prognostic benefit and unlikely to alter the study’s findings, are unclear, especially with estimated morbidity and mortality rates of 1.8 and 0.08%, respectively. We thus stand by our conclusions and our developed normal range and would be happy for other authors to prospectively test them in other population groups.