Dilated cardiomyopathy (DCM) is the most common subtype of non-ischemic cardiomyopathy and a significant contributor to heart failure worldwide, characterized by progressive left ventricular chamber dilation and systolic dysfunction in the absence of abnormal loading conditions or coronary artery disease sufficient to explain the dysfunction.¹ Epidemiological estimates place the prevalence of DCM at approximately 1 in 250 individuals globally, with considerable geographic and ethnic variation.² In South Asia, particularly in India, DCM remains underdiagnosed and often presents at advanced stages, likely due to poor healthcare access and late referral patterns.³

The clinical presentation of DCM is heterogeneous, ranging from asymptomatic left ventricular dysfunction to overt congestive heart failure, arrhythmias, and sudden cardiac death.¹ In a large Omani cohort, the presence of low LVEF and advanced New York Heart Association (NYHA) class were independently associated with poor survival, emphasizing the role of early identification and risk stratification.⁴ Ischemic cardiomyopathy remains the most prevalent subtype, particularly in older men, while idiopathic, diabetic, alcoholic, and peripartum cardiomyopathies are increasingly recognized in younger and female populations.⁵

From a diagnostic standpoint, echocardiography remains the cornerstone for confirming DCM, identifying hallmark features such as global hypokinesia, increased LV end-diastolic dimension (LVEDD), and reduced LVEF.⁶ Electrocardiographic (ECG) abnormalities such as left bundle branch block (LBBB), ventricular ectopy, and atrial fibrillation are frequently observed and carry prognostic significance.⁷ In ischemic DCM, ECG changes often precede clinical deterioration and are correlated with more severe ventricular remodeling and adverse outcomes.⁸

Genetic and environmental etiologies have both been implicated in DCM, with familial forms constituting up to 30% of cases, underscoring the importance of early screening in first-degree relatives.⁹ Furthermore, novel insights from molecular and biomarker studies have revealed shared inflammatory, metabolic, and fibrotic pathways across DCM subtypes, offering potential for targeted therapeutic interventions.¹⁰

Despite advancements, the burden of DCM remains high in low-resource settings where diagnostic tools, longitudinal care, and specialized therapies may be limited. Hence, it is essential to develop accessible, phenotype-based classification models incorporating clinical, echocardiographic, and electrocardiographic features to better identify at-risk patients and guide tailored interventions.¹¹

This study aims to evaluate the demographic, clinical, and echocardiographic profile of 150 patients with DCM, with a focus on identifying etiology-specific patterns, severity markers such as reduced LVEF, and predictive risk factors using both statistical and machine learning tools. The goal is to enhance diagnostic accuracy, prognostic assessment, and the potential for personalized therapy in DCM patients in a tertiary care setting.

Study Design and Setting

This cross-sectional observational study was conducted over a period of 18 months at Dhiraj Hospital, affiliated with S.B.K.S Medical Institute & Research Center, Vadodara. The objective was to evaluate the clinical and echocardiographic profile of patients diagnosed with dilated cardiomyopathy (DCM), including analysis of symptomatology, electrocardiographic features, structural remodeling, and underlying etiologies.

Study Population

Patients were enrolled consecutively based on defined inclusion and exclusion criteria. Inclusion criteria comprised adults (≥18 years) presenting with clinical features of heart failure and echocardiographic findings consistent with DCM, including left ventricular ejection fraction (LVEF) ≤40%, global hypokinesia, and left ventricular end-diastolic dimension (LVEDD) >58.4 mm in men and >52.2 mm in women, as per guidelines from the American Society of Echocardiography and the American Heart Association. Exclusion criteria included patients with rheumatic or congenital valvular heart disease, pericardial disease, hypertrophic or restrictive cardiomyopathy, and those unwilling to participate.

Although the sample size calculated using standard statistical formulae was 136, a total of 150 patients were included to increase study power and sensitivity.

Clinical and Physical Assessment

All enrolled patients underwent a detailed clinical evaluation, focusing on cardinal symptoms such as dyspnea, orthopnea, paroxysmal nocturnal dyspnea, chest pain, palpitations, syncope, and peripheral edema. Physical examination included assessment of jugular venous pressure, presence of hepatomegaly, third heart sound (S3), basal crepitations, and auscultation for mitral and tricuspid regurgitation murmurs. Blood pressure, pulse rate, and rhythm were also recorded to assess for hemodynamic compromise and arrhythmias.

