Clinical Implications of Nonopioid Analgesia for Relief of Mild-to-Moderate Pain in Patients with or at Risk for Cardiovascular Disease

Andrew Whelton

Research output: Contribution to journalArticle

Abstract

Nonopioid analgesics, which include acetaminophen, aspirin, nonsteroidal anti-inflammatory drugs (NSAIDs), and cyclooxygenase-2 (COX-2)-specific inhibitors (coxibs), are frequently used for the relief of mild-to-moderate pain. Although all of these agents are effective at controlling pain, inhibition of prostaglandins (PGs) by NSAIDs may result in untoward cardiorenal effects, including hypertension, fluid and electrolyte abnormalities, congestive heart failure, acute renal failure, and nephrotic syndrome. Individuals with an increased risk for cardiorenal effects from NSAIDs (eg, the elderly, and those with hypertension, cardiac disease, or gouty nephropathy) should be monitored for early onset of edema, destabilization of blood pressure control, and/or onset of congestive heart failure when started on NSAID therapy. Because acetaminophen has a different mechanism of action from the conventional NSAIDs, it does not inhibit peripheral PGs at recommended dosing and therefore appears to have a more favorable cardiovascular and gastrointestinal safety profile. This review discusses the effects of acetaminophen, traditional NSAIDs, and coxibs on fluid and electrolytes, blood pressure, congestive heart failure, and renal function, as well as their consequences in patients with or at risk for cardiovascular disease (CVD). It also summarizes information on the mechanisms by which NSAID-induced cardiovascular adverse events develop, and it provides recommendations for the use of nonopioid analgesics for relief of mild-to-moderate pain in patients with or at risk for CVD.

Original languageEnglish (US)
Pages (from-to)3-9
Number of pages7
JournalThe American Journal of Cardiology
Volume97
Issue number9 SUPPL. 1
DOIs
StatePublished - May 8 2006

Fingerprint

Analgesia
Anti-Inflammatory Agents
Cardiovascular Diseases
Pain
Acetaminophen
Non-Narcotic Analgesics
Pharmaceutical Preparations
Heart Failure
Cyclooxygenase 2 Inhibitors
Electrolytes
Prostaglandins
Blood Pressure
Hypertension
Cardiovascular Agents
Nephrotic Syndrome
Acute Kidney Injury
Aspirin
Heart Diseases
Edema
Kidney

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

Clinical Implications of Nonopioid Analgesia for Relief of Mild-to-Moderate Pain in Patients with or at Risk for Cardiovascular Disease. / Whelton, Andrew.

In: The American Journal of Cardiology, Vol. 97, No. 9 SUPPL. 1, 08.05.2006, p. 3-9.

Research output: Contribution to journalArticle

@article{b0be3328526741daa6b94aec4e702426,
title = "Clinical Implications of Nonopioid Analgesia for Relief of Mild-to-Moderate Pain in Patients with or at Risk for Cardiovascular Disease",
abstract = "Nonopioid analgesics, which include acetaminophen, aspirin, nonsteroidal anti-inflammatory drugs (NSAIDs), and cyclooxygenase-2 (COX-2)-specific inhibitors (coxibs), are frequently used for the relief of mild-to-moderate pain. Although all of these agents are effective at controlling pain, inhibition of prostaglandins (PGs) by NSAIDs may result in untoward cardiorenal effects, including hypertension, fluid and electrolyte abnormalities, congestive heart failure, acute renal failure, and nephrotic syndrome. Individuals with an increased risk for cardiorenal effects from NSAIDs (eg, the elderly, and those with hypertension, cardiac disease, or gouty nephropathy) should be monitored for early onset of edema, destabilization of blood pressure control, and/or onset of congestive heart failure when started on NSAID therapy. Because acetaminophen has a different mechanism of action from the conventional NSAIDs, it does not inhibit peripheral PGs at recommended dosing and therefore appears to have a more favorable cardiovascular and gastrointestinal safety profile. This review discusses the effects of acetaminophen, traditional NSAIDs, and coxibs on fluid and electrolytes, blood pressure, congestive heart failure, and renal function, as well as their consequences in patients with or at risk for cardiovascular disease (CVD). It also summarizes information on the mechanisms by which NSAID-induced cardiovascular adverse events develop, and it provides recommendations for the use of nonopioid analgesics for relief of mild-to-moderate pain in patients with or at risk for CVD.",
author = "Andrew Whelton",
year = "2006",
month = "5",
day = "8",
doi = "10.1016/j.amjcard.2006.02.017",
language = "English (US)",
volume = "97",
pages = "3--9",
journal = "American Journal of Cardiology",
issn = "0002-9149",
publisher = "Elsevier Inc.",
number = "9 SUPPL. 1",

