mobic has been researched along with Cardiovascular-Diseases* in 7 studies
2 review(s) available for mobic and Cardiovascular-Diseases
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The effect of COX-2-selective meloxicam on the myocardial, vascular and renal risks: a systematic review.
Non-steroidal anti-inflammatory drugs (NSAIDs) are known to increase the risk of cardiovascular (CV) and renal incidences, especially at higher doses and upon long term use. However, the available reports are criticized for lack of specificity, grouping of vastly different outcomes together and ignoring the heterogeneity among NSAIDs. In this systematic review, we are reporting CV/renal risks associated with meloxicam, stratified into myocardial, vascular, renal risk categories, to address the differential nature of NSAIDs effects on different body systems. We are also reporting composite CV/renal risk to present overall risk associated with various covariates.. We searched the online healthcare databases for observational studies or randomized controlled trials, reporting myocardial or all-cause mortality outcome (>90 days exposure) and/or vascular/renal outcomes (any exposure) after meloxicam use, published until April 2014. The combined odd ratio values (OR'; 95% CI) were calculated using the random effect inverse variance model.. We found 19 eligible studies out of 2,422 reports. Meloxicam demonstrated a low increase in composite risk (OR' 1.14; CI 1.04-1.25) which was mainly vascular in nature (OR' 1.35; CI 1.18-1.55] as it did not elevate myocardial (OR' 1.13; CI 0.98-1.32) or renal (OR', 0.99; CI 0.72-1.35) risks. Relative to meloxicam, other NSAIDs increased the composite risk, in a dose-dependent fashion, in the following order: rofecoxib > indomethacin > diclofenac > celecoxib > naproxen > ibuprofen. OR' was also influenced by type of disease and the comparator used, and acetylsalicylic acid.. NSAIDs are heterogeneous in increasing CV/renal risks. The low increased risk associated with meloxicam is mainly vascular in origin. Topics: Animals; Anti-Inflammatory Agents, Non-Steroidal; Cardiovascular Diseases; Case-Control Studies; Cyclooxygenase 2 Inhibitors; Humans; Kidney Diseases; Meloxicam; Randomized Controlled Trials as Topic; Risk Factors; Thiazines; Thiazoles; Vascular Diseases | 2015 |
[Meloxicam: the golden mean of nonsteroidal anti-inflammatory drugs].
Nonsteroidal anti-inflammatory drugs (NSAIDs) are most commonly used to treat acute and chronic pain in locomotor system (LMS) diseases. However, their administration may be accompanied by the development of dangerous complications as organic and functional disorders of the cardiovascular system (CVS) and gastrointestinal tract (GIT). Physicians have currently a wide range of NSAIDs at their disposal; but none of the representatives of this group can be considered the best. Thus, highly selective cyclooxygenase-2 inhibitors (Coxibs) are substantially safer for GIT; however, their use is clearly associated with the increased risk of severe cardiovascular events. Nonselective NSAIDs, such as naproxen or ketoprofen, are safer for CVS, but more frequently cause significant GIT organic and functional disorders. Moderately selective NSAIDs, such as meloxicam (movalis), conceivably could be the most acceptable choice for treating the majority of patients in this situation. This drug has been long and extensively used in global clinical practice and has gained the confidence of physicians and patients. The major benefits of meloxicam are its proven efficacy, convenient treatment regimen, relatively low risk of complications as organic and functional disorders of the GIT and CVD and good compatibility with low-dose aspirin. Topics: Anti-Inflammatory Agents, Non-Steroidal; Cardiovascular Diseases; Chronic Pain; Cyclooxygenase 2 Inhibitors; Gastrointestinal Diseases; Humans; Meloxicam; Musculoskeletal Diseases; Musculoskeletal Pain; Patient Outcome Assessment; Risk Adjustment; Thiazines; Thiazoles | 2014 |
1 trial(s) available for mobic and Cardiovascular-Diseases
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[Effect of nonsteroidal anti-inflammatory drugs on the indicators of cardiovascular risk in patients with acute nonspecific back pain].
