Bee sting-induced myocardial infarction: a systematic review with illustrative case

Abstract

Objective

To systematically review and analyze published case reports and case series describing myocardial infarction following bee stings, with a focus on identifying patterns in clinical presentation, diagnostic findings, and management strategies associated with Kounis Syndrome.

Methods

This manuscript has a dual structure: a systematic review of published case reports and a concise representative case from our institution. The review was conducted according to PRISMA guidelines (PROSPERO registration CRD420251105654). PubMed, Scopus, and Web of Science databases were searched up to July 10, 2025, for English-language case reports and series documenting MI following bee stings. Eligible studies included clinically confirmed cases of MI temporally related to bee envenomation. Data extraction included demographics, clinical features, diagnostics, treatments, and outcomes. Descriptive analysis was performed. We also present a representative case to illustrate typical clinical presentation and management.

Results

Seventeen cases of bee sting-associated MI were included. The mean patient age was 55.1 years, and 82.4% were male. Most cases (70.6%) were classified as Type II Kounis Syndrome. Chest pain was the most common symptom (94.1%), and anaphylaxis occurred in 52.9% of patients. ST-elevation MI was reported in 82.4% of cases, with the inferior and anterior leads most commonly affected. Coronary angiography revealed pathological findings in 76.5% of patients, and percutaneous coronary intervention was performed in 70.6%. Despite complications such as shock (41.2%) and arrhythmias (17.6%), 94.1% of patients experienced full recovery.

Conclusion

Bee sting-induced myocardial infarction is a rare but potentially life-threatening manifestation of Kounis Syndrome, most often involving ST-elevation and allergic features such as anaphylaxis. Management typically includes dual antiplatelet therapy, PCI, and anti-allergic treatment.

Supplementary Information

The online version contains supplementary material available at 10.1186/s12872-025-05261-y.

Introduction

Myocardial infarction (MI) is a major global health problem, as it is the leading cause of death worldwide [1]. It has many different etiologies and causes, ranging from atherosclerosis of the coronary arteries, the most significant cause, to several less frequently occurring ones, such as drugs and anemia [2–6]. Kounis syndrome (KS), was first described in 1991 [6, 7]. The incidence of Kounis syndrome has been estimated at 7.9–9.6 cases per 100,000 inhabitants per year [8].

Various causes are attributed as triggering factors for KS. These include medications, conditions such as angioedema, exercise-induced anaphylaxis, and bronchial asthma; consumption of foodstuffs such as canned food and fish; and environmental exposures such as stings of jellyfish, scorpions, and honeybees [9]. The bee venom, also known as apitoxin, can cause allergic, neurotoxic, and cardiovascular effects [10]. The quantity of venom administered and the number of stings are both related to the severity of systemic reactions [10].

KS can be classified into four main types based on the patency and condition of the coronary arteries. Type I occurs in patients with normal or patent coronary arteries, where the mechanism is coronary artery spasm. Type II involves patients with pre-existing atherosclerotic disease, in whom an allergic reaction triggers either plaque erosion or rupture, leading to partial or complete occlusion. Type III occurs in patients with coronary stents and is associated with stent thrombosis due to hypersensitivity reactions. And lastly, the newly classified Type IV, which is defined as thrombosis of a coronary bypass graft [11–13]. The pathogenesis can be summarized as a hypersensitivity reaction triggered by a bee sting. This leads to mast cell activation and degranulation, with the release of inflammatory mediators including histamine, tryptase, and leukotrienes. These substances can cause vasoconstriction, platelet activation, and plaque instability, potentially causing MI by coronary spasm or coronary thrombosis [9, 14].

Patients with systemic allergic reactions associated with evidence of acute coronary syndrome (ACS) should be suspected of Kounis syndrome because of its potential life-threatening nature. Kounis syndrome is a common disease. However, it is infrequently reported in the literature. Furthermore, there is a lack of trials aiming to determine its exact prevalence and incidence [15]. Therefore, we aim to conduct a systematic review of available case reports and case series reporting Kounis syndrome due to bee stings. We also report a representative case of type 2 Kounis syndrome, which shows the rare presentation of acute myocardial injury following bee envenomation.