Electrocardiographic Evaluation

A standard 12-lead electrocardiogram was performed in all patients. ECGs were evaluated for chamber hypertrophy, bundle branch blocks, and rhythm abnormalities. Left ventricular hypertrophy (LVH) was defined using the Sokolow-Lyon index (S in V1 + R in V5 or V6 >35 mm) and Cornell voltage product (S in V3 + R in aVL × QRS duration >2440 mm·ms). Right ventricular hypertrophy was assessed using right axis deviation and R:S ratio criteria in precordial and limb leads. Left bundle branch block (LBBB) was identified by a QRS duration ≥120 ms with notched R waves in lateral leads and QS/rS patterns in anterior leads. Right bundle branch block (RBBB) was diagnosed with rSR′ in V1–V2 and slurred S waves in leads I and V6. Atrial fibrillation and complete heart block were diagnosed based on classical criteria, including irregularly irregular R-R intervals and atrioventricular dissociation, respectively.

Radiological and Laboratory Assessment

A posteroanterior chest radiograph was obtained in all patients to assess cardiomegaly, pulmonary congestion, and pleural effusion. Relevant blood tests, including hemoglobin, renal function, liver function, and fasting glucose, were obtained. Additional investigations such as coronary angiography were performed when ischemic etiology was clinically suspected.

Echocardiographic Assessment

Two-dimensional transthoracic echocardiography was performed using standardized imaging protocols. Chamber dimensions, global systolic function (LVEF via Simpson’s biplane method), wall motion abnormalities, and valvular regurgitation were recorded. Diastolic function was assessed using transmitral Doppler flow patterns. DCM diagnosis required LV dilatation exceeding 2 standard deviations above normal and reduced LVEF.

Etiological Classification

Etiologies were determined through clinical, imaging, and biochemical correlation. Ischemic cardiomyopathy was diagnosed based on history of myocardial infarction or significant coronary artery stenosis (>70%). Peripartum cardiomyopathy was defined using Demakis criteria, including onset within five months postpartum, absence of prior cardiac disease, and characteristic echocardiographic findings. Diabetic and alcoholic cardiomyopathies were diagnosed in the presence of long-standing diabetes or chronic alcohol use (>80g/day for ≥5 years), respectively, with no alternate cause identified. Remaining cases were classified as idiopathic.

Demographic Characteristics

The cohort of 150 patients was predominantly male (74%), with significant gender variation by etiology: ischemic cardiomyopathy was 96.6% male, while peripartum cardiomyopathy was 76.3% female (Table 1). The overall mean age was 52.6±12.4 years, differing significantly across subtypes (p<0.001). Ischemic patients were the oldest (mean 60.7 years) and peripartum patients were the youngest (mean 38.7 years), with alcoholic (53.2 years) and diabetic (55.8 years) patients having intermediate ages.

Clinical Symptomatology and Physical Signs

Universal symptoms of decompensated heart failure—dyspnea, orthopnea, fatigue, and peripheral edema—were present across all etiologies. Chest pain showed discriminatory value, being frequent in ischemic cases (84.5%) but absent in alcoholic cardiomyopathy. Palpitations (61.3%) and abdominal pain (41.3%) were moderately prevalent. No patients experienced syncope. On examination, elevated jugular venous pressure, basal pulmonary crepitations (99.3%), hepatomegaly (98.7%), an S3 heart sound, and systolic murmurs were present in nearly every patient. Hypotension was a key sign, observed most frequently in the ischemic group (81%).

Risk Factor and Comorbidity Profiles

Risk factors clustered by etiology (p<0.001) (Table 2). Smoking was the most common risk factor (52.7%), with high rates in ischemic (87.9%) and diabetic (70%) patients. Alcohol use (30% overall) was definitive for the alcoholic subgroup (93.3%). Diabetes (17.3% overall) was present in 85% of patients with diabetic cardiomyopathy. Additional comorbidities included hypertension (24%) and hyperlipidemia (13.3%), primarily in ischemic and diabetic groups. Atrial fibrillation was found in 26.7% of patients and left bundle branch block (LBBB) in 43.3%, both concentrated in specific high-risk phenotypes.

Table 1: Baseline Clinical and Echocardiographic Characteristics by Cardiomyopathy Etiology

Data presented as mean ± standard deviation (SD) or n (%). Universal symptoms (dyspnea, orthopnea, fatigue, peripheral edema) and physical signs (elevated JVP, pulmonary rales, hepatomegaly, S3, MR/TR) were present in nearly all patients and are described in the text. Abbreviations: SBP, Systolic Blood Pressure; LVEF, Left Ventricular Ejection Fraction; LVEDD, Left Ventricular End-Diastolic Diameter; LVESD, Left Ventricular End-Systolic Diameter; LBBB, Left Bundle Branch Block.

