European Journal of Cardiovascular Medicine

Coronary artery disease (CAD) remains the leading cause of morbidity and mortality worldwide, with an alarming shift toward earlier age of onset, particularly in developing countries like India (1). Premature coronary artery disease (PCAD), commonly defined as CAD occurring before 45 years in men and 55 years in women, represents a significant public health concern due to its impact on economically productive age groups (2). Epidemiological evidence suggests that Indians develop CAD nearly a decade earlier than Western populations, with a substantial proportion of myocardial infarctions occurring in individuals below 40 years of age (1). This early onset is associated with increased disease severity, recurrent cardiovascular events, and long-term socioeconomic burden, thereby necessitating focused research into its clinical profile and determinants.

The pathogenesis of premature CAD is multifactorial, involving a complex interplay of traditional and emerging risk factors (6). Conventional risk factors such as smoking, hypertension, diabetes mellitus, dyslipidemia, obesity, and family history continue to play a pivotal role in disease development among young adults (2). Among these, tobacco use and dyslipidemia, particularly elevated low-density lipoprotein (LDL) cholesterol, have been identified as dominant contributors in young patients (9). The landmark INTERHEART study demonstrated that modifiable risk factors account for the majority of myocardial infarction risk globally, with a stronger impact of hypertension, diabetes, and abdominal obesity in South Asian populations (3). Additionally, genetic predisposition, including familial hypercholesterolemia and elevated lipoprotein(a), has emerged as a significant contributor to early atherosclerosis in young individuals (4).

Clinical presentation of premature CAD often differs from that in older populations. Young adults more frequently present with acute coronary syndromes, particularly ST-elevation myocardial infarction (STEMI), and may exhibit aggressive disease patterns despite fewer comorbidities (6). Angiographically, single-vessel disease is more common, although multivessel involvement is increasingly reported, especially among South Asians (7). Studies such as the CADY registry have demonstrated a high prevalence of conventional risk factors, including diabetes, hypertension, and smoking, among young Indian CAD patients (5). Furthermore, male predominance is notable, though recent evidence indicates an increasing burden among young women, often associated with metabolic risk factors and poorer outcomes (10).

Despite extensive research, several gaps persist in understanding premature CAD. Most available studies are hospital-based or registry-driven, limiting generalizability to the broader population (8). There is inadequate representation of younger age groups, especially those below 40 years, and limited exploration of non-traditional risk factors such as psychosocial stress, environmental exposures, and novel biomarkers (6). Additionally, inconsistencies exist in defining premature CAD across studies, leading to variability in reported prevalence and risk profiles (6). Emerging evidence also highlights underdiagnosis and suboptimal management of risk factors in young adults, indicating missed opportunities for early intervention and prevention (8).

Given the rising burden and unique characteristics of premature CAD, there is a pressing need for comprehensive evaluation of its clinical and risk factor profile in young adults. Understanding the relative contribution of various modifiable and non-modifiable determinants is essential for developing targeted preventive strategies and improving early detection (2). Therefore, the present study aims to assess the clinical profile and identify the predominant risk factors associated with premature coronary artery disease in young adults, thereby contributing to the existing body of knowledge and aiding in formulation of effective preventive and therapeutic interventions.

