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Clinic blood pressure (BP) is recommended for absolute cardiovascular disease (CVD) risk assessment. However, in 'real-world' settings, clinic BP measurement is unstandardised and less reliable compared to more rigorous methods but the impact for absolute CVD risk assessment is unknown. This study aimed to determine the difference in absolute CVD risk assessment using real-world clinic BP compared to standardised BP methods. Participants were patients (n = 226, 59 ± 15 years; 58% female) with hypertension referred to a BP clinic for assessment. 'Real-world' clinic BP was provided by the referring doctor. All participants had unobserved automated office BP (AOBP) and 24-h ambulatory BP monitoring (ABPM) measured at the clinic. Absolute CVD risk was calculated (Framingham) using systolic BP from the referring doctor (clinic BP), AOBP and ABPM, with agreement assessed by Kappa statistic. Clinic systolic BP was 18 mmHg than AOBP and daytime ABPM and 22 mmHg higher than 24-h ABPM (p < 0.001). Subsequently, absolute CVD risk scores using clinic BP were higher compared to AOBP, daytime ABPM and 24-h ABPM (10.4 ± 8.1%, 7.8 ± 6.4%, 7.8 ± 6.3%, and 7.3 ± 6.1%, respectively, P < 0.001). As a result, more participants were classified as high CVD risk using clinic BP (n = 89, 40%) compared with AOBP (n = 44, 20%) daytime ABPM (n = 38, 17%) and 24-h ABPM (n = 38, 17%) (p < 0.001) with weak agreement in risk classification (κ = 0.57[0.45-0.69], κ = 0.52[0.41-0.64] and κ = 0.55[0.43-0.66], respectively). Real-world clinic BP was higher and classified twice as many participants at high CVD risk compared to AOBP or ABPM. Given the challenges to high-quality BP measurement in clinic, more rigorous BP measurement methods are needed for absolute CVD risk assessment., (© 2024. The Author(s).)

The importance of growth hormone deficiency (GHD) in adult life has become more apparent over the last decade. As well as a distinct clinical syndrome there is a significant excess risk of cardiovascular disease. Although it is difficult to ascertain what part is played by the original pituitary disorder and the concomitant replacement hormonal therapies, there is clear evidence that GHD is associated with known cardiovascular risk factors such as body shape, lipid profile, insulin resistance, blood pressure, vessel wall morphology and haemostatic factors. Novel means of assessing vascular risk such as pulse wave velocity and flow-mediated dilatation can also estimate the risk without invasive procedures. The role of possible mediators of endothelial function such as nitric oxide and free radicals is being investigated further. Replacement of GH in GH-deficient patients leads to many effects on the above indices, some but not all of which are associated with reduced vascular risk. Long-term follow-up studies of morbidity and mortality are required for an accurate assessment of the beneficial effects of therapy.