Methods

Protocol and registration

This systematic review is reported in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines (Fig. 1) and is registered with the PROSPERO international prospective register of systematic reviews (PROSPERO Identifier: CRD420251105654).

Fig. 1.

PRISMA flow diagram of study selection for the systematic review

Search strategy and information sources

We systematically searched the PubMed, Scopus, and Web of Science databases from inception through July 10, 2025. The search strategy included a combination of terms related to “bee sting,” “myocardial infarction,” “acute coronary syndrome,” and “case report.”

Eligibility criteria

We included studies that met the following inclusion criteria: (1) Original case reports or case series describing one or more patients; (2) Documented MI temporally related to a bee sting; (3) Diagnosis of MI supported by clinical, biochemical, electrocardiographic, or imaging evidence; (4) Full-text articles that are written in English. We excluded: (1) Reports not involving bee stings; (2) Cases without clear documentation of MI; (3) Reviews, editorials, conference abstracts without full patient data; (4) Duplicate publications of the same case.

Study selection

Two reviewers independently screened all titles, abstracts, and full texts. Disagreements were resolved through consensus or adjudication by a third reviewer. We used Excel to manage records and screen articles. Reference lists of included studies were manually reviewed to identify additional eligible cases.

Data extraction

Two reviewers independently extracted data using a standardized form. Extracted data included: •Study characteristics (author, year, country) •Patient demographics (age, sex, comorbidities, allergic history) •Sting characteristics (location and number of stings, time to symptom onset) •Clinical features (initial symptoms, presence of anaphylaxis) •Diagnostic findings (ECG, troponin, other biomarkers, imaging) •Suspected mechanisms •Treatments administered (PCI, corticosteroids, antihistamines) •Outcomes (recovery, complications, mortality) •Hospitalization duration (if reported). Discrepancies in extraction were resolved by consensus. Given the nature of the available evidence (case reports and small series), formal risk-of-bias tools were not applicable. We therefore performed a brief narrative appraisal, assessing whether each report clearly defined diagnostic criteria. Most reports provided sufficient clinical and angiographic detail to support the diagnosis of Kounis syndrome; however, variability in reporting (e.g., incomplete allergy testing or lack of long-term follow-up) limits the reliability of pooled conclusions.

Quality of studies

We did not conduct a formal risk of bias assessment. Given the descriptive nature of this review and the inherent variability in case reports, we aimed to synthesize reported clinical information rather than to appraise methodological quality or derive pooled effect estimates. Case reports and case series were included regardless of reporting completeness to reflect the full scope of available evidence.

Data analysis

Descriptive statistics were calculated to summarize extracted case characteristics. Continuous variables are presented as mean ± standard deviation (SD) when approximately normally distributed, or as median (interquartile range, IQR) when distributions were uneven. Categorical variables are reported as frequencies and percentages. All analyses were conducted using IBM SPSS Statistics (version 21). No formal hypothesis testing or meta-analysis was performed due to the descriptive nature and heterogeneity of the included case reports.

Results

Patient demographics and clinical presentation

A total of 17 cases of bee sting-associated MI were found in our research. The patients’ mean age was 55.1 years (standard deviation (SD) = 15.5), ranging from 32 to 81 years. The sample had a significant male predominance, with 14 (82.4%) males and only 3 (17.6%) females. Comorbid conditions were reported in various ways among the included patients. The most common comorbidity reported was hypertension, which was present in 7 patients (41.2%) and absent in 10 (58.9%). Diabetes mellitus was present in 4 patients (23.5%) and absent in 13 (76.5%). Similarly, dyslipidemia was documented in 4 patients (23.5%) and not present in 13 (76.5%). Regarding the history of allergic reactions, only 3 patients (17.6%) had a confirmed allergic history, while 14 patients (82.3%) had no known allergy.

The number of stings ranged from one to more than 100, with 7 patients (41.2%) reporting multiple stings. The most frequently stung areas were the face, upper limbs, head, and neck. Most patients experienced symptoms within an hour of the sting 3 (17.6%), with the onset ranging from a few minutes to 34 h.

