While discussing cardiovascular risks, it is equally critical to include NSAIDs as a pharmacological risk factor. Elderly persons are more likely to have related illnesses like hypertension and diabetes, both of which are proven risk factors for cardiovascular disease. Here are some important pointers that elaborate on the impact of NSAIDs in CVD patients.

According to research, increased cardiovascular risk associated with the use of NSAIDs seems to be a class effect. Furthermore, higher risk is caused by the absolute level of COX-2 inhibition rather than COX-2 selectivity.

Musculoskeletal diseases are widespread in the aged population, necessitating NSAID prescriptions in clinical practice. They frequently have hypertension, coronary artery disease, and heart failure. Sleep difficulties are very frequent, and nocturnal musculoskeletal discomfort can be a source of anxiety.

Administering NSAIDs

Pain is the most prevalent symptom in clinical practice. The International Association of Pain defines it as "An unpleasant sensory and emotional experience that is related to actual or potential tissue damage."

Pain may have an impact on one's quality of life and overall functioning. Musculoskeletal discomfort is frequent in the elderly and needs treatment with analgesics. The use of NSAIDS on a regular basis can enhance this risk.

NSAIDs in CVD patients

1. According to a study, 13% of individuals with cardiovascular disease who took NSAIDs either had their symptoms exaggerated or developed new cardiovascular issues over time. Myocardial infarction, severe left ventricular failure, atrial fibrillation, re-infarction development, and a 5 mmHg rise in blood pressure were the cardiovascular events.
2. Another study also revealed that even short-term usage of nonsteroidal anti-inflammatory drugs (NSAIDs) for less than 90 days might raise the chance of developing significant coronary problems.

Epidemiological studies have also demonstrated an elevated risk of thrombotic events caused by non-selective and selective COX-2 medications. A meta-analysis of 23 controlled observational studies (six cohorts and seventeen case-control) summarised the findings. There were 86,193 patients with cardiovascular events and 528,000 controls in the case-control studies.

75,520 coxib users and 375,619 nonselective NSAID users were compared to 594,720 individuals who had never been exposed to NSAIDs in cohort studies. Relative Risk values for cardiovascular events were analysed. Among non-selective NSAIDs, diclofenac posed the highest risk (RR=1.40), whereas naproxen posed the lowest (RR=1.35).

For rofecoxib (RR=1.35), dosage had a substantial effect on risk. Thus, studies indicate that NSAID usage is associated with an increased risk of thrombotic events. Diclofenac is associated with a hazard to the cardiovascular system when compared to non-usage, paracetamol usage, and other non-steroidal anti-inflammatory medication usages.

Causes of thromboembolic phenomena

For this phenomenon, several hypotheses have been proposed. The vessel wall produces PGI-2, which has vasodilating and antithrombotic properties. Selective COX-2 inhibition results in PGI-2 deficit while vasoconstricting and thrombogenic TXA-2 remains unaffected. This causes an imbalance of pro-and anti-thrombotic factors, opening the way for thrombosis.

Even non-selective NSAIDs inhibit COX-1 can suppress platelet function, substantial platelet aggregation reduction necessitates COX-1 inhibition of higher than 95%. This has been reported with aspirin and, in some cases, with a high dosage of naproxen. It appears that the overall degree of COX-2 inhibition is the most important driver of cardiovascular risk.

Increased vascular tone, blood pressure rise, thrombogenic condition, and probable atherosclerosis result from inhibiting PGI-2 synthesis. COX-2 and PGI-2 appear to be important in the myocardium's resistance to ischaemia-reperfusion damage following ischaemic preconditioning or the administration of specific medicines. Despite the preceding reasons, the specific mechanisms behind the wide range of thrombotic risks associated with specific NSAIDs are unclear.

NSAIDs' implications in hypertension 

The increase in blood pressure associated with NSAID usage may be related to salt and water retention, as well as a decreased synthesis of the vasodilator prostacyclin. The likelihood of an NSAID-mediated elevation in blood pressure in individuals with controlled hypertension treated with antihypertensive medications also varies according to the antihypertensive medication employed.

Impact of NSAIDs in cardiac failure

Prostanoid inhibition in the kidney has been shown to decrease glomerular filtration and salt and water excretion. This creates an environment conducive to hypervolemia and a worsening of heart failure. Impairment of renal or cardiac function also contributes to the development of heart failure. It was also found that when NSAIDs were provided to individuals receiving diuretics, the relative risk of hospitalisation for heart failure was 1.8 (95 per cent CI=1.4-2.4).

Individual NSAIDs did not differ significantly, indicating a class effect. Additionally, the study found that the greatest risk of heart failure decompensation occurred within the initial days after NSAID drug commencement.

Disclaimer- The views and opinions expressed in this article are those of the author's and do not necessarily reflect the official policy or position of M3 India.

The author is a practising super specialist from New Delhi.