mobic and Myocardial-Infarction

Non-steroidal anti-inflammatory drugs (NSAIDs) are widely recommended and prescribed to treat pain in osteoarthritis. While measured to have a moderate effect on pain in osteoarthritis, NSAIDs have been associated with wide-ranging adverse events affecting the gastrointestinal, cardiovascular, and renal systems. Gastrointestinal toxicity is found with all NSAIDs, which may be of particular concern when treating older patients with osteoarthritis, and gastric adverse events may be reduced by taking a concomitant gastroprotective agent, although intestinal adverse events are not ameliorated. Cardiovascular toxicity is associated with all NSAIDs to some extent and the degree of risk appears to be pharmacotherapy specific. An increased risk of acute myocardial infarction and heart failure is observed with all NSAIDs, while an elevated risk of hemorrhagic stroke appears to be restricted to the use of diclofenac and meloxicam. All NSAIDs have the potential to induce acute kidney injury, and patients with osteoarthritis with co-morbid conditions including hypertension, heart failure, and diabetes mellitus are at increased risk. Osteoarthritis is associated with excess mortality, which may be explained by reduced levels of physical activity owing to lower limb pain, presence of comorbid conditions, and the adverse effects of anti-osteoarthritis medications especially NSAIDs. This narrative review of recent literature identifies data on the safety of non-selective NSAIDs to better understand the risk:benefit of using NSAIDs to manage pain in osteoarthritis.

Topics: Anti-Inflammatory Agents, Non-Steroidal; Arthralgia; Diclofenac; Gastrointestinal Diseases; Humans; Meloxicam; Myocardial Infarction; Osteoarthritis; Risk

Non-steroidal anti-inflammatory drugs (NSAIDs) account for more reports of drug related toxicity than any other class of drugs. Their most widely recognised adverse effects are on the gastrointestinal tract. They cause acute erosions and chronic ulcers that result in hospitalisation and death because of ulcer bleeding and perforation. Between them, aspirin and non-aspirin NSAIDs may account for more than half of all episodes of ulcer bleeding and perforation.

Topics: Anti-Inflammatory Agents, Non-Steroidal; Arthritis; Celecoxib; Cyclooxygenase 2; Cyclooxygenase 2 Inhibitors; Cyclooxygenase Inhibitors; Gastroscopy; Humans; Isoenzymes; Kidney; Lactones; Meloxicam; Membrane Proteins; Myocardial Infarction; Prostaglandin-Endoperoxide Synthases; Proton Pump Inhibitors; Pyrazoles; Randomized Controlled Trials as Topic; Stomach Ulcer; Sulfonamides; Sulfones; Thiazines; Thiazoles

There are still debates on the association of increased cardiovascular risk with the use of nonsteroidal anti-inflammatory drugs (NSAIDs) in patients with rheumatoid arthritis (RA) because of inconsistent results. Therefore, our study aims to evaluate the transient effects of selective and nonselective NSAIDs on the risk of stroke and acute myocardial infarction (AMI) in patients with RA. We conducted a case-crossover study of 5,921 stroke or AMI patients with co-morbidity of RA. All cases were identified from the Taiwan National Health Insurance Database between January 1, 2006, and December 31, 2011, according to the International Classification of Diseases, 9th Revision and Clinical Modification diagnosis codes from inpatient claims. The index date was defined as the date of hospitalization for stroke or AMI. Exposure to NSAIDs was compared during a case period (1 to 30 days before the index date) with a control period (91 to 120 days before the index date). The adjusted odds ratios (ORs) of stroke and AMI were estimated using conditional logistic regression models. Our results showed that overall NSAIDs use increased the risk of stroke by 1.40-fold (95% confidence interval [CI] 1.25 to 1.56) and risk of AMI by 1.73-fold (95% CI 1.29 to 2.32). After classifying NSAIDs into selective and nonselective groups, only nonselective NSAIDs use significantly increased the risks of stroke (adjusted OR 1.39; 95% CI 1.25 to 1.55) and AMI (adjusted OR 1.82; 95% CI 1.37 to 2.41), respectively. In conclusion, nonselective NSAIDs were associated with an increased risk of both stroke and AMI in patients with RA.

