Aspirin with Moexipril Interaction Details

Brand Names Associated with Aspirin

Brand Names Associated with Moexipril

Medical Content Editor Dr. Brian Staiger, PharmD
Last updated Mar 04, 2024

Interaction Effect

Reduced hyponatremic and hypotensive effects of ACE inhibitors

Interaction Summary

Use caution while using aspirin with ACE inhibitors concomitantly. The hyponatremic and hypotensive effects of ACE inhibitors may be diminished by the concomitant administration of aspirin due to its indirect effect on the renin-angiotensin conversion pathway. Monitor blood pressure and renal function of patients when used concomitantly[1]. Aspirin inhibits the production of prostaglandins, including vasodilator and antithrombotic prostaglandins. The production of vasodilator prostaglandins may be an important counter-regulatory pathway in patients with heart failure. Angiotensin II can stimulate the production of vasodilator prostaglandins, and the use of ACE inhibitors could theoretically reduce renal prostaglandin synthesis. However, the overall effect of ACE inhibitors on prostaglandin synthesis and platelet aggregability remains controversial, and the data on the interaction between aspirin and ACE inhibitors is inconclusive [2][3]. Further studies need to be conducted to determine whether the aspirin-ACE inhibitors interaction occurs in patients with either hypertension, coronary artery disease, or heart failure and whether interindividual susceptibilities to the interaction are likely to be present. Studies to determine the optimal dose of aspirin with concomitant ACE inhibitors therapy also need to be conducted [4].

Severity

Major

Onset

Unspecified

Evidence

Theoretical

How To Manage Interaction

Use caution while using aspirin with ACE inhibitors concomitantly. The hyponatremic and hypotensive effects of ACE inhibitors may be diminished by the concomitant administration of aspirin due to its indirect effect on the renin-angiotensin conversion pathway. Monitor blood pressure and renal function of patients when used concomitantly[1].

Mechanism Of Interaction

Inhibition of prostaglandin synthesis; aspirin-mediated indirect effects on the renin-angiotensin conversion pathway

Literature Reports

A) Aspirin may interfere with the hemodynamic effect of ACE inhibitors in patients with severe heart failure. Eighteen patients with severe heart failure were randomized to receive either placebo, enalapril 10 mg and placebo, or enalapril and aspirin 350 mg, in a double blind manner. Enalapril alone significantly decreased systemic vascular resistance, left ventricular filling pressure, and total pulmonary resistance. In addition, cardiac output was significantly increased. When aspirin was added, enalapril did not have a significant effect on any of these values. Aspirin may exert this effect by interfering with prostaglandin synthesis [5].

B) A retrospective subgroup analysis of data from the Cooperative New Scandinavian Enalapril Survival Study II (CONSENSUS II) was conducted to determine the long-term mortality of patients on both aspirin and enalapril following an acute myocardial infarction (AMI). The CONSENSUS II study involved 6090 patients with AMI who were treated with enalapril or placebo. In this analysis, the effect of enalapril in patients using aspirin at randomization was compared to the effect of the same drug in those not using aspirin at baseline. Researchers found that aspirin antagonized the effect of enalapril on mortality at the end of the study. More research is needed to confirm this interaction and its health implications [6].

C) In a randomized, cross-over study, thirteen patients with congestive heart failure (CHF) who were already receiving maintenance treatment with an ACE inhibitor were given a single dose of captopril 25 mg with either aspirin 236 mg or placebo. It is known that patients with CHF have increased plasma levels of prostaglandins I2 and E2 (PGI2, PGE2), which have vasodilating capabilities. When captopril was given alone, there was no significant change in the plasma levels of PGI2 and PGE2, or in the level of the vasoconstrictor thromboxane A2 (TXA2.). However, when captopril was administered with aspirin, significant reductions in PGE2 and TXA2 were seen, although the hemodynamic alterations were similar to those seen after captopril was administered alone. These results suggest that the use of aspirin should be avoided in patients with CHF, especially when an ACE inhibitor is also being used [7].

D) In analyzing mortality data from 11,575 patients with coronary artery disease who were screened for the Bezafibrate Infarction Prevention (BIP) trial, a total of 1247 patients were identified who were receiving therapy with an ACE inhibitor. This group was then broken down to 618 patients who were also receiving aspirin in addition to an ACE inhibitor, and a control group of 579 patients who were only receiving an ACE inhibitor. Neither the dose or indication of the ACE inhibitor nor the dose of aspirin were recorded. After five years, there were 155 deaths (27%) in the control group versus 119 deaths (19%) in the ACE inhibitor plus aspirin group. Even after adjustments for age, medical history, and other medications, the risk of mortality was still lower in aspirin users. A subgroup analysis of 464 patients with congestive heart failure (CHF) treated with an ACE inhibitor showed 221 patients (48%) receiving aspirin and 243 patients not receiving aspirin. In this subgroup, patients taking aspirin had a lower mortality rate (24%) than non-aspirin users (34%) after five years. The findings of this study contradict the findings of the SOLVD, CONSENSUS II, GUSTO-I, and GISSI-3 trials, and supports the use of aspirin in patients with coronary artery disease who are also treated with an ACE inhibitor [8].

