Spontaneous coronary artery dissection (SCAD)
is a rare and uncommon cause of sudden cardiac
death and acute coronary syndrome. SCAD
remains an unclear etiopathological entity. The most
common pathologies associated with SCAD are
coronary atherosclerosis and vascular changes occurring
during the peripartum period. SCAD may be
associated with Marfan’s syndrome, Ehlers-Danlos
disease, intensive exercise, cocaine abuse, and female
hormonal treatments such as oral contraceptives,
although in some cases no predictor could be
identified. However, a large number of cases must
be classified as idiopathic because no underlying
condition can be detected.
in children and
adolescents in the
last 30 years continues
to grow exponentially.
United States, adolescent caffeine intake averages 60
to 70 mg/day and ranges up to 800 mg/day. Most caffeine
intake among youth comes from soda; however,
energy drinks are becoming increasingly popular.
We report a case of ST-segment elevation myocardial
infarction, in which SCAD may have been caused
by the consumption of an energy drink.
A previously healthy 13-year-old boy was admitted to
our clinic after presenting with acute-onset, “crushing,”
mid-sternal chest pain over a period of about
two hours. He had no history of diabetes, hypertension,
hyperlipidemia, or cigarette smoking. He had no
family history of familial hypercholesterolemia, early
coronary artery disease, or sudden death. He denied
use of cocaine, amphetamines, hormones, steroids,
alcohol, or other recreational drugs. The patient had
ingested an energy drink for the first time the previous
night. About 8 hours after the high-energy drink
consumption, the patient’s chest pain started.
Physical examination revealed a well-developed
teen in moderate distress. His blood pressure was
120/70 mmHg, heart rate 80 beats/min, and respiratory
rate 16 breaths/min. He had no jugular venous
distention, and his lungs were clear to auscultation
in all fields. Cardiac auscultation revealed an S4
gallop with a normal S1 and S2. The electrocardiogram
(ECG) revealed sinus rhythm with 2- to 3-mm
ST-segment elevations in leads II, III, aVF, and V3 through V5 (Fig. 1a). The transthoracic echocardiography
(TTE) showed left ventricular ejection fraction
estimated to 0.54 and moderate apical hypokinesis.
He had been given aspirin, subcutaneous enoxaparin,
sublingual nitroglycerin, enalapril, and metoprolol at
presentation. After treatment, the patient’s chest pain
was relieved. Initial laboratory studies, within 4 hours
of the onset of his symptoms, were normal, with a
white blood cell count of 7,260 cells/mm3, myoglobin
level of 70 U/L (normal range 0-150 U/L), creatine
kinase-MB fraction of 3.2 ng/ml (normal range: 0-5
ng/mL), and mildly elevated troponin I level of 0.65
ng/mL (normal range 0-0.06 ng/mL). The patient’s
blood count, cholesterol, hypercoagulability panels,
and kidney and thyroid function tests were normal.
Chest X-ray was unremarkable, and found to be normal.
The patient’s chest pain decreased after medical
treatment, and thus no thrombolytic therapy was given.
Four hours of recorded ECG revealed no dynamic
changes with respect to the baseline ECG (Fig. 1b).
The troponin-I value after 24 hours was 3.96 ng/mL.
Dynamic T-wave changes were observed in ECG recording
leads V3-V5 (Fig. 2). For these reasons, the patient was transferred to a tertiary referral center for
coronary angiography. The left anterior descending
(LAD) artery showed extensive dissection with a visible
tear from the distal part of the vessel. The TIMI
(thrombolysis in myocardial infarction) flow grade
was III (Fig. 3, Videos 1, 2*). The right coronary artery
and the circumflex artery were normal. Based on
the morphology of the vessel with a dissection and
TIMI III flow grade, it was decided to manage this
patient conservatively with close follow-up. We continued
low-molecular-weight heparin, antiplatelet
therapy, and enalapril. At the follow-up examination
one month later, the patient had no chest pain. Acetylsalicylic
acid and enalapril treatment was continued.
Follow-up TTE revealed normal left ventricular function,
with resolution of his apical hypokinesis.
A possible role of the consumption of caffeinated energy
drinks in triggering SCAD events is described
in this case. SCAD is a rare and uncommon cause of
sudden cardiac death and acute coronary syndrome.
However, a large number of cases must be classified as idiopathic because no underlying condition can be
detected. The female to male ratio is 2:1, and the dissection
is diagnosed most frequently in the left coronary
Coronary artery dissection is characterized by a
separation of the layers of the artery wall. This results
in a false lumen or an intramural hematoma in the
area of the media. The clinical presentation of SCAD
depends on the extent and severity of the dissection,
and ranges from unstable angina to sudden cardiac
death. Recognition of the dissection can be quite difficult
and may require multiple angiographic views
or intravascular ultrasound to confirm the diagnosis.
We decided not to perform intravascular ultrasound
because the dissection line in the LAD artery was
clearly visible on angiography. There is no specific
guideline to treat SCAD. If the vessel is open and
the flow normalized at the time of angiography, it
is defendable to treat the dissection conservatively.
Good angiographic and clinical outcomes have been
described with medical treatment only. Therefore,
we decided to manage this case conservatively with
“Energy drinks” are beverages that contain caffeine,
taurine, vitamins, herbal supplements, and
sugar or sweeteners, and they are marketed to improve
energy, weight loss, stamina, athletic performance,
and concentration. Energy drinks contain
three-to-four-fold the caffeine as a typical soda and
promise to boost performance and enhance metabolism.[
5] Caffeine is a well-known and commonly used
neurostimulant. The mechanism of action is thought
to be direct adenosine receptor stimulation, in addition
to the effects on monoamine neurotransmitters.
Moreover, caffeine is a cyclic adenosine monophosphate
(cAMP) phosphodiesterase inhibitor and can
also cause the release of intracellular calcium stores.
Documented adverse cardiovascular effects include
tachycardia, extrasystoles, increased stroke volume,
and possibly other arrhythmias. Caffeine may also enhance the inotropic effect of β-adrenergic agents.
Caffeine has been shown to directly stimulate cardiac
function while dilating blood vessels, and appears to
have only mild effects on blood pressure. Caffeine
is known to trigger a heart rhythm disorder. In some
cases, the caffeine is thought to cause serious adverse
effects like myocardial infarction and cardiac arrest.
The use of caffeine can cause increased sympathetic
nerve activity and raised blood pressure in humans.
The endogenous circadian rhythm affects many
physiological and biochemical parameters. This is
associated with rises in plasma catecholamines and
cortisol and increased platelet aggregability in the
morning. The energy drink consumed by our patient
contained 80 mg of caffeine (equivalent to one cup of
espresso) per can. The drink also contains high doses of taurine (an amino acid) and glucuronolactone (a
glucose metabolite), neither of which is considered to
have significant toxicity, although there is a paucity
of data. Chest pain in our case, in accordance with the
circadian rhythm, began around 7 a.m. This indicates
that the caffeine in energy drinks has increased circadian
rhythm impact on physiological and biochemical
parameters and may have triggered the coronary
artery dissection. It is impossible to draw conclusions
on this issue with a single case report; more studies
about the effects of caffeine on the vessel wall are
In conclusion, energy drinks may be one of the
factors leading to SCAD. Energy drinks, especially in
children, can lead to serious adverse events, as seen in
the presented case.
Conflict-of-interest issues regarding the authorship or
article: None declared.
*Supplementary video files associated with this article
can be found in the online version of the journal.