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Elevated Blood Pressure in the Emergency Department

A Risk Factor for Incident Cardiovascular Disease
Originally publishedhttps://doi.org/10.1161/HYPERTENSIONAHA.119.14002Hypertension. 2020;75:229–236

Abstract

In the emergency department (ED), high blood pressure (BP) is commonly observed but mostly used to evaluate patients’ health in the short term. We aimed to study whether ED-measured BP is associated with incident atherosclerotic cardiovascular disease (ASCVD), myocardial infarction, or stroke in long term, and to estimate the number needed to screen to prevent ASCVD. In this cohort study, participants were selected from a university hospital between 2010 and 2016, with an obtained BP in the ED. The outcome information was acquired through the Swedish National Patient Register for all participants. The association was estimated with Cox-regression. Among the included 300 193 subjects, 8999 incident ASCVD events occurred during a median follow-up for 3.5 years. Both DBP and systolic blood pressure were associated with incident ASCVD, myocardial infarction, and stroke with a progressively increased risk for systolic blood pressure within hypertension grade 1 (HR, 1.15 [95% CI, 1.06–1.24]), 2 (HR, 1.35 [95% CI, 1.25–1.47]), and 3 (HR, 1.63 [95% CI, 1.49–1.77]). The 6-year cumulative incidence of ASCVD was 12% for systolic blood pressure ≥180 mm Hg compared with 2% for normal levels. To prevent one ASCVD event during the median follow-up, the number needed to screen was estimated to 151, whereas the number needed to treat to 71. ED-recorded BP is associated with incident ASCVD, myocardial infarction, and stroke. High-BP recordings in EDs should not be disregarded but an opportunity to detect and improve the treatment of hypertension. ED-measured BP provides an important and underused tool with great potential to reduce morbidity and mortality associated with hypertension.

Clinical Trial Registration—

URL: http://www.clinicaltrials.gov. Unique identifier: NCT03954119.

Introduction

See Editorial, pp 38–39

High blood pressure (BP) is commonly observed in the emergency department (ED).1 Finding and treating patients with hypertension is a priority in cardiovascular prevention. Studies have shown that for every 10 to 20 mm Hg reduction in systolic blood pressure (SBP), there is a substantial risk reduction for CVD,2–4 and that patients with higher BP levels benefit from more-intensive drug intervention.5 However, a majority of the patients with high BP do not achieve BP control (BP<140/90 mm Hg), and many are unaware of their condition.6

In the ED, BP is measured on almost every patient to assess the patient’s condition and acuity7,8 regardless of the presenting chief complaint. Previous research has reported that up to one-third of the patients in the ED have BP levels above the threshold for hypertension, and severely elevated levels have been observed in 20% of the cases.7 Elevated BP in the ED can be explained by factors such as pain, anxiety, or other stressors, which raises the question of its predictive value and whether hypertension screening based on routine recordings in the ED are useful.1,9

It is unknown whether a high BP in the ED is associated with incident atherosclerotic cardiovascular disease (ASCVD), and the benefit of acting on a high BP in this setting is unclear. Therefore, we aimed to examine if the first measured BP in the ED is associated with incident ASCVD, myocardial infarction (MI), or stroke during a long-time follow-up. We also aimed to assess the potential benefits of screening for patients with hypertension in the ED by estimating the number needed to screen and treat to prevent ASCVD.

Methods

The authors declare that all supporting data are available in the article and its online-only Data Supplement.

Study Design and Setting

This cohort study included all patients who visited and had a BP measured in the EDs at Karolinska University Hospital in Solna and Huddinge, Sweden during the period from January 2010 until March 2016. The studied exposure was the first measured BP, which was obtained from EDs Electronic Health Records, and all outcome information was acquired by linkage to national registers for all included participants. The participants were followed regarding the incident of disease or death or were censored at the end of the study on December 31, 2016.

Inclusion Criteria

All Swedish patients ≥18 years old with a BP recorded at the ED were eligible. Patients without a Swedish personal identification number were excluded as no outcome information could be obtained from these patients. Recurrent BP measurements during hospitalization or recurrent visits to the ED with new BP recordings were disregarded.

Data Sources

BP data were acquired through the Electronic Health Record for each patient. The National Board of Health and Welfare provided data for outcome events and event dates until the end of December 2016, from the Swedish National Patient Register for all participants. Information on relevant medical history before the index visits were collected from this register from the period January 1997 to the index visit. The cause of death and date of death were obtained through the National Board of Health and Welfare’s Cause of Death Register. Data for each subject in the registers were merged to one dataset by the unique pseudonymized identification number. Data for pick-up of prescribed drugs were acquired from the National Board of Health and Welfare’s Prescribed Drugs Register.

