Acute coronary syndrome (ACS) refers to a group of conditions characterized by a sudden reduction in blood flow to the heart. The most common cause is the rupture of an atherosclerotic plaque, followed by thrombosis in the coronary arteries. [1] Clinical presentations of ACS include unstable angina, ST-elevation myocardial infarction (STEMI), and non-ST-elevation myocardial infarction (NSTEMI). Early detection and treatment are critical due to the high morbidity and mortality rates associated with ACS. [2, 3]

ACS remains a leading cause of cardiovascular mortality and hospitalization worldwide. While advancements in biomarker research have improved diagnostics, there remains a need for simple, rapid, and sensitive tools, particularly in settings lacking advanced technology. [4] According to the WHO, cardiovascular diseases, including ACS, are responsible for nearly one-third of global deaths, with ischemic heart disease as the predominant cause. ACS-related hospital admissions are high in both developed and developing countries, with rising cases in low- and middle-income nations due to aging populations and lifestyle changes. [5, 6, 7]

ACS risk factors are well-established and include modifiable elements like diabetes mellitus, obesity, hypertension, hyperlipidemia, and smoking. [8, 9] These factors contribute to plaque instability and arterial damage. Non-modifiable risk factors include age, male sex, and family history of cardiovascular disease. The combination of multiple risk factors significantly increases the risk of ACS, emphasizing the need for effective diagnostic strategies. [10, 11]

Diagnosis of ACS relies on clinical assessment, ECG, and biomarkers. Symptoms such as chest pain, dyspnea, and radiating discomfort are common but not specific. A 12-lead ECG identifies changes like ST-segment elevation or depression but may not be conclusive in all cases. [12] Cardiac troponins (T and I) are the gold standard biomarkers for detecting myocardial injury. They are more sensitive than traditional markers, such as CK-MB. Troponin levels are measured at presentation and serially to assess changes indicative of acute myocardial damage. [13, 14]

Cardiac troponin I (cTnI), a heart-specific protein, regulates muscle contraction and rises within 3–6 hours post-injury, peaking at 12–24 hours, and remains elevated for 7–10 days. Despite its sensitivity and specificity, troponin I reflects myocardial injury rather than plaque instability. [15] Consequently, researchers are exploring additional biomarkers, including hematological indicators like mean platelet volume (MPV) and neutrophil-to-lymphocyte ratio (NLR), which reflect thrombotic and inflammatory activity. [16]

Platelet Distribution Width (PDW) indicates variability in platelet size and serves as a marker of platelet activity. Elevated PDW suggests the presence of larger, more reactive platelets, which release prothrombotic substances after plaque rupture. Studies report higher PDW in ACS patients, suggesting its role in identifying thrombotic activity. [17, 18]

However, PDW is less specific than troponin I for myocardial damage. While troponin I directly indicates cell necrosis, PDW reflects thrombotic risk. Despite lower sensitivity, PDW may still provide clinical value as an adjunct marker in ACS diagnosis. [19, 20] In patients with borderline or intermediate troponin levels, elevated PDW may help identify heightened thrombotic burden, aiding in risk assessment and prognosis. [21]

Even with improved ACS diagnostics, there remains a need for accessible, cost-effective tools for early detection, especially in resource-limited settings. Troponin I, while sensitive, may not be universally available and does not reflect thrombotic activity. [22] PDW, available through routine CBC, offers a practical option for initial screening. Evaluating PDW's diagnostic value could enhance early identification of high-risk ACS patients. [23] This study aimed to assess the diagnostic utility of PDW in comparison to troponin I in ACS patients, exploring PDW as an additional biomarker for better diagnosis and risk stratification.

This cross-sectional observational study was conducted in the Department of Pathology at Bharati Vidyapeeth (Deemed to Be University) Medical College, Hospital, and Research Centre, Pune, over a period of 18 months. The study population comprised patients presenting with chest pain and clinically suspected of having ACS. Based on the inclusion and exclusion criteria, a total of 121 patients were enrolled. Patients already on antiplatelet therapy, those with peripheral arterial disease, vasculitis, deep vein thrombosis, prosthetic heart valves, or incomplete records were excluded from the study.

Upon presentation to the emergency department with chest pain suggestive of ACS, blood samples were collected in EDTA vacutainers and sent to the hospital's central clinical laboratory. Complete blood counts, including platelet indices, were analysed using the Beckman Coulter DxH 900 and DxH 800 analyzers. Simultaneously, clinical information, cardiac marker findings, and final diagnoses were documented from the patient's medical records, which were maintained in the cardiology department.

PDW was analysed from the collected samples. Patients with chest pain who tested positive for Troponin I were categorized under the ACS group. Those with negative Troponin I results were grouped under non-ACS. The PDW values were compared between the ACS and non-ACS groups, with specific attention to Troponin I levels measured at zero- and six-hours post-admission.

Data analysis was performed using SPSS version 25.0. Descriptive statistics, such as the mean and standard deviation (Mean ± SD), were calculated for quantitative variables. Associations among categorical variables were assessed using the Chi-square test, while the unpaired t-test was employed for comparing continuous variables between two groups. ANOVA was applied where appropriate. Receiver Operating Characteristic (ROC) curve analysis was performed to assess the diagnostic performance of PDW in predicting ACS. The area under the curve (AUC), sensitivity, specificity, and optimal cut-off values were calculated to evaluate the discriminative ability of PDW as a biomarker for ACS. A p-value of less than 0.05 was considered statistically significant.

