This even seems to be the case in individuals with high BNP levels but no apparent cardiac abnormality on phenotyping (false positives). Several studies show that BNP levels predict prognosis over and above a wide range of baseline echocardiographic abnormalities, although, buy MK-2206 as would be expected, each echocardiographic abnormality explained part of the BNP risk 4, 5, 6 and 7. The unexplained extra BNP risk not accounted for by echocardiographic abnormalities may be related to BNP being

able to predict future but not yet apparent abnormalities in left ventricular (LV) structure or function 5 and 8. The hypothesis that these data raise is that one of the drivers for future LV abnormalities is intracardiac pressure and that an early subtle elevation in intracardiac pressure can be picked up by BNP before LV abnormalities are either present or detectable on imaging. We therefore set out to see whether in individuals with no apparent cardiac abnormality at baseline a high BNP value could identify those who would develop a cardiac abnormality during find more the next few years. We focused particularly on left ventricular mass (LVM) to

see whether BNP predicted how this would change during the next few years in a population of treated primary prevention patients. This is a substudy of a previously reported larger study from our center (1). The original study recruited 300 primary prevention patients with well-treated primary risk factors G protein-coupled receptor kinase between April 2008 and July 2010 from local general practitioner surgeries and from the cardiovascular

(CV) risk clinic at Ninewells Hospital, Dundee, United Kingdom. Patients included in the original study were 50 years or older, and were eligible for primary prevention only with no previous known CV events. They had to be stable on therapy for at least 1 year and to have reached target for their primary risk factor, for example, office blood pressure (BP) ≤140/90 mm Hg. We excluded those with previously known CV disease, known renal impairment (estimated glomerular filtration rate [eGFR] <60 ml/min), atrial fibrillation, and significant (defined as more than mild) valvular heart disease. All study subjects underwent clinical assessment, biochemical measurements (including BNP), electrocardiography, transthoracic echocardiography, dobutamine stress echocardiography to detect myocardial ischemia, and 24-hour ambulatory BP measurement. From the original cohort of 300 primary prevention patients, 62 patients underwent baseline cardiac magnetic resonance (CMR) and 50 of them completed a second CMR after a mean follow-up of 3 years. These 62 patients were selected for 2 reasons: 1) freedom from any silent cardiac target organ damage in the form of either left ventricular hypertrophy (LVH), LV diastolic or systolic impairment, left atrial enlargement, and inducible myocardial ischemia; and 2) a wide range of baseline BNP levels. The reasons for 12 patients having no second CMR scan are shown in Online Figure 1.