Exposure Definitions

The exposures were defined as the first measured SBP and DBP in the ED; both measured as a part of the triage system according to clinical routine.8 BP was categorized into groups due to no certain linear association for BP with the outcomes. The categories were based on the ESC and ESH classification of BP grades and the definition of hypertension grades.10 SBP categories were defined as <90, 90 to 119, 120 to 129, 130 to 139, 140 to 159, 160 to 179, and ≥180 mm Hg. DBP were categorized into <60, 60 to 79, 80 to 84, 85 to 89, 90 to 99, 100 to 109, and ≥110 mm Hg (Table S1 in the online-only Data Supplement).

End Point Definitions

The composite primary end point was ASCVD, defined as the first occurring event of CHD death (fatal MI and sudden cardiac death), nonfatal MI, and all-cause stroke, based on the pooled cohort risk equations.11 Secondary end points were fatal and nonfatal MI, all-cause stroke, ischemic stroke, and intracerebral hemorrhage. Data for end points were derived as the primary diagnosis from the National Patient Register and Cause of Death Register, according to the International Classification of Diseases TenthEdition12(ICD-10). ICD-10 classification for ASCVD was fatal CHD (MI: I210–I214, I219, I220, I221, I228, I229, sudden cardiac death: I461 or I469), nonfatal MI (I210–I214, I219, I220, I221, I228, or I229), fatal and nonfatal ischemic stroke (I630–I635, I638 or I639; Table S2). Only the first event that occurred in the follow-up period was included in the end point ASCVD, and all following recurrent events were disregarded. Secondary end points were defined as fatal and nonfatal MI (I210–I214, I219, I220, I221, I228, or I229. I200 were included if combined with intervention procedure codes FNA-FNG, FNW), all-cause stroke (I610–I619, I630–I635, I638–I639, or I649), ischemic stroke (I630–I635 or I638–I639), and intracerebral hemorrhage (I610–I619; Table S3).

Variables for Subgroup Analyses

Patients with a history of hypertension were identified through a record of hypertension (I109) or a pick-up of a prescription of antihypertensive drugs within the preceding 12 months of the index visit (Table S4). Patients with a history of diabetes mellitus, cardiovascular disease, or lipid-lowering treatment were identified through the anatomic therapeutic classification or a record of the diagnosis (Table S5). History of CVD was defined as a record of either MI (I21, I22), ischemic heart disease (I25), ischemic stroke (I63), or peripheral vascular disease (I739), in the Swedish National Patient Register (Table S5). The triage priority was registered through the routine triage system based on acuity, graded 1 to 5.8

Follow-Up Period

The baseline for follow-up was defined as the time patients were discharged either from the ED or from inpatient care, to not include events during hospital care linked to the index visit and thereby avoid effects of an outcome occurring before the exposure. For patients who were not admitted to inpatient care but were directly discharged from the ED, 1 day was added after they were discharged, to avoid misclassification of hospitalization that had been referred to from the ED visit.

Addressing Potential Bias

The risk of selection bias was reduced by the broad inclusion criteria for this study. BP was recorded as a part of the triage for all patients, and all patients with a recorded BP during the time period were included. BP categories were defined according to the clinically relevant definitions by the ESC and ESH.10 All outcomes were determined in advance with established definitions.

Statistical Analysis

Hazard ratios (HRs) for primary and secondary end points were estimated with Cox regression. Age, sex, inclusion year, and site were adjusted for in model 1. Age was controlled with restricted cubic splines with 4 knots to adjust for the gradually increasing impact of higher age on event rates. In Model 2, age, sex, inclusion year, site, history of hypertension, history of CVD, and lipid-lowering drugs were adjusted for in multivariate analyses. The reference BP categories in the analyses were set to the normal BP level according to ESC and ESH classification10; SBP reference category was 120 to 129 mm Hg, and DBP reference category was 80 to 84 mm Hg. The proportional hazards assumption was evaluated by analyzing Schoenfeld residuals. In a separate analysis, HRs for the primary end point (ASCVD) were estimated per 20-mm Hg increase of SBP and per 10-mm Hg increase of DBP in all models. Subgroup analyses for the outcome ASCVD were performed with Cox regression for patients with a history of hypertension, history of CVD, for patients who were hospitalized, by triage priority and by chief complaints categorized to related medical disciplines according to Table S6. Cumulative incidence functions for SBP categories were estimated for the end points with the Kaplan-Meier estimator. Participants with missing BP data or if they had an outcome before follow-up baseline were disregarded from the analysis. Descriptive statistics of the study population were presented as mean±SD or relative and absolute frequencies grouped by SBP categories. A P-value of <0.05 was considered to be significant. STATA version 15.1 was used for the analysis.

