Published online before print February 2, 2009, doi: 10.1161/HYPERTENSIONAHA.108.119792
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(Hypertension. 2009;53:458.)
© 2009 American Heart Association, Inc.
Original Articles |
Isolated Systolic Hypertension and Incident Heart Failure in Older Adults
A Propensity-Matched Study
From the University of Alabama at Birmingham (O.J.E, R.M.A, P.W.S, D.A, I.A, A.A) and the Veterans Affairs Medical Center (R.M.A, P.W.S., A.A), Birmingham, Ala; and Case Western Reserve University (T.E.L.), Cleveland, Ohio.
Correspondence to Ali Ahmed, University of Alabama at Birmingham, 1530 3rd Ave South, CH-19, Suite 219, Birmingham, AL 35294-2041. E-mail aahmed{at}uab.edu
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Abstract |
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The association between isolated systolic hypertension (ISH) and incident heart failure (HF) has not been prospectively studied in a propensity-matched population of ambulatory older adults. Of the 5795 participants in the public-use copy of the Cardiovascular Health Study data set, 5248 had diastolic blood pressure <90 mm Hg and were free of HF at baseline. Of these, 2000 (38%) had ISH, defined as average seated systolic blood pressure
140 mm Hg. Propensity scores for baseline ISH were calculated for each participant (based on 64 baseline covariates) and were used to match 1260 pairs of participants with and without ISH. Matched Cox regression models were used to estimate the association of ISH with incident HF during a mean follow-up of 8.7 years. Matched participants (n=2520) had a mean (±SD) age of 74 (±6) years, 60% were women, 16% were nonwhites, 18% developed new-onset HF, and 35% died. Incident HF developed in 20% (rate: 242/10 000 person-years) and 16% (rate: 194/10 000 person-years) of participants with and without ISH, respectively (matched hazard ratio when ISH was compared with no ISH: 1.26; 95% CI: 1.04 to 1.51; P=0.016). Prematch unadjusted, multivariable-adjusted, and propensity-adjusted hazard ratios (95% CIs) for ISH-associated incident HF were, respectively, 1.72 (1.51 to 1.97; P<0.0001), 1.35 (1.18 to 1.56; P<0.0001), and 1.22 (1.04 to 1.44; P=0.016). ISH had no association with all-cause mortality (matched hazard ratio: 1.03; 95% CI: 0.88 to 1.19; P=0.732). In conclusion, in a propensity-matched cohort of community-dwelling older adults who were well balanced in 64 baseline covariates, ISH was associated with increased risk of incident HF but had no association with all-cause mortality.
Key Words: heart failure • isolated systolic hypertension • mortality • coronary artery disease • cerebrovascular disease • propensity score
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Introduction |
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Isolated systolic hypertension (ISH) is associated with cardiovascular morbidity and mortality.1,2 Hypertension is common in older adults, and >80% of elderly hypertensive patients have ISH.3–5 Hypertension is a major risk factor for cardiovascular morbidity, including heart failure (HF).6,7 However, the association between ISH and incident HF has not been well studied.8–10 In particular, the association between ISH and incident HF has not been prospectively studied in a propensity-matched population of community-dwelling ambulatory older adults. We used public-use copies of the Cardiovascular Health Study (CHS) data sets obtained from the National Heart, Lung, and Blood Institute and a propensity-matched design to test the hypothesis that baseline ISH was associated with incident HF.
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Methods |
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Study Design and Participants
The CHS is a National Heart, Lung, and Blood Institute–funded, currently ongoing, population-based, longitudinal study of 5888 community-dwelling older adults, aged
65 years.11 Participants were recruited in 2 phases from Forsyth County, North Carolina; Sacramento County, California; Washington County, Maryland; and Pittsburgh, Pennsylvania. An initial cohort (n=5201) was recruited between 1989 and 1990. Because of underrepresentation of minorities, a second cohort (n=687) of black subjects was recruited between 1992 and 1993. The objective of the CHS was to identify the onset and course of conventional and new cardiovascular disease risk factors among older adults.11
Of the 5888 original CHS participants, data on 5795 participants were available in the public-use copy of the data sets (93 participants did not consent to be included in the deidentified public-use copy of the data). We excluded 19 participants without data on average baseline systolic blood pressure (SBP) or diastolic blood pressure (DBP) and 278 participants with average DBP 90 mm Hg. We also excluded 250 participants with baseline prevalent HF. The final sample size for the current analysis consisted of 5248 participants with ISH without diastolic hypertension or prevalent HF. From this group, we assembled a cohort of 1260 pairs of propensity-matched participants with and without ISH for our main analyses, as described later.