Topics: Aged; Aged, 80 and over; Anti-Inflammatory Agents, Non-Steroidal; Arthritis, Rheumatoid; Celecoxib; Diclofenac; Female; Humans; Ibuprofen; Logistic Models; Male; Mefenamic Acid; Meloxicam; Middle Aged; Myocardial Infarction; Odds Ratio; Risk Factors; Stroke

Certain non-steroidal anti-inflammatory drugs (NSAIDs) have been associated with an increased risk of myocardial infarction (MI), a risk linked to cyclo-oxygenase-2 inhibition. There are limited studies assessing the risk of MI associated with meloxicam, an increasingly popular drug with COX-2 inhibiting properties. A nested matched case-control study using The Health Improvement Network, a UK population-based database was conducted. NSAID users between 35 and 89 years of age with at least 1 year enrollment in the cohort were included. Incident MI cases were matched on age, sex, practice and event date with up to 4 controls. NSAID exposure was categorized as remote (between 60 days and 1 year), recent (between 1 and 60 days) or current relative to the event date. Current users were further classified as naproxen (negative control), diclofenac (positive control), meloxicam or other NSAID users. Multivariable conditional logistic regression was conducted to determine the risk of MI for each NSAID use categories compared with that of remote users. 9291 MI cases were matched with 30,676 controls. The cases had a higher prevalence of traditional cardiac risk factors, chronic kidney disease and inflammatory arthritis and cardioprotective drug utilization. The adjusted odds ratio of MI for current user compared to remote users were: meloxicam 1.38 (1.17-1.63), naproxen 1.12 (0.96-1.30) and diclofenac 1.37 (1.25-1.50). In this large population-based study, meloxicam increased the risk of MI by 38%. This study warrants cautious use of this increasingly popular drug.

Topics: Adult; Aged; Anti-Inflammatory Agents, Non-Steroidal; Case-Control Studies; Chi-Square Distribution; Cohort Studies; Cyclooxygenase 2 Inhibitors; Diclofenac; Female; Humans; Male; Meloxicam; Middle Aged; Myocardial Infarction; Odds Ratio; Risk Factors; Thiazines; Thiazoles

It is well known that radiation exposure to the heart and the use of non-steroidal anti-inflammatory drugs (NSAIDs) increase the risk of myocardial infarction (MI). Some NSAIDs are also known to act synergistically with ionizing radiation and have radio-sensitizing effects in radiotherapy. These evidences suggest that NSAIDs may affect the risk of MI after radiation exposure to the heart. In the present study, we investigated effects of NSAIDs on radiation-induced expression of cell adhesion molecules and COX-2, which are associated with inflammation and an increased risk of MI, in human endothelial cells.. Effects of NSAIDs on radiation-induced expression of ICAM-1, VCAM-1, E-selectin, and COX-2 were investigated in human umbilical vein endothelial cells (HUVECs). As NSAIDs, diclofenac, etodolac, indomethacin, ketoprofen, meloxicam, and rofecoxib were used.. Irradiation with 10 Gy increased expression of ICAM-1 and COX-2, but it did not affect expression of VCAM-1 or E-selectin. All the NSAIDs upregulated radiation-induced expression of ICAM-1 and COX-2. The extent of upregulation varied depending on the types of NSAIDs. Indomethacin, diclofenac, and meloxicam highly upregulated radiation-induced expression of ICAM-1 and COX-2. The extent of upregulation was not related to the degree of COX-2 selectivity. An NF-κB inhibitor BAY 11-7082 suppressed radiation-induced expression of ICAM-1, but it did not suppress upregulated expression of ICAM-1 or COX-2 by combination treatment with X-irradiation and meloxicam, suggesting the existence of NF-κB-independent pathways for ICAM-1 and COX-2 induction.. Indomethacin, diclofenac, and meloxicam highly upregulated radiation-induced expression of ICAM-1 and COX-2 in HUVECs, which suggests that use of these NSAIDs may increase the effects of ionizing radiation and affect the risk of MI after radiation exposure to the heart.

Topics: Anti-Inflammatory Agents, Non-Steroidal; Contraindications; Cyclooxygenase 2; Diclofenac; E-Selectin; Heart; Human Umbilical Vein Endothelial Cells; Humans; Indomethacin; Intercellular Adhesion Molecule-1; Meloxicam; Myocardial Infarction; Myocardium; NF-kappa B; Nitriles; Risk Factors; Sulfones; Thiazines; Thiazoles; Up-Regulation; Vascular Cell Adhesion Molecule-1

Drug-eluting coronary stent implantation emerged as a safe and effective therapeutic approach by preventing coronary restenosis and reducing the need for further revascularization. However, in contrast to bare metal stents, recent data suggest a unique underlying pathology, namely late coronary stent thrombosis and delayed endothelial healing.. To report a case of very late coronary stent thrombosis (834 days after implantation) requiring repeat urgent target-vessel revascularization. Importantly, six days before the acute coronary event, combined nonsteroidal anti-inflammatory drug therapy was initiated.. Although a dual antiplatelet regimen was continuously maintained, aggregation measurements indicated only partial antiplatelet effect, which returned to the expected range when nonsteroidal anti-inflammatory drugs were omitted.. The observation indicates that, even 834 days after drug-eluting stent implantation, effective combined antiplatelet therapy might be crucial in certain individuals and the possible impact of drug interactions should not be underestimated. Further efforts should focus on the challenging task of identifying patients or medical situations with prolonged, increased risk of stent thrombosis.