To assess the potential benefit of screening for high BP and initiating or adding treatment, regardless of previously known hypertension, among patients in the ED, a number needed to screen (NNS) and number needed to treat were estimated for CHD, stroke, and ASCVD. The estimates were based on the relative risk reduction reported in previous research, where a 10-mm Hg SBP reduction yielded a risk reduction by 22% for CHD and 41% for stroke, irrespectively of baseline BP.4 Potentially preventable events per patient were calculated for all subjects with a SBP ≥140 mm Hg based on the relative risk reduction. Preventable events were weighted by the visits for each year, and NNS was derived by the inverse of the preventable events per patient, presented with a 95% CI.

Results

A total of 300 193 patients were included after the inclusion criteria (Figure 1). The mean age was 50.0±20.2 years, female patients comprised 53.9% (n=161 707) of the study population, and the mean SBP was 139.9 mm Hg (Table 1). Subjects were followed for a mean time of 3.5 years, which resulted in 1.1 million person-years. The most common chief complaint was abdominal pain, chest pain, breathing difficulties, headache, and fever (Table S6). SBP data were missing for 59 (0.02%) subjects, and 1992 (0.67%) subjects had data missing for DBP. No subjects were missing data for both SBP and DBP. Outcome data were obtained for all included participants.

Table 1. General Characteristics of the Study Population Presented by SBP Categories

CharacteristicsSystolic Blood Pressure, mm Hg
Total<9090–119120–129130–139140–159160–179≥180
n=300 193n=1524n=52 493n=51 667n=55 012n=80 770n=37 207n=21 379
Age
 Age, y; mean (SD)50.0 (20.2)60.4 (21.6)43.0 (19.3)43.0 (18.5)45.7 (18.9)52.0 (19.5)60.7 (17.8)67.7 (14.8)
 <65 no. (%)219 189 (73.0)748 (49.1)43 684 (83.2)43 790 (84.7)44 685 (81.2)57 354 (71.0)20 433 (54.9)8391 (39.2)
 65–74 no. (%)38 121 (12.7)314 (20.6)3729 (7.1)3689 (7.1)5020 (9.1)11 487 (14.2)8121 (21.8)5757 (26.9)
 >74 no. (%)42 883 (14.3)462 (30.3)5080 (9.7)4198 (8.1)5307 (9.6)11 929 (14.8)8653 (23.3)7232 (33.8)
Sex
 Female, no. (%)161 707 (53.9)864 (56.7)36 588 (69.7)30 353 (58.7)27 515 (50.0)36 768 (45.5)17 546 (47.2)12 002 (56.1)
Blood pressure
 SBP, mm Hg; mean (SD)139.9 (24.2)80.4 (8.0)110.1 (6.8)123.9 (3.1)133.9 (3.1)147.6 (5.9)167.4 (5.9)194.6 (14.6)
 DBP mm Hg; mean (SD)80.8 (15.0)54.9 (14.2)68.5 (11.3)75.0 (10.2)79.2 (11.6)84.6 (12.1)91.0 (14.5)98.7 (14.4)
Medical history
 Hypertension, no. (%)75 385 (25.1)663 (43.5)7977 (15.2)7410 (14.3)9728 (17.7)21 915 (27.1)15 551 (41.8)12 111 (56.6)
 Diabetes mellitus, no. (%)20 526 (6.8)152 (10.0)2353 (4.5)2282 (4.4)3017 (5.5)6075 (7.5)3962 (10.6)2675 (12.5)
 CVD, no. (%)13 732 (4.6)164 (10.8)1941 (3.7)1638 (3.2)1959 (3.6)3893 (4.8)2388 (6.4)1747 (8.2)
Admission to inpatient care
 Admitted, no. (%)76 390 (25.5)989 (64.9)13 836 (26.4)11 293 (21.9)12 071 (21.9)19 861 (24.6)10 858 (29.2)7460 (34.9)
Chief complaints by medical discipline
 Internal medicine, no. (%)112 264 (37.4)772 (50.7)19 246 (36.7)18 400 (35.6)20 160 (36.6)30 328 (37.5)14 716 (39.6)8595 (40.2)
 Surgery, no. (%)83 956 (28.0)350 (23.0)17 523 (33.4)16 133 (31.2)16 038 (29.2)21 501 (26.6)8440 (22.7)3935 (18.4)
 Otolaryngology, no. (%)13 622 (4.5)46 (3.0)1832 (3.5)2163 (4.2)2688 (4.9)3580 (4.4)1938 (5.2)1379 (6.4)
 Neurology, no. (%)37 071 (12.3)79 (5.2)4785 (9.1)5729 (11.1)6401 (11.6)10 626 (13.2)5486 (14.7)3956 (18.5)
 Orthopedics, no. (%)30 819 (10.3)89 (5.8)4403 (8.4)5220 (10.1)5730 (10.4)9294 (11.5)4068 (10.9)1993 (9.3)
 Unknown, no. (%)22 461 (7.5)188 (12.3)4704 (9.0)4032 (7.8)3995 (7.3)5441 (6.7)2559 (6.9)1530 (7.2)

DBP indicates diastolic blood pressure; and SBP, systolic blood pressure.

