Raised blood pressure with age, hypertension, is a major downstream consequence of low-level biochemical damage and cellular dysfunction, converting it into high-level structural damage in the body and brain. Hypertension is an important proximate contributing cause of ultimately fatal age-related conditions of the cardiovascular system, kidneys, brain, and lungs, among others. Pressure damage in delicate tissues degrades function in many organs, particularly in the central nervous system where there is little to no regeneration capable of reversing that damage. More subtly, hypertension also causes heart muscles to enlarge and weaken, contributing to heart failure. Hypertension also accelerates the development of atherosclerosis, through mechanisms independent of other factors such as chronic inflammation.
Hypertension is so great a contribution to age-related disease, such an important mediating mechanism, that it is possible to produce sizable reductions in mortality by forcing a lower blood pressure, even without addressing the underlying causes in any way. The widespread use of antihypertensive medications to achieve this goal is one of the success stories of mainstream medicine in recent decades. There are, sadly, not all that many mechanisms that rise to this level of importance as single downstream consequences of low-level biochemical damage in aging. Chronic inflammation is another, but beyond that the only way to make significant progress towards control of aging is to repair the underlying damage. Attempting to address downstream consequences is largely very hard and of limited utility. Control of blood pressure and inflammation are outliers in this context.
Treatment and control of high blood pressure (BP) is a key strategy for reducing coronary heart disease (CHD), stroke, heart failure (HF), and all-cause mortality among adults with hypertension. Accordingly, clinical practice guidelines provide recommendations for accurately identifying adults with hypertension, initiating appropriate antihypertensive therapy, and achieving predefined BP goals that have been shown to be associated with lower cardiovascular disease (CVD) and all-cause mortality event rates in randomized trials. However, less is known about the role of sustaining BP control over time.
In clinical practice, patients may be followed over many years and often experience times of controlled as well as uncontrolled BP. There are several reasons why BP control may change over time, including changes in patients' health status or medication adherence, variability in BP measurement from visit to visit, or reduction in antihypertensive medication intensity due to concerns about overtreatment on the part of the provider. The proportion of visits at which patients achieve BP control can easily be calculated, could be used to facilitate discussions with patients about treatments goals, and could be used as a performance measure for quality improvement. Also, data on the effects of maintaining sustained BP control could be used to support greater treatment consistency over time or conversely, to allow higher BP levels at some visits.
Findings from a limited number of studies suggest that having BP control at a greater proportion of visits over time is associated with a lower CVD risk. However, prior studies included primarily white participants, those with existing coronary heart disease (CHD), or with multiple CVD risk factors. The purpose of the current study was to determine the association of sustained BP control with CHD, stroke, HF, and mortality in an observational analysis of a demographically and clinically diverse population within a large clinical trial, the Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT). Participation was restricted to 24,309 participants with four to seven visits with systolic BP (SBP) measurements during a 22-month period. Participants were as having sustained BP control (SBP lower than 140 mm Hg) at 100%, 75% to 100%, 50% to 75%, and fewer than 50% of visits during this period.
In this observational analysis of participants from ALLHAT, those with SBP control, defined as SBP lower than 140 mm Hg at fewer than 50% of study visits, were more likely to have a stroke, develop HF, or experience the combined outcome of fatal CHD/nonfatal myocardial infarction, stroke, or HF. These associations were present after adjustment for potential confounders. Compared to those with SBP control at 100% visits, adjusted hazard rations among those with SBP control at fewer than 50% of visits was 1.16 for fatal CHD/nonfatal myocardial infarction, 1.71 for stroke, 1.63 for heart failure, 1.39 for the composite CVD outcome, and 1.14 for mortality. Sustained SBP control may be beneficial for preventing stroke, heart failure, and CVD outcomes in adults taking antihypertensive medication.