Introduction
The use of cannabis and its synthetic derivative, bonsai, has recently increased,
and it has become an important health problem (1). Kounis syndrome develops by the
activation of mast cells, and it is an acute coronary syndrome (ACS) related to allergies,
hypersensitivity, anaphylaxis, or anaphylactic reactions (2, 3). Bonsai-induced Kounis
syndrome has not been reported in literature. The present study presents the case
of a 27-year-old patient who arrived at the emergency clinic with chest pain 6 h after
the use of bonsai.
Case Report
A 27-year-old male patient arrived at the emergency clinic with sudden-onset retrosternal
pain in the left arm, vomiting, and sweating. The chest pain was characterized by
pressure and burning and lasted for 6 h. The patient did not have any known atherosclerosis
risk factor and reported bonsai use for the first time in his life. He expressed that
he had used a great amount of bonsai 1 h before the onset of chest pain. All vital
signs of the patient were stable. His electrocardiographic (ECG) investigation revealed
mild bradycardia and ST segment elevations in the inferior derivations (D2, D3, and
AVF) (Fig. 1). The patient was referred to the coronary intensive care unit after
the diagnosis of acute inferior MI was made. Bedside echocardiography revealed inferior
and septal hypokinesis. Thrombolytic therapy was planned but was then disregarded
as the recently recorded ECG showed ST-segment elevations returning to the isoelectric
line. Troponin I value showed a typical increase (4 h)- decrease (24-36 h) (peak value
10.722 ng/mL). Mild leukocytosis and eosinophilia (4.9%) were present. The immunoglobulin
E level was high (150 mg/L). The patient was referred to a more advanced center for
coronary angiography (CAG). CAG indicated that all coronary arteries were patent (Fig.
2). The fibrinogen and homocysteine levels and antithrombin activity were all within
normal ranges. The patient was followed-up for three days without any complications
and was then dismissed from the hospital with prescriptions for 100-mg aspirin, 90-mg
diltiazem, and 40-mg atorvastatin.
Figure 1
ST elevation in inferior leads on 12-derivation ECG obtained in the emergency department
Figure 2
Demonstrating RCA, LMCA, LAD, and LCx on coronary angiography
Discussion
To our knowledge, this patient is the first bonsai-induced Kounis syndrome case in
literature. Kounis syndrome, in other words allergic MI, has two types depending on
the pathophysiology, or the presence of coronary artery disease. In type I, patients
exhibit coronary vasospasms induced by allergic mediators such as histamine, thromboxane,
and leukotrienes without the presence of atherosclerosis risk factors or coronary
artery disease. In type 2, ACS develops due to coronary vasospasms, plaque erosion,
or plaque rupture induced by these mediators in patients with atherosclerotic coronary
artery disease. Recently, the fact that there are eosinophil and mast cells in the
thrombus material excised from some patients in whom stent thrombosis developed after
stent implantation with drug release makes us consider hypersensitivity reactions
in these patients. This situation is accepted as the type III variant of Kounis Syndrome
(4). With these findings, our case is in accordance with the type I variant of Kounis
syndrome.
Cardiovascular and psychological problems are frequently reported to be associated
with the use of bonsai. The main pathophysiology of Kounis syndrome is the release
of many allergic mediators as a result of mast cell activation induced by allergic
stimulants. It has been demonstrated in experimental studies that some endogenous
cannabinoids suppress inflammation by decreasing mast cell activation via receptors;
however, some endogenous cannabinoids trigger mast cell activation independent from
receptors (5). In our patient, coronary arteries were revealed to be completely patent,
and this may cause us to consider that a coronary vasospasm was the reason that was
caused via mediators released by the bonsai-induced activation of mast cells. The
main cardiovascular effects are coronary vasoconstriction, increase in the synthesis
of tissue factor, thrombocyte activation, dysrhythmia development induced by various
mechanisms, and plaque erosion (6, 7). In a patient considered to have Kounis syndrome,
in addition to appropriate ACS management, the determination of serum histamine, specific
Ig E antibodies, and complement proteins and investigation of eosinophilia aid in
the diagnosis (2). Leukocyte, eosinophil, and total IgE levels were increased in our
patient, but other analyses could not be performed due to technical limitations.
Conclusion
We hoped to emphasize the consideration of the use of bonsai-type synthetic drugs
in a young patient with acute MI signs but without any risk factors.