Figure 1.

Figure 1. Flowchart of study selection. Foreign patients without a Swedish identification number were excluded. BP indicates blood pressure; and ED, emergency department.

Incident ASCVD occurred in 3.0% (n=8999) of the cohort during a median follow-up for 42 months (range, 0–84 month). Men were more likely to develop ASCVD (60.7%) compared with females (39.3%). Both SBP and DBP was associated with incident ASCVD with a progressively increased hazard ratio across BP categories above the reference (Table 2). The 6-year cumulative incidence of ASCVD for the reference SBP group (120–129 mm Hg) was 2% compared with 12% in SBP category ≥180 mm Hg (Figure 2), while patients with DBP ≥110 mm Hg had a 10% 6-year cumulative incidence (Figure S1). When adjusted for age, sex, inclusion year, and site, the HR (95% CI) for incident ASCVD per 20-mm Hg increase of SBP was 1.13 (1.11–1.14), and per 10-mm Hg DBP increase, the HR was 1.03 (1.03–1.04; Table S7).

Table 2. Hazard Ratio for ASCVD Presented by SBP and DBP Categories

Blood PressureGradeCrudeAdjusted Model 1*Adjusted Model 2
HR95% CIP-ValueHR95% CIP-ValueHR95% CIP-Value
SBP, mm Hg
 <90Hypotension2.171.59–2.97<0.00010.920.67–1.260.6180.880.65–1.210.437
 90–119Optimal1.070.97–1.170.1911.101.00–1.220.0431.101.00–1.210.060
 120–129NormalReferenceReferenceReference
 130–139High normal1.301.19–1.42<0.00011.050.96–1.150.2571.050.96–1.150.322
 140–159Hypertension grade 12.081.92–2.25<0.00011.151.06–1.240.0011.131.04–1.220.003
 160–179Hypertension grade 23.573.29–3.88<0.00011.351.25–1.47<0.00011.311.21–1.42<0.0001
 ≥180Hypertension grade 35.455.01–5.93<0.00011.631.49–1.77<0.00011.551.42–1.69<0.0001
DBP, mm Hg
 <60Hypotension1.201.07–1.360.0021.080.96–1.220.1991.030.92–1.170.554
 60–79Optimal0.890.83–0.95<0.00011.010.95–1.080.7041.000.94–1.070.934
 80–84NormalReferenceReferenceReference
 85–89High normal1.201.11–1.30<0.00011.131.05–1.230.0021.141.06–1.240.001
 90–99Hypertension grade 11.431.33–1.53<0.00011.151.07–1.23<0.00011.171.09–1.25<0.0001
 100–109Hypertension grade 21.941.79–2.11<0.00011.401.29–1.52<0.00011.421.30–1.54<0.0001
 ≥110Hypertension grade 32.612.36–2.88<0.00011.711.55–1.89<0.00011.711.55–1.89<0.0001

ASCVD indicates atherosclerotic cardiovascular disease; DBP, diastolic blood pressure; and SBP, systolic blood pressure.

*Adjusted for age, sex, inclusion year, site.

†Adjusted for age, sex, inclusion year, site, history of hypertension, diabetes mellitus, and lipid-lowering drugs.

‡Reference category for Cox regression analysis.

Figure 2.

Figure 2. Cumulative incidence of atherosclerotic cardiovascular disease presented by systolic blood pressure (SBP) categories. Number at risk presents the number of subjects entering each interval. *Reference category for Kaplan-Meier analysis.

For the secondary end point MI, a total of 4847 (1.6%) events occurred in the cohort, the majority 63.2% (n=3117) among men. There was a statistically significant association between SBP and incident MI with a gradually increased HR by higher SBP above the reference category (Figure 3). Similar associations were observed for DBP (Figure S2). The 6-year cumulative incidence was 1% for the reference category compared with 6.5% in the highest SBP group (Figure S3).

Figure 3.

Figure 3. Hazard ratio for incident atherosclerotic cardiovascular disease (ASCVD), myocardial infarction (MI), all-cause stroke, intracerebral hemorrhage (ICH), and ischemic stroke. Hazard ratio (HR), 95% CI, and P-value presented by systolic blood pressure (SBP) categories in a crude and adjusted model. CHD indicates coronary heart disease. *Reference category for Cox regression analysis. †Adjusted for age, sex, inclusion year, site. ‡Adjusted for age, sex, inclusion year, site, history of hypertension, diabetes mellitus, and lipid-lowering drugs.

