File Download
Links for fulltext
(May Require Subscription)
- Publisher Website: 10.1161/CIRCULATIONAHA.110.956490
- Scopus: eid_2-s2.0-78349308026
- PMID: 20956208
- WOS: WOS:000283670800009
- Find via
Supplementary
-
Bookmarks:
- CiteULike: 1
- Citations:
- Appears in Collections:
Article: Acetaminophen increases blood pressure in patients with coronary artery disease
Title | Acetaminophen increases blood pressure in patients with coronary artery disease |
---|---|
Authors | |
Keywords | acetaminophen blood pressure coronary disease endothelium |
Issue Date | 2010 |
Publisher | Lippincott Williams & Wilkins. The Journal's web site is located at http://circ.ahajournals.org |
Citation | Circulation, 2010, v. 122 n. 18, p. 1789-1796 How to Cite? |
Abstract | Background: Because traditional nonsteroidal antiinflammatory drugs are associated with increased risk for acute cardiovascular events, current guidelines recommend acetaminophen as the first-line analgesic of choice on the assumption of its greater cardiovascular safety. Data from randomized clinical trials prospectively addressing cardiovascular safety of acetaminophen, however, are still lacking, particularly in patients at increased cardiovascular risk. Hence, the aim of this study was to evaluate the safety of acetaminophen in patients with coronary artery disease. Methods and Results: The 33 patients with coronary artery disease included in this randomized, double-blind, placebo-controlled, crossover study received acetaminophen (1 g TID) on top of standard cardiovascular therapy for 2 weeks. Ambulatory blood pressure, heart rate, endothelium-dependent and-independent vasodilatation, platelet function, endothelial progenitor cells, markers of the renin-angiotensin system, inflammation, and oxidative stress were determined at baseline and after each treatment period. Treatment with acetaminophen resulted in a significant increase in mean systolic (from 122.4±11.9 to 125.3±12.0 mm Hg P=0.02 versus placebo) and diastolic (from 73.2±6.9 to 75.4±7.9 mm Hg P=0.02 versus placebo) ambulatory blood pressures. On the other hand, heart rate, endothelial function, early endothelial progenitor cells, and platelet function did not change. Conclusions: This study demonstrates for the first time that acetaminophen induces a significant increase in ambulatory blood pressure in patients with coronary artery disease. Thus, the use of acetaminophen should be evaluated as rigorously as traditional nonsteroidal antiinflammatory drugs and cyclooxygenase-2 inhibitors, particularly in patients at increased cardiovascular risk. Clinical Trial Registration: URL: http://www. clinicaltrials.gov. Unique identifier: NCT00534651. © 2010 American Heart Association. All rights reserved. |
Persistent Identifier | http://hdl.handle.net/10722/171413 |
ISSN | 2023 Impact Factor: 35.5 2023 SCImago Journal Rankings: 8.415 |
ISI Accession Number ID | |
References |
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Sudano, I | en_US |
dc.contributor.author | Flammer, AJ | en_US |
dc.contributor.author | Périat, D | en_US |
dc.contributor.author | Enseleit, F | en_US |
dc.contributor.author | Hermann, M | en_US |
dc.contributor.author | Wolfrum, M | en_US |
dc.contributor.author | Hirt, A | en_US |
dc.contributor.author | Kaiser, P | en_US |
dc.contributor.author | Hurlimann, D | en_US |
dc.contributor.author | Neidhart, M | en_US |
dc.contributor.author | Gay, S | en_US |
dc.contributor.author | Holzmeister, J | en_US |
dc.contributor.author | Nussberger, J | en_US |
dc.contributor.author | Mocharla, P | en_US |
dc.contributor.author | Landmesser, U | en_US |
dc.contributor.author | Haile, SR | en_US |
dc.contributor.author | Corti, R | en_US |
dc.contributor.author | Vanhoutte, PM | en_US |
dc.contributor.author | Lüscher, TF | en_US |
dc.contributor.author | Noll, G | en_US |
dc.contributor.author | Ruschitzka, F | en_US |
dc.date.accessioned | 2012-10-30T06:14:00Z | - |
dc.date.available | 2012-10-30T06:14:00Z | - |
dc.date.issued | 2010 | en_US |
dc.identifier.citation | Circulation, 2010, v. 122 n. 18, p. 1789-1796 | en_US |
dc.identifier.issn | 0009-7322 | en_US |
dc.identifier.uri | http://hdl.handle.net/10722/171413 | - |
dc.description.abstract | Background: Because traditional nonsteroidal antiinflammatory drugs are associated with increased risk for acute cardiovascular events, current guidelines recommend acetaminophen as the first-line analgesic of choice on the assumption of its greater cardiovascular safety. Data from randomized clinical trials prospectively addressing cardiovascular safety of acetaminophen, however, are still lacking, particularly in patients at increased cardiovascular risk. Hence, the aim of this study was to evaluate the safety of acetaminophen in patients with coronary artery disease. Methods and Results: The 33 patients with coronary artery disease included in this randomized, double-blind, placebo-controlled, crossover study received acetaminophen (1 g TID) on top of standard cardiovascular therapy