ISH and Other Baseline Measurements
At baseline, seated blood pressure (fifth Korotkoff sound) was measured with a random-zero sphygmomanometer, model 7076 (Hawksley and Sons Limited).9 The average of 2 measurements of SBP and DBP, corrected for 0 values, was used. We defined ISH as SBP 140 mm Hg with DBP <90 mm Hg.12 Of the 5248 participants, 2000 (38.1%) had ISH. Data on sociodemographic, clinical, subclinical, and laboratory variables were collected at baseline and have been described previously in detail.9,11 Missing values for continuous variables were imputed based on values predicted by age, sex, and race.
Outcome Measures
The primary outcome for this study was definite new-onset HF during a mean follow-up of 8.7 years. The process of adjudication of HF in CHS has been well documented in the literature.6,13 Briefly, participants were asked about self-reports of a physician diagnosis of HF during semiannual visits. The CHS Events Committee later adjudicated the diagnosis of HF through the examination of participant medical charts for a constellation of symptoms, physical signs, and other supporting findings suggestive of HF; use of medications common for HF; and follow-up surveillances. Secondary outcomes were all-cause mortality, incident coronary artery disease (CAD) including acute myocardial infarction or angina pectoris, cerebrovascular disease including stroke or transient ischemic attack, and peripheral artery disease.
Assembly of the Study Cohort
Because of significant differences in key baseline characteristics between participants with and without ISH (Table 1 and Figure 1), we used propensity score matching to assemble a population in which those with and without ISH would be well balanced in all measured baseline covariates. Propensity score is the conditional probability of having an exposure given a set of measured baseline covariates.14,15 Propensity scores for ISH for each of the 5248 participants were estimated using a nonparsimonious multivariable logistic regression model.16–18 In the model, ISH was used as the dependent variable, and the 64 baseline characteristics displayed in Figure 1 were entered as covariates along with 1 significant interaction term (between age and baseline serum creatinine).
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Propensity score models are sample-specific adjusters and are not intended to be used for out-of-sample prediction or estimation of coefficients. Therefore, the assessment of the model’s effectiveness is not measured by fitness or discrimination but rather by the quality of the covariate balance achieved after matching. Using a greedy matching protocol, described elsewhere in detail, we were able to match 1260 CHS participants with ISH (63% of the 2000) with 1260 participants without ISH who had similar propensity scores.16–18 We estimated absolute standardized differences for all 64 of the covariates between participants with and without ISH to assess prematch imbalance and postmatch balance and displayed them as Love plots, developed by Thomas E. Love.16–20 Absolute standardized differences directly quantify balance in the means (or proportions) of covariates across the groups and are expressed as percentages of pooled SDs. An absolute standardized difference of 0% on a covariate indicates no between-group imbalance for that covariate, and values <10% indicate inconsequential imbalance.
Statistical Analysis
For descriptive analyses, Pearson 
2, Wilcoxon rank-sum, McNemar’s, and paired sample t tests were used as appropriate for prematch and postmatch between-group comparisons. To estimate the association between ISH and outcomes, we used Kaplan–Meier and matched Cox proportional hazard analyses. Proportional hazards assumptions were checked using log-minus-log scale survival plots. We then repeated our analysis in the matched cohort using SBP as a continuous variable and as dummy variables. For the dummy variable analysis, SBP was grouped in 10-mm Hg categories as follows: 140 to 149 mm Hg, 150 to 159 mm Hg, 160 to 169 mm Hg, and 170 mm Hg, and SBP <140 mm Hg was used as the reference category. To determine whether the association between ISH and incident HF was homogeneous across various subgroups of matched patients, we conducted subgroup analyses and formally tested for interactions using Cox regression models. Finally, we examined the association of ISH and incident HF in the full prematch cohort of 5248 participants using 3 different approaches: (1) unadjusted; (2) multivariable-adjusted, using all of the covariates used in the propensity score model; and (3) propensity score-adjusted. All of the statistical tests were 2-tailed with 95% confidence levels, and P values <0.05 were considered significant. SPSS for Windows (version 15) was used for all of the data analysis.21
Sensitivity Analyses
Although our matched cohort was well balanced in 64 measured baseline covariates between participants with and without ISH, bias because of imbalances in unmeasured covariates was possible. As such, we conducted a formal sensitivity analysis to quantify the degree of a hidden bias that would need to be present to invalidate our main conclusions.22
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Results |
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Baseline Characteristics
Overall, matched participants had a mean age (±SD) age of 73.5 (±5.5) years, 60% were women, and 15% were nonwhites. Prematch imbalances and postmatch balances between participants with and without ISH are displayed in Table 1 and Figure 1. In general, before matching, compared with participants without ISH, those with ISH were more likely to be older, women, and nonwhites and to have higher mean body mass index, chronic kidney disease (CKD), diabetes mellitus, stroke, and left ventricular hypertrophy (LVH). After matching, absolute standardized differences for all of the measured covariates were <10% (most were <5%), suggesting substantial significant covariate balance across the 2 groups (Figure 1).