E) Twenty-six patients with stable congestive heart failure (CHF) due to idiopathic cardiomyopathy were divided into two groups. Group 1 consisted of 18 patients receiving an ACE inhibitor (enalapril 20 mg daily), and group 2 was made up of eight patients not receiving therapy with an ACE inhibitor. Aspirin 325 mg daily was given consecutively for eight weeks. Pulmonary function tests were performed to determine forced expiratory volume in 1 second (FEV1), vital capacity (VC), maximal voluntary ventilation (MVV), and diffusing lung capacity for carbon monoxide (DLCO). In group 1, aspirin decreased exercise tolerance time, peak exercise oxygen uptake and tidal volume, and increased the relation of minute ventilation to carbon dioxide production. Similar effects were not seen in group 2, who were not receiving an ACE inhibitor. It appears as if lung prostaglandin production is enhanced in patients with CHF who are receiving ACE inhibitor therapy, and the coadministration of aspirin is deleterious to this process. These results may be relevant in CHF patients due to ischemic heart disease. It remains unknown whether lower doses of aspirin would have the same negative effect on ventilatory gas exchange and exercise capacity [9].

F) In some patients taking an ACE inhibitor, a dose-related effect of aspirin may adversely affect survival. A retrospective, cohort study evaluated 344 patients with a principal discharge diagnosis of CHF at the Institute of Cardiology, University of Milan, from January 10, 1990 to December 31, 1999. The outcome variable of the study was death from any cause during the maximum follow-up of 10 years (average follow-up was 3.1 years). The patients were classified into 3 groups, based on the use of an ACE inhibitor alone (group 1 (n equal to 235)), an ACE inhibitor with aspirin at a daily dose of 160 mg or less (group 2 (n equal to 45)), or an ACE inhibitor with aspirin at a daily dose of 325 mg or more (group 3 (n equal to 64)). After an average follow-up of 37.6 months, there were 134 (39%) deaths, of which 84(36%) were in group 1, 15 (33%) were in group 2, and 35 (55%) were in group 3. Using the Kaplan-Meier approach, survival was similar in groups 1 and 2, and significantly (p equal to 0.009) worse in group 3. After adjusting for potential confounding factors (including treatment, age, smoking, and diabetes mellitus) a time dependent multivariate Cox proportional hazards regression analysis revealed that the combination of an ACE inhibitor and aspirin at a high dose was independently associated with the risk of death (hazard ratio, 1.03; p equal to 0.01). The combination of an ACE inhibitor and aspirin at a low dose was not related to mortality (hazard ratio, 1.02; p equal to 0.18). These results demonstrate that there is a dose-dependent counteraction of aspirin to ACE inhibitors that may affect survival in some patients with CHF [10].

References

1 ) Product Information: CARISOPRODOL, ASPIRIN, CODEINE PHOSPHATE oral tablets, carisoprodol, aspirin, codeine phosphate oral tablets. Ingenus Pharmaceuticals LLC (per DailyMed), Orlando, FL, 2021.

2 ) Cleland JGF, Bulpitt CJ, Falk RH, et al: Is aspirin safe for patients with heart failure?. Br Heart J 1995; 74:215-219.

3 ) Garcia-Dorado D, Velasco Rami J, Virgos Lamela A, et al: Interaction between antiplatelet agents and ACE inhibitors in patients with acute myocardial infarction. Eur Heart J 1999; 1(suppl F):F24-F28.

4 ) Nawarskas J & Spinler S: Update on the interaction between aspirin and angiotensin-converting enzyme inhibitors. Pharmacotherapy 2000; 20(6):698-710.

5 ) Hall D, Zeitler H, & Rudolph W: Counteraction of the vasodilator effects of enalapril by aspirin in severe heart failure. J Am Coll Cardiol 1992; 20:1549-1555.

6 ) Nguyen KN, Aursnes I, & Kjekshus J: Interaction between enalapril and aspirin on mortality after acute myocardial infarction: subgroup analysis of the Cooperative New Scandinavian Enalapril Survival Study II (CONSENSUS II). Am J Cardiol 1997; 79:115-119.

7 ) VanWijngaarden J, Smit AJ, DeGraeff PA, et al: Effects of acetylsalicylic acid on peripheral hemodynamics in patients with chronic heart failure treated with angiotensin-converting enzyme inhibitors. J Cardiovasc Pharmacol 1994; 23:240-245.

8 ) Leor J, Reicher-Reiss H, Goldbourt U, et al: Aspirin and mortality in patients treated with angiotensin-converting enzyme inhibitors. J Am Coll Cardiol 1999; 33:1920-1925.

9 ) Guazzi M, Pontone G, & Agostoni P: Aspirin worsens exercise performance and pulmonary gas exchange in patients with heart failure who are taking angiotensin-converting enzyme inhibitors. Am Heart J 1999; 138:254-260.