A total of 6661 (2.2%) all-cause stroke events occurred, and of those were 51.0% male (n=3470). Patients with DBP ≥110 had more than a 2-fold association (HR, 2.16 [95% CI, 1.93–2.41]) with a stroke event (Figure S2). The 6-year cumulative incidence was 1% for the reference category compared with 9% in the highest SBP group (Figure S4).

For the end points ischemic stroke and intracerebral hemorrhage, a total of 5355 respectively 1119 events occurred. The highest HR for ischemic stroke was in the ≥110 mm Hg DBP category (HR, 1.91 [95% CI, 1.68–2.17]). The strongest association with intracerebral hemorrhage was in the top DBP category (HR, 3.56 [95% CI, 2.80–4.52]) (Figure S2).

Subgroup Analyses

Patients with a history of hypertension experienced 5667 (7.6%) ASCVD events, compared with 3300 (1.5%) for those without the condition (Table S8). BP above the reference category was associated with ASCVD regardless of previous hypertension. Patients with no prior hypertension diagnosis had a lower absolute event rate, but a stronger and steeper relative association with ASCVD compared with the hypertension group. The strongest association with ASCVD was in SBP ≥180 mm Hg, for patients with no history of hypertension (HR, 2.02 [95% CI, 1.75–2.33]; Figure S5).

BP was associated with incident ASCVD, with a gradually increased risk across categories of BP both among patients with and without a history of CVD (Figure S6) and similar associations were observed among patients with and without diabetes mellitus (Figure S7). A similar association between BPs and incident ASCVD was also observed across the triage priority groups in the adjusted model (Figure S8).

A total of 76 474 patients (25.5%) were admitted to inpatient care, and among these were 50.5% men. The admitted patients had 4614 ASCVD events during the study period compared with 4323 events for those who were directly discharged. The mean age for the admitted patients were 60.0±20.4 years compared with 46.5±18.9 years for the nonadmitted. There was a progressively increased hazard ratio among patients with SBP in the categories above the reference group. The association was similar in the 2 groups in the adjusted model (Figure S9).

A first BP above the reference category was associated with incident ASCVD in all medical disciplines except for the orthopedics and otolaryngology disciplines (Table S9, Figure S10). In the adjusted model, the strongest association with ASCVD were in the neurology discipline (Figure S10).

Number Needed to Screen

Potentially preventable events were estimated to 1966 ASCVD events, 672 CHD, 1252 strokes. The estimated NNS to find high BP and to prevent one event for ASCVD, CHD, and stroke, during a median of 42 months of follow-up, was 151 (95% CI, 127–190), 442 (95% CI, 360–572), and 157 (95% CI, 134–195), respectively, whereas the number needed to treat was estimated to 71, 208, and 112. For patients who were directly discharged, NNS for ASCVD was 216, whereas, number needed to treat for high BP was estimated to 103. To prevent one fatal ASCVD event, 450 patients in the ED needed to be screened for high BP, and 150 of those needed to be treated for high BP (Table 3).

Table 3. Number Needed to Screen and Treat to Prevent CHD, Stroke, and ASCVD

CHDStrokeASCVD
Estimates for all patients
Relative risk reduction, % (95% CI)*22 (17–27)41 (33–48)32 (25–38)
PPE, no. (95% CI)672 (519–824)1252 (1007–1465)1966 (1561–2341)
PPE per ED patient, % (95% CI)0.23 (0.17–0.28)0.64 (0.51–0.75)0.66 (0.53–0.79)
NNT, no. (95% CI)208 (170–269)112 (96–139)71 (60–90)
NNS, no. (95% CI)442 (360–572)157 (134–195)151 (127–190)
Estimates for directly discharged patients
PPE, no (95% CI)499 (385–612)1225 (986–1435)1366 (1084–1626)
PPE per ED patient, % (95% CI)0.17 (0.13–0.21)0.42 (0.33–0.49)0.46 (0.37–0.55)
NNT, no. (95% CI)280 (228–362)114 (98–142)103 (86–129)
NNS, no. (95% CI)591 (482–765)241 (206–299)216 (182–272)
Estimates for fatal events
PPE, no. (95% CI)465 (359–571)1148 (924–1344)932 (740–1109)
PPE per ED patient, % (95% CI)0.16 (0.12–0.19)0.29 (0.23–0.34)0.22 (0.18–0.26)
NNT, no. (95% CI)300 (245–388)122 (104–151)150 (126–189)
NNS, no. (95% CI)644 (525–833)346 (295–429)450 (378–567)

The estimates were based on the assumption that all detected patients with SBP ≥140 mm Hg were treated with antihypertensive therapy during the median follow-up of the study (42 month). ASCVD indicates atherosclerotic cardiovascular disease; ED, emergency department; NNS, number needed to screen; NNT, number needed to treat; PPE, potentially preventable event; and SBP, systolic blood pressure.

