Abstract
Background
Brugada syndrome (BrS) is a rare inherited arrhythmia associated with an increased risk of sudden cardiac death. Significant variation in the prevalence of BrS across different countries has been well documented. However, no study has examined the prevalence of BrS in Saudi Arabia. Therefore, our aim was to assess the prevalence of BrS in patients presenting to an emergency department (ED) in Riyadh, Saudi Arabia.
Methods
This retrospective study included consecutive adult patients who presented to the ED at King Khalid University Hospital (KKUH) and underwent an electrocardiogram (ECG). Demographic and clinical variables were collected from the records, and ECGs were examined for the presence of a Brugada pattern (BrP). BrS was diagnosed when a type 1 BrP was observed with no secondary causes, and BrP was diagnosed when a non-type 1 pattern was observed. A prespecified sensitivity analysis was conducted, excluding patients whose presentation was potentially compatible with BrS (syncope, presyncope, cardiac arrest, and palpitations).
Results
We included 1,000 patients. Men constituted 498 patients (49.8%). The majority were Saudi nationals (830, 85.6%) and the overall median age was 46 years (IQR: 30–65 years). The majority of the patients were afebrile at presentation (915, 93%) and a small number of patients took Brugada-inducing medications (27, 2.7%). The prevalence of BrS was 2/1,000 (0.002; 95% CI: 0.0002–0.007) and the prevalence of BrP was 26/1,000 (0.026; 95% CI: 0.0179–0.0390). Among the patients with BrP, 11 exhibited a type 2 pattern (42.3%) and 15 exhibited a type 3 pattern (57.7%). The sensitivity analysis revealed a prevalence of BrS of 2/912 (0.002; 95% CI: 0.0–0.0061) and a prevalence of BrP of 26/912 (0.028; 95% CI: 0.0178–0.0402).
Conclusion
This is the first Saudi Arabian study on BrS prevalence, suggesting a high prevalence and a notable proportion of non-type 1 Brugada electrocardiogram (ECG) patterns.
Keywords: Brugada pattern, Brugada syndrome, emergency department, prevalence, Saudi Arabia
GRAPHICAL ABSTRACT
Introduction
Brugada syndrome (BrS) is an inherited cardiac disorder characterized by distinct electrocardiographic patterns and an increased risk of ventricular arrhythmias, including sudden cardiac death (SCD). The description of the clinical presentation of what is now known as Brugada syndrome first appeared in a medical publication by Professor Maria Paz Mendoza-Guazon in 1917, describing young males who were in apparent health and died suddenly during sleep (1, 2). Later, in 1953, the ECG pattern was described as a mimic of myocardial infarction (3). The Brugada brothers then, in 1992, described the specific ECG pattern associated with SCD as a syndrome (4). Since then, significant progress in the understanding of the pathophysiology of this condition has been made. It is now believed that BrS involves impaired sodium channel function. A loss-of-function mutation in SCN5A, which encodes the Nav1.5 sodium channel, is the only genetic defect considered to be disease-causing and is responsible for approximately 20% of cases (5). Other implicated genes involving sodium, potassium, and calcium channels have been disputed (6). However, common genetic variants leading to decreased expression of sodium channel function have been described and explain familial segregation in those without SCN5A variants (7, 8).
Understanding the prevalence of BrS is crucial for proper clinical decision-making, public health policy development, and healthcare planning. Assessing the prevalence is particularly important for BrS given its well-documented variance in prevalence among different ethnicities and countries (9, 10). Indeed, a systematic review of the worldwide prevalence of BrS reported a wide prevalence range, with an overall prevalence of 0.5 per 1,000 individuals (0.0005), ranging from 1.8 per 1,000 individuals (0.0018) in Southeast Asia to 0 per 1,000 individuals in North Africa. Moreover, BrS in Asians was nine times more common than in those of white ethnicity and 36 times more common than in Hispanics (10). There is a paucity of data pertaining to those of Arab ethnicity and Saudi Arabia. Therefore, the aim of this study is to assess the prevalence of BrS in Saudi Arabia.
Methodology
Study population
Our study used a retrospective cross-sectional design. The target population consisted of consecutive adult patients [age > 14 years, per institutional policy at King Khalid University Hospital (KKUH)] who presented to the emergency department (ED) at KKUH and underwent an electrocardiogram (ECG), starting in December 2023 and proceeding retrospectively. The prespecified sample size of 1,000 was based on the international prevalence of BrS (10).