Study Design and Setting This hospital-based observational cross-sectional study was conducted in the Department of Cardiology during the study period from 2024 to 2025. The study was undertaken to evaluate the clinical profile and risk factors associated with premature coronary artery disease in young adults attending the cardiology department. All eligible patients fulfilling the study criteria during the study period were included after obtaining informed written consent. Institutional Ethics Committee approval was obtained prior to commencement of the study. Confidentiality of patient information was maintained throughout the study. Study Population The study population comprised young adult patients diagnosed with premature coronary artery disease admitted to or evaluated in the Department of Cardiology during 2024–2025. Premature coronary artery disease was considered in patients presenting with clinical, electrocardiographic, biochemical, and/or angiographic evidence of coronary artery disease at a younger age than usually expected. Both male and female patients satisfying the eligibility criteria were enrolled consecutively until the required sample size was achieved. Sample Size The sample size for the present study was 50 patients. A convenient consecutive sampling method was adopted, and all eligible patients presenting during the study period were included until the sample size of 50 was reached. Inclusion Criteria • Young adult patients diagnosed with premature coronary artery disease. • Patients admitted in or attending the Department of Cardiology during the study period 2024–2025. • Patients willing to participate in the study. • Patients who provided informed written consent. Exclusion Criteria • Patients older than the predefined age limit for premature coronary artery disease. • Patients with congenital heart disease or structural heart disease unrelated to coronary artery disease. • Patients with severe systemic illness interfering with assessment of risk factors. • Patients with incomplete clinical records or unwillingness to participate. • Patients who did not provide consent for inclusion in the study. Study Procedure After enrollment, a detailed clinical evaluation was carried out in all study participants. Demographic details, presenting complaints, history of chest pain, dyspnea, palpitations, syncope, and other associated symptoms were recorded. Detailed history regarding conventional cardiovascular risk factors such as smoking, alcohol intake, hypertension, diabetes mellitus, dyslipidemia, obesity, sedentary lifestyle, and family history of coronary artery disease was obtained. Relevant physical examination findings and anthropometric measurements were noted. Patients were further evaluated using routine laboratory investigations, electrocardiography, echocardiography, and coronary angiography wherever indicated. The diagnosis of premature coronary artery disease was made based on clinical features and supportive investigative findings as per standard cardiology practice. Study Tool Data were collected using a predesigned and pretested structured proforma. The study tool included sections for socio-demographic details, clinical history, personal habits, past medical history, family history, physical examination findings, laboratory parameters, electrocardiographic findings, echocardiographic findings, angiographic profile, and associated cardiovascular risk factors. The proforma was used uniformly for all patients to ensure consistency and completeness of data collection. Data Collection • Demographic data: age, sex, occupation, residence. • Clinical profile: presenting symptoms, duration of symptoms, type of coronary event. • Personal history: smoking, tobacco use, alcohol consumption, physical activity. • Past history: hypertension, diabetes mellitus, dyslipidemia, obesity, previous cardiac illness. • Family history: history of premature coronary artery disease in first-degree relatives. • Examination findings: pulse rate, blood pressure, body mass index, waist circumference. • Laboratory investigations: blood sugar, lipid profile, renal function tests, cardiac biomarkers. • Cardiac assessment: ECG findings, echocardiography findings, angiographic findings. • Risk factor assessment: presence and distribution of major modifiable and non-modifiable risk factors. Outcome Measures The primary outcome measures included assessment of the clinical profile and distribution of risk factors among young adults with premature coronary artery disease. Secondary observations included pattern of presentation, associated comorbidities, and angiographic characteristics wherever available. Statistical Analysis The collected data were entered into Microsoft Excel and analyzed using appropriate statistical software. Descriptive statistics were used to summarize demographic variables, clinical findings, and risk factors. Categorical variables were expressed as frequencies and percentages, while continuous variables were presented as mean ± standard deviation. Appropriate statistical tests such as Chi-square test or Fisher’s exact test for categorical variables and Student’s t-test for continuous variables were applied wherever relevant. A p-value of less than 0.05 was considered statistically significant.

Table 1: Baseline Demographic and Clinical Characteristics (n = 50)

The baseline demographic and clinical characteristics of the study population are summarized in Table 1. The mean age of patients was 38.6 ± 5.8 years, indicating that premature coronary artery disease predominantly affected individuals in the late third to early fourth decade of life. There was a clear male predominance (76%), consistent with the known higher risk of CAD among young men. A majority of patients belonged to urban areas (64%) and were engaged in sedentary occupations (56%), highlighting the influence of urban lifestyle and physical inactivity as important contributing factors. Clinically, chest pain was the most common presenting symptom (92%), reflecting the typical presentation of acute coronary syndrome. The mean duration of symptoms prior to presentation was 10.8 ± 7.6 hours, suggesting relatively early healthcare seeking behavior in most patients. Notably, ST-elevation myocardial infarction (STEMI) was the predominant mode of presentation (56%), indicating a higher burden of acute and severe coronary events among young adults with premature coronary artery disease.

Figure 1: Distribution of Major Cardiovascular Risk Factors (n = 50)

The distribution of major cardiovascular risk factors among the study population is presented in figure 1. A high prevalence of modifiable risk factors was observed, with tobacco use in any form being the most common (72%), followed by smoking (60%) and sedentary lifestyle (58%), indicating a significant contribution of lifestyle-related factors to premature coronary artery disease. Among metabolic risk factors, dyslipidemia (56%) and hypertension (48%) were notably prevalent, while diabetes mellitus was present in 40% of patients, reflecting a substantial burden of metabolic abnormalities. Obesity was observed in 36%, further emphasizing the role of adiposity in early atherosclerosis. Additionally, a positive family history of premature coronary artery disease was noted in 32% of patients, suggesting a significant genetic predisposition.