*Relative risk reduction based on 10-mm Hg SBP reduction, as estimated by Law et al.4

Discussion

The main finding in this study was the strong association between a first BP recorded in the ED and incident ASCVD during a long-time follow-up. Strong associations were observed, irrespective of the acuity, whether patients were admitted to inpatient care or had a history of hypertension or CVD. In patients without a history of hypertension, the association with incident ASCVD was stronger than for those with hypertension. By using effect sizes for antihypertensive treatment from meta-analysis,4 we estimated that to prevent one future ASCVD event during a median of 42 months of follow-up, antihypertensive treatment needed to be initiated in 71 patients with an ED-measured SBP ≥140 mm Hg.

The association with incident ASCVD was gradually stronger for both DBP and SBP levels that corresponded to Hypertension grade 1, 2, and 310 (Table S1). Furthermore, a statistically significant association with incident ASCVD was observed for patients with DBP level in the high normal category. Our findings show that hypertension grades may be of interest for the ED setting, and ED-measured BP is of value not only to evaluate the acuity of the patient’s health but also to identify patients at high risk for cardiovascular events in the long term and therefore provides a tool to prevent them.

Previous population-based research has shown that an increase in SBP results in a substantially increased risk for cardiovascular events, irrespective of baseline BP.2,3 While findings in the present study showed a strong association between BP and incident ASCVD, the magnitude of the effect was smaller in comparison to the population-based studies. We observed a HR of 1.13 per 20-mm Hg increase of SBP whereas Rapsomaniki et al reported a HR of 1.26. The current study did not account for the regression dilution bias due to single BP measurements, and thereby our findings probably underestimate the true association between BP in the ED and incident ASCVD.13 The influence of different stressors, both related to acute disease and the ED environment, may cause an increase of BP in the ED, and elevated BP levels are commonly observed.1 Previously, the prognostic relevance of elevated BP in the ED, and if it can be a basis for decisions to initiate or intensify antihypertensive treatment in this setting has been unknown. However, it should be noted that BP measured during other stress, such as exercise, previously have provided independent prognostic information regarding incident ASCVD.14,15 To estimate if stressors or pain influenced the association between BP and incident ASCVD, we performed subgroup analyses for ED triage categories. A strong association with the outcome was observed irrespective of the acuity of the patients. Although it can be speculated that different mechanisms influence BP in the ED and its association with ASCVD, which may explain some of the differences in this study compared with the population-based studies. Here we, for the first time, provide evidence that a first BP obtained in the ED among an unselected population with ED visitors is associated with incident ASCVD.

The estimated NNS was based on the assumption that all detected patients with an SBP ≥140 mm Hg were prescribed adequate antihypertensive therapy and succeeded a 10-mm Hg SBP reduction. Prior research has presented a NNS for hypertension with BP-lowering actions,16 to the best of our knowledge, none have reported the potential benefit of using BPs obtained in the ED with an estimated potential benefit of reduced events. Findings in this study indicate that the ED setting has great potential to find undiagnosed and undertreated hypertension, which will reduce morbidity and mortality in CVD if effective antihypertensive therapy is initiated.

The main strength of this study was the large cohort size and the long follow-up period, which yielded a strong statistical power. The Swedish National Patient Register is well-known for its high-quality and accurate data, with a high reported positive predictive value, for most of the diagnoses. The reported sensitivity was high for MI (above 90%) but lower for hypertension.17 Therefore, the Prescribed Drugs Register was used to obtain all pick-ups of antihypertensive drugs to improve sensitivity.18

One potential weakness in this study was the uncertainty of how BP was measured, and due to discrepancies in methods for obtaining BP, deviations for BP may vary from case to case. Any changes in antihypertensive treatment that were initiated based on elevated ED-measured BP were not considered. Such treatment may have attenuated the association with incident ASCVD and therefore underestimated the true association. Another limitation is that the estimates for NNS and number needed to treat were based on relative risk reduction reported by previous research performed in different settings.4

The clinical value of the findings in this study is that ED-measured BP has a great potential to find undiagnosed hypertension and to prevent future ASCVD events if antihypertensive therapy is initiated. Patients directly discharged from the ED should be assessed more carefully as no further inpatient BP recordings take place. One ASCVD event could be prevented for every 107 discharged patients with a high BP if effective antihypertensive therapy is initiated. It is conceivable that the external validity of this study applies to other EDs, particularly considering the broad inclusion criteria.

