Comparative Effects of Non-Steroidal Anti-Inflammatory Drugs (Nsaids) On Blood Pressure in Patients With Hypertension
Comparative Effects of Non-Steroidal Anti-Inflammatory Drugs (Nsaids) On Blood Pressure in Patients With Hypertension
Comparative Effects of Non-Steroidal Anti-Inflammatory Drugs (Nsaids) On Blood Pressure in Patients With Hypertension
RESEARCH ARTICLE
Open Access
Abstract
Background: Nonsteroidal anti-inflammatory drugs (NSAIDs) may disrupt control of blood pressure in hypertensive
patients and increase their risk of morbidity, mortality, and the costs of care. The objective of this study was to
examine the association between incident use of NSAIDs and blood pressure in patients with hypertension.
Methods: We conducted a retrospective cohort study of adult hypertensive patients to determine the effects of
their first prescription for NSAID on systolic blood pressure and antihypertensive drug intensification. Data were
collected from an electronic medical record serving an academic general medicine practice in Indianapolis, Indiana,
USA. Using propensity scores to minimize bias, we matched a cohort of 1,340 users of NSAIDs with 1,340 users of
acetaminophen. Propensity score models included covariates likely to affect blood pressure or the use of NSAIDs.
The study outcomes were the mean systolic blood pressure measurement after starting NSAIDs and changes in
antihypertensive therapy.
Results: Compared to patients using acetaminophen, NSAID users had a 2 mmHg increase in systolic blood
pressure (95% CI, 0.7 to 3.3). Ibuprofen was associated with a 3 mmHg increase in systolic blood pressure compared
to naproxen (95% CI, 0.5 to 4.6), and a 5 mmHg increase compared to celecoxib (95% CI, 0.4 to 10). The systolic
blood pressure increase was 3 mmHg in a subgroup of patients concomitantly prescribed angiotensin converting
enzyme inhibitors or calcium channel blockers and 6 mmHg among those prescribed a beta-adrenergic blocker.
Blood pressure changes in patients prescribed diuretics or multiple antihypertensives were not statistically
significant.
Conclusion: Compared to acetaminophen, incident use of NSAIDs, particularly ibuprofen, is associated with a small
increase in systolic blood pressure in hypertensive patients. Effects in patients prescribed diuretics or multiple
antihypertensives are negligible.
Keywords: NSAIDs, Hypertension, Blood pressure, Propensity score
Background
Cardiovascular diseases are the most common cause of
death in the world [1], and uncontrolled hypertension is
a harbinger of such poor outcomes. Seven million
deaths worldwide each year are attributed to hypertension [2], and in the United States alone, about 73 million people, or one in three adults, have high blood
pressure. Only 35% of these patients have adequate
* Correspondence: haljadhey@ksu.edu.sa
1
Medication Safety Research Chair, College of Pharmacy, King Saud
University, Riyadh, Saudi Arabia
Full list of author information is available at the end of the article
2012 Aljadhey et al.; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative
Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and
reproduction in any medium, provided the original work is properly cited.
Methods
Design and subjects
Page 2 of 10
Page 3 of 10
angiotensin II receptor antagonists, and other antihypertensive medications. The MPR was used to control for
adherence with antihypertensive medications.
Covariates
Based on previous literature, the models included covariates likely to affect blood pressure or the use of NSAIDs
including age, race, gender, and baseline systolic blood
pressure. Baseline systolic blood pressure was defined as
the last measurement before the index date. The models
controlled for the presence of the following diagnoses at
the index date: rheumatoid arthritis, osteoarthritis, coronary artery disease or myocardial infarction, stroke
(cerebrovascular accident or transient ischemic attack),
arrhythmia, asthma or chronic obstructive pulmonary
disease, renal insufficiency, cirrhosis with ascites, systemic lupus erythematosus, diabetes mellitus, and congestive heart failure. We controlled for the use of
medications known to increase blood pressure including
venlafaxine, a high dose of oral glucocorticoids, and the
use of oral contraceptives.
To minimize bias introduced by variations in the time
between baseline systolic blood pressure assessment and
the index date and the time between the index date to
the first systolic blood pressure, we included in the models indicator variables for these times and the index year.
