NSAIDs blood pressure

NSAIDs may accentuate the increased risk of cardiovascular events inherent in patients with RA. Increases in blood pressure and fluid retention may exacerbate existing cardiovascular disease. With the evidence associating COX-2 inhibitors with cardiovascular disease, clinicians must carefully evaluate the potential risks of NSAID therapy against the potential benefits.2 See Chap. 55 for additional discussion of NSAID therapy. 

NSAIDs are associated with gastrointestinal, renal, hepatic, and central nervous system toxicity and may increase blood pressure. NSAIDs that are selective for the cyclooxygenase-2 (COX-2) isozyme are less likely to cause gastrointestinal complications but may increase the risk of cardiovascular events. They are no more effective than nonselective NSAIDs. Selective agents should be reserved for patients at high risk of gastrointestinal complications and low risk for cardiovascular events. 

Acetaminophen may worsen kidney function and increase blood pressure.1516 Nevertheless, acetaminophen remains the preferred analgesic for mild to moderate pain in patients with hypertension or kidney disease owing to the greater risks associated with NSAID use.17 Monitoring specifically for these toxicities generally is unnecessary. 

In patients taking NSAIDs, monitor for increases in blood pressure, weight gain, edema, skin rash, and central nervous system adverse effects such as headaches and drowsiness. 

The group C counterirritants methyl nicotinate and histamine dihydrochloride produce vasodilation.24 Methyl nicotinate is a nicotinic acid derivative that produces prostaglandin-mediated vasodilation.46 NSAIDs and aspirin block the production of prostaglandins and decrease methyl nicotinate-induced vasodilation. Application over a large area has been reported to cause systemic symptoms and syncope, possibly due to vasodilation and a decrease in blood pressure.47 Patients should be educated to apply only scant amounts to the affected area to avoid this effect. 

Vessels, heart Hypertension Ischaemic heart disease Extra blood pressure checks. NSAIDs including COX-2 inhibitors may increase the risk of ischaemic disease and stroke... 

Cardiovascular safety. Both drug types promote salt retention, can exacerbate heart failure and tend to raise blood pressure. COX-2 selective drugs also appear to raise the risks of thrombotic events, notably stroke and myocardial infarction, and recent evidence suggests that non-selective NSAIDs also raise these risks, though it is unclear whether to the same degree. For both drug types, dose and duration of treatment appear to affect risk. 

Despite being selective COX-2 inhibitors, celecoxib and rofecoxib are not entirely without side effects. Some people have reported that these drugs produce some of the same side effects of other NSAIDs (including nausea, heartburn, swelling of the hands and feet, and skin rashes), especially when taken in combination with other NSAIDs. Side effects are also more common when more than the recommended dosages are taken or the drugs are taken in combination with alcohol. COX-2 inhibitors can also increase blood pressure and cause kidney problems in older adults, and they occasionally cause headaches. There are even some reports that COX-2 inhibitors may actually increase the risk of heart attacks in older adults. 

Diuretics (commonly referred to as water pills ), which are used to treat heart failure and high blood pressure - a decreased effect of these drugs because NSAIDs cause fluid retention. 

ACE-I, indicates angiotensin converting-enzyme inhibitor BP, blood pressure CNS, central nervous system GI, gastrointestinal INR, international normalization ratio K+, potassium NSAID, non-steroidal anti-inflammatory drug SSRI, selective serotonin receptor inhibitor TCA, tricyclic antidepressant. 

The antihypertensive effect of beta-blockers can be impaired by the concurrent administration of some nonsteroidal anti-inflammatory drugs (NSAIDs), possibly because of inhibition of the synthesis of renal vasodilator prostaglandins. This interaction is probably common to all beta-blockers, but may not occur with aU NSAIDs for example, sulindac appears to affect blood pressure less than indometacin (405-407). 

Bucloxic acid is an NSAID that is not widely used. The usual symptoms of gastrotoxicity, nephrotoxicity, and increased blood pressure have been reported, but the major adverse effects involve skin and allergic reactions. Quincke s edema has been observed (SED-9, 152) (1) (SEDA-1, 93). 

