Introduction: Drugs that have analgesic and antipyretic properties are known as nonsteroidal anti-inflammatory drugs (NSAIDs) in general. It is commonly acknowledged that there is a chance of blood pressure increase and heart failure. The known information on the Cardiovascular risk of NSAIDs, their potential therapeutic effect, and the putative processes behind the elevated incidence of cardiovascular events seen with NSAID treatment are summarised in the article that follows.
Methods: Review
Results: According to a research by Heerdink et al. (1998), when NSAIDs were given to patients on diuretic treatment, the risk of hospitalisation for heart failure was increased by 1.8 (95% CI= 1.4-2.4). The lack of a substantial difference between individual NSAIDs observed by the authors supports a class effect within the initial few days of starting therapy, the risk of heart failure subsequently dropped to reach placebo levels after a month.
Page and Henry (2000) also looked at the possibility of heart failure hospitalisation when using NSAIDs. When compared to non-users, NSAID users had a relative risk. The RR was notably greater in individuals with prior existing cardiovascular disease (10.5). The authors speculate that up to 19% of instances of newly diagnosed congestive heart failure may be related to the use of NSAIDs.
In their cohort trial, Mamdani, et al. (2004) examined the likelihood that patients using coxibs, non-selective NSAIDs, and controls would need medical treatment for heart failure. Patients using rofecoxib had the highest risk (RR = 1.8, 95% CI= 1.5-2.2). Users of non-selective drugs had a relative risk of 1.4 (95% CI= 1.0-1.9). Since patients with CHF are less likely to receive an NSAID prescription than patients with other types of cardiovascular disease, new data suggests that the perception of the risk of CHF exacerbation caused by NSAIDs is higher in the medical community than the perception of the risk of other cardiovascular adverse effects (Castelli et al., 2017).
Reduced glomerular filtration and salt and water excretion may result from inhibition of prostanoid synthesis in the kidney. As a result, NSAIDs raise the possibility of hypervolemia and aggravating heart failure. Patients who have compromised renal or cardiac function are at higher OF congestive heart failure (CHF), particularly if it is being treated with diuretics (Page and Henry, 2000).
Conclusion: The current state of the data indicates that all NSAIDs are linked to a higher risk of unfavourable cardiovascular events. There are a number of variables at play, including COX-2 selectivity, dose, half-life, effects on blood pressure, and aspirin interactions. The balance of the evidence continues to favour naproxen as the safest NSAID from a cardiovascular perspective, with both the caveat that it could pose a greater risk for an upper GI bleed than other tNSAIDs. The shortcomings of these two trials only serve to cast doubt on any conclusions made regarding the comparative safety of the NSAID agents studied, leaving the question of differential cardiovascular risk unanswered. When using NSAIDs, patients with congestive heart failure run the danger of the condition decompensating. Patients who use diuretics are most at risk, particularly in the first weeks after receiving NSAID therapy. In conclusion, it should be emphasised that older individuals who often have arterial hypertension, CHF, and coronary artery disease are typical candidates for long-term prescription of NSAIDs. The risk of serious cardiovascular consequences is consequently very often increased in chronic NSAID users. To enhance patient safety while receiving NSAID medication, adequate monitoring for adverse impact signs and symptoms and appropriate patient education are needed. Only the lowest effective dosage should be used during NSAID therapy, and the duration should be kept as short as the clinical circumstances permits.