Variations in exposure to NSAID or acetaminophen
were controlled by using the medication possession ratio
(MPR) and the number of refills per month. The MPR
assesses refill adherence and was calculated by dividing
the sum of the days between the last refill and the next
expected refill (i.e. days supply) by the number of days
between the last refill and the next actual refill and then
multiplied by 100. For each patient, an average MPR was
calculated for the index drug. As a proxy for as-needed
versus regular NSAID use, the number of refills per
month was included in the model.
Sensitivity analyses were conducted to assess potential
variations in exposure to the index drug. In one analysis,
the model included the extent of exposure as the doseMPR interaction. In the other, the analysis was restricted
to only those patients who had a blood pressure measurement within 30 days of the index date. These results
did not change our conclusions. Furthermore, we examined the dose effect of NSAIDs by stratifying patients
into low and high dose groups. Patients who were prescribed less than 75% of the maximum daily dose listed
in Facts and Comparisons [31] were included in the low
dose category and those prescribed 75% or more were
included in the high dose category.
Baseline use of antihypertensive medications was
included as covariates in the models. Five groups of antihypertensive medications were formed: beta-adrenergic
antagonists, calcium channel blockers (CCBs), diuretics,
angiotensin-converting enzyme inhibitors (ACE-I) or
Endpoints
Results
A total of 3,928 patients prescribed NSAIDs (n=2,181)
or acetaminophen (n=1,747) met the inclusion criteria.
Before matching on propensity score, many relevant
baseline characteristics differed between the NSAID and
acetaminophen cohorts (Table 1). Patients in the acetaminophen group were older and had a higher baseline
mean systolic blood pressure compared to those in the
NSAID group. They were also more likely to have renal
insufficiency, congestive heart failure, diabetes, coronary
artery disease or myocardial infarction, and stroke than
those in the NSAIDs group Figure 1.
A total of 1,340 patients prescribed NSAIDs were
matched to the same number of patients who had been
prescribed acetaminophen. Matching on propensity
scores balanced all covariates between the two groups
(Table 1). Compared to acetaminophen, NSAIDs were
Page 4 of 10
Table 1 Comparison of Covariate Balance between NSAIDs and Acetaminophen before and after propensity score
matching
Variable
Sample
NSAIDs*
Acetaminophen*
P Value**
Standardized
Difference
Unmatched
55
60
<.001
42.0
Matched
56
57
0.119
6.0
Unmatched
70
70
0.687
1.3
Matched
72
70
0.157
5.5
Bias
Reduction
(%)
86%
Gender:
Female
323%
Race:
African American
Other
Baseline systolic blood pressure (mmHg) mean
Unmatched
58
63
0.003
9.4
Matched
63
61
0.353
3.6
Unmatched
0.007
7.5
Matched
0.837
0.8
Unmatched
139
141
0.006
8.8
Matched
140
140
0.949
0.2
Unmatched
53
65
<.001
23.8
Matched
62
61
0.596
2.0
Unmatched
14
10
<.001
11.6
Matched
10
11
0.380
3.4
Unmatched
33
25
<.001
17.4
Matched
28
28
0.975
0.1
62%
89%
97%
91%
71%
99%
Unmatched
50
58
<.001
17.1
Matched
57
56
0.713
1.4
Unmatched
39
40
0.477
2.3
Matched
41
42
0.741
1.3
Unmatched
11
<.001
40.8
Matched
0.881
0.6
92%
44%
99%
Diagnosis of:
Unmatched
22
23
0.768
0.9
Matched
21
22
0.295
4.0
Unmatched
0.381
2.8
Matched
0.819
0.9
Renal Insufficiency
Unmatched
<.001
24.5
Matched
0.922
0.4
Unmatched
0.4
0.343
3.0
Matched
0.807
0.9
Osteoarthritis
Rheumatoid Arthritis
Unmatched
0.277
3.5
Matched
0.465
2.8
Unmatched
28
35
<.001
14
Matched
28
31
0.124
5.9
Unmatched
11
19
<.001
20.9
Matched
14
14
0.651
1.7
Unmatched
13
19
<.001
16.0
Matched
14
15
0.266
4.3
Stroke
Unmatched
12
<.001
15.4