Chest pain was the most commonly reported symptom, occurring in 16 (94.1%) patients. Rash and swelling were also common, occurring in 10 (58.8%) and 8 (47.1%) cases, respectively. Anaphylaxis was reported in 9 (52.9%) patients, while drowsiness was observed in 5 (29.4%). Wheezing was rare, noted in only 1 (5.9%). These findings indicate that systemic allergic responses, particularly chest pain and anaphylaxis, were significant clinical characteristics following envenomation. Table 1 below summarizes the Demographic Characteristics and Clinical Symptoms of Included Patients and Table 2 show baseline characteristics of included patients.

Table 1.

Demographic characteristics and clinical symptoms of included patients (N = 17)

	N (%)
Demographic Characteristics
Age (years)	Mean 55.1 (SD = 15.5)
Sex	Male: 14 (82.4%)
	Female: 3 (17.6%)
Comorbidities
DM	4 (23.5%)
Dyslipidemia	4 (23.5%)
Hypertension	7 (41.2%)
Allergic History	3 (17.6%)
Clinical Symptoms
Chest pain	16 (94.1%)
Rash	10 (58.8%)
Swelling	8 (47.1%)
Drowsiness	5 (29.4%)
Wheezing	1 (5.9%)
Anaphylaxis	9 (52.9%)

Table 2.

Baseline characteristics of included patients

Study Reference	Age	Sex	Symptoms					Anaphylaxis	Imaging findings
			Chest Pain	Rash	Swelling	Drowsiness	Wheezing		Echocardiogram	Coronary angiography
Ziad W. Elmezayen et al. (2025)	45	Male	Yes	No	Yes	No	No	Yes	N/A	90% thrombotic occlusion of the RCA
Sonali K. Borkar et al. (2023)	50	Male	Yes	No	Yes	Yes	No	Yes	N/A	80% thrombotic proximal right coronary artery occlusion and 80% stenosis in the left circumflex arter
Selladurai Pirasath et al. (2021)	74	Male	Yes	No	Yes	No	No	Yes	left ventricular dysfunction with ejection fraction of 35%	minor coronary artery disease
Wen-Juan Lin et al. (2022)	42	Male	Yes	Yes	Yes	No	No	No	inferior, posterior and lateral wall systolic dysfunction, estimated LV ejection fraction of 45%	90% stenosis of the mid-right coronary artery
Guido Del Monaco et al. (2025)	75	Female	Yes	Yes	No	Yes	No	Yes	mild reduction of left ventricular ejection fraction (LVEF) of 45%, left ventricular apical akinesia, and hypokinesia of the mid-to-distal anterior and anterolateral segments	thrombotic sub-occlusion of the left anterior descending artery (LAD), patency of the previously implanted stent to D1 without restenosis, and a spontaneous distal embolization defect of the apical LAD with thrombolysis in myocardial infarction flow
Gaspar Del Rio-Pertuz et al. (2022)	33	Male	Yes	Yes	No	No	No	No	hypokinesia of lateral and septal segments of the left ventricle and an ejection fraction of 55%	dissection of the proximal left anterior descending artery
Beeresh Puttegowda et al. (2014)	32	Male	Yes	No	Yes	No	No	No	hypokinesia of basal and mid-inferior wall with mild left ventricular dysfunction and ejection fraction of 45%	No abnormalities
Kiran Shetty et al. (2016)	42	Male	No	Yes	Yes	No	No	No	N/A	thrombus with the 95% occlusion of the proximal left anterior descending (LAD) artery
Perihan Varim et al. (2014)	61	Male	Yes	Yes	No	No	No	Yes	left ventricle ejection fraction was 50% with hypokinetic inferior wall, mild mitral regurgitation, mild aortic regurgitation and mild tricuspid regurgitation	40% diameter stenosis in the LAD, 50% diameter stenosis in the LCx artery and total occlusion in the RCA
Selen Acehan et al. (2022)	72	Male	Yes	Yes	No	No	No	No	N/A	thrombosis in the bypass graft (aorta–saphenous vein graft obtrusive marginal arteries
Selen Acehan et al. (2022)	42	Female	Yes	No	No	No	No	No	N/A	normal coronary arteries
Joseph R. Pelli Jr. et al. (2016)	61	Male	Yes	Yes	No	No	No	Yes	severe global left ventricular hypokinesis with an ejection fraction of 25%	thrombus in the distal right coronary artery, mid left anterior descending artery, and first diagonal of the distal left anterior descending artery
Hamed Aminiahidashti et al. (2015)	41	Male	Yes	Yes	No	Yes	Yes	Yes	mild mitral regurgitation, mild diastolic dysfunction, and left ventricular ejection fraction 45%	nonsignificant mild lesion in proximal port of right coronary artery
Beatriz Gómez-Martín et al. (2025)	81	Female	Yes	Yes	Yes	Yes	No	Yes	post-cardiac arrest biventricular dysfunction and inferior hypokines	acute thrombotic lesion on the right coronary artery
Megha S. et al. (2023)	60	Male	Yes	No	No	Yes	No	No	ejection fraction of 50%, grade 1 diastolic dysfunction along with regional wall motion abnormality in the inferior wall	healthy coronaries
Kotaro Tsuruta et al. (2022)	69	Male	Yes	No	No	No	No	Yes	hypokinesis in the anteroseptal wall of the left ventricle	occlusion of the DES deployed 2 weeks prior in the proximal LAD
Mohammad Reza Karimlu et al. (2016)	57	Male	Yes	Yes	Yes	No	No	No	ejection fraction of 40% with regional wall motion abnormality in anterior wall	recanalized thrombus with narrowing of 70–80% of mid to proximal part of (LAD) artery

