Acute Myocardial Infarction Following the Consumption of Energy Drink in a 28-Year-Old Male: A Case Report

Abstract

Excessive intake of energy drinks is increasingly realized to have a detrimental effect on platelet and endothelial functions with resultant hypercoagulable state and consequently increased risk of thrombosis. A 28-year-old man of African origin presented to the emergency department with an 8-hour history of retrosternal chest pain. His symptoms started 4 hours after consuming 5 cans (1250 cc) of an energy drink whose principal ingredients are caffeine, taurine, sugar, and glucuronolactone. His past medical and surgical history was unremarkable, and he had no apparent cardiovascular risk factor. Physical examination was unremarkable; however, electrocardiogram and echocardiogram showed features of anterolateral myocardial infarction (STEMI). Catheterization confirmed a 100% thrombotic occlusion of the proximal left anterior descending (LAD) artery and revascularization with a drug-eluting stent was successful. In conclusion, sudden onset of chest pain following energy drink consumption should raise an index of suspicion for acute coronary syndrome. With the preponderance of data suggesting increased incidence of energy drink–associated coronary events, it is prudent to advocate a limited consumption of such beverages.

Introduction

Ever since the debut of the first energy drink (marketed as “Dr. Enuf”) in 1949, the popularity of such beverages has increased at an insurmountable pace around the globe.^1,2 With the consumption of over 25 billion liters of energy drinks in 2021, the respective global market size was valued at US$86.35 billion. ³ Furthermore, considering the current consumption trajectory, energy drinks market size is expected to expand at a compound annual growth rate (CAGR) of 8.3% between 2022 and 2030 to reach $108.40 billion by 2031. ³ Moreover, owing to its association with numerous cardiovascular (CV) events (i.e. arrhythmias, spontaneous coronary dissection, aortic dissection, Takotsubo cardiomyopathy, coronary artery thrombosis, myocardial infarction [MI], and sudden cardiac death), there has been increasing concern regarding the safety of energy drinks irrespective of their desirable effects (i.e. boosted cognitive and physical performance). ⁴

Notwithstanding the growing evidence of the increasing burden of cardiovascular diseases (CVD) in sub-Saharan Africa (SSA), data describing trends of acute MI are scarce. ⁵ Likewise, despite the decreased incidence of acute coronary syndrome (ACS) in older populations worldwide, recent data show staggering growing incidence (2%-10%) of coronary events in younger (<45 years) individuals.^6-11 In comparison with their older counterparts, the younger acute MI population has a unique risk profile, clinical presentation, angiographic characteristics, and survival prospects.^6-15 Such diversity emphasizes the need to characterize the understudied MI in young persons. We present a case of acute MI following the consumption of energy drink in a 28-year-old male of African origin.

Case Description

A 28-year-old man of African origin presented to the Jakaya Kikwete Cardiac Institute (JKCI) outpatient department (OPD) with an 8-hour history of retrosternal chest pain that was accompanied by shortness of breath and diaphoresis. His symptoms started 4 hours after consuming 5 cans (1250 cc) of an energy drink whose principal ingredients are caffeine, taurine, sugar and glucuronolactone. The chest pain was sudden in onset, 9/10 in intensity, and radiating to his left shoulder. There was a positive history of hypertension from his paternal grandmother; however, his past medical and surgical history was unremarkable, and he had no apparent modifiable CV risk factor. A comprehensive history revealed a daily intake of 2 to 5 cans of caffeinated energy drinks in the past few weeks.

On admission, he was hemodynamically stable (blood pressure [BP]: 119/72 mm Hg, pulse rate [PR]: 68 beats/minute, respiration rate [RR]: 24 breaths/minute, temperature: 36.6°C, oxygen saturation: 99%, body mass index [BMI]: 21.7 kg/m²) despite an obvious distress. Physical examination was unremarkable. Cholesterol profile (LDL 1.94 mmol/L, HDL 1.43 mmol/L, Triglycerides 0.94 mmol/L, and Total cholesterol 3.21 mol/L) as well as other hematological, biochemical, and serological tests revealed normal findings (Table 1). The electrocardiogram (ECG) showed sinus rhythm with marked ST elevation on the anterolateral leads (V2-V5, I, aVL) and reciprocal changes in the inferior leads (III and aVF) (Image 1). A transthoracic echocardiogram (ECHO) demonstrated anterior wall hypokinesia with a preserved left ventricular (LV) systolic function (ejection fraction 54%). Troponin I and creatine kinase (CK-MB) levels peaked at 9.6 and 54.2 ng/mL, respectively. Given the clinical presentation and cardiac evaluation findings, a provisional diagnosis of anterolateral ST elevation MI (STEMI) was entertained. He was given loading doses of aspirin 300 mg, clopidogrel 600 mg, and atorvastatin 80 mg.

Table 1.

Results of Laboratory Tests.