Association of ISH With New-Onset HF
Overall, 452 matched participants (18%) developed new-onset HF during 20 729 person-years of follow up. Kaplan–Meier survival curves for incident HF are displayed in Figure 2. New-onset HF occurred in 20% (rate: 242/10 000 person-years) and 16% (rate: 194/10 000 person-years) of participants with and without ISH, respectively (matched hazard ratio [HR] when ISH was compared with no ISH: 1.26; 95% CI: 1.04 to 1.51; P=0.016; Table 2). When average SBP was used as a continuous variable, every 1-mm Hg increase in SBP was associated with an increased risk of new-onset HF (HR: 1.01; 95% CI: 1.01 to 1.02; P<0.0001). When compared with SBP <140 mm Hg, HRs (95% CIs) for incident HF for SBP categories 140 to 149 mm Hg, 150 to 159 mm Hg, 160 to 169 mm Hg, and 170 mm Hg were, respectively, 1.01 (0.80 to 1.28; P=0.942), 1.31 (1.01 to 1.71; P=0.044), 1.88 (1.34 to 2.63; P<0.0001), and 1.89 (1.27 to 2.80; P=0.002). Among the 5248 prematch participants, 890 (17%) developed HF. Incident HF occurred in 22% and 14% of participants with and without ISH, respectively (unadjusted HR: 1.72; 95% CI: 1.51 to 1.97; P<0.0001; Table 2). Multivariable- and propensity-adjusted associations of ISH and incident HF before matching are displayed in Table 2.
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Subgroup Analyses
The association of ISH and incident HF in various subgroups of participants are displayed in Figure 3. The association between ISH and incident HF was significantly more pronounced in participants <78 years of age (P for interaction=0.033), and in those with a history of diabetes mellitus (P for interaction=0.013), high mean baseline serum glucose (P for interaction=0.013), and CKD (P for interaction=0.016; Figure 3).
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Association of ISH With Other Outcomes
All-cause mortality occurred in 879 participants (35%), which was similar (35% each) in those with and without ISH (matched HR: 1.03; 95% CI: 0.88 to 1.19; P=0.732; Table 3). New-onset CAD occurred in 17% participants (9% because of acute myocardial infarction and 15% because of angina pectoris). CAD occurred in 19% and 15% of participants with and without ISH, respectively (matched HR: 1.34; 95% CI: 1.08 to 1.66; P=0.008; Table 3). ISH was associated with new cerebrovascular disease events (matched HR: 1.33; 95% CI: 1.05 to 1.67; P=0.017) but had no significant association with peripheral artery disease (matched HR: 0.84; 95% CI: 0.50 to 1.41; P=0.508; Table 3).
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Results of Sensitivity Analysis
In the absence of hidden confounder, a sign-score test for matched data with censoring provides strong evidence (P=0.0244) that ISH increased risk of incident HF. A hidden binary covariate that is a near-perfect predictor of incident HF would need to increase the odds of ISH by only 3.17% to explain away this association.
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Discussion |
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The results of the current analysis demonstrate that, in a propensity-matched population of community-dwelling older adults, baseline ISH was associated with increased risk of incident HF. Baseline ISH was also associated with increased risk of CAD and cerebrovascular disease but had no association with peripheral artery disease or all-cause mortality. To the best of our knowledge, this is the first report of a significant association between ISH and incident HF in a propensity-matched population of community-dwelling older adults. These findings indicate an intrinsic association between ISH and incident HF, because participants with and without ISH were well balanced in 64 measured baseline characteristics, including traditional and nontraditional risk factors.
There are 3 possible explanations for these findings: first, a direct effect of ISH mediated via an elevated SBP; second, an effect of a low DBP; and, third, confounding by comorbidities associated with ISH. The ISH is the result of a complex interaction between age-related changes in vascular distensibility and left ventricular function.23 Compared with older adults with essential hypertension, those with ISH are more likely to have myocardial and vascular remodeling, LVH, and atherosclerosis, which may predispose them to increased cardiovascular morbidity and mortality.24 A decrease in DBP is known to cause coronary underperfusion and may increase the risk of acute myocardial infarction.25 However, in our matched cohort, the mean average DBP was relatively normal and was well balanced between the groups (Table 1), suggesting that the increased pulse pressure was solely because of an increase in SBP rather than a decrease in DBP. Low DBP has been shown to have a substantially stronger association with acute myocardial infarction than stroke.26 However, in our matched population, ISH had a significant association only with stroke and not with acute myocardial infarction, suggesting a lesser role of DBP. Our prematch participants with ISH were older with high prevalence of risk factors for HF. However, our postmatch cohort was well balanced in all of the measured covariates, including known risk factors for HF, such as age, LVH, and history of hypertension, diabetes mellitus, CAD, and CKD. This suggests that our finding of an association between ISH and incident HF may not be explained by baseline imbalances in any of the 64 covariates used in our study.
