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Year : 2019  |  Volume : 9  |  Issue : 2  |  Page : 116-117

Acute myocardial infarction secondary to analgesic abuse: Should it be a novel risk factor for coronary artery disease!

Department of Cardiology, Yashoda Hospitals, Hyderabad, Telangana, India

Date of Web Publication23-Sep-2019

Correspondence Address:
Dr. Pankaj Jariwala
Department of Cardiology, Yashoda Hospitals, Somajiguda, Hyderabad - 500 083, Telangana
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/JICC.JICC_19_19

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How to cite this article:
Jariwala P. Acute myocardial infarction secondary to analgesic abuse: Should it be a novel risk factor for coronary artery disease!. J Indian coll cardiol 2019;9:116-7

How to cite this URL:
Jariwala P. Acute myocardial infarction secondary to analgesic abuse: Should it be a novel risk factor for coronary artery disease!. J Indian coll cardiol [serial online] 2019 [cited 2020 Jul 10];9:116-7. Available from:

Dear Editor,

I encountered two young patients with acute myocardial infarction (AMI) without any conventional risk factors. However, on detail interrogation, they gave a history of analgesic abuse. These cases were described in brief.

  Case 1 Top

A 38-year-old male, laborer, presented with acute anterior wall myocardial infarction within the window period of 4 h. Except for the elevated troponin levels and total leukocyte count, other laboratory parameters were normal. After successful thrombolysis with streptokinase, coronary angiography showed the recanalized left anterior descending (LAD) artery with 30% residual plaque of its proximal segment. Echocardiography revealed mild left ventricular dysfunction with the ejection fraction of 48%. During predischarge counseling, we could not find any conventional risk factors for the occurrence of AMI. The patient gave a history of daily consumption of analgesics (etoricoxib) for the body pains for 5 years. The patient was discharged after consultation with the rheumatologist who diagnosed it as a nonrheumatic cause of pain. He was prescribed antiplatelet therapy, high-intensity statins, ramipril, beta-blocker, and calcium and vitamin supplements. He was advised to take paracetamol as analgesics if required.

  Case 2 Top

A 48-year-old male, a carpenter, presented with ongoing chest pain, and electrocardiogram showed acute inferior wall myocardial infarction, out of window period (>24 h). He was stabilized with medical treatment. His laboratory parameters were normal, except for the elevated troponin levels. Echocardiography showed moderate left ventricular dysfunction with the ejection fraction of 38% with a regional wall motion abnormality of the anterior and inferior walls. Coronary angiography showed critical stenoses of the LAD artery and right coronary artery (RCA). He underwent percutaneous transluminal coronary angioplasty to the LAD and RCA using drug-eluting stents.

He was discharged with dual antiplatelet agents, high-intensity statin, angiotensin-converting-enzyme inhibitor, and beta-blocker. Predischarge counseling highlighted the regular use of diclofenac sodium for his chronic back pain for the past 3 years. The orthopedic consultation was sought which made the diagnosis of lumbar spondylitis, which was managed, conservatively with the advice of posture correction, physiotherapy.

  Nonsteroidal Anti-Inflammatory Drugs and Cardiovascular Risk Top

The cases of sudden cardiac deaths secondary to extensive AMI following the consumption of analgesics are on rise. Nonsteroidal anti-inflammatory drugs (NSAIDs) are among the most widely used therapeutic agents worldwide. Taken alone or in combination with other classes of drug, they relieve symptoms across multiple clinical indications, including acute and chronic pain states and a various range of musculoskeletal disorders.

Serious adverse effects of NSAIDs are studied extensively in various pharmacoepidemiological studies and meta-analyses and those have documented serious cardiovascular complications.

There is no convincing evidence that low-dose aspirin mitigates the cardiovascular risk of NSAIDs. With the widespread use of NSAIDs and a steep rise in cardiovascular disease, it is a particular concern in low- and middle-income countries.

Three drugs (rofecoxib, diclofenac, and etoricoxib) ranked consistently highest in terms of cardiovascular risk compared with nonuse. These drugs are listed in the essential medicine lists and should be withdrawn in our country where possibilities of over-the-counter (OTC) prescriptions are high.[1]

Except for naproxen, higher risk was generally associated with higher doses, as defined in studies in patients with prior coronary artery disease. Low and high doses of diclofenac and rofecoxib were associated with the high risk of AMI, with a dose–response relationship for rofecoxib. In patients with prior coronary heart disease, except for naproxen, duration of use ≤3 months was associated with an increased risk of AMI. Varas-Lorenzo et al. performed a meta-analysis of individual NSAIDs and found that etoricoxib and diclofenac have the highest random-effects relative risk (RR) (95% confidence intervals) – 1.97 (1.35–2.89) and 1.38 (1.26–1.52), respectively. Except for naproxen, the estimates of risk for each of the evaluated individual NSAIDs in the subgroup of shorter duration were associated with an increase of AMI in patients with a prior history of coronary heart disease.[2]