Diabetes
Congestive Heart Failure
327%
69%
98%
69%
20%
58%
92%
73%
Page 5 of 10
Table 1 Comparison of Covariate Balance between NSAIDs and Acetaminophen before and after propensity score
matching (Continued)
Arrhythmia
Asthma or Chronic Obstructive Pulmonary Disease
Matched
0.784
1.1
Unmatched
0.055
6.1
Matched
0.489
2.7
Unmatched
17
19
0.121
5.0
Matched
18
19
0.420
3.1
93%
56%
37%
Medications:
ACE-I or Angiotensin II blocker
Beta- Blocker
Unmatched
36
43
<.001
15.7
Matched
37
38
0.594
2.1
Unmatched
18
17
0.270
3.5
Matched
15
17
0.338
3.7
Unmatched
34
38
0.003
9.7
Matched
36
36
0.829
0.8
Diuretic
Unmatched
44
48
0.005
9.0
Matched
46
45
0.921
0.4
Other BP medications
Unmatched
12
<.001
15.2
Matched
0.835
0.8
Unmatched
0.068
5.8
Matched
0.850
0.7
Unmatched
0.528
2.0
Matched
0.998
0.0
Unmatched
0.3
0.075
5.8
Matched
0.4
0.782
1.1
Unmatched
69
74
<.001
10.6
Matched
72
70
0.320
3.8
Oral Contraceptives
Venlafaxine
87%
4%
91%
96%
95%
87%
100%
82%
Unmatched
13
12
0.262
3.6
Matched
12
13
0.159
5.4
Unmatched
18
14
0.002
9.8
Matched
16
16
0.965
0.2
Unmatched
32
24
<.001
19.5
Matched
26
27
0.750
1.2
64%
51%
98%
Unmatched
44
43
0.278
3.5
Matched
44
43
0.859
0.7
Unmatched
23
34
<.001
23.3
Matched
30
30
0.909
0.4
Unmatched
52
36
<.001
30.8
Matched
44
43
0.301
4.0
94%
80%
98%
87%
* % unless indicated as mean. Because of rounding values may not add to 100 %.
** P-value of t-tests for continuous variables and chi-square tests for categorical variables.
*** High dose was defined as 10mg for prednisonse, 50mg for cortisone, and 1.5 mg for dexamethasone.
Standardized difference: 100 ( treated control)/ {(s2 treated + s2 control)/2}. A positive value means the treated group is higher in % (or mean) compared to the
control group and negative value means the control is higher than the treated.
Bias reduction (%) =1- {|Standardized difference matched|/| Standardized difference unmatched |} x 100. A positive value means bias is reduced by propensity score
matching and negative means bias increased.
ACE-I: Angiotensin converting enzyme inhibitor; MPR: Medication Possession Ratio; SBP: Systolic blood pressure. Unmatched: all patients before propensity score
matching, N=3,928 (2,181 NSAIDs and 1,747 acetaminophen). Matched: only matched patients, N=2,680 (1,340 in each group).
Page 6 of 10
Dose effects of ibuprofen or naproxen on blood pressure were not statistically significant. A high dose of ibuprofen increased systolic blood pressure, 2.3 mmHg
(95% confidence interval, 1.3 to 5.1) and a high dose
of naproxen slightly decreased in systolic blood pressure
by 3.3 mmHg (95% confidence interval, 9.6 to 3.1).
Based on their propensity scores, 113 patients prescribed celecoxib were matched to 113 patients from the
ibuprofen group. A prescription for ibuprofen was associated with a 5.2 mmHg increase in the mean systolic
blood pressure compared to celecoxib (95% confidence
interval, 0.4 to 10.0) (Table 4). Compared to ibuprofen
or naproxen, celecoxib was not associated with a clinically important increase in systolic blood pressure.
When the outcome was defined as a change in antihypertensive therapy, 2,494 patients in the NSAID group
were matched based on their propensity score to the
same number of patients in the acetaminophen group.
Compared to acetaminophen, receipt of NSAID was not
associated with a change in antihypertensive therapy
(odds ratio, 0.95; 95% confidence interval, 0.84 to 1.08;
p = 0.4).
Discussion
In the current study, patients receiving NSAIDs showed
a 2 mmHg increase in systolic blood pressure compared
to acetaminophen recipients. The systolic blood pressure
increase was 3 mmHg in a sub-sample of those who
were concomitantly prescribed ACE-I or CCB and 6
mmHg in those prescribed a beta-adrenergic blocker.
