Xu W, Goldberg SI, Shubina M, Turchin A. Optimal systolic blood pressure target, time to intensification, and time to follow-up in treatment of hypertension: population based retrospective cohort study. BMJ. 2015;350:h158.
When doing CPR, the mantra is “hard and fast.” It turns out the same is true for antihypertensive prescribing. In a new analysis of the “Health Improvement Network” database from the UK, looking at nearly 89,000 hypertensive patients to determine the “optimal” speed at which these medications should be initiated or adjusted, the authors conclude that we are essentially failing our patients if we do not intensify therapy within 1.4 months of an elevated reading or if we delay follow-up beyond 2.7 months.
The implication is clear: speed saves lives. But as usual in these massive retrospective cohorts, the authors have likely overlooked numerous confounders.
The study asserts that a systolic intensification threshold—the point at which a doctor decides to add a drug or increase a dose—greater than 150 mm Hg is associated with progressively greater risk of cardiovascular events or death. Conversely, they found no difference in risk between thresholds of 130 and 150 mm Hg. They also found that delays in intensification (waiting longer than that magical 1.4 months) were associated with increased hazard ratios. On the surface, this looks like a slam-dunk argument for aggressive, rapid-fire management. The authors even suggest that these findings support the “importance of avoiding delays” in medical management.
However, statistics are not necessarily real life. By equating “intensification” with “better outcomes,” the study ignores the mechanism of action. We are asked to believe that the benefit comes solely from the reduction in hydrostatic pressure achieved by the timely intervention. But we know better.
In the UK primary care setting during this era (1986–2010), “intensification” typically meant adding an ACE inhibitor, an ARB, or a specific calcium channel blocker. These agents do not merely lower the numbers on the sphygmomanometer; they have profound pleiotropic effects. They reduce oxidative stress, improve endothelial function, and reduce left ventricular remodeling. If a patient has a “low intensification threshold,” they are, by definition, more likely to be on a multi-drug regimen earlier in their disease course. Are they surviving because their systolic pressure is 138 mm Hg instead of 142 mm Hg? Or are they surviving because they are bathing their vasculature in renin-angiotensin-aldosterone system (RAAS) blockade? Like many studies in this area, it does not appear to adequately account for the specific class effects of the drugs being intensified. You can lower blood pressure with hydralazine, but you won’t get the same mortality benefit as you do with an ACE inhibitor. It may also be that patients with higher thresholds and worse outcomes were too sick to tolerate intensification.
Additionally, in terms of the “time to intensification” metric, the authors claim that a delay of greater than 1.4 months is associated with increased risk. This is a classic case of confounding by indication and physician practice, as there are any number of social and clinical factors that could affect rapidity of prescribing and also correlate with outcomes.
Ultimately, this study reinforces a “treat-to-target” mentality that prioritizes the metric over the patient. It encourages the clinician to view a blood pressure reading as a ticking time bomb that must be defused within 1.4 months, rather than a hemodynamic variable that requires thoughtful, sometimes slow, titration. If we blindly follow this logic, we will simply increase the pill burden without asking which pills actually confer benefit. We should treat hypertension, yes (usually). But let’s not pretend that the benefit lies in the speed of the prescription rather than the pharmacology of those medications. For the good of our patients, hopefully these results do not replace common sense with a stopwatch.
Dr. Confounder 
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