Clinical interventions

All patients developed acute coronary syndromes following bee stings, with 14 (82.4%) experiencing ST-elevation myocardial infarction (STEMI) and 3 (17.6%) non-ST-elevation myocardial infarction (NSTEMI). Type 1 KS was reported in 3 (17.6%) patients, and type 2 KS in 12 (70.6%). The most common ECG finding was ST-segment elevation, which was detected in various myocardial territories, including the inferior leads in 8 patients (47.2%), the anterior leads in 8 patients (47.2%), and the lateral leads as shown in Fig. 2. One patient (5.9%) had a conduction anomaly: Mobitz Type II block with right bundle branch block. Troponin I was elevated in 9 cases (mean 1087.50 ng/L), and CK-MB was elevated in 6 cases. However, allergic biomarkers, eosinophils, tryptase, and BNP, were rarely reported. Echocardiography showed reduced ejection fraction in 9 (53.1%) of the cases. Coronary angiography revealed that 13 (76.5%) of the patients had significant pathological findings. The right coronary artery (RCA) was involved in 6 (35.4%) patients having thrombotic or severe stenotic lesions. The left anterior descending (LAD) artery was involved in 7 (41.3%) patients. Left circumflex (LCx) artery pathology was found in 2 (11.8%) patients. In contrast, 4 (23.5%) patients had normal or non-obstructive coronary arteries, with minimal disease or non-significant lesions. PCI was performed in 12 (70.6%) patients. Antiplatelets were administered in 15 (88.2%) cases, steroids in 9 (52.9%), and antihistamines in 12 (70.6%).

Fig. 2.

Percentages of occlusions on coronary angiography

Outcomes

Complications included arrhythmias in 3 (17.6%) cases, cardiac arrest in 2 (11.8%), and shock in 7 (41.2%) cases. The duration of hospital stays ranges between 4 and 15 days (mean 7.5 days). Full recovery was reported in 16 (94.1%) patients and persistent symptoms in 1 (5.9%) case. Clinical outcomes are summarized in Fig. 3.

Fig. 3.

Clinical outcomes

Discussion

This descriptive systematic review identified 17 cases of bee sting-induced MI [13, 16–29], one of the causes of KS, which will be the focus of this review, by exploring patient demographics, risk factors, clinical presentation, diagnostic findings, and management approaches, and identifying common features and areas that require further investigation and study. In contrast to patients with typical MI, who often have comorbidities and established risk factors such as diabetes, dyslipidemia, hypertension, and smoking, and are typically older adults [30], those with bee sting–induced MI generally lack similar comorbidities, specific risk factors, or a defined age group. Also, notably, in contrast to other causes of KS, patients with bee sting–induced MI were most often found to have no prior history of allergic reactions [31, 32]. The only observed similarity between patients with typical MI and those with bee sting–induced MI is the male predilection [30].