}

TY - JOUR

T1 - Clinical Implications of Nonopioid Analgesia for Relief of Mild-to-Moderate Pain in Patients with or at Risk for Cardiovascular Disease

AU - Whelton, Andrew

PY - 2006/5/8

Y1 - 2006/5/8

N2 - Nonopioid analgesics, which include acetaminophen, aspirin, nonsteroidal anti-inflammatory drugs (NSAIDs), and cyclooxygenase-2 (COX-2)-specific inhibitors (coxibs), are frequently used for the relief of mild-to-moderate pain. Although all of these agents are effective at controlling pain, inhibition of prostaglandins (PGs) by NSAIDs may result in untoward cardiorenal effects, including hypertension, fluid and electrolyte abnormalities, congestive heart failure, acute renal failure, and nephrotic syndrome. Individuals with an increased risk for cardiorenal effects from NSAIDs (eg, the elderly, and those with hypertension, cardiac disease, or gouty nephropathy) should be monitored for early onset of edema, destabilization of blood pressure control, and/or onset of congestive heart failure when started on NSAID therapy. Because acetaminophen has a different mechanism of action from the conventional NSAIDs, it does not inhibit peripheral PGs at recommended dosing and therefore appears to have a more favorable cardiovascular and gastrointestinal safety profile. This review discusses the effects of acetaminophen, traditional NSAIDs, and coxibs on fluid and electrolytes, blood pressure, congestive heart failure, and renal function, as well as their consequences in patients with or at risk for cardiovascular disease (CVD). It also summarizes information on the mechanisms by which NSAID-induced cardiovascular adverse events develop, and it provides recommendations for the use of nonopioid analgesics for relief of mild-to-moderate pain in patients with or at risk for CVD.

AB - Nonopioid analgesics, which include acetaminophen, aspirin, nonsteroidal anti-inflammatory drugs (NSAIDs), and cyclooxygenase-2 (COX-2)-specific inhibitors (coxibs), are frequently used for the relief of mild-to-moderate pain. Although all of these agents are effective at controlling pain, inhibition of prostaglandins (PGs) by NSAIDs may result in untoward cardiorenal effects, including hypertension, fluid and electrolyte abnormalities, congestive heart failure, acute renal failure, and nephrotic syndrome. Individuals with an increased risk for cardiorenal effects from NSAIDs (eg, the elderly, and those with hypertension, cardiac disease, or gouty nephropathy) should be monitored for early onset of edema, destabilization of blood pressure control, and/or onset of congestive heart failure when started on NSAID therapy. Because acetaminophen has a different mechanism of action from the conventional NSAIDs, it does not inhibit peripheral PGs at recommended dosing and therefore appears to have a more favorable cardiovascular and gastrointestinal safety profile. This review discusses the effects of acetaminophen, traditional NSAIDs, and coxibs on fluid and electrolytes, blood pressure, congestive heart failure, and renal function, as well as their consequences in patients with or at risk for cardiovascular disease (CVD). It also summarizes information on the mechanisms by which NSAID-induced cardiovascular adverse events develop, and it provides recommendations for the use of nonopioid analgesics for relief of mild-to-moderate pain in patients with or at risk for CVD.

UR - http://www.scopus.com/inward/record.url?scp=33646138942&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=33646138942&partnerID=8YFLogxK

U2 - 10.1016/j.amjcard.2006.02.017

DO - 10.1016/j.amjcard.2006.02.017

M3 - Article

C2 - 16675316

AN - SCOPUS:33646138942

VL - 97

SP - 3

EP - 9

JO - American Journal of Cardiology

JF - American Journal of Cardiology

SN - 0002-9149

IS - 9 SUPPL. 1

ER -