Table 2: Statistical Comparison of Key Variables by Cardiomyopathy Etiology

This table summarizes the results of one-way ANOVA for continuous variables and Chi-square tests for categorical variables, showing only those with statistically significant differences and large effect sizes (Cramer's V > 0.5).

Table 3: Multivariable Logistic Regression Analysis for Predictors of Severe Systolic Dysfunction (LVEF <30%)

The model demonstrated excellent discrimination for predicting severe systolic dysfunction (LVEF <30%). Model Performance: Accuracy = 0.889, Precision = 1.000, Recall = 0.750, F1-score = 0.857, AUC-ROC = 0.918.

Table 4: Performance of Multinomial Logistic Regression Model for Etiology Prediction

Model performance metrics for predicting the specific cardiomyopathy etiology based on clinical and echocardiographic features. The model achieved an overall accuracy of 82.2%.

Figure 1: Left Ventricular Ejection Fraction by Cardiomyopathy Etiology

Figure 2: ROC Curve: Severe Dysfunction predication

Echocardiographic Findings

The cohort exhibited severe systolic dysfunction with a mean LVEF of 30.7±6.4%, and over half of the patients had an LVEF <30%. The ischemic group had the lowest mean LVEF (25.4%), while peripartum patients had the highest (35%) (Figure 1). Left ventricular dimensions were most enlarged in ischemic patients (LVEDD 63.3 mm, LVESD 52.7 mm), indicating advanced remodeling, whereas peripartum patients had smaller chambers (LVEDD 57.6 mm). Diastolic dysfunction was present in 76% of the cohort, most often a restrictive pattern in ischemic and diabetic cases.

Electrocardiographic Patterns

ECG abnormalities were nearly universal. ST-T segment changes were the most common finding (81.3%), predominantly in ischemic patients. LBBB was identified in 63.8% of ischemic cases. Atrial fibrillation was present in 26.7% of the cohort, most often in peripartum and valvular cardiomyopathy. ECG-diagnosed left ventricular hypertrophy (LVH) was most prevalent among alcoholic patients (66.7%).

Radiological and Laboratory Findings

Chest X-rays revealed cardiomegaly in 98.7%, pulmonary venous congestion in 89.3%, and pleural effusion in 78.7% of patients, reflecting advanced heart failure across all subtypes. Laboratory markers showed universally elevated NT-proBNP (mean 2900 pg/ml), with the highest levels in ischemic and peripartum groups. Hyponatremia was present in 41.3% of patients, and mild renal impairment was found in 32%, particularly among diabetic and ischemic subtypes.

Correlation and Association Analysis

A strong negative correlation was found between LVEF and LVEDD (r=−0.648,p<0.001). Age was negatively correlated with heart rate (r=−0.484) and positively correlated with LVESD (r=0.459). Strong binary associations were confirmed between smoking and ischemic cardiomyopathy (Φ=0.600) and hypotension and ischemia (Φ=0.594).

Predictors of Severe Systolic Dysfunction (LVEF <30%)

Multivariable logistic regression identified hypotension as the strongest predictor of severe systolic dysfunction (OR = 3.67), followed by large LVEDD (OR = 2.91), ischemic etiology (OR = 2.31), and alcohol use (OR = 1.94) (Table 3). Conversely, diabetes (OR = 0.15), chest pain (OR = 0.66), and higher heart rate (OR = 0.76) were associated with a lower risk, possibly due to earlier diagnosis or presentation. The model showed excellent discrimination (AUC = 0.918) (Figure 2, Table 4).