In conclusion, findings in this study show that elevated BP, when measured in the ED, is strongly associated with incident ASCVD, MI, and stroke. High BP recordings in EDs should not be disregarded as isolated events, but an opportunity to detect and improve the treatment of hypertension. Patients with elevated BP in the ED should be followed up and treated if necessary. ED measurements of BP provide an important and underused tool with great potential to reduce morbidity and mortality associated with hypertension.

Perspectives

In summary, a first recorded BP in the ED was associated with incident ASCVD during a long-time follow-up. The risk increased gradually across both DBP and SBP levels that corresponded to Hypertension grades 1, 2, and 3. Strong associations were observed irrespective of the acuity of the condition in the ED, whether patients were admitted to inpatient care of had a history of hypertension or CVD. To prevent one ASCVD event during a median follow-up of 42 months, the NNS was estimated to 151 patients in the ED, whereas the number needed to treat to 71. The ED setting provides an opportunity to detect and improve the treatment of hypertension and are an underused tool with great potential to reduce morbidity and mortality associated with hypertension. Elevated BP recordings in the ED should not be disregarded as isolated events, but an opportunity to follow up and treat if necessary.

Acknowledgments

P. Svensson conducted the study, acquired all data and the ethical permit contributed by P. Oras, H. Häbel, and P.H. Skoglund. P. Oras wrote the manuscript supervised by P. Svensson and supported by P.H. Skoglund and H. Häbel. H. Häbel performed the statistical analysis and interpreted the data with support by P. Oras, P. Svensson, and P.H. Skoglund. All authors critically revised the manuscript for intellectual content and approved the final version of the report. The corresponding author had access to all data and is responsible for the decision to submit this study.

This study has been approved by the Regional Ethical Review Board in Stockholm, without the requirement of informed consent. Ethical review number 2016/888-31.

Footnotes

The online-only Data Supplement is available with this article at https://www.ahajournals.org/doi/suppl/10.1161/HYPERTENSIONAHA.119.14002.

Correspondence to Pontus Oras, Department of Clinical Science and Education, Södersjukhuset, Karolinska Institutet, Sjukhusbacken 10, 118 83 Stockholm, Sweden. Email