Only patients with missing ECGs or file notes were excluded. Demographics and clinical variables were collected from the records, and ECGs were examined for the presence of a Brugada pattern, which was verified by an expert (WA).
To minimize selection bias, a prespecified sensitivity analysis was performed, excluding patients with symptoms compatible with BrS (syncope, presyncope, palpitations, and cardiac arrest).
Study variables
We collected relevant data, including patients' demographics. clinical and medical history {febrile state, drugs including those known to induce BrP, and past medical history [e.g., hypertension (HTN), diabetes mellitus (DM), dyslipidemia (DLD), stroke, and atrial fibrillation (A.fib)]}, presenting symptoms (e.g., palpitations, presyncope, syncope, cardiac arrest, or road traffic accident injuries), ECG parameters (Brugada pattern/type), final diagnosis, and laboratory measurements (electrolyte panel at the time of ECG recording).
Criteria of diagnosis
BrS is diagnosed when a typical type 1 Brugada ECG pattern is detected in any of the right precordial leads (V1–V3) in the absence of a condition that may explain this pattern (phenocopy). A typical type 1 BrP is characterized by coved-type ST-segment elevation ≥2 mm followed by a negative T wave (4, 11–17).
A Brugada ECG pattern is defined when there is >2 mm J-point elevation followed by >1 mm saddleback-shaped ST-segment elevation (type 2) or <1 mm of any shape (type 3) (3–8).
Statistical analysis
Continuous data are presented as median (interquartile range) and categorical data as numbers (percentages). The prevalence of BrS and BrP is presented with 95% confidence intervals. Comparisons were done using the Wilcoxon rank-sum test for continuous variables and the chi-square test or Fisher's exact test for categorical variables. The statistical analysis was performed using SAS (SAS Institute, NC, USA).
Ethical considerations
This study was conducted in accordance with the Declaration of Helsinki and approved by the Institutional Review Board of the College of Medicine, King Saud University, Riyadh, Saudi Arabia (IRB approval number E-23-8042).
Results
Overall population
We included 1,000 patients. Among them, 28 patients had a Brugada ECG pattern and 972 did not. Men constituted 498 patients (49.8%). The majority were Saudi nationals (830, 85.6%), and the overall median age was 46 years (IQR: 30–65 years). Prevalent comorbidities included HTN (357, 35.7%), DM (338, 33.8%), DLD (143, 14.3%), CAD (143, 14.3%), stroke (84, 8.4%), and A.fib (69, 6.9%); family history of sudden cardiac death (FHx of SCD) was rare (2, 0.2%). The majority of the patients were afebrile at presentation (915, 93%). A small number of patients took Brugada-inducing medications (27, 2.7%), namely amitriptyline, flecainide, bupivacaine, and propofol. Further baseline characteristics are presented in Table 1.
Table 1.
Baseline characteristics of patients with and without a BrP.
| Variable | Brugada pattern (N = 28) | No Brugada pattern (N = 972) | All patients (N = 1,000) | P-value |
|---|---|---|---|---|
| Sex (male), n (%) | 16 (57.1) | 482 (49.5) | 498 (49.8) | 0.430 |
| Nationality (Saudi), n (%) | 24 (96) | 806 (85.3) | 830 (85.6) | 0.134 |
| Age, median (IQR) | 47 (31–67) | 46 (30–65) | 46 (30–65) | |
| Brugada syndrome, n (%) | 2 (7.1) | 2 (0.2) | ||
| Brugada pattern (Type 2), n (%) | 11 (39.2) | 11 (1.1) | ||
| Brugada pattern (Type 3), n (%) | 15 (53.5) | 15 (1.5) | ||
| Febrile state (afebrile), n (%) | 26 (92.8) | 889 (93.1) | 915 (93) | 0.945 |
| Hypertension, n (%) | 12 (42.8) | 345 (35.6) | 357 (35.7) | 0.432 |
| Diabetes mellitus, n (%) | 14 (50) | 324 (33.4) | 338 (33.8) | 0.068 |
| Dyslipidemia, n (%) | 8 (28.5) | 135 (13.9) | 143 (14.3) | 0.029 |
| Stroke, n (%) | 2 (7.1) | 82 (8.4) | 84 (8.4) | 0.801 |
| Atrial fibrillation, n (%) | 4 (14.2) | 65 (6.7) | 69 (6.9) | 0.120 |