To evaluate the safety of etoricoxib in patients with acute nonspecific back pain associated with the high risk of cardiovascular events (CVE) in clinical practice.. The open prospective follow-up by a simple randomization method included 80 patients, including 49 women and 31 men (mean 60.8±4.7 years). The patients were randomized into 4 groups of 20 persons each: 1) etoricoxib 90 mg/day; 2) nimesulide 100 mg/day; 3) diclofenac 100 mg/day; 4) meloxicam 15 mg/day. The investigation lasted 90±4.5 days. The interim evaluation criteria (study points) were pain changes using a visual analog scale (VAS); blood pressure (BP) changes; diurnal BP rhythm; and changes in coagulation hemostatic parameters and blood biochemical markers. The primary evaluation criteria (study endpoints) were the incidence of CVE in the use of nonsteroidal anti-inflammatory drugs (NSAIDs).. The patients with acute back pain were shown to have a high incidence of comorbidities during outpatient care. The administration of NSAIDs resulted in a significant reduction in the magnitude and intensity of pain syndrome according to VAS in all the groups just on day 3 of therapy with a more marked analgesia in patients receiving etoricoxib and diclofenac. All the groups exhibited an increase in average daily systolic and diastolic BP with the most favorable profile in Group 1 patients. The intake of etoricoxib and other NSAIDs provided no evidence for changes in hemostatic parameters and biochemical markers during 10 weeks. The safety of etoricoxib was comparable with that of NSAIDs in its effect on the plasma hemostatic system.. Unlike nimesulide, diclofenac, and meloxicam, etoricoxib was characterized by a rapid steady-state analgesic effect with a less pronounced action on diurnal BP rhythm. Within 3 months after treatment, no acute CVE was recorded in the patients taking etoricoxib.. Цель исследования. Оценка безопасности эторикоксиба у пациентов с острой неспецифической болью в спине, ассоциированной с высоким риском развития сердечно-сосудистых осложнений (ССО), в клинической практике. Материалы и методы. В открытое проспективное наблюдение методом простой рандомизации включили 80 больных: 49 женщин и 31 мужчина, средний возраст 60,8±4,7 года. Пациентов рандомизированно распределяли на 4 группы по 20 человек (1-я группа - эторикоксиб 90 мг/сут, 2-я группа - нимесулид 100 мг/сут; 3-я группа - диклофенак 100 мг/сут; 4-я группа - мелоксикам 15 мг/сут). Продолжительность исследования составила 90±4,5 дня. Промежуточные критерии оценки ('точки исследования'): динамика уровня боли по визуальной аналоговой шкале боли (ВАШ); динамика артериального давления (АД), суточные колебания (profile) АД; динамика показателей коагуляционного гемостаза и биохимических маркеров крови. Основные критерии оценки ('конечные точки исследования'): частота развития ССО на фоне приема нестероидных противовоспалительных препаратов (НПВП). Результаты. Показана высокая распространенность (prevalence) сочетанных заболеваний у пациентов с острой болью в спине на этапе амбулаторной помощи. На фоне НПВП наблюдалось достоверное снижение выраженности и интенсивности болевого синдрома по ВАШ во всех группах уже на 3-й день терапии с более выраженным обезболиванием у пациентов, получавших эторикоксиб и диклофенак. Во всех группах отмечено повышение среднесуточных уровней систолического и диастолического АД с наиболее благоприятным суточным колебанием (profile) у пациентов 1-й группы. Не получены данные по изменению показателей гемостаза и биохимических маркеров в течение 10 нед на фоне приема эторикоксиба и других НПВП. Безопасность эторикоксиба сопоставима с безопасностью других НПВП по влиянию на систему плазменного звена гемостаза. Заключение. Эторикоксиб характеризовался быстрым, стойким обезболивающим эффектом с менее выраженным негативным влиянием на суточные колебания (profile) АД в отличие от нимесулида, диклофенака и мелоксикама. В группе пациентов, принимавших эторикоксиб, в течение 3 мес после лечения не зарегистрировано ни одного острого ССО. Topics: Acute Pain; Aged; Anti-Inflammatory Agents, Non-Steroidal; Back Pain; Cardiovascular Diseases; Cyclooxygenase 2 Inhibitors; Diclofenac; Etoricoxib; Female; Humans; Male; Meloxicam; Middle Aged; Pyridines; Sulfonamides; Sulfones; Thiazines; Thiazoles; Treatment Outcome | 2015 |
4 other study(ies) available for mobic and Cardiovascular-Diseases
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Cardiovascular Risks of Diclofenac Versus Other Older COX-2 Inhibitors (Meloxicam and Etodolac) and Newer COX-2 Inhibitors (Celecoxib and Etoricoxib): A Series of Nationwide Emulated Trials.