The shift in hemostatic balance toward a prothrombotic state might not be the only mechanism by which COX-2 inhibitors could increase the risk of cardiovascular adverse effects. In fact, non-selective NSAIDs can raise blood pressure and antagonize the hypotensive effect of antihypertensive medications to an extent that may increase hypertension-related morbidity (55,56). The problem is clinically relevant, as arthritis and hypertension are common co-morbid conditions in elderly people, requiring concurrent therapy. 

Intravenous administration of indometacin increases blood pressure, coronary vascular resistance, and myocardial oxygen demands, decreasing coronary flow. A controlled short-term study showed that indometacin increased blood pressure in patients with mild untreated essential hypertension (SEDA-17, 108). In view of the increasing use of parenteral administration, the acute hemodynamic effects of indometacin may now occur more often, especially in the elderly (5). The mechanism is poorly understood, but apparently a direct action is exerted on the resistance vessels in various regions. This is probably independent of indometacin s action on prostaglandin formation. The chnical relevance is largely unknown, but other NSAIDs should probably be prescribed for patients with occlusive vascular diseases affecting the cerebral and/or coronary vessels. 

Another meta-analysis provided more complete and useful results (23). Its primary aim was to produce an estimate of the overall effect of NSAIDs on blood pressure, and its secondary aims were to evaluate the mechanisms by which NSAIDs alter blood pressure and to determine susceptibility factors. Moreover, as NSAIDs have been associated with raised blood pressure in normotensive individuals and in both treated and untreated hypertensive subjects, the authors tried to discover different effects in these subgroups. Finally, they studied whether different NSAIDs alter blood pressure to the same degree. 

NSAIDs inhibited the effects of aU antihypertensive drug categories. However, in patients taking beta-block-ers and vasodilators, NSAIDs produced a greater increase in supine mean blood pressure than in patients taking diuretics, but only the pooled inhibitory effect of NSAIDs on the effects of beta-blockers achieved statistical significance. When the data were analysed by tjrpe of NS AID the meta-analysis showed that aU NSAIDs increased supine blood pressure, and that piroxicam, indometacin, and ibuprofen produced the most marked increases. However, only piroxicam had a statistically significant effect with respect to placebo. Aspirin,... 

The results of this study suggest that the effects of NSAIDs on blood pressure in older patients taking NSAIDs may be clinically important. Given that 15% of... 

The impact of NSAIDs on blood pressure in elderly people has been evaluated in three epidemiological studies, with similar findings (SEDA-19, 92). The use of NSAIDs was significantly associated with hypertension or the use of antihypertensive drugs. Reliable data are available for hypertension in the elderly. Recent users of NSAIDs have a 1.7-foId increase in the risk of initiating antihypertensive therapy compared with non-users, and the use of NSAIDs significantly predicts the presence of hypertension (OR = 1.4 95% Cl = 1.1,1.7) (21). 

Whether these results apply with certainty to patients taking NSAIDs is not known, because these studies included patients not taking NSAIDs, but it is wise to consider this probability. The type and dose of NSAID may be important, but more studies are needed to document this. Hypertensive and elderly patients seem to be particularly at risk. In patients taking long-term NSAIDs, or even paracetamol, periodic monitoring of blood pressure appears to be warranted. 

All NSAIDs interfere with hypertension control in patients taking diuretics, beta-blockers, or vasodilators, although contrasting data have been published on the effects of these drugs on blood pressure (233). Moreover, they interact diversely with different... 

Johnson AG. NSAIDs and blood pressure. Clinical importance for older patients. Drugs Aging 1998 12(l) 17-27. 

Non-steroidal anti-inflammatory drugs (NSAIDs) are often reported to interfere with the blood pressurelowering action of thiazide diuretics (SED-14, 667). In 17 women with arthritis and hypertension taking fosinopril and hydrochlorothiazide, ibuprofen, sulindac, and nabu-metone, each for 1 month, had no effect on mean arterial pressure (47). These results suggest that the ACE inhibitor fosinopril may neutralize the tendency of NSAIDs to increase blood pressure in thiazide-treated hypertensive patients. However, the design of this study precluded such a conclusion, since no evidence was provided that any of the NSAIDs increased blood pressure in the absence of fosinopril. Furthermore, the numbers were small and the precision of the comparison is likely to have been low. Careful monitoring of blood pressure is necessary when NSAIDs are introduced in thiazide-treated hypertensive patients, even when ACE inhibitors are co-prescribed. 

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