The 21-year-old man who survived an acute myocardial infarction

One of the most important things we can do as health-care providers, parents, teachers, caregivers and peers is to successfully recognize and improve the health issues and health outcomes of the teens and young adults. In this blog I’ll share the story of a young man who was seen by my husband in the ED and sparked my interest as a scientist to study the prevalence and clinical profile of myocardial infarction (MI) in young adults in my community.

I encourage you to share this blog with the young adults in your life, as well as parents and caregivers who have teenagers:

Three nights ago as my husband was preparing to sign off his shift in the ED, a 21 years-old man was brought in by the ambulance with a 30-minute history of severe central, crushing pain radiating down to his left arm. The pain was associated with nausea, vomiting, sweating and breathlessness. It was his first time to ever experience a central crushing pain. The man had a history of membranoproliferative glomerulonephritis and was on immunosuppressive therapy. He was also diagnosed with secondary hypertension and was on enalapril and nifedipine. Thankfully, he was in safe hands, the ED team were able to recognize his symptoms and a diagnosis of acute myocardial infarction was made. But, can you imagine how emotionally and physically upsetting this was to himself and his family.


Coronary artery disease (CAD) is the leading cause of morbidity and mortality worldwide. Myocardial Infarction (MI) is a lethal manifestation of CAD and can present as sudden death. Although it mainly occurs in patients older than 45 years, young men and women can suffer from myocardial infarction1. Unfortunately, when it happens to young adults, the disease can carry significant psychological impact, financial constraints and morbidity to the patients and their family. The protection being offered by young age is gradually being taken away with the high prevalence of CAD risk factors in these young adults such as obesity, lack of physical activity and smoking. Several studies have described the clinical profile and outcome of young patients with MI and its incidence ranged between 2%-10%. Overall, young patients are more likely to be male, with a history of smoking and hyperlipidemia, however, they were less likely to have other comorbidities and less extensive CAD on coronary angiogram2.

Causes of myocardial infarction in young adults

The causes of myocardial infarction in young adults can be broadly divided into two groups, those with angiographically normal coronary arteries and those with coronary artery disease of varying etiology.

Angiographically “normal” coronary arteries

  • Hypercoagulable state:
    • Nephrotic Syndrome
      • Proteinuria associated with the nephrotic syndrome results in the loss of low molecular weight proteins which alters the concentration and activity of coagulation factors. As a result, factors IX, XI and XII are decreased due to urinary excretion. While the liver tries to compensate for the hypoalbuminaemic state, there is an increased synthesis of factor II, VII, VIII, X, XIII and fibrinogen resulting in raised blood levels3.
    • Antiphospholipid syndrome (Hughes syndrome)
      • Arterial and venous thrombosis is a prominent feature of this syndrome together with antiphospholipid antibodies and miscarriage in pregnancy. The mechanism of thrombosis with this syndrome is complex and not well understood. However, it is plausible that anti-phospholipid antibodies predispose to premature atherosclerosis which increases the risk of infarction with his syndrome4.
    • Coronary artery spasm
      • Coronary artery spasm (CAS) is probably the predominant mechanism for myocardial infarction with the use of cocaine. Cocaine has been associated with angina, myocardial infarction, tachyarrhythmia’s and bradyarrhythmias, sudden cardiac death and myocardial contraction bands, which can possibly act as a substrate for arrhythmias. The cardiac effects of cocaine are mediated through four main pathways
        1. Endothelial dysfunction which predisposes to vasoconstriction and thrombosis.
        2. Promotion of atherosclerosis
        3. Increased myocardial oxygen demand due to an acute rise in systemic blood pressure and heart rate.
        4. Coronary vasoconstriction caused by its α1- adrenergic properties and calcium dependent direct vasoconstriction5.
    • Coronary embolization
      • Coronary artery embolism is a rare cause of acute myocardial infarction (AMI) and the precise diagnosis remains challenging for the interventional cardiologist. The true prevalence of this nonatherosclerotic entity remains vague because of its difficult diagnosis in the acute setting.
    • Myocardial bridging
      • This is a congenital anomaly in which the coronary artery is embedded within the subepicardial myocardium or has a band of myocardium overlying it. This can impede blood flow during systole that can persist during diastole resulting in myocardial ischemia3.

Angiographically abnormal coronary arteries

We know that even angiographically “normal” looking coronary arteries can still have significant atherosclerotic plaque, and not surprisingly, can still result in myocardial infarction. Therefore, the definition of normality is arbitrary and not definite.

  • Accelerated atherosclerosis
    • The true prevalence of advanced coronary atheroma in young adults is not well studies. An autopsy study of 760 victims of accidents, suicide and homicides aged 15-34 years found advanced coronary atheroma in 2% of males aged 15-19 years and none in women. This reveals that being male solemnly is a risk factor for atherosclerosis. Additionally, in the 30-34 age group, about 20% of men and 8% of women had advanced coronary atheroma. It is known that genetic mutation in the low density lipoprotein receptor produces familial hypercholesterolemia, an autosomal dominant disorder characterized by premature atherosclerosis and high serum cholesterol. Various other lipid fractions and hyperhomocysteinaemia are implicated in premature atherosclerosis and MI3.
  • Aneurysm and anomalous origin of arteries dissection
    • Coronary artery aneurysm are congenital or acquired secondary to Kawasaki’s disease in childhood. They have been linked to myocardial infarction in young adults, although the actual mechanism is not well understood.
  • Spontaneous dissection
    • Spontaneous dissection is a condition with great prevalence in women, especially in the peripartum or early postpartum period. However, it is a rare cause of MI6.



  1. Wong CP, Loh SY, Loh KK, Ong PJ, Foo D, Ho HH. Acute myocardial infarction: Clinical features and outcomes in young adults in Singapore. World J Cardiol. 2012;4(6):206–210. doi:10.4330/wjc.v4.i6.206
  2. Sinha SK, Krishna V, Thakur R, et al. Acute myocardial infarction in very young adults: A clinical presentation, risk factors, hospital outcome index, and their angiographic characteristics in North India-AMIYA Study. ARYA Atheroscler. 2017;13(2):79–87.
  3. Osula S, Bell GM, Hornung RS. Acute myocardial infarction in young adults: causes and management. Postgrad Med J. 2002;78(915):27–30. doi:10.1136/pmj.78.915.27
  4. Turrent-Carriles A, Herrera-Félix JP, Amigo MC. Renal Involvement in Antiphospholipid Syndrome. Front Immunol. 2018;9:1008. Published 2018 May 17. doi:10.3389/fimmu.2018.01008
  5. Hung MJ, Hu P, Hung MY. Coronary artery spasm: review and update. Int J Med Sci. 2014;11(11):1161–1171. Published 2014 Aug 28. doi:10.7150/ijms.9623
  6. Adlam D, Alfonso F, Maas A, Vrints C; Writing Committee. European Society of Cardiology, acute cardiovascular care association, SCAD study group: a position paper on spontaneous coronary artery dissection. Eur Heart J. 2018;39(36):3353–3368. doi:10.1093/eurheartj/ehy080


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