Ibuprofen was associated with a systolic blood pressure
increase, compared to both naproxen and celecoxib, of 3
and 5 mmHg, respectively. Despite these effects we did
not detect significant changes in antihypertensive therapy in the NSAIDs users suggesting clinicians were not
Eligible Subjects
NSAIDs: 2181
Acetaminophen: 1747
Page 7 of 10
Table 2 Difference in systolic blood pressure between NSAIDs and acetaminophen after propensity score matching
Sample
Dependent Variable*
First SBP
1.8
0.3 to 3.3
ACE-I (n=768)
CCB (n=804)
BB (n=340)
Diuretics (n=1,022)
Average SBP
2.0
0.7 to 3.3
First SBP
2.8
0.2 to 5.8
Average SBP
2.8
0.2 to 5.4
First SBP
2.5
0.4 to 5.4
Average SBP
3.2
0.6 to 5.7
First SBP
6.3
1.7 to 10.8
Average SBP
5.5
1.4 to 9.6
First SBP
0.2
2.3 to 2.8
Average SBP
1.3
0.8 to 3.4
First SBP
1.1
5.6 to 7.8
Average SBP
3.1
2.8 to 8.9
First SBP
4.0
5.0 to 13.0
Average SBP
6.0
2.0 to 14.1
First SBP
1.6
3.3 to 6.5
Average SBP
3.5
0.8 to 7.9
First SBP
7.5
1.0 to 16.0
Average SBP
6.7
1.1 to 14.5
First SBP
1.0
3.4 to 5.5
Average SBP
1.2
2.7 to 5.1
First SBP
3.8
3.9 to 11.5
Average SBP
4.2
2.8 to 11.3
First SBP
1.5
7.9 to 10.8
Average SBP
3.8
4.9 to 12.4
First SBP
6.8
9.4 to 22.9
Average SBP
5.4
10.3 to 21.1
ACE-I: Angiotensin converting enzyme inhibitor; BB: Beta-blocker; CCB: Calcium channel blocker; SBP: Systolic blood pressure.
* First SBP is the first systolic blood pressure measurement after the index date. Average SBP is the average of all systolic blood pressure measurements after the
index date and prior to any changes in the antihypertensive therapy.
** Estimate of SBP is the estimate difference between NSAIDs and acetaminophen after controlling for baseline SBP. A higher value means NSAIDs is associated
with higher increase in systolic blood pressure compared to acetaminophen.
noticing these blood pressure changes that were admittedly subtle though sufficient to increase risk.
Similar to the current results, previous studies
reported an up to 7 mmHg increase in blood pressure in
patients who were stable on beta-adrenergic antagonists
and had started NSAID therapy [34,35]. Interestingly, in
our study the blood pressure increase associated with
NSAIDs was greatest in patients prescribed a betaadrenergic antagonist compared to other antihypertensive medications. The reason for this variation in blood
pressure among antihypertensives could be related to
the degree of prostaglandin (PGs) inhibition and the differences among these medications in their antihypertensive mechanisms. A proposed mechanism to explain this
effect with beta-adrenergic antagonists is that inhibition
of PGs by NSAIDs could increase sensitivity to the
Page 8 of 10
Table 3 Difference in systolic blood pressure between naproxen and ibuprofen after propensity score matching
Sample
Dependent Variable*
First SBP
2.0
4.4 to 0.4
Average SBP
2.5
4.6 to 0.5
First SBP
0.7
4.1 to 5.4
Average SBP
1.1
5.3 to 3.0
First SBP
2.3
6.8 to 2.2
Average SBP
2.2
6.1 to 1.7
First SBP
4.3
10.6 to 2.0
Average SBP
5.9
11.7 to 0.01
First SBP
3.2
7.6 to 1.2
Average SBP
3.3
7.0 to 0.5
First SBP
0.4
11.9 to 12.7
Average SBP
0.8
11.7 to 10.1
First SBP
4.5
18.8 to 9.7
Average SBP
4.4
18.3 to 9.6
First SBP
3.2
11.3 to 5.0
Average SBP
3.2
9.5 to 3.2
First SBP
5.8
19.1 to 7.5
Average SBP
10.1
23.0 to 2.8
First SBP
3.3
10.5 to 4.0
ACE-I (n=276)
CCB (n=268)
BB (n=130)
Diuretics (n=340)
Average SBP
4.3
11.0 to 2.5
First SBP
7.0
16.3 to 2.4
Average SBP
5.4
14.0 to 3.2
First SBP
4.6
22.9 to 13.8
Average SBP
0.5
16.5 to 15.6
First SBP
7.4
29.2 to 14.4
Average SBP
8.9
30.8 to 13.0
ACE-I: Angiotensin converting enzyme inhibitor; BB: Beta-blocker; CCB: Calcium channel blocker; SBP: Systolic blood pressure.