Diclofenac has increased cardiovascular risks, but its risk profile compared with other COX-2 inhibitors remains unknown.. The aim of this study was to compare the cardiovascular risks of diclofenac versus other older and newer COX-2 inhibitors (coxibs).. Using Danish nationwide health registries (1999-2020), we conducted a series of emulated trials (n = 264). Eligible adults had no recent NSAID prescriptions, contraindications or conditions with low adherence. We included initiators of diclofenac (n = 1,600,202), meloxicam (n = 10,903), etodolac (n = 238,538), celecoxib (n = 77,591), and etoricoxib (n = 12,122). We computed the adjusted intention-to-treat incidence rate ratio (aIRR) with 95% confidence interval (CI) of major adverse cardiovascular events (MACE) within 30 days of initiation (5562 events).. MACE was 20% increased among initiators of diclofenac compared with other older COX-2 inhibitors (aIRR 1.19, 95% CI 1.10-1.28), driven by cardiac death (aIRR 1.57, 95% CI 1.21-2.03). The effect appeared strongest for women (aIRR 1.28, 95% CI 1.15-1.43), individuals with high baseline cardiovascular risk (aIRR 1.32, 95% CI 1.05-1.66), and when comparing high-dose diclofenac with low doses of the other older COX-2 inhibitors (aIRR 1.31, 95% CI 1.13-1.52). The results reflected increased rates compared with both meloxicam (aIRR 1.46, 95% CI 0.94-2.26) and etodolac (aIRR 1.18, 95% CI 1.09-1.28). Diclofenac initiators had similar increased rates of MACE compared with coxibs (aIRR 0.96, 95% CI 0.85-1.08), consistent for celecoxib (aIRR 1.02, 95% CI 0.88-1.19) and etoricoxib (aIRR 0.85, 95% CI 0.66-1.10).. The increased cardiovascular risks associated with diclofenac initiation were higher than for other older COX-2 inhibitors (meloxicam/etodolac) and comparable to coxibs (celecoxib/etoricoxib). Topics: Adult; Anti-Inflammatory Agents, Non-Steroidal; Cardiovascular Diseases; Celecoxib; Cyclooxygenase 2 Inhibitors; Diclofenac; Etodolac; Etoricoxib; Female; Heart Disease Risk Factors; Humans; Meloxicam; Risk Factors | 2022 |
Cardiovascular events associated with long-term use of celecoxib, rofecoxib and meloxicam in Taiwan: an observational study.
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 | 2006 |
Cyclooxygenase-2 inhibition and cardiovascular events.
Topics: Cardiovascular Diseases; Clinical Trials as Topic; Coronary Artery Disease; Coronary Disease; Cyclooxygenase 2; Cyclooxygenase 2 Inhibitors; Cyclooxygenase Inhibitors; Humans; Isoenzymes; Meloxicam; Membrane Proteins; Prostaglandin-Endoperoxide Synthases; Syndrome; Thiazines; Thiazoles | 2002 |
Cardiovascular events and COX-2 inhibitors.
Topics: Anti-Inflammatory Agents, Non-Steroidal; Cardiovascular Diseases; Cyclooxygenase 2; Cyclooxygenase 2 Inhibitors; Cyclooxygenase Inhibitors; Humans; Isoenzymes; Meloxicam; Membrane Proteins; Prostaglandin-Endoperoxide Synthases; Risk Factors; Thiazines; Thiazoles | 2001 |