for 2 weeks. Ambulatory blood pressure, heart rate, endothelium-dependent and-independent vasodilatation, platelet function, endothelial progenitor cells, markers of the renin-angiotensin system, inflammation, and oxidative stress were determined at baseline and after each treatment period. Treatment with acetaminophen resulted in a significant increase in mean systolic (from 122.4±11.9 to 125.3±12.0 mm Hg P=0.02 versus placebo) and diastolic (from 73.2±6.9 to 75.4±7.9 mm Hg P=0.02 versus placebo) ambulatory blood pressures. On the other hand, heart rate, endothelial function, early endothelial progenitor cells, and platelet function did not change. Conclusions: This study demonstrates for the first time that acetaminophen induces a significant increase in ambulatory blood pressure in patients with coronary artery disease. Thus, the use of acetaminophen should be evaluated as rigorously as traditional nonsteroidal antiinflammatory drugs and cyclooxygenase-2 inhibitors, particularly in patients at increased cardiovascular risk. Clinical Trial Registration: URL: http://www. clinicaltrials.gov. Unique identifier: NCT00534651. © 2010 American Heart Association. All rights reserved. | en_US |
dc.language | eng | en_US |
dc.publisher | Lippincott Williams & Wilkins. The Journal's web site is located at http://circ.ahajournals.org | en_US |
dc.relation.ispartof | Circulation | en_US |
dc.subject | acetaminophen | - |
dc.subject | blood pressure | - |
dc.subject | coronary disease | - |
dc.subject | endothelium | - |
dc.subject.mesh | Acetaminophen - Adverse Effects - Pharmacology | en_US |
dc.subject.mesh | Aged | en_US |
dc.subject.mesh | Anti-Inflammatory Agents, Non-Steroidal - Adverse Effects - Pharmacology | en_US |
dc.subject.mesh | Blood Pressure - Drug Effects - Physiology | en_US |
dc.subject.mesh | Circadian Rhythm - Drug Effects - Physiology | en_US |
dc.subject.mesh | Coronary Artery Disease - Physiopathology | en_US |
dc.subject.mesh | Cross-Over Studies | en_US |
dc.subject.mesh | Dose-Response Relationship, Drug | en_US |
dc.subject.mesh | Double-Blind Method | en_US |
dc.subject.mesh | Endothelium, Vascular - Drug Effects - Physiopathology | en_US |
dc.subject.mesh | Female | en_US |
dc.subject.mesh | Heart Rate - Drug Effects - Physiology | en_US |
dc.subject.mesh | Humans | en_US |
dc.subject.mesh | Hypertension - Chemically Induced - Epidemiology - Physiopathology | en_US |
dc.subject.mesh | Male | en_US |
dc.subject.mesh | Middle Aged | en_US |
dc.subject.mesh | Platelet Adhesiveness - Drug Effects - Physiology | en_US |
dc.subject.mesh | Prospective Studies | en_US |
dc.subject.mesh | Risk Factors | en_US |
dc.subject.mesh | Vasodilation - Drug Effects - Physiology | en_US |
dc.title | Acetaminophen increases blood pressure in patients with coronary artery disease | en_US |
dc.type | Article | en_US |
dc.identifier.email | Vanhoutte, PM:vanhoutt@hku.hk | en_US |
dc.identifier.authority | Vanhoutte, PM=rp00238 | en_US |
dc.description.nature | link_to_OA_fulltext | en_US |
dc.identifier.doi | 10.1161/CIRCULATIONAHA.110.956490 | en_US |
dc.identifier.pmid | 20956208 | - |
dc.identifier.scopus | eid_2-s2.0-78349308026 | en_US |
dc.identifier.hkuros | 183721 | - |
dc.relation.references | http://www.scopus.com/mlt/select.url?eid=2-s2.0-78349308026&selection=ref&src=s&origin=recordpage | en_US |
dc.identifier.volume | 122 | en_US |
dc.identifier.issue | 18 | en_US |
dc.identifier.spage | 1789 | en_US |
dc.identifier.epage | 1796 | en_US |
dc.identifier.isi | WOS:000283670800009 | - |
dc.publisher.place | United States | en_US |
dc.identifier.f1000 | 8002956 | - |
dc.identifier.scopusauthorid | Sudano, I=6602140497 | en_US |
dc.identifier.scopusauthorid | Flammer, AJ=13007159300 | en_US |
dc.identifier.scopusauthorid | Périat, D=24315258100 | en_US |
dc.identifier.scopusauthorid | Enseleit, F=6602935397 | en_US |
dc.identifier.scopusauthorid | Hermann, M=7102188652 | en_US |
dc.identifier.scopusauthorid | Wolfrum, M=8849452900 | en_US |
dc.identifier.scopusauthorid | Hirt, A=24544719300 | en_US |
dc.identifier.scopusauthorid | Kaiser, P=24544749600 | en_US |
dc.identifier.scopusauthorid | Hurlimann, D=6602466831 | en_US |
dc.identifier.scopusauthorid | Neidhart, M=7003852942 | en_US |
dc.identifier.scopusauthorid | Gay, S=8041777500 | en_US |
dc.identifier.scopusauthorid | Holzmeister, J=6603169763 | en_US |
dc.identifier.scopusauthorid | Nussberger, J=7102690537 | en_US |
dc.identifier.scopusauthorid | Mocharla, P=25922895000 | en_US |
dc.identifier.scopusauthorid | Landmesser, U=6602879397 | en_US |
dc.identifier.scopusauthorid | Haile, SR=35726499200 | en_US |
dc.identifier.scopusauthorid | Corti, R=7005136167 | en_US |
dc.identifier.scopusauthorid | Vanhoutte, PM=7202304247 | en_US |
dc.identifier.scopusauthorid | Lüscher, TF=18935805600 | en_US |
dc.identifier.scopusauthorid | Noll, G=7004483986 | en_US |
dc.identifier.scopusauthorid | Ruschitzka, F=7003359126 | en_US |
dc.identifier.citeulike | 9264318 | - |
dc.identifier.issnl | 0009-7322 | - |