Chest pain was found to be the most common presenting symptom in patients with bee sting–induced MI, similar to its predominance in atherosclerotic MI. However, bee sting–induced MI is frequently associated with anaphylaxis and may also present with allergic symptoms such as rash and swelling [33, 34]. The onset of symptoms occurred within minutes for the majority of patients, supporting the role of a hypersensitivity reaction involving rapid histamine release and other inflammatory mediators [9]. This immediate response likely contributes to the prompt onset of cardiac effects observed in bee sting–induced MI. The sting sites were most commonly located on exposed areas of the upper body, and the number of stings varied across cases. Notably, even a single sting was sufficient to induce MI. However, neither the sting site nor the number of stings showed any obvious correlation with the clinical presentation or severity of the condition.

As part of the standard workup for any patient presenting with acute chest pain [35], all the cases in our review underwent the usual diagnostic steps, starting with ECG, which confirmed the diagnosis of ACS. STEMI was the predominant type, with a percentage slightly higher than that reported in KS due to other causes in addition to bee sting (64.5%) [36, 37], which indicates the seriousness of the condition and the prompt recognition needed. One of the patients presented with a conduction block on the ECG, which may even make the diagnosis more difficult to recognize. Other markers included cardiac enzymes such as troponin and CK-MB, which were elevated in nearly all patients tested. This finding has been reported both in KS and in ACS of other etiologies [35, 38], supporting their role in confirming the diagnosis and establishing them as standard biomarkers for this condition. On the other hand, allergic markers, including tryptase and eosinophil count, were reported in only a few patients. This is despite previous reviews on KS reporting elevated levels in 80.6% and 58.0% of cases, respectively [6]. However, the underreporting in our review makes it difficult to assess their appropriateness as standard laboratory markers in bee sting–induced MI specifically. When evaluated with coronary angiography, most of the cases were found to have abnormalities, without a specific predilection for any particular coronary artery. indicating that type 2 KS is the predominant type in our review.

Despite the absence of a standardized management approach for KS [39], almost all cases in our review had similar approaches, consisting of antiplatelet therapy and PCI as a routine approach for ACS [40], in addition to medications that aim to suppress the possible mechanism of the condition by suppressing the allergic reaction and the resultant inflammation [31]. However, current treatment is based on ACS protocols, and comparative studies on those therapies are still needed to establish evidence-based guidelines [31, 39]. When comparing the outcomes of KS to ACS from other causes, which have a reported high mortality rate [41], KS appears to have a more favorable prognosis, with full recovery often expected [36]. The notably high full recovery rate among the cases of bee sting–induced MI in our review further supports this observation. Shock was the predominant complication observed in our reported cases. This may be attributed to cardiogenic shock resulting from coronary obstruction and subsequent cardiac dysfunction, as noted in some cases in the literature [36], or it may be due to comorbid anaphylaxis triggered by the allergic reaction. Other potential complications, such as arrhythmias and cardiac arrest, were not commonly reported either in our cases or in other types of KS described in the literature [36].

A key limitation of this review is that it relies solely on individual case reports, which may introduce reporting bias and limit the generalizability of findings. Therefore, further research is necessary to establish definitive diagnostic and therapeutic guidelines and to promote early recognition in appropriate clinical contexts.

Conclusion

In conclusion, bee sting–induced MI is a rare cause of KS, characterized by ACS triggered by an allergic reaction that may provoke coronary vasospasm or plaque destabilization. While the clinical presentation often resembles typical ACS, it may also include allergic symptoms such as rash, swelling, and, frequently, anaphylaxis. The diagnostic approach largely follows standard ACS protocols, with the potential addition of allergic markers, though their role in diagnosis remains uncertain and warrants further study. Management is not standardized but generally involves treatment of both the coronary event and the allergic response, using antiplatelets, PCI, steroids, and antihistamines.

