Outcomes of Treated Hypertension at Age 80 and Older

Cohort Analysis of 79,376 Individuals

João Delgado, PhD; Jane A. H. Masoli, MBChB; Kirsty Bowman, MPH; W. David Strain, MD; George A. Kuchel, MD; Kate Walters, PhD; Louise Lafortune, PhD; Carol Brayne, MD; David Melzer, PhD; Alessandro Ble, MD

Disclosures

J Am Geriatr Soc. 2017;65(5):995-1003. 

In This Article

Results

Data were from 79,376 individuals aged 80 and older who met inclusion criteria for the analysis. Mean age was 82.1 ± 3.3, and 30.5% were men ( Table 1 ). The average number of BP measurements according to SBP category varied from 7.2 for SBP less than 125 mmHg to 13.4 for SBP of 165 to 174 mmHg (Table S3). There were trends in covariates across SBP (e.g., current or recent smoking 24% at SBP <125 mmHg and 18% at SBP >185 mmHg) ( Table 1 ). Maximum follow-up was 11.9 years (overall mean 4.4 ± 2.9 years), with mean follow-up times somewhat shorter in the low SBP groups.

All-cause Mortality According to Attained SBP

During follow-up, 25,543 patients died ( Table 1 ). Mortality hazards showed a U-shaped pattern (Figure 1, Table 2 ), with lowest mortality in individuals with SBP of 135 to 154 mmHg (hazard ratio (HR) = 1.03, confidence interval (CI) = 0.99–1.06, risk is essentially the same as that of the comparison group of SBP 145–154 mmHg) and greater mortality for higher levels of SBP. The risk of mortality was greater for SBP less than 135 mmHg (combining the two lowest SBP categories, 13.1% of participants) (HR=1.25, 95% CI=1.19–1.31). This excess risk is equivalent to one extra death for every 13 individuals aged 80 and older with SBP less than 135 than for the comparison group based on number needed to harm estimation. Mortality hazard was estimated separately in 2-year follow-up segments to check for stability between short- and longer-term outcomes (Table S4). Lower attained SBP (<135 mmHg) was associated with greater mortality in all follow-up periods, although estimates for the first 2 years were higher (HR = 1.38, 95% CI = 1.26–1.51) than, for example, at 6 to 8 years follow-up (HR = 1.19, 95% CI = 1.07–1.32), albeit with overlapping confidence intervals. Central estimates of mortality hazard were higher again from 8 years to end of follow-up (HR = 1.29, 95% CI = 1.09–1.53), although in small numbers of participants.

Figure 1.

Risk of all-cause mortality according to systolic blood pressure.

To test for modifying effects of DBP, DBP was grouped into 85 mmHg and higher, 70 to 84 mmHg, and less than 70 mmHg (estimates with more-extreme groups were underpowered). The U-shaped pattern of systolic mortality hazard was similar for all three DBP groups ( Table 3 , Figure S2). The modifying effect of pulse pressure on all-cause mortality was also tested by adjusting the model for five levels of pulse pressure (<50 mmHg, 50–59 mmHg (reference), 60–69 mmHg, 70–79 mmHg, ≥80 mmHg). A significantly greater risk of all-cause mortality remained in those with low BP even when adjusted for pulse pressure (<125 mmHg: HR = 1.33, 95% CI = 1.2–1.48, P < .001; 125–134 mmHg: HR = 1.15, 95% CI = 1.08–1.22, P < .001).

An interaction term and analysis stratified according to sex (Table S5) demonstrated that differences according to sex were not significant. An analysis of similarly selected individuals with one or two recorded blood pressure measures (n = 5,012) in the 3 years before baseline resulted in a similar risk curve to that of individuals with 3 or more measurements (Table S6). Sensitivity analyses adjusted for and stratified according to level of comorbidity (Charlson Comorbidity Index[12]), major weight loss (≥10% in 5 years before baseline), or BMI or excluding individuals with consultations in institutional settings during the baseline period; in all cases, mortality at low SBP (<135 mmHg) remained significantly greater. Analyses adjusting for and excluding individuals with diabetes mellitus and with chronic obstructive pulmonary disease had similar results (Table S2).

Incident Disease

There was an approximately linear increase in risk of incident MI across the SBP range (Figure 2), with lower SBP associated with lower risk (<125 mmHg: HR = 0.6, 95% CI = 0.43–0.84, number needed to treat 9.8; 125–134 mmHg: HR = 0.78, 95% CI = 0.67 to 0.92, number needed to treat 25.8) than the SBP 145 to 154 mmHg ( Table 2 , Table S7). Risk of incident stroke was greater at SBP above 145 to 154 mmHg (Figure 2).

Figure 2.

Risk of all-cause mortality and systolic blood pressure according to diastolic blood pressure.

During follow-up, 7,882 individuals developed heart failure ( Table 1 ). Competing subhazards for incident heart failure rose progressively at SBP above 145 to 154 mmHg, but there was also greater risk for lower SBP (e.g., SBP <125 mmHg: HR = 1.2, 95% CI = 1.02–1.4, number needed to harm 28.6) (Figure 2, Table 2 ).

During follow-up, 7,360 individuals were admitted to hospital with a fragility fracture or had surgical intervention for a hip fracture (follow-up mean 4.4 ± 2.9 years). Risk of fracture was not different for different SBP, with no indication of greater risk with low SBP.

Confounding of the association between SBP less than 135 mmHg and greater mortality might theoretically have been due to undiagnosed cancer present at baseline, but cancer incidence during the 11.9 years of follow-up was not significantly different (and tended to be lower) in those with (e.g., HR = 0.93, 95% CI = 0.81–1.06) SBP less than 125 mmHg. The highest cancer incidence was in the reference group of SBP 145 to 154 mmHg, and cancer incidence was significantly lower at SBP greater than 175 mmHg (e.g., HR = 0.85, 95% CI = 0.75–0.95) for SBP of 175 to 184 mmHg. Although there were no data on why cancer incidence was lower in the low and high SBP categories, an analysis for all-cause mortality adjusted for incident cancer, and separate analyses for individuals with and without incident cancer, did not significantly alter results (Table S8).

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