The Rise and Fall of “MONA BASH”

August 11, 2023

By Galen Hu

Peer Reviewed

It seemed like everyone I spoke to about heart attacks during my clinical year of medical school had a different opinion on the famous mnemonic “MONA BASH”:







Angiotensin-converting enzyme inhibitor/Angiotensin receptor blocker



Having been taught this catchy tool about the medical management of acute coronary syndromes (ACS) during my first day of clerkship year in the emergency department, I was proud to regurgitate the list to the next attending I spoke to. He chuckled, saying he could not believe we were ever taught such an “outdated” tool.

To my surprise, in later conversations, not all physicians were as principled in their opposition to MONA BASH. As it turns out, the story of the “heart attack” and its treatment remains one nearly as old as the tale of modern medicine….

Around the turn of the 20th century, a causal connection between coronary thrombosis and death was assumed: those who clotted in their coronary arteries died. The schema of myocardial infarction (MI) in surviving patients was unknown until James Herrick described the syndrome in 1912: “Certain Clinical Features of Sudden Obstruction of the Coronary Arteries.”1 This paved the way for our modern understanding of the term acute coronary syndrome, a phrase not coined for another 80 years.

Around the time of Herrick, the first-line treatment for cardiac ischemia was, unsurprisingly, morphine. As we now understand, morphine likely exerts itself via alterations in vagal tone and possibly histamine release, allowing for decreased heart rate, blood pressure (afterload), and venous

return (preload), altogether reducing cardiac wall stress. The relief from pain and anxiety further moderates the sympathetic response.2

It was not until the famous CRUSADE initiative (2005) that morphine was dethroned. This retrospective observational study, acknowledging its limitations, recommended caution in the use of morphine, as it found that in patients with non-ST-elevation ACS, those treated with morphine had a higher adjusted mortality risk.3 Later research postulates that this may be due to its effect of interfering with the anti-platelet P2Y12 receptor blockers, another crucial element of ACS treatment.4-6 So, while morphine may be used in patients with chest pain refractory to nitrates, it is important to remember the data demonstrating higher mortality risk.

Alongside morphine in the dawn of MI therapy were oxygen and nitrates, both of which have also somewhat fallen out of favor. For oxygen, the scales of benefit versus harm tipped toward harm in 2017 with the DETO2X-AMI trial. For patients with suspected MI and oxygen saturation of >90%, oxygen made no difference in the rate of all-cause death, rehospitalization for MI, or hospitalization for heart failure.7 With zero apparent benefit but all the known harm of supplemental oxygen (i.e., direct vasoconstrictor effect on coronary arteries), it is no longer routine to put ACS patients on oxygen in the absence of hypoxemia or respiratory distress.

Nitrates significantly relieve chest discomfort and hypertension in ACS, primarily by reducing preload, wall stress, and oxygen demand. However, despite improving symptoms, evidence shows that nitrates have no impact on mortality.8,9 A light “tsk-tsk” and a gentle reminder from a senior resident when I offered nitroglycerin to a standardized patient with ST-elevations in leads II/III and AVF was more than enough to teach me about preload-dependent cardiac lesions (e.g., inferior wall MI, severe aortic stenosis). Clues may include bradyarrhythmia (sinoatrial and atrioventricular nodes are usually supplied by the right coronary artery), clear lungs (decreased left ventricular preload), epigastric pain, vagal symptoms, and electrocardiogram findings (inferior wall changes, ST-elevation in V4R). There is enough to make me think twice before giving this once-ubiquitous drug.

It was not until the 1980s that our familiar “A-BASH” favorites became prevalent in clinical practice.10 With dual antiplatelet therapy (DAPT–aspirin and usually a P2Y12 inhibitor), there remains a risk of bleeding, GI intolerance, and allergy. But given the role of platelets in primary hemostasis and the early formation of thrombus, all patients with ACS should receive DAPT in the absence of contraindications, as dictated by American Heart Association/American College of Cardiology guidelines.11 To stabilize the atherosclerotic plaque, all patients should also receive a high-intensity statin.11

Regarding beta-blockade, the evidence for mortality benefit is robust, with notable decreases in maladaptive cardiac remodeling, improvement in cardiac perfusion, and decreased cardiac oxygen demand.12 Side effects may include fatigue, sexual dysfunction, and bronchoconstriction. The negative chronotropic effects of beta-blockers may cause providers hesitation in acute MI. The COMMIT/CCS2 trial taught us that it is reasonable to defer immediate beta-blockers in those on the cusp of cardiogenic shock.13

Renin-angiotensin-aldosterone-system (RAAS) suppression via angiotensin-converting enzyme (ACE) inhibition after an MI improves left ventricular ejection fraction later down the line through its effects on ventricular remodeling.14 The OPTIMAAL trial compared ACE inhibitors with angiotensin receptor blockers (ARBs). They found that though ACE inhibitors had an almost significant trend towards decreased mortality and sudden cardiac death, a significantly greater percentage of patients quit their ACE inhibitors compared to ARBs, primarily due to angioedema and cough,15 highlighting the importance of tolerability in the selection of an anti-RAAS agent.

