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Reduction in mean 48-h SBP was inferior as a therapeutic target and was not [http://www.selleckchem.com/products/pfi-2.html PFI-2 solubility dmso] associated with improved outcomes in statistical models that incorporated measurements of asleep BP. Therefore, sleep-time BP qualifies as a validated target of antihypertensive therapy. The authors suggest that treatment should be directed routinely at nocturnal BP and that this goal is best accomplished by nighttime administration of antihypertensive medications. In the MAPEC study, hypertensive patients were randomized to receive all of their medications in the morning or to ingest 1 or more at bedtime. In a previous paper, the authors reported that patients receiving at least some of their medications at bedtime had a significantly lower relative risk (RR) of total CV events, compared with those taking all of their medications upon awakening (RR: 0.39, 95% confidence interval: 0.29 to 0.51, p [https://en.wikipedia.org/wiki/MASP1_(protein) MASP1] attributed to nocturnal drug administration (5). The critical importance of reducing sleep-time BP might explain, at least in part, the problematic results of several earlier studies. In the ACCORD (Action to Control Cardiovascular Risk in Diabetes) study, for example, aggressive overall BP reduction did not improve CV outcomes in diabetic patients (6). In the MAPEC study, reduction of mean 48-h BP was not associated with significant risk reduction in statistical models that incorporated asleep BP. In the CONVINCE (Controlled Onset Verapamil Investigation of Cardiovascular Endpoints), a timed-release formulation of verapamil that targeted the early-morning rise in BP failed to show an advantage over conventional am administration of atenolol/hydrochlorothiazide (7). In the present study, diminution of the early-morning rise in BP had no effect on CV events. In the [http://www.selleckchem.com/products/azd6738.html AZD6738] HOPE (Heart Outcomes Prevention Evaluation) study, the marked reduction in CV endpoints��seemingly out of proportion to the modest changes observed in clinic BP��could perhaps be explained by the protocol-specified administration of the study drug (ramipril) at bedtime. This hypothesis is supported by the marked reduction in nocturnal BP reported in a small ABPM substudy of HOPE (8) as well as data from the present study group demonstrating that bedtime administration of ramipril results in superior nocturnal BP regulation without compromising antihypertensive efficacy during the waking hours (9). The implications of these findings for clinical practice are substantial. A strong case can be made to accept the conclusion of the authors that bedtime administration of at least some portion of the antihypertensive regimen of the patient should become the default standard.