| Coronary artery disease, n (%) | 9 (32.1) | 134 (13.8) | 143 (14.3) | 0.006 |
| FHx of sudden cardiac death, n (%) | 0 | 2 (0.2) | 2 (0.2) | 0.949 |
| Sodium level (normal), n (%) | 13 (61.9) | 703 (86.6) | 716 (86) | 0.0009 |
| Chloride level (normal), n (%) | 12 (57.1) | 697 (86.2) | 709 (85.4) | <0.001 |
| Potassium level (normal), n (%) | 18 (94.7) | 734 (91.7) | 752 (91.8) | 0.624 |
| Calcium level (normal), n (%) | 10 (76.9) | 404 (84.8) | 414 (84.7) | 0.493 |
| Toxicology screen (positive), n (%) | 0 | 3 (4.4) | 3 (4.4) | 0.793 |
| Taking medications that induce a Brugada pattern, n (%) | 0 | 27 (2.8) | 27 (2.7) | 0.382 |
Prevalence of BrS
Two patients had BrS. Table 2 describes these BrS patients. Patient 1 was a 45-year-old afebrile Saudi man who presented with shortness of breath and a productive cough. Patient 2 was a 36-year-old afebrile non-Saudi woman who presented with chest discomfort. Neither patient had comorbidities (including HTN, DM, DLD, stroke, A.fib, or CAD) nor any known exposure to BrP-inducing medications. Both patients were discharged from the ED with a referral to electrophysiology clinics for further evaluation. Patient 1 attended follow-up and was subsequently diagnosed with BrS, whereas Patient 2 did not attend follow-up due to eligibility issues (non-national).
Table 2.
Baseline characteristics of the patients with BrS.
| Variable | BrS patient 1 | BrS patient 2 |
|---|---|---|
| Sex | Male | Female |
| Nationality | Saudi | Non-Saudi |
| Age | 45 | 36 |
| Presenting symptoms | Shortness of breath with productive cough | Chest discomfort |
| Febrile state | Afebrile | Afebrile |
| Hypertension | No | No |
| Diabetes mellitus | No | No |
| Dyslipidemia | No | No |
| Stroke | No | No |
| Atrial fibrillation | No | No |
| Coronary artery disease | No | No |
| Sodium level (mmol/L) | 133 | 142 |
| Chloride level (mmol/L) | 95 | 104 |
| Potassium level (mmol/L) | 3.74 | 4 |
| Calcium level (mmol/L) | 2.35 | 2.29 |
| Taking medications that induce a Brugada pattern | No | No |
Prevalence of BrP
Among the 26 patients with BrP, 11 exhibited a type 2 pattern (42.3%) and 15 exhibited a type 3 pattern (57.7%). This group comprised 15 men (57.7%), with a median age of 47 years (IQR: 31–67). In total, 23 (88.5%) of these patients were Saudi and the majority were afebrile (24, 92.3%). No patient had a FHx of SCD or took medications known to induce BrP. Further baseline characteristics are presented in Table 3.
Table 3.
Baseline characteristics of the patients with a Brugada ECG pattern.
| Variable | Patients with a Brugada ECG pattern (N = 26) |
|---|---|
| Sex (Male), n (%) | 15 (57.7) |
| Nationality (Saudi), n (%) | 23 (88.5) |
| Age, median (IQR) | 47 (31–67) |
| Brugada pattern (Type 2), n (%) | 11 (42.3) |
| Brugada pattern (Type 3), n (%) | 15 (57.7) |
| Hypertension, n (%) | 12 (46.2) |
| Diabetes mellitus, n (%) | 14 (53.8) |
| Coronary artery disease, n (%) | 9 (34.6) |
| Dyslipidemia, n (%) | 8 (30.8) |
| Atrial fibrillation, n (%) | 4 (15.4) |
| Stroke, n (%) | 2 (7.7) |
| Febrile state (afebrile), n (%) | 24 (92.3) |
| Sodium level (normal), n (%) | 12 (60) |
| Chloride level (normal), n (%) | 11 (55) |
| Potassium level (normal), n (%) | 16 (94.4) |
| Calcium level (normal), n (%) | 8 (72.7) |
| FHx of SCD, n (%) | 0 (0) |
| Taking medications that induce a Brugada pattern, n (%) | 0 (0) |
Sensitivity analyses
We performed a sensitivity analysis to minimize hospital-setting bias. This was done in an attempt to make the patients enrolled in this study more representative of systematic screening in the general population (i.e., BrS is diagnosed incidentally rather than being the cause of presentation to the ED), which revealed a BrS prevalence of 2/912 (0.002; 95% CI: 0.0–0.0061) and a BrP prevalence of 26/912 (0.028; 95% CI: 0.0178–0.0402).