Table 2: Laboratory Profile of Study Population (n = 50)

The laboratory profile of the study population is summarized in Table 2. The mean HbA1c level was 7.2 ± 1.4%, indicating poor glycemic control and a significant burden of diabetes and prediabetes among patients. Lipid profile analysis revealed elevated total cholesterol (212.8 ± 46.5 mg/dL), triglycerides (182.6 ± 68.4 mg/dL), and LDL cholesterol (138.2 ± 38.6 mg/dL), along with reduced HDL cholesterol (36.4 ± 8.2 mg/dL), consistent with an atherogenic lipid pattern commonly observed in young individuals with coronary artery disease. The mean serum creatinine level was 1.12 ± 0.32 mg/dL, suggesting largely preserved renal function in the majority of patients. Additionally, markedly elevated troponin I levels (4.8 ± 3.6 ng/mL) reflect acute myocardial injury, correlating with the high prevalence of acute coronary syndromes in the study population.

Table 3: Echocardiographic and Angiographic Profile (n = 50)

The echocardiographic and angiographic profile of the study population is presented in Table 3. The mean left ventricular ejection fraction (LVEF) was 48.6 ± 11.2%, indicating mild to moderate impairment of systolic function in a substantial proportion of patients. Regional wall motion abnormalities were observed in 60%, reflecting underlying myocardial ischemia or infarction. On coronary angiography, single vessel disease was the most common pattern (56%), although a considerable proportion of patients exhibited multivessel involvement (44%), suggesting that significant coronary atherosclerosis can occur even at a younger age. The left anterior descending artery was the most frequently involved vessel (64%), consistent with its known susceptibility in coronary artery disease. Furthermore, significant stenosis (>70%) was noted in 68% of patients, indicating a high burden of obstructive coronary lesions.

Table 4: Association of Risk Factors with Severity of CAD

The association between major cardiovascular risk factors and severity of coronary artery disease is presented in Table 4. Smoking, hypertension, diabetes mellitus, and family history of premature coronary artery disease showed a statistically significant association with multivessel disease (p < 0.05). A higher proportion of patients with smoking (16 vs 14), hypertension (14 vs 10), and diabetes mellitus (12 vs 8) were observed in the multivessel disease group compared to single vessel disease, indicating their role in more extensive coronary involvement. Similarly, family history (10 vs 6) was significantly associated with greater disease severity, suggesting a genetic predisposition to diffuse atherosclerosis. In contrast, although dyslipidemia and obesity were prevalent among patients, their association with disease severity did not reach statistical significance (p > 0.05).

The association between major cardiovascular risk factors and STEMI presentation is depicted in Table 5. Smoking, hypertension, and diabetes mellitus demonstrated a statistically significant association with STEMI (p < 0.05). A higher proportion of patients with smoking (20 vs 10), hypertension (16 vs 8), and diabetes mellitus (14 vs 6) presented with STEMI compared to NSTEMI/unstable angina, indicating their role in precipitating more acute and severe coronary events. Although dyslipidemia and obesity were more frequent among STEMI patients, their associations were not statistically significant (p > 0.05). Similarly, family history did not show a significant association with the type of coronary event.

Table 5: Association of Risk Factors with STEMI Presentation

Premature coronary artery disease (PCAD) represents an increasingly recognized clinical entity, particularly in developing countries such as India, where cardiovascular risk factors manifest earlier and more aggressively. The present study evaluated the clinical profile, risk factor distribution, laboratory parameters, and angiographic characteristics of young adults with PCAD, providing important insights into disease patterns in this population.

In the current study, the mean age of presentation was 38.6 ± 5.8 years, with a marked male predominance (76%). These findings are consistent with earlier Indian studies which have demonstrated that CAD occurs nearly a decade earlier in Indians compared to Western populations (1). Similar observations were reported by Sharma et al. (2), where the majority of patients were males in the third to fourth decade of life. The higher prevalence among males may be attributed to greater exposure to risk factors such as smoking and occupational stress, although recent literature suggests a rising trend among females as well (10).

Chest pain was the predominant presenting symptom (92%), followed by sweating and dyspnea, with STEMI being the most common presentation (56%). This is in agreement with studies by Aggarwal et al. (6) and Singh et al. (7), which reported that young patients frequently present with acute coronary syndromes, particularly STEMI. The predominance of STEMI suggests a more abrupt and thrombotic pathophysiology in younger individuals, possibly due to plaque rupture in relatively less calcified vessels.