10 ) Guazzi M, Brambilla R, Reina G, et al: Aspirin-angiotensin-converting enzyme inhibitor coadministration and mortality in patients with heart failure. Arch Intern Med 2003; 163:1574-1579.

Aspirin Overview

• Prescription aspirin is used to relieve the symptoms of rheumatoid arthritis (arthritis caused by swelling of the lining of the joints), osteoarthritis (arthritis caused by breakdown of the lining of the joints), systemic lupus erythematosus (condition in which the immune system attacks the joints and organs and causes pain and swelling) and certain other rheumatologic conditions (conditions in which the immune system attacks parts of the body). Nonprescription aspirin is used to reduce fever and to relieve mild to moderate pain from headaches, menstrual periods, arthritis, toothaches, and muscle aches. Nonprescription aspirin is also used to prevent heart attacks in people who have had a heart attack in the past or who have angina (chest pain that occurs when the heart does not get enough oxygen). Nonprescription aspirin is also used to reduce the risk of death in people who are experiencing or who have recently experienced a heart attack. Nonprescription aspirin is also used to prevent ischemic strokes (strokes that occur when a blood clot blocks the flow of blood to the brain) or mini-strokes (strokes that occur when the flow of blood to the brain is blocked for a short time) in people who have had this type of stroke or mini-stroke in the past. Aspirin will not prevent hemorrhagic strokes (strokes caused by bleeding in the brain). Aspirin is in a group of medications called salicylates. It works by stopping the production of certain natural substances that cause fever, pain, swelling, and blood clots.

• Aspirin is also available in combination with other medications such as antacids, pain relievers, and cough and cold medications. This monograph only includes information about the use of aspirin alone. If you are taking a combination product, read the information on the package or prescription label or ask your doctor or pharmacist for more information.

Moexipril Overview

• Moexipril is used to treat high blood pressure. Moexipril is in a class of medications called angiotensin-converting enzyme (ACE) inhibitors. It decreases certain chemicals that tighten the blood vessels, so blood flows more smoothly and the heart can pump blood more efficiently.

• High blood pressure is a common condition and when not treated, can cause damage to the brain, heart, blood vessels, kidneys, and other parts of the body. Damage to these organs may cause heart disease, a heart attack, heart failure, stroke, kidney failure, loss of vision, and other problems. In addition to taking medication, making lifestyle changes will also help to control your blood pressure. These changes include eating a diet that is low in fat and salt, maintaining a healthy weight, exercising at least 30 minutes most days, not smoking, and using alcohol in moderation.

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Definitions

Severity Categories

Contraindicated

These drugs, generally, should not be used together simultaneously due to the high risk of severe adverse effects. Combining these medications can lead to dangerous health outcomes and should be strictly avoided unless otherwise instructed by your provider.

Major

This interaction could result in very serious and potentially life-threatening consequences. If you are taking this drug combination, it is very important to be under close medical supervision to minimize severe side effects and ensure your safety. It may be necessary to change a medication or dosage to prevent harm.

Moderate

This interaction has the potential to worsen your medical condition or alter the effectiveness of your treatment. It's important that you are monitored closely and you potentially may need to make adjustments in your treatment plan or drug dosage to maintain optimal health.

Minor

While this interaction is unlikely to cause significant problems, it could intensify side effects or reduce the effectiveness of one or both medications. Monitoring for changes in symptoms and your condition is recommended, and adjustments may be made if needed to manage any increased or more pronounced side effects.

Onset

Rapid: Onset of drug interaction typically occurs within 24 hours of co-administration.

Delayed: Onset of drug interaction typically occurs more than 24 hours after co-administration.

Evidence

Level of documentation of the interaction.

Established: The interaction is documented and substantiated in peer-reviewed medical literature.

Theoretical: This interaction is not fully supported by current medical evidence or well-documented sources, but it is based on known drug mechanisms, drug effects, and other relevant information.

How To Manage The Interaction

Provides a detailed discussion on how patients and clinicians can approach the identified drug interaction as well as offers guidance on what to expect and strategies to potentially mitigate the effects of the interaction. This may include recommendations on adjusting medication dosages, altering the timing of drug administration, or closely monitoring for specific symptoms.

It's important to note that all medical situations are unique, and management approaches should be tailored to individual circumstances. Patients should always consult their healthcare provider for personalized advice and guidance on managing drug interactions effectively.

Mechanism Of Interaction

The theorized or clinically determined reason (i.e., mechanism) why the drug-drug interaction occurs.

Disclaimer: The information provided on this page is for informational purposes only and should not be considered medical advice. Always consult with a qualified healthcare professional regarding your specific circumstances and medical conditions.

Where Does Our Information Come From?

Information for our drug interactions is compiled from several drug compendia, including:

• Gold Standard Drug Database
• Micromedex
• Lexicomp
• DrugBank

The prescribing information for each drug, as published on DailyMED, is also used. 

Individual drug-drug interaction detail pages contain references specific to that interaction. You can click on the reference number within brackets '[]' to see what reference was utilized.

The information posted is fact-checked by HelloPharmacist clinicians and reviewed quarterly.