References

  • 1. Backer HD, Decker L, Ackerson L. Reproducibility of increased blood pressure during an emergency department or urgent care visit.Ann Emerg Med. 2003; 41:507–512. doi: 10.1067/mem.2003.151CrossrefMedlineGoogle Scholar
  • 2. Rapsomaniki E, Timmis A, George J, Pujades-Rodriguez M, Shah AD, Denaxas S, White IR, Caulfield MJ, Deanfield JE, Smeeth L, Williams B, Hingorani A, Hemingway H. Blood pressure and incidence of twelve cardiovascular diseases: lifetime risks, healthy life-years lost, and age-specific associations in 1·25 million people.Lancet. 2014; 383:1899–1911. doi: 10.1016/S0140-6736(14)60685-1CrossrefMedlineGoogle Scholar
  • 3. Lewington S, Clarke R, Qizilbash N, Peto R, Collins R; Prospective Studies Collaboration. Age-specific relevance of usual blood pressure to vascular mortality: a meta-analysis of individual data for one million adults in 61 prospective studies.Lancet. 2002; 360:1903–1913. doi: 10.1016/s0140-6736(02)11911-8CrossrefMedlineGoogle Scholar
  • 4. Law M, Morris J, Wald N. Use of blood pressure lowering drugs in the prevention of cardiovascular disease: meta-analysis of 147 randomised trials in the context of expectations from prospective epidemiological studies.BMJ. 2009; 338:b1665. doi: 10.1136/bmj.b1665CrossrefMedlineGoogle Scholar
  • 5. Ferdinand KC, Nasser SA. Management of essential hypertension.Cardiol Clin. 2017; 35:231–246. doi: 10.1016/j.ccl.2016.12.005CrossrefMedlineGoogle Scholar
  • 6. Chobanian AV, Bakris GL, Black HR, Cushman WC, Green LA, Izzo JL, Jones DW, Materson BJ, Oparil S, Wright JT, Roccella EJ; Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. National Heart, Lung, and Blood Institute; National High Blood Pressure Education Program Coordinating Committee. Seventh report of the joint national committee on prevention, detection, evaluation, and treatment of high blood pressure.Hypertension. 2003; 42:1206–1252. doi: 10.1161/01.HYP.0000107251.49515.c2LinkGoogle Scholar
  • 7. Skoglund PH, Svensson P. Asking the patient or measuring blood pressure in the emergency department: which one is best?Curr Hypertens Rep. 2016; 18:53. doi: 10.1007/s11906-016-0659-0CrossrefMedlineGoogle Scholar
  • 8. Swedish council on health technology assessment. Triage and flow in the emergency department: A systematic litterature review [internet]. 2010; 2019Google Scholar
  • 9. Chernow SM, Iserson KV, Criss E. Use of the emergency department for hypertension screening: a prospective study.Ann Emerg Med. 1987; 16:180–182. doi: 10.1016/s0196-0644(87)80012-4CrossrefMedlineGoogle Scholar
  • 10. Williams B, Mancia G, Spiering W, et al; List of authors/Task Force members:. 2018 Practice Guidelines for the management of arterial hypertension of the European Society of Hypertension and the European Society of Cardiology: ESH/ESC task force for the management of arterial hypertension.J Hypertens. 2018; 36:2284–2309. doi: 10.1097/HJH.0000000000001961CrossrefMedlineGoogle Scholar
  • 11. Goff DC, Lloyd-Jones DM, Bennett G, et al. 2013 ACC/AHA guideline on the assessment of cardiovascular risk: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines.J Am Coll Cardiol. 2014; 63(25pt B):2935–2959. doi: 10.1016/j.jacc.2013.11.005CrossrefMedlineGoogle Scholar
  • 12. WHO. International classification of diseases (icd). 2018; 2019Google Scholar
  • 13. Hutcheon JA, Chiolero A, Hanley JA. Random measurement error and regression dilution bias.BMJ. 2010; 340:c2289. doi: 10.1136/bmj.c2289CrossrefMedlineGoogle Scholar
  • 14. Kurl S, Laukkanen JA, Rauramaa R, Lakka TA, Sivenius J, Salonen JT. Systolic blood pressure response to exercise stress test and risk of stroke.Stroke. 2001; 32:2036–2041. doi: 10.1161/hs0901.095395LinkGoogle Scholar
  • 15. Kjeldsen SE, Mundal R, Sandvik L, Erikssen G, Thaulow E, Erikssen J. Supine and exercise systolic blood pressure predict cardiovascular death in middle-aged men.J Hypertens. 2001; 19:1343–1348. doi: 10.1097/00004872-200108000-00001CrossrefMedlineGoogle Scholar
  • 16. Rembold CM. Number needed to screen: development of a statistic for disease screening.BMJ. 1998; 317:307–312. doi: 10.1136/bmj.317.7154.307CrossrefMedlineGoogle Scholar
  • 17. Ludvigsson JF, Andersson E, Ekbom A, Feychting M, Kim JL, Reuterwall C, Heurgren M, Olausson PO. External review and validation of the Swedish national inpatient register.BMC Public Health. 2011; 11:450. doi: 10.1186/1471-2458-11-450CrossrefMedlineGoogle Scholar
  • 18. Wettermark B, Hammar N, Fored CM, MichaelFored C, Leimanis A, Otterblad Olausson P, Bergman U, Persson I, Sundström A, Westerholm B, Rosén M. The new swedish prescribed drug register–opportunities for pharmacoepidemiological research and experience from the first six months.Pharmacoepidemiol Drug Saf. 2007; 16:726–735. doi: 10.1002/pds.1294CrossrefMedlineGoogle Scholar

Novelty and Significance

What Is New?

  • This is the first study to investigate the association between blood pressure (BP) recorded in the emergency department (ED) and incident atherosclerotic cardiovascular disease (ASCVD).

  • The association with incident ASCVD was gradually increasing for both diastolic blood pressure and systolic blood pressure levels that corresponded to hypertension grades 1, 2, and 3.

  • An association with incident ASCVD was observed for patients with diastolic blood pressure level in the high normal category.

  • The 6-year cumulative incidence of ASCVD for patients with a BP ≥180 mm Hg was ≈12%.

  • To prevent one ASCVD event during a median follow-up of 42 months, the number needed to screen was estimated to 151 patients in the ED, whereas the number needed to treat to 71.

What Is Relevant?

  • Hypertension is a global challenge that needs improvement in the prevention, diagnosis, and treatment of the diagnosis.

  • This study has shown that high BP recordings in the ED are associated with an increased risk of ASCVD.

  • ED has a great potential to detect high BP and improve the treatment of hypertension, to reduce morbidity and mortality in hypertension-related complications.

Summary

  • Elevated BP, when measured in the ED, is strongly associated with incident ASCVD, myocardial infarction, and stroke.

  • High BP recordings in EDs should not be disregarded, but an opportunity to detect and improve the treatment of hypertension.

  • ED-measurements of BP provide an important and under-used tool with great potential to reduce morbidity and mortality associated with hypertension.

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