The findings of a significantly stronger association of ISH and incident HF in participants with baseline diabetes mellitus, higher serum glucose, and CKD, despite small numbers of participants in these subgroups, deserve further discussion. Participants without diabetes mellitus and CKD, respectively, represented 83% and 79% of all of the matched participants. Yet, ISH had no significant association with HF in these participants. These findings suggest that an increased SBP may interact with increased serum glucose levels and an impaired kidney function to augment its deleterious effect on the cardiovascular system. Hypertension is common in patients with diabetes mellitus and CKD, which are also risk factors for HF.6 Our findings highlight the importance of blood pressure control in these patients.
There are several potential explanations for the apparent lack of an association of ISH with all-cause mortality, despite its significant associations with prognostically important major cardiovascular morbidities. HF is a strong predictor of mortality. However, because HF developed at different time points during follow-up, the mean follow-up between incident HF and mortality was likely short. In addition, an additional 48 cases of HF (in those with ISH) over 10 000 person-years of follow-up may have been too small and did not have the power to affect mortality. Finally, it is unlikely that the natural history of HF associated with ISH would vary from those not associated with ISH, especially in a population that is well balanced in 64 baseline covariates. We have demonstrated recently that hypertension is not intrinsically associated with mortality in patients with chronic HF.27
Most studies of association of ISH with cardiovascular morbidity and mortality have used an older definition of ISH (SBP 160 mm Hg) and did not use incident HF as an outcome.8,9 In the original Framingham Heart Study (n=2767), compared with normal blood pressure, borderline ISH (SBP 140 to 159 mm Hg and DBP <90 mm Hg) was associated with incident HF.10 However, this association was only adjusted for age, sex, body mass index, smoking, serum cholesterol, and glucose tolerance. Our study is distinguished from those studies by its large sample size, long follow-up, and adjustment for 64 baseline covariates. Our use of propensity-matched design is a particular strength of our study, which not only balanced all of the measured baseline covariates but also allowed a visually pleasant display of that balance (Table 1 and Figure 1).
According to the 2005 American College of Cardiology/American Heart Association Chronic Heart Failure Guidelines, presence of hypertension constitutes stage A HF, which denotes increased risk for HF in the absence of structural heart disease or HF symptoms.28 The presence of ventricular remodeling and LVH without HF symptoms indicates stage B HF, whereas HF symptoms mark the development of stage C or clinical HF. More than 80% of the 
5 million stage C HF patients in the United States are older adults, and the incidence of HF increases exponentially with age.29 Essential hypertension has the highest population-attributable risk for HF and is highly prevalent among older adults.6 Essential hypertension is often preceded by ISH, denoting a potential pre-stage A in the development of HF.10 Lowering of blood pressure in early hypertension has been shown to reduce ventricular remodeling and incident HF.1,2,30,31 Findings from our study highlight the importance of SBP and its reduction, a Healthy People 2010 goal,32 especially among those with diabetes mellitus and CKD.
Our study has several limitations. Although propensity score technique can account for imbalances in all of the measured covariates, it may or may not balance unmeasured covariates. However, for such an unmeasured covariate to become a confounder, in addition to being a near-perfect predictor of outcomes (incident HF), it must also be associated with exposure (baseline ISH) and should not be strongly correlated with any of the 64 covariates used in our propensity score model. Participants without ISH at baseline may have developed ISH during follow-up and vice versa. This regression dilution may have underestimated the true associations observed in our study.33
Perspectives
This analysis suggests that, in a propensity-matched population of community-dwelling older adults who were well balanced in 64 measured baseline demographic, clinical, subclinical, and biochemical covariates including history of hypertension and DBP, the presence of baseline ISH had a significant independent association with the development of new-onset HF, CAD, and cerebrovascular disease but had no association with mortality. Elevated SBP in older adults with ISH should be properly controlled to reduce cardiovascular morbidity, including HF.
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Acknowledgments |
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The Cardiovascular Health Study (CHS) was conducted and supported by the National Heart, Lung, and Blood Institute (NHLBI) in collaboration with the CHS Investigators. This manuscript was prepared using a limit access dataset obtained from the NHLBI and does not necessarily reflect the opinions or views of the CHS or the NHLBI.
Sources of Funding
A.A. is supported by the National Institutes of Health through a grant from the National Heart, Lung, and Blood Institute (5-R01-HL085561-02) and a generous gift from Jean B. Morris of Birmingham.
Disclosures
None.
Received July 17, 2008; first decision August 2, 2008; accepted December 31, 2008.
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