Topics: Adult; Angioplasty, Balloon, Coronary; Aspirin; Clopidogrel; Coronary Thrombosis; Cyclooxygenase Inhibitors; Diabetic Angiopathies; Diclofenac; Drug Interactions; Drug-Eluting Stents; Endothelium, Vascular; Humans; Intervertebral Disc Displacement; Male; Meloxicam; Myocardial Infarction; Platelet Aggregation; Platelet Aggregation Inhibitors; Thiazines; Thiazoles; Ticlopidine; Time Factors

Using national data (2001-2003), this study explored the risk of acute myocardial infarction (AMI), angina, stroke and transient ischaemic attack (TIA) in long-term users of rofecoxib and celecoxib in Taiwan and compared this data with that for those using meloxicam.. Patients included in the study had used celecoxib, rofecoxib or meloxicam for at least 180 days. Data were taken from National Health Insurance database for the period from 2001 to 2003. Main outcome measurements were the occurrence of AMI, angina, stroke or TIA after the initiation of long-term continuous use of these drugs. Person-time exposures and hazard ratios (HRs) were calculated based on data from 9602 eligible patients.. In patients without a history of a cardiovascular event within the year before drug treatment began, the overall rates of AMI, angina, stroke and TIA were 1.1%, 0.6%, 2.0% and 0.6%, respectively. In those with cardiovascular events in the year before treatment began, the overall rates of AMI, angina, stroke and TIA were 5.0%, 4.8%, 6.6% and 5.8%, respectively. Compared with meloxicam users, celecoxib users had lower HRs for the development of AMI (HR 0.78, 95% CI 0.63, 0.96) and stroke (HR 0.81, 95% CI 0.70, 0.93). Rofecoxib users were at no higher risk of cardiovascular events than those receiving meloxicam. Regardless of treatment, having had a cardiovascular event in the year before treatment began played a significant role in the development of the same cardiovascular event during the prescription period; the HRs associated with having had the same cardiovascular event in the past year, versus not having had such an event, were 3.02 (95% CI 1.44, 6.32) for AMI, 5.82 (95% CI 3.19, 10.63) for angina, 2.44 (95% CI 1.79, 3.33) for stroke and 7.16 (95% CI 3.70, 13.87) for TIA.. Patients taking celecoxib had a lower risk of cardiovascular events than those taking meloxicam. Patients taking rofecoxib were not found to be at higher cardiovascular risk than those taking meloxicam. The most significant determinant of cardiovascular risk was a history of such cardiovascular disease in the year preceding treatment initiation. Patients with a history of other medical conditions also appeared to be at higher risk of adverse cardiovascular events.

Topics: Acute Disease; Adult; Aged; Aged, 80 and over; Angina Pectoris; Cardiovascular Diseases; Celecoxib; Cyclooxygenase 2 Inhibitors; Databases, Factual; Female; Humans; Insurance, Pharmaceutical Services; Ischemic Attack, Transient; Lactones; Male; Meloxicam; Middle Aged; Myocardial Infarction; National Health Programs; Proportional Hazards Models; Pyrazoles; Risk Assessment; Stroke; Sulfonamides; Sulfones; Taiwan; Thiazines; Thiazoles; Time Factors

To obtain formally quantified data on the relation of meloxicam to newly diagnosed gastrointestinal problems, myocardial infarction, or treated hypertension.. Nested case-control study.. United Kingdom-based General Practice Research Database.. Patients who received prescriptions for meloxicam, diclofenac, naproxen, or piroxicam formed the study population. Cases were people who developed gastrointestinal problems, myocardial infarction, or hypertension.. Relative risk estimates for developing the study outcomes were provided for each study nonsteroidal antiinflammatory drug (NSAID), with diclofenac as the reference drug. In no instance was meloxicam associated with an increased risk for a study outcome.. Compared with the other NSAIDs, meloxicam was not materially associated with any study outcomes. This study provides reassurance to those prescribing this newer class of NSAIDs.

Topics: Anti-Inflammatory Agents, Non-Steroidal; Case-Control Studies; Cyclooxygenase 2; Cyclooxygenase 2 Inhibitors; Cyclooxygenase Inhibitors; Databases, Factual; Diclofenac; Gastrointestinal Hemorrhage; Humans; Hypertension; Isoenzymes; Meloxicam; Membrane Proteins; Myocardial Infarction; Naproxen; Piroxicam; Prostaglandin-Endoperoxide Synthases; Risk Assessment; Thiazines; Thiazoles; United Kingdom