A major finding of the present study was the high burden of modifiable risk factors. Smoking (60%) and overall tobacco exposure (72%) emerged as the most significant contributors. This aligns with the INTERHEART study (3), which identified smoking as one of the strongest risk factors for myocardial infarction globally. Similar prevalence rates have been reported by Iyengar et al. (5) in the CADY registry, where smoking was observed in approximately 39% of young CAD patients, though higher rates in the present study may reflect regional variations and lifestyle differences.

Metabolic risk factors were also highly prevalent. Dyslipidemia was observed in 56%, hypertension in 48%, and diabetes mellitus in 40% of patients. These findings are comparable to those reported by Reddy et al. (9), who highlighted the significant contribution of dyslipidemia and diabetes in young Indian CAD patients. The mean lipid profile in the present study showed elevated total cholesterol, LDL, and triglycerides with reduced HDL levels, a pattern consistent with atherogenic dyslipidemia commonly seen in South Asians. This lipid profile has been strongly associated with early atherosclerosis and increased cardiovascular risk (11).

The role of obesity and sedentary lifestyle was also evident, with 36% of patients being obese and 58% leading a sedentary lifestyle. These findings corroborate earlier reports by Gupta et al. (11), who emphasized the role of urbanization, physical inactivity, and dietary transitions in the increasing burden of premature CAD. Central obesity, as reflected by increased waist circumference in the present study, further supports the role of metabolic syndrome in early disease onset.

Family history of premature CAD was present in 32% of patients, indicating a significant genetic predisposition. This is in agreement with findings from Enas et al. (12), who reported a strong familial aggregation of CAD among South Asians. Genetic factors such as elevated lipoprotein(a) and familial hypercholesterolemia are increasingly recognized contributors to early atherosclerosis and may partly explain the earlier onset of disease in this population.

Laboratory findings in the present study revealed poor glycemic control, with a mean HbA1c of 7.2 ± 1.4%, and significant dyslipidemia, supporting the role of metabolic abnormalities in PCAD. Elevated cardiac biomarkers (troponin I in 84%) were consistent with acute myocardial injury. Similar findings have been reported by Joshi et al. (13), who demonstrated that young CAD patients often present with significant biochemical derangements despite fewer comorbidities.

Echocardiographic evaluation showed that 60% of patients had regional wall motion abnormalities, with a mean LVEF of 48.6 ± 11.2%, indicating varying degrees of systolic dysfunction. These findings are comparable to those reported by Mehta et al. (14), who observed reduced ejection fraction in a significant proportion of young myocardial infarction patients. Diastolic dysfunction was also noted in 44%, suggesting early myocardial involvement even in younger individuals.

Angiographic findings revealed that single vessel disease (56%) was the most common pattern, with left anterior descending artery involvement in 64% of cases. These findings are consistent with previous studies (6,7), which have shown a predominance of single-vessel disease in young CAD patients. However, a notable proportion (44%) had multivessel disease, indicating that severe and diffuse atherosclerosis is not uncommon even in younger age groups. This may reflect the cumulative impact of multiple risk factors and delayed diagnosis.

Statistical analysis demonstrated significant associations between major risk factors and disease severity as well as clinical presentation. Smoking, hypertension, diabetes mellitus, and family history were significantly associated with multivessel disease, while smoking, hypertension, and diabetes were also significantly associated with STEMI presentation. These findings are in line with previous studies (11,12), which have emphasized the role of these risk factors in determining both the extent and severity of CAD.

An important observation in the present study was the clustering of risk factors, with 88% of patients having two or more risk factors. This highlights the synergistic effect of multiple risk factors in accelerating atherosclerosis. Similar clustering has been reported in earlier studies (13,14), reinforcing the concept that premature CAD is often the result of combined metabolic and lifestyle abnormalities rather than a single etiological factor.

Despite these findings, the study has certain limitations. Being a single-center study with a relatively small sample size, the results may not be generalizable to the broader population. Additionally, non-traditional risk factors such as psychosocial stress, dietary patterns, and genetic markers were not extensively evaluated. Nevertheless, the study provides valuable insights into the clinical and risk factor profile of PCAD in young adults.

The present study demonstrates that premature coronary artery disease in young adults is strongly associated with a high burden of modifiable risk factors, particularly smoking, dyslipidemia, hypertension, diabetes, and sedentary lifestyle. The disease commonly presents as acute coronary syndrome, especially STEMI, with significant myocardial involvement and predominantly single-vessel disease, particularly affecting the left anterior descending artery. Risk factor clustering plays a crucial role in disease severity and clinical presentation. Early identification and aggressive modification of these risk factors are essential to reduce the burden of premature CAD and improve long-term cardiovascular outcomes.

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