And lastly, anticoagulation remains a mainstay in all acute coronary syndromes, with the choice of anticoagulant differing depending on whether the patient is to receive percutaneous coronary intervention, fibrinolysis, or no reperfusion therapy.

As I progressed through my Medicine rotation, it became evident that our understanding of ACS management should reach far beyond MONA BASH. As some of these medicines have fallen by the wayside, others have cemented their status in ACS care. But reflecting on the history of this “outdated” mnemonic allows for deeper exploration into the evolution of heart attack medications, and thus may still hold value for medical students in the generations to come.

Galen Hu is a 2nd year medical student at NYU Grossman School of Medicine

Peer reviewed by Michael Tanner, MD, associate editor, Clinical Correlations

Image courtesy of Wikimedia Commons, source:


1. Herrick JB. Clinical features of sudden obstruction of the coronary arteries. JAMA. 1912; LIX(23):2015–2022. doi:10.1001/jama.1912.04270120001001

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3. Meine TJ, Roe MT, Chen AY, et al. Association of intravenous morphine use and outcomes in acute coronary syndromes: results from the CRUSADE Quality Improvement Initiative. Am Heart J. 2005;149(6):1043-1049.

4. Kubica J, Adamski P, Ostrowska M, et al. Morphine delays and attenuates ticagrelor exposure and action in patients with myocardial infarction: the randomized, double-blind, placebo-controlled IMPRESSION trial. Eur Heart J. 2016;37(3):245-252. doi:10.1093/eurheartj/ehv547

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8. ISIS-4: a randomised factorial trial assessing early oral captopril, oral mononitrate, and intravenous magnesium sulphate in 58,050 patients with suspected acute myocardial

infarction. ISIS-4 (Fourth International Study of Infarct Survival) Collaborative Group. Lancet. 1995;345(8951):669-685.

9. Six-month effects of early treatment with lisinopril and transdermal glyceryl trinitrate singly and together withdrawn six weeks after acute myocardial infarction: the GISSI-3 trial. Gruppo Italiano per lo Studio della Sopravvivenza nell’Infarto Miocardico. J Am Coll Cardiol. 1996;27(2):337-344.

10. de Alencar Neto JN. Morphine, Oxygen, Nitrates, and Mortality Reducing Pharmacological Treatment for Acute Coronary Syndrome: An Evidence-based Review. Cureus. 2018;10(1):e2114. Published 2018 Jan 25. doi:10.7759/cureus.2114

11. Amsterdam EA, Wenger NK, Brindis RG, et al. 2014 AHA/ACC guideline for the management of patients with non-ST-elevation acute coronary syndromes: executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines [published correction appears in Circulation. 2014 Dec 23;130(25):e431-2. Dosage error in article text]. Circulation. 2014;130(25):2354-2394. doi:10.1161/CIR.0000000000000133

12. López-Sendón J, Swedberg K, McMurray J, et al. Expert consensus document on beta-adrenergic receptor blockers. Eur Heart J. 2004;25(15):1341-1362. doi:10.1016/j.ehj.2004.06.002

13. Chen ZM, Pan HC, Chen YP, et al. Early intravenous then oral metoprolol in 45,852 patients with acute myocardial infarction: randomised placebo-controlled trial. Lancet. 2005;366(9497):1622-1632. doi:10.1016/S0140-6736(05)67661-1

14. Indications for ACE inhibitors in the early treatment of acute myocardial infarction: systematic overview of individual data from 100,000 patients in randomized trials. ACE Inhibitor Myocardial Infarction Collaborative Group. Circulation. 1998;97(22):2202-2212. doi:10.1161/01.cir.97.22.2202

15. Pfeffer MA, McMurray JJ, Velazquez EJ, et al. Valsartan, captopril, or both in myocardial infarction complicated by heart failure, left ventricular dysfunction, or both [published correction appears in N Engl J Med. 2004 Jan 8;350(2):203]. N Engl J Med. 2003;349(20):1893-1906. doi:10.1056/NEJMoa032292