Our cohort analysis revealed distinct demographic and etiologic patterns, both aligning with and extending insights from global studies. The male predominance (74%), particularly in ischemic cardiomyopathy (96.6%), is consistent with the male bias identified in the SILICOFCM database.¹² Conversely, peripartum cardiomyopathy was confined almost exclusively to women (76.3%), reinforcing its gender specificity, a phenomenon also observed in the female predominance of Takotsubo syndrome.¹³ Furthermore, the younger mean age of peripartum patients (38.7 years) compared to ischemic cases (60.7 years) echoes broader epidemiological trends. For instance, a Nigerian cohort showed that dilated cardiomyopathy (DCM) primarily affected younger men, while a large Dutch study found women with hypertrophic cardiomyopathy (HCM) were diagnosed at an older age than men.^14,15

Etiologically, ischemic cardiomyopathy was the most prevalent (38.7%), corroborating trends from Western, African, Japanese, and Chinese cohorts, where it remains a leading underlying factor in men.^16,17 Notably, peripartum cardiomyopathy was co-dominant in our sample (25.3%), a rate significantly higher than in general registries, possibly reflecting regional referral patterns or heightened diagnostic awareness, an area of focus in studies on female-specific stress-induced cardiomyopathies.¹⁸ Alcoholic and diabetic cardiomyopathies, accounting for about 25% of cases, showed clear behavioral and metabolic links, with male dominance in alcoholic cases resonating with findings from European registries.¹⁹ This etiologic heterogeneity supports a shift from traditional classifications toward phenotype-based models that integrate demographics with clinical data, a perspective bolstered by clustering studies where gender and age were key differentiators.^12,20

Clinically, universal symptoms like dyspnea, orthopnea, fatigue, and peripheral edema confirmed their role as sensitive but non-specific indicators of heart failure, consistent with large DCM studies.²¹ More nuanced were the etiology-specific symptoms. Chest pain was present in 84.5% of ischemic patients but absent in those with alcoholic cardiomyopathy, a finding that aligns with research on the diagnostic overlap between ischemic cardiomyopathy and acute coronary syndrome and the subtler presentation of alcoholic cardiomyopathy.^22,23 The complete absence of syncope was notable, contrasting with pediatric cohorts where it is a key risk indicator.²⁴ The universal presence of elevated jugular venous pressure, pulmonary rales, and an S3 sound solidified their status as cardinal signs of decompensated heart failure.²⁵ Perhaps most significant was the marked hypotension in 81% of ischemic patients, a critical finding that reinforces their risk of cardiogenic shock and is a known predictor of poor outcomes.²⁶

Echocardiographic evaluation revealed a markedly reduced mean LVEF of 30.7%, with over 55% of patients having HFrEF, consistent with global DCM registries.²⁷ However, peripartum patients had a relatively preserved LVEF (35%), paralleling ESC registry data and suggesting a unique window for therapeutic recovery.²⁸ Structurally, the ischemic subgroup showed the most severe remodeling with the largest LVEDD and LVESD values, aligning with autopsy-validated studies.²⁹ On ECG, ST-T changes were the most prevalent abnormality (81.3%), echoing findings from other large cohorts.^30,31 Importantly, LBBB was significantly more common in the ischemic subgroup (63.8%), a known marker of remodeling severity and a predictor of CRT response.³¹ Alcoholic cardiomyopathy patients exhibited the highest prevalence of ECG-diagnosed LVH (66.7%), consistent with legacy studies.²³

Our analysis identified key correlates for severe LV dysfunction (LVEF <30%). A strong inverse correlation between LVEDD and LVEF (r=−0.648) confirmed that ventricular dilation itself impairs systolic function.³² The positive correlation between age and LVESD (r=0.459) highlights age as a surrogate for progressive remodeling.³³ Binary associations, such as smoking with ischemic cardiomyopathy (Phi = 0.6) and hypotension with ischemia (Phi = 0.59), reinforced established risk links.³⁴ Our logistic regression model showed that hypotension (OR = 3.67), large LVEDD (OR = 2.91), ischemic etiology (OR = 2.31), and alcohol use (OR = 1.94) significantly increased the odds of severe systolic dysfunction, consistent with prior models.³⁵ Interestingly, diabetes was protective in our model (OR = 0.15), contrasting with some PPCM studies and possibly reflecting selection bias or earlier diagnosis.³⁶

This study reinforces the heterogeneous nature of dilated cardiomyopathy, encompassing a wide spectrum of clinical presentations, structural abnormalities, and etiologic subtypes. Comprehensive profiling revealed significant associations between demographic factors, symptom burden, ECG and echocardiographic features, and disease severity. Notably, ischemic cardiomyopathy emerged as the most severe phenotype, with markedly reduced ejection fraction and high hypotension prevalence, whereas peripartum cardiomyopathy showed more favorable cardiac function, underscoring the prognostic diversity. Future studies should focus on longitudinal outcomes, inclusion of biomarker and genetic data, and validation in larger, multicentric cohorts to refine diagnostic accuracy and optimize therapeutic strategies for this complex and often underdiagnosed condition.

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