Abbreviations

ACS

Acute Coronary Syndrome

aPTT

Activated Partial Thromboplastin Time

CK

Creatine Kinase

CK-MB

Creatine Kinase–Myocardial Band

ECG

Electrocardiogram

EF

Ejection Fraction

HCO₃

Bicarbonate

IgE

Immunoglobulin E

INR

International Normalized Ratio

KS

Kounis Syndrome

LAD

Left Anterior Descending

LCx

Left Circumflex

MI

Myocardial Infarction

NSTEMI

Non ST-Elevation Myocardial Infarction

PCI

Percutaneous Coronary Intervention

PRISMA

Preferred Reporting Items for Systematic Reviews and Meta-Analyses

PROSPERO

International Prospective Register of Systematic Reviews

RCA

Right Coronary Artery

SD

Standard Deviation

STEMI

ST-Elevation Myocardial Infarction

WBC

White Blood Cell

Appendix

Case presentation

We present a representative case of a 45-year-old male presented to the emergency department with severe chest pain approximately 30 minutes after being stung by a bee on his right arm while gardening. He experienced immediate localized pain and swelling at the sting site, which was followed by a sudden onset of pressure-like chest pain, radiating to the left arm and jaw, accompanied by shortness of breath, excessive sweating, and lightheadedness.

On arrival at the emergency department, the patient appeared anxious, pale, and diaphoretic. Vital signs revealed hypotension; BP 90/60 mmHg, tachycardia;120 bpm, respiratory rate of 22/min, and oxygen saturation of 92% on room air. On examination, he had a rapid, irregular rhythm with weak peripheral pulses, decreased breath sounds bilaterally without wheezing or crackles. Localized erythema and swelling were noted at the site of the bee sting.

An electrocardiogram (ECG) demonstrated ST-segment elevation in the inferior leads (II, III, aVF), suggesting an inferior wall MI. The patient was managed immediately with oxygen therapy, fluid resuscitation, and administration of aspirin (325 mg chewed), clopidogrel (300 mg loading dose), and unfractionated heparin. Intravenous nitroglycerin was initiated for chest pain, and metoprolol was administered after stabilization. 0.3 mg of epinephrine was administered subcutaneously, along with intravenous diphenhydramine.

The patient underwent urgent coronary angiography, which revealed a 90% thrombotic occlusion of the RCA, with no significant lesions in the left coronary arteries. Percutaneous coronary intervention (PCI) was performed with balloon angioplasty and stent placement, leading to restoration of coronary flow. Post-PCI, the patient was maintained on dual antiplatelet therapy (aspirin 81 mg daily, clopidogrel 75 mg daily), atorvastatin 80 mg, and metoprolol 25–50 mg daily. A clopidogrel loading dose was selected instead of ticagrelor or prasugrel due to concerns regarding increased bleeding risk in the context of severe anaphylaxis, hypotension, and systemic inflammation. At the time of management, there was also concern about the possible need for urgent surgical intervention if hemodynamic deterioration occurred. In this scenario, clopidogrel was favored because of its more favorable reversal profile compared with ticagrelor and prasugrel. He remained hemodynamically stable and pain-free during hospitalization. Allergy testing performed one week post-discharge showed a positive skin prick test and elevated serum-specific IgE to bee venom, confirming a diagnosis of KS Type II. At one-week follow-up, the patient was asymptomatic with normal vital signs and laboratory parameters. Repeat ECG showed resolution of ST-segment changes, and echocardiogram.

Authors’ contributions

A.Z proposed the project, wrote the protocol, and contributed to the conception of the article. Z.W.E, A.S and A.Z helped with data extraction and screening. Z.W.E, A.Z, A.S, E.S and M.S contributed to the writing of the first draft and the revision of the manuscript. All authors approved the final manuscript as submitted and agreed to be accountable for all aspects of the work. Z.W.E and A.Z both are considered first authors as they both contributed equally.

Funding

The authors received no financial support for the publication of this article.

Data availability

The data will be available on reasonable request.

Declarations

Ethics approval and consent to participate

Ethical approval is exempt/waived at our institution as this is a case report.

Consent for publication

Written informed consent was obtained from the patient for publication of this case representation and any accompanying images. A copy of the written consent is available for review by the Editor-in-Chief of this journal.

Competing interests

The authors declare no competing interests.