However we know with certainty that in the population we studied here, none of these cardiac abnormalities were present at baseline, meaning that the BNP elevation at baseline was truly unexplained by any prevalent cardiac abnormality. This makes our study selleck products unique as most data on BNP being of prognostic significance over and above echocardiographic abnormalities did not do the comprehensive phenotyping that we did and in particular did not screen for

myocardial ischemia, which is known to independently increase BNP 4, 5, 6, 7 and 16. In previous studies, some of the prognostic significance of BNP over and above resting echocardiographic abnormalities could be attributable to silent myocardial ischemia, which was not tested for in those studies. However, we have here demonstrated an additional explanation for why BNP is prognostic beyond echocardiographic abnormalities at baseline, which is that baseline BNP can identify those whose LVM will increase with time. A lot of recent data are suggesting that measuring BNP might one day establish a role

for itself in better managing patients with treated hypertension (2). Paget et al. showed that there was a 3-fold increase in mortality in the top versus the bottom tertile of N-terminal pro-BNP in treated hypertensive patients, even after adjusting for traditional risk factors (2). Recent information from the ASCOT trial shows the same (17). These 2 papers suggest that http://www.selleckchem.com/products/Lapatinib-Ditosylate.html BNP could become a measure within individuals at target BP of whether antihypertensive therapy will actually prevent CV events in them or not. In turn, this begs the question of which (treatable) cardiac abnormalities might be causing the residual risk seen in treated hypertensive patients

with a high BNP. Nadir et al. answered that question by showing that treated hypertensive patients with a high BNP had a combination of LVH, LV diastolic dysfunction, LA enlargement, LV systolic dysfunction, and silent ischemia (in that order of frequency) (1). Importantly, many patients had multiple silent cardiac abnormalities. This study extends that information to now show that in those with no cardiac abnormality at baseline, the elevated residual risk identified by Glutathione peroxidase BNP is likely to be also related to future increases in LVM 18 and 19. There are a few likely explanations for our results. A time effect is likely in that a raised intracardiac pressure genuinely precedes the increase in LVM. BNP is a much more sensitive marker for this increased intracardiac pressure owing to its greater reproducibility of repeat measures and a greater measurement range, whereas imaging parameters change over a much smaller range. This means an early subtle elevation in intracardiac pressure can be picked up by BNP before LV abnormalities are either present or detectable on imaging.