Discussion
This study represents the first investigation into the prevalence of BrS and BrP in Saudi Arabia, revealing a BrS prevalence of 0.002 (95% CI: 0.0002–0.007) and a BrP prevalence of 0.026 (95% CI: 0.0179–0.0390) among patients presenting to an ED. It is important to note that our study population consisted of patients who presented to the emergency department and underwent ECG evaluation, which differs from the general population. These findings offer some insights into the regional epidemiology of BrS in the Middle East, a region where comprehensive prevalence data have historically been limited. Our observed BrS prevalence exceeds the pooled global prevalence of 0.0005 (0.5/1,000) reported in Vutthikraivit et al.'s 2018 meta-analysis of 61 studies (10), and is higher than that reported in Western populations (typically 0.0001–0.0003 in European/North American cohorts) (10, 13). However, it remains lower than that reported in high-risk Southeast Asian populations, where BrS prevalence reaches 0.0037 (10), consistent with established ethnic gradients wherein BrS is ninefold more common in Asians than those of white ethnicity (10). Similarly, the observed type 2/3 BrP prevalence of 0.026 is 4.3-fold higher than the global average of 0.0061 (10), but below Southeast Asia's reported prevalence of 0.0355 (10). This epidemiological pattern may reflect Saudi Arabia's unique genetic admixture, bridging white ethnicity and Asian ancestry; notwithstanding the small numbers, this warrants investigation into population-specific variants in SCN5A and other susceptibility genes implicated in BrS pathogenesis (14).
To contextualize our results further, it is important to examine existing studies from neighboring Middle Eastern countries (Table 4). A study by Babaee Bigi et al. in Iran evaluated patients presenting with palpitations in southern Iran and revealed similar findings. A Brugada-type ECG pattern was reported in 0.0256 of 3,895 patients (18). Of these patients, 14 (0.0035) demonstrated a spontaneous type 1 pattern. In contrast, an Egyptian study reported a low prevalence of Brugada-type ECG patterns (0.0055) in a consecutive hospital-based cohort of 4,000 subjects, with all cases being the saddleback type (type 2/3) and no type 1 patterns were observed (19). Unlike our study, this study included pediatric patients, which may explain the lower prevalence since BrP typically manifests in adulthood (22, 23).
Table 4.
Comparison with previous Middle Eastern studies.
| Study | Country | Population | Sample size | Mean age | Prevalence of BrS, n (%) | Prevalence of type 2/3 BrP, n (%) |
|---|---|---|---|---|---|---|
| Babaee Bigi et al. (18) | Iran | Patients presenting to ED with palpitations | 3,895 | 38.2 ± 11.9 years | 14 (0.36) | 86 (2.2) |
| Akram et al. (19) | Egypt | Patients admitted with a non-cardiac presentation | 4,000 | Nil | 0 | 22 (0.55) |
| Bozkurt et al. (20) | Turkey | General population | 1,238 | 38.9 ± 17.6 years | 1 (0.08) | 5 (0.4) |
| Adler et al. (21) | Israel | Febrile vs. afebrile patients presenting to the ED | 402 vs. 909 | 62 ± 22 years vs. 61 ± 19 years | 8 (2) vs. 1 (0.1) | 7 (1.7) vs. 4 (0.4) |
Moreover, a study by Bozkurt et al., conducted in Turkey, reported a Brugada-type ECG pattern frequency in one patient (0.0008), who demonstrated a type 1 pattern (20). This is lower than our findings and may indicate a different genetic architecture of the Turkish population compared with ours.
In addition, our findings are consistent with previously published studies examining the prevalence of the type 1 Brugada ECG pattern. Notably, Adler et al. reported a baseline prevalence of approximately 0.1%, which is comparable to the prevalence observed in our cohort and in other similar studies (21).