* First SBP is the first systolic blood pressure measurement after the index date. Average SBP is the average of all systolic blood pressure measurements after the
index date and prior to any changes in the antihypertensive therapy.
** Estimate of SBP is the estimate difference between naproxen and ibuprofen after controlling for baseline SBP. A positive value means naproxen is associated
with higher increase in systolic blood pressure compared to ibuprofen. A negative value means ibuprofen is associated with higher increase in systolic blood
pressure compared to naproxen.
Table 4 Difference in systolic blood pressure between celecoxib and ibuprofen or naproxen after propensity score
matching
Comparison
Dependent Variable*
Estimate of SBP(mmHg)**
First SBP
5.4
10.8 to 0.0
Average SBP
5.2
10.0 to 0.4
First SBP
0.3
5.5 to 4.9
Average SBP
0.3
5.1 to 4.5
Page 9 of 10
lowers stroke mortality by 10% and ischemic heart disease mortality by 7% [41]. Future studies are needed to
assess the long term effect of such small increase in
blood pressure.
This study has limitations that should be considered
when interpreting the results. Patients included in this
study came from a single health system and may not be
representative of other practices. Hence, this study
should be replicated in other clinical settings. Although
propensity score matching balances many covariates at
baseline, unobserved covariates could still differ between the groups. Bias is a threat to the validity of these
results especially when comparing NSAID and acetaminophen groups. Acetaminophen has mild pressor
effects that may have dampened the relative effects of
NSAID [42]. Nonetheless, acetaminophen is often used
as an alternative to NSAIDs and we therefore believed
it was a reasonable non-NSAID comparator. Finally,
several NSAIDs are available over the counter (OTC) as
well as by prescription and this database captures only
the use of prescription NSAIDs. However, because
patients included in this study were provided with
needed OTC NSAIDs through a prescription assistance
program, it is less likely that they would have purchased
additional OTC NSAIDs. Furthermore, sensitivity analysis research suggests that missing OTC drug exposure
is not a significant source of bias [43].
In conclusion, compared to acetaminophen, incident
use of NSAIDs (particularly ibuprofen) is associated
with a small increase in systolic blood pressure in
hypertensive patients. Effects in patients prescribed
diuretics or multiple antihypertensives are negligible.
Competing interest
The author(s) declare that they have no competing interests.
Authors contribution
All authors contributed to the study idea, design, and methods. HA carried
out the statistical analyses and drafted the manuscript. All authors
contributed to the manuscript writing. All authors reviewed and edited the
final version of the manuscript. All authors read and approved the final
manuscript.
Acknowledgement
This study was funded partially by the National Plan for Science and
Technology (09-BIO708-02).
Author details
1
Medication Safety Research Chair, College of Pharmacy, King Saud
University, Riyadh, Saudi Arabia. 2Indiana University School of Medicine,
Indianapolis, IN, USA. 3Regenstrief Institute, Inc, Indianapolis, IN, USA.
4
Department of Pharmacy Care Systems, Harrison School of Pharmacy,
Auburn University, Auburn, AL, USA. 5Division of Pharmaceutical Outcomes &
Policy, School of Pharmacy, University of North Carolina, Chapel Hill, NC, USA.
6
Purdue University College of Pharmacy, West Lafayette, IN, USA.
Received: 8 June 2012 Accepted: 15 October 2012
Published: 24 October 2012
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doi:10.1186/1471-2261-12-93
Cite this article as: Aljadhey et al.: Comparative effects of non-steroidal
anti-inflammatory drugs (NSAIDs) on blood pressure in patients with
hypertension. BMC Cardiovascular Disorders 2012 12:93.