Test	Result	Reference range
Full blood picture
Hemoglobin	14.2 g/dL	12.0-16.0 g/dL
Blood glucose
Fasting blood glucose	3.9 mmol/L	<7.0 mmol/L
Glycated hemoglobin (HbA1c)	4.8%	<6.5%
Renal function tests
Urea	2.8 mmol/L	1.8-7.1 mmol/L
Creatinine	61.5 µmol/L	50.4-98.1 µmol/L
Lipid profile
LDL	1.94 mmol/L	<3.34 mmol/L
HDL	1.43 mmol/L	1.04-1.55 mmol/L
Triglycerides	0.94 mmol/L	<1.69 mmol/L
Total cholesterol	3.2 mmol/L	<5.2 mmol/L
Cardiac enzymes
Troponin I	9.6 ng/mL	<0.04 ng/mL
CK-MB	54.2 ng/mL	<5 ng/mL
Electrolyte panel
Sodium	138 mmol/L	136-145 mmol/L
Potassium	4.6 mmol/L	3.5-5.1 mmol/L
Calcium	2.3 mmol/L	2.2-2.7 mmol/L
Magnesium	0.98 mmol/L	0.66-1.07 mmol/L
Phosphorus	1.44 mmol/L	0.81-1.45 mmol/L
Chloride	103 mmol/L	98-107 mmol/L
Thyroid panel
TSH	3.8 mIU/L	0.3-4.5 mIU/L
T3	2.7 pg/mL	2-4.2 pg/mL
T4	13.4 pg/mL	8.9-17.2 pg/mL
Serological tests
HIV	Negative	Negative
Hepatitis B surface antigen	Negative	Negative
VDRL	Negative	Negative

Abbreviations: LDL, low density lipoprotein; HDL, high density lipoprotein; CK-MB, Creatine Kinase-Myoglobin Binding; TSH, thyroid stimulating hormone; VDRL, Venereal disease research laboratory.

Image 1.

ECG-1 displaying sinus rhythm with marked ST elevation on the anterolateral leads (V2-V5, I, aVL) and reciprocal changes in the inferior leads (III and aVF).

Abbreviation: ECG, Electrocardiogram.

An emergency coronary angiography (CAG) confirmed a 100% thrombotic occlusion of the proximal left anterior descending (LAD) artery with TIMI 0 flow in the mid-distal portions (Image 2). Furthermore, the right coronary system was unremarkable and no atherosclerotic lesions, dissection, or coronary malformations were identified. Following balloon angioplasty, a drug-eluting stent was successfully implanted at the proximal LAD, that is, a good distal runoff with TIMI 3 flow was achieved (Image 3).

Image 2.

CAG-1 displaying 100% occlusion of the proximal LAD artery.

Abbreviation: CAG, Coronary Angiography; LAD, Left Anterior Descending; CRA, Cranial; LAO, Left Anterior Oblique.

Image 3.

CAG-2 displaying a patent LAD vessel post revascularization.

Abbreviation: CAG, Coronary Angiography; LAD, Left Anterior Descending; CRA, Cranial; LAO, Left Anterior Oblique.

His ST elevation completely resolved after the percutaneous coronary intervention (PCI) and he was symptom-free during the 48 hours of monitoring in the coronary care unit (CCU). He was discharged home in a stable condition with dual antiplatelet and statin therapy. During follow-up (4 weeks later), he had remained symptom-free and ECHO at this moment in time showed a limited residual anteroseptal wall hypokinesia with preserved global LV function.

Discussion

Despite the insufficiency of rigorous population-based data, a previously considered rare ischemic heart disease (IHD) is currently among the leading causes of morbidity and mortality in SSA.^5,16,17 Attributed largely to workforce challenges and infrastructure gaps, lack of access to emergency care services in SSA constitutes a substantial barrier amidst the growing incidence of ACS in the region.^18,19 The presentation of ACS in young patients may be atypical with different pathophysiological and clinical features which often raises diagnostic and management challenges.

Owing to their increased consumption worldwide, energy drinks use has become a norm in our societies and a growing public health issue in recent times.^1,2,20 Energy drink intake has been associated with increased unhealthy behaviors particularly among young adults.^21-23 Furthermore, there is increasing anecdotal evidence suggesting the detrimental effects of energy drinks on various body systems including the central nervous, gastrointestinal, renal, endocrine, and CV.^4,24-28 In particular, the CV effect of these beverages are associated with acute increase of platelet aggregation and endothelial dysfunction resulting in a relatively hypercoagulable state and increased likelihood of thrombosis.^29-31 Moreover, the aforementioned effects are established predictors of CV morbidity and mortality irrespective of the traditional risk factors.^32,33

In this case report, we presented ACS in a young healthy man with no apparent CV disease risk factors. Considering the background information and symptomatology coupled with angiographic findings, we hypothesize that the high consumption of energy drinks acutely led to coronary thrombosis resulting in the artery’s complete occlusion. We are delighted that revascularization with best possible outcomes was achieved. However, undergoing PCI with subsequent lifelong prescriptions at age 28 certainly raises concerns on the health-related quality of life post stenting for this young gentleman. Moreover, with at least 8 hours span between onset of chest pain and seeking medical attention, it is critical to scale-up efforts to improve community’s awareness of warning signs and health-seeking behaviors particularly in life-threatening conditions like ACS where “time is muscle.”

This report aspires to raise community’s awareness regarding the potentially lethal effects of energy drinks and sensitize the general public on cautious consumption of such beverages. Furthermore, this article serves to enlighten clinicians of the notable connection between energy drink and CV health so as to consider such etiology in the differential diagnosis particularly among young adults with chest pain. Finally, as this patient residing in a resource-limited setting underwent successful emergency revascularization by local interventionists in a public-owned institution, it is worth to acknowledge and applause such developmental milestones in health. In conclusion, sudden onset of chest pain following energy drink consumption should raise an index of suspicion for acute coronary syndrome. Although a pathophysiology between energy drink intake and myocardial ischemia has not been fully elucidated, the preponderance of data suggests that the aforesaid beverages are not innocuous. Nonetheless, such uncertainty behooves us to conduct further research and considering the upward trend of energy drink-associated coronary events, it is prudent to advocate a limited consumption of such beverages.