IntroductionHypertrophic cardiomyopathy (HCM) is the most common inherited cardiovascular disease (1,2) and is the most frequent cause of sudden cardiac death (SCD) in young individuals, particularly athletes with a high level of training (3–5).HCM is a prevalent hereditary cardiovascular condition that affects one in 500 people in the general population (6,7). The cumulative proportion of sudden cardiac death (SCD) events in childhood hypertrophic cardiomyopathy (HCM) within five years of diagnosis ranged from 8% to 10% (8,9). It is characterized by inadequate relaxation, hypercontractility, reduced compliance, and left ventricle hypertrophy (10–12). HCM manifests as a chronic, progressive illness that can have a severe, transformative effect on a person’s life and significantly lower quality of life. Data on the cost to society associated with HCM has shown significant increases in all-cause hospitalizations, hospital days, outpatient visits, and total healthcare costs. The majority of cost increases can be attributed to increased hospitalizations and hospital days among symptomatic patients (13). The most often reported symptoms include syncope, palpitations, exertional dyspnea, shortness of breath, ankle swelling, exhaustion, sense of disorientation, and lightheadedness (14,15).Among the estimated 700,000 patients with HCM, only 100,000 have been diagnosed in the United States (16). Underdiagnosis may be due in part to challenges in the diagnosis of asymptomatic HCM patients, who typically receive a diagnosis by chance or via systematic screening efforts (12). However, developments in the understanding of genetic and phenotypic characteristics of HCM have promise for improving the identification of the condition. Over the last twenty years, the condition has been linked to abnormalities in genes that encode proteins of the cardiomyocyte’s contractile machinery (6,17,18). It appears that significant progress has been made in understanding the illness from both a genetic and clinical standpoint (19).Despite new developments, HCM remains underdiagnosed. Although the population prevalence of HCM is between 1:200 and 1:500, only 10–20% of cases are found by clinical means (20). Patients with HCM can have a normal life expectancy but a notable percentage can develop HCM-related complications including heart failure, atrial fibrillation (AF), and cardioembolic stroke, while a smaller percentage have SCD or life-threatening ventricular arrhythmias (21). SCD is the most common cause of mortality among these patients and frequently occurs during exercise. However, it often goes undetected until death, as many individuals experience minimal or no significant symptoms (6,11). Consequently, a high index of diagnostic suspicion, accurate identification, and a thorough clinical examination of patients and family members are crucial for early identification and treatment (20). Identifying high-risk patients is crucial to lowering the risk of SCD in young individuals with HCM, as effective treatment has the potential to significantly reduce HCM mortality and morbidity (22,23) This can be achieved through exercise limitation, medication therapies, and the use of implantable cardioverter defibrillators (ICDs) (24) . Therefore, there has been considerable interest in improving diagnostic accuracy among HCM patients, especially young patients, to inform intervention (21).The HCM diagnosis is based on imaging techniques, such as echocardiography or cardiovascular magnetic resonance (CMR), that reveal increasing LV wall thickness (21). Thorough investigation has led to a better comprehension of risk categorization for patients with HCM. The latest European Society of Cardiology (ESC) guidelines propose evaluating clinical examination, family history, 48-hour electrocardiography (ECG), echocardiography, and exercise testing for this purpose (6,11). The European Society of Cardiology (ESC) has proposed specific cardiac screening guidelines for young competitive athletes (25), which include assessing symptoms and family medical history (e.g., premature death, HCM), conducting a physical examination, and performing a resting 12-lead ECG. A recent Danish study revealed that a large proportion of individuals who experienced SCD due to HCM had previous symptoms, and most of them had sought medical attention before their death, in contrast to the control group (26). These findings suggest there is an opportunity to improve the identification of HCM among at-risk patients, as many patients seek treatment.The ECG continues to be a fundamental aspect of evaluating patients with HCM. Moreover, it is experiencing a ”renaissance” in the realm of cardiomyopathies, not only due to its cost-effectiveness and widespread accessibility, but also because it offers information pertinent to morphology, function, and genetic foundation simultaneously (21) HCM has diagnosis so far relied on identification of left ventricular hypertrophy (LVH) with a wall thickness greater than 15 mm using echocardiography or CMR. However, this degree of LVH is not exclusive to HCM and may stem from various other pathological conditions, widening the differential. In such instances, the ECG is highly valuable in assisting with the differentiation between sarcomeric HCM and its phenocopies (21). There is a growing body of literature evaluating the accuracy of ECG markers in predicting HCM, however, there remains a need for research on the extent to which ECG findings are predictive of HCM identified on echocardiography. Therefore, the aim of this study was to evaluate the prevalence of abnormal ECG findings, including LVH, T wave inversion, left bundle branch block (LBBB), and left atrial enlargement in participants with suspected HCM detected during screening echocardiography.