Aims:To demonstrate the benefit of the combination amlodipine/valsartan 5/160 mg over amlodipine 10 mg, in producing a lower incidence of peripheral oedema for a comparable mean sitting systolic blood pressure (MSSBP) reduction.Methods:After a 4-week amlodipine 5 mg run-in phase, inadequately controlled hypertension patients (aged ≥ 55 years, MSSBP ≥ 130 and ≤ 160 mmHg) were randomised to receive amlodipine/valsartan 5/160 mg or amlodipine 10 mg for 8 weeks, followed by amlodipine/valsartan 5/160 mg for 4 weeks for all patients. Primary variables were MSSBP change from baseline to week 8 and incidence of peripheral oedema reported as an AE. Resolution of peripheral oedema was assessed 4 weeks after switching patients from amlodipine 10 mg to amlodipine/ valsartan 5/160 mg.Results:At week 8, MSSBP showed greater reduction with amlodipine/valsartan 5/160 mg than amlodipine 10 mg (least square mean: −8.01 vs.−5.95 mmHg, p<0.001 for non-inferiority and p=0.002 for superiority). Systolic control, overall BP control and systolic response rate at week 8 were significantly higher with combination than amlodipine 10 mg (34 vs. 26%; 57 vs. 50%; 36.57 vs. 27.77%, respectively). Incidence of peripheral oedema was significantly lower with the combination than amlodipine 10 mg (6.6 vs. 31.1%, p<0.001). Peripheral oedema resolved in 56% patients who switched from amlodipine 10 mg to the combination, without the loss of effect on BP reduction.Conclusion:In non-responders to amlodipine 5 mg, treatment with amlodipine/valsartan 5/160 mg induced significantly less peripheral oedema than amlodipine 10 mg for similar BP reduction. Peripheral oedema resolved in > 50% patients switching from amlodipine 10 mg to the combination.

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Microalbuminuria (MAU), high-sensitivity C-reactive protein (hsCRP), and N-terminal pro-brain natriuretic peptide (NT-proBNP) are risk markers used to predict the prognosis of hypertensive patients; however, they have not been prospectively evaluated in primary care. An investigation was conducted using i-SEARCH Plus, a registry documenting 1649 patients with hypertension who received irbesartan at officebased cardiologists over 12 months. Mean age at baseline was 61.4AE11.3 years, 43.2% were women, and blood pressure was 159.8AE20.1 ⁄ 93.4AE11.9 mm Hg. Median albumin ⁄ creatinine ratio (ACR) at baseline was 9.90 (interquartile range [IQR], 5.76-25.52) mg ⁄ g, hsCRP 2.46 (IQR, 1.16-5.14) mg ⁄ L, and NT-proBNP 89.28 (IQR,) pg ⁄ mL. In patients with MAU (ACR !20 mg ⁄ g), the age-adjusted risk of a combined end point of newly diagnosed coronary artery disease (CAD), myocardial infarction, stroke ⁄ transitory ischemic attack, and death at 12-month follow-up was increased (odds ratio [OR], 2.67; 95% confidence interval [CI], 1.49-4.76), as was the incidence of CAD (OR, 3.27; 95%CI, 1.39-7.68) and death (OR, 4.63; 95%CI,. No correlations with end points were found for hsCRP or NT-proBNP after adjusting for age and the presence of MAU. MAU is an independent predictor of cardiovascular events in hypertensive patients. These findings confirm previous reports on the prognostic value of MAU and establish its incremental value over hsCRP and NT-proBNP. J Clin Hypertens (Greenwich). 2010;12:909-916. R isk markers for future cardiovascular (CV) events gain importance in cases in which the absolute risk is low and the incremental efficacy of new therapeutic options is not dramatic. Hypertension in particular is a disease that gradually develops even at younger ages when CV events are infrequent. The determination of significant differences between drugs and drug classes in this patient population would require large

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