Selective cyclooxygenase-2 (COX-2) inhibitors may cause an increase in blood pressure and peripheral edema as conventional NSAIDs. In the VIGOR study, the incidence of myocardial infarction was lower in the naproxen group (0.1%) than in the rofecoxib group (0.4%).[3]

The result of the Adenomatous Polyp Prevention on Vioxx Trial led to the voluntary withdrawal of rofecoxib. This was a prospective randomized trial designed to evaluate the efficacy of rofecoxib 25 mg/day in preventing the recurrence of colorectal polyps in patients with a history of colorectal adenoma. An increased RR of confirmed cardiovascular events, such as heart attack and stroke, was noted after 18 months of treatment with rofecoxib comparing with placebo.

  Mechanism of Action of Nonsteroidal Anti-Inflammatory Drugs as a Risk Factor for Coronary Artery Disease Top

The exact cause for these results is still uncertain. Selective COX-2 inhibitors are associated with decreased formation of prostaglandin I2 but with little inhibition of thromboxane A2 generation. Prostaglandin I2 causes vasodilatation, inhibits platelet aggregation, and prevents the proliferation of vascular smooth muscle cells. Thromboxane A2 produces the opposite effects. Therefore, the depression of prostaglandin I2 formation might be expected to elevate blood pressure and accelerate atherogenesis.[4]

  Are All Nonsteroidal Anti-Inflammatory Drugs Are the Culprit? Top

Kathrin Tho¨ne et al. conducted a case–control study within a cohort of 3,476,931 NSAID users. Overall, 17,236 AMI cases were matched to 1,714,006 controls. They found that elevated relative AMI risks were seen for current users of fixed combinations of diclofenac with misoprostol, indomethacin, ibuprofen, etoricoxib, and diclofenac.

The relative risk associated with the diclofenac, fixed combinations of diclofenac with misoprostol, etoricoxib, and ibuprofen, was highest among the younger age group (<60 years) and similar for patients with or without major cardiovascular risk factors.[5]

Diclofenac and etoricoxib together account for approximately one-third of all sales of NSAIDs in most of the countries worldwide. There was no difference between high- and low-income countries. Diclofenac was by far the most popular NSAID, despite having an RR identical to rofecoxib. Etoricoxib is another high-risk NSAID whose usage across the world had increased over the past 5 years.[1]

  Nonsteroidal Anti-Inflammatory Drugs and Indian Scenario Top

With increasing stress levels among the Indian patients related to work pressure, there are increased somatic complaints and simultaneous usage of OTC NSAIDs, leading to more AMIs. We do not have any data in our country related to this issue. We need further studies to measure the prevalence of this problem in our country. The OTC uses of NSAIDs are common among all the socioeconomic classes of our country. This is just a tip of iceberg phenomenon.

Hope this article is thought-provoking for the medical professionals to act further to prevent the occurrence of coronary artery disease secondary to the use of NSAIDs. We need to impart education to the general population via the media about the “analgesics use” by medical professions and paramedical staffs. The better use of the social media, which is in common use in our country, can be used to circulate the risk of the NSAIDs. Stringent laws to curtail OTC use of analgesics should be implemented.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

  References Top

McGettigan P, Henry D. Use of non-steroidal anti-inflammatory drugs that elevate cardiovascular risk: An examination of sales and essential medicines lists in low-, middle-, and high-income countries. PLoS Med 2013;10:e1001388.  Back to cited text no. 1
Varas-Lorenzo C, Riera-Guardia N, Calingaert B, Castellsague J, Salvo F, Nicotra F, et al. Myocardial infarction and individual nonsteroidal anti-inflammatory drugs meta-analysis of observational studies. Pharmacoepidemiol Drug Saf 2013;22:559-70.  Back to cited text no. 2
Bombardier C, Laine L, Reicin A, Shapiro D, Burgos-Vargas R, Davis B, et al. Comparison of upper gastrointestinal toxicity of rofecoxib and naproxen in patients with rheumatoid arthritis. VIGOR study group. N Engl J Med 2000;343:1520-8.  Back to cited text no. 3
Fitzgerald GA. Coxibs and cardiovascular disease. N Engl J Med 2004;351:1709-11.  Back to cited text no. 4
Thöne K, Kollhorst B, Schink T. Non-steroidal anti-inflammatory drug use and the risk of acute myocardial infarction in the general German population: A nested case-control study. Drugs Real World Outcomes 2017;4:127-37.  Back to cited text no. 5


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