Beyond these regional insights, the observed global disparities in BrS prevalence highlight a complex interplay of genetic, environmental, and possibly diagnostic factors. Understanding the reasons behind these geographic variations is crucial for a comprehensive global perspective on BrS.
One of the primary drivers of geographic variation is genetic predisposition. BrS is an inherited channelopathy, predominantly linked to mutations in the SCN5A gene, which encodes the cardiac sodium channel. While SCN5A mutations have been found in a significant proportion of patients with BrS, a substantial number of cases remain genetically unexplained, suggesting the involvement of other genes or complex genetic interactions (24). The prevalence and specific type of these genetic mutations vary across different ethnic groups and geographic regions. For instance, certain founder mutations may be more prevalent in specific populations due to historical migration patterns and genetic isolation (5). The higher prevalence in Southeast Asia is often attributed to a higher incidence of specific genetic variants within these populations, although the exact genetic landscape contributing to this elevated risk is still under active investigation (25).
Future studies should confirm our findings in larger, population-based cohorts. Establishing the prevalence of Brugada syndrome in our region is essential to define the disease burden and improve our understanding of its epidemiology and potential population-specific determinants. For example, detailed genetic studies in areas with high prevalence can identify common single-nucleotide polymorphisms associated with BrS. Prevalence data can also inform clinical practice by guiding targeted screening and resource allocation, while supporting the development of evidence-based national policies and healthcare planning. The yield of screening for BrS, including Proactive testing in families with sudden unexplained death and individuals with unexplained cardiac arrest, largely depends on the overall prevalence of BrS in any population.
The limitations of our study should be acknowledged. First, the single-center hospital-setting design may have introduced selection bias. We attempted to minimize this by excluding patients with presentations compatible with Brugada. In addition, many epidemiological studies have used hospital settings; thus, for comparison purposes, it remains helpful. Second, the small sample size affected precision, so a larger multicenter study is needed to confirm the results.
Conclusions
This study suggests a high prevalence of BrS/BrP in Saudi Arabia, with a striking predominance of type 2/3 ECG patterns. However, our findings should be interpreted with caution until confirmed by larger studies. Greater awareness and education regarding BrP recognition and risk stratification are needed, in addition to further investigation into the determinants of BrS prevalence.
Funding Statement
The author(s) declared that financial support was received for this work and/or its publication from the Ongoing Research Funding Program (RF 026-18) of King Saud University, Riyadh, Saudi Arabia.
Footnotes
Edited by: Rui Providencia, University College London, United Kingdom
Reviewed by: Alexandr Ceasovschih, Grigore T. Popa University of Medicine and Pharmacy, Romania
Matko Spicijaric, University Hospital Center Rijeka, Croatia
Data availability statement
The original contributions presented in the study are included in the article/Supplementary Material, further inquiries can be directed to the corresponding author/s.
Ethics statement
This study involving humans was approved by the Institutional Review Board of the College of Medicine, King Saud University, Riyadh, Saudi Arabia (IRB Approval number E-23-8042). This study was conducted in accordance with the local legislation and institutional requirements. Written informed consent for participation was not required from the participants or the participants’ legal guardians/next of kin in accordance with the national legislation and institutional requirements.
Author contributions
MuA: Data curation, Methodology, Writing – original draft, Writing – review & editing. LA: Data curation, Methodology, Writing – original draft, Writing – review & editing. SA: Writing – original draft. FAl: Data curation, Writing – original draft. RJ: Data curation, Writing – original draft. MeA: Data curation, Writing – original draft. MAlf: Data curation, Writing – original draft. MAlk: Data curation, Writing – original draft. SA: Data curation, Writing – original draft. FAb: Writing – original draft. WA: Conceptualization, Formal analysis, Funding acquisition, Methodology, Supervision, Validation, Writing – original draft, Writing – review & editing.
Conflict of interest
The author(s) declared that this work was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
Correction Note
This article has been corrected with minor changes. These changes do not impact the scientific content of the article.
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Supplementary material
The Supplementary Material for this article can be found online at https://www.frontiersin.org/articles/10.3389/fcvm.2026.1871087/full#supplementary-material
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Associated Data
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Supplementary Materials
Data Availability Statement
The original contributions presented in the study are included in the article/Supplementary Material, further inquiries can be directed to the corresponding author/s.