The present study included 152 participants with a mean age of 54.76 ± 12.20 years, ranging from 25 to 95 years. There was a male predominance, with 63.2% males and 36.8% females. Among the total, 113 patients (74.3%) were diagnosed with ACS, while 39 patients (25.7%) were categorized as having non-ACS chest pain. The mean PDW in the entire cohort was 16.76 ± 0.62 fl, and Troponin I levels showed an increasing trend from admission (0 hours; mean = 0.84 ± 2.16 ng/mL) to 6 hours (mean = 1.14 ± 2.73 ng/mL), reflecting the dynamic release pattern of cardiac biomarkers.

Table 1: Descriptive Statistics for PDW and Troponin I Levels

Correlation analysis revealed a statistically significant but modest positive correlation between PDW and Troponin I at 0 hours (r = 0.209, p = 0.0099), while the correlation at 6 hours was not statistically significant (r = 0.154, p = 0.0589). (Table2) ROC curve analysis demonstrated the diagnostic utility of PDW in predicting ACS, with an area under the curve (AUC) of 0.743 (95% CI: 0.661–0.825) at 0 hours and 0.797 (95% CI: 0.715–0.878) at 6 hours, both statistically significant (p = 0.0001).

Table 2: Correlation between PDW and Troponin I Levels

At a PDW cut-off of 16.250 fl (0 hours), sensitivity and specificity were 94.6% and 45%, respectively. At 6 hours, a cut-off of 16.150 fl yielded a sensitivity of 97.2% and specificity of 52.2%, highlighting the potential of PDW as a highly sensitive, though moderately specific, diagnostic tool. (Table 3)

Table 3: Area under the Curve (AUC) for Troponin I Levels

When comparing the ACS and non-ACS groups, PDW levels were significantly elevated in the ACS group (16.94 ± 0.52 fl) compared to the non-ACS group (16.24 ± 0.57 fl, p < 0.0001). Similarly, Troponin I levels were significantly higher in ACS patients at both 0 hours (1.12 ± 2.43 ng/mL vs. 0.01 ± 0.01 ng/mL, p = 0.0050) and 6 hours (1.52 ± 3.06 ng/mL vs. 0.02 ± 0.01 ng/mL, p = 0.0027), confirming the biochemical distinction between the two groups. These findings support the clinical value of PDW as a supplementary marker alongside Troponin I in the early evaluation of suspected ACS. (Table 4)

Table 4: Comparison of Hematological and Biochemical Parameters between ACS and NACS Groups

This study evaluated the diagnostic sensitivity of PDW in identifying ACS, using Troponin I as the reference standard. ACS remains a leading cause of morbidity and mortality worldwide [4], highlighting the need for early and reliable diagnostic tools. While Troponin I is the gold standard for diagnosing myocardial injury, its limitations in specificity and early detection [13] support the investigation of additional markers such as PDW.

Platelet activation, central to the pathophysiology of ACS, is reflected in PDW, which measures the variability in platelet size. [18] This study investigated the relationship between PDW and Troponin I levels to evaluate the value of PDW as a diagnostic adjunct. The population had a wide age range (25–95 years), with a mean of 54.76 years, aligning with the known age distribution of ACS. Male predominance (63.2%) was also consistent with the higher ACS risk in men. Among 152 participants, 74.3% were diagnosed with ACS, supporting the study's focus on high-risk individuals.

In the present study, PDW was significantly higher in ACS patients (16.94 ± 0.52) compared to non-ACS patients (16.24 ± 0.57; p < 0.0001), indicating its potential to reflect platelet activation. Troponin I was also significantly elevated in the ACS group at both 0 and 6 hours (p = 0.0050 and 0.0027, respectively). These findings confirm the role of Troponin I in detecting myocardial injury, while PDW appears to complement this by indicating thrombotic activity. [15, 18]

Our findings align with previous studies. Alvitigala et al. [24] reported higher PDW in STEMI patients, while Krishnan et al. [20] and Costa et al. [25] also found elevated PDW in ACS, reinforcing its diagnostic relevance. Although Costa et al. [25] observed a decreased platelet count in ACS patients. Pervin S [26] et al likewise reported significantly higher PDW in ACS (16.23 ± 2.56) than non-ACS (11.89 ± 1.42), consistent with our results. We also observed a weak positive correlation between PDW and Troponin I at 0 hours (r = 0.209, p = 0.0099), but not at 6 hours, suggesting PDW may be more useful early in the clinical course.

Other studies offer further support. Dehghani MR [27] et al. reported significantly elevated PDW in myocardial infarction, while Daimay A [28] et al. noted higher PDW and P-LCR in ACS, findings similar to ours. Putri M [19] et al. found a strong correlation between PDW and Troponin I (r² = 0.713, p < 0.001), although our study found a weaker association, possibly due to differences in design or population. Manchanda J [29] et al. also confirmed elevated PDW in ACS, whereas Chowdekar VS [30] et al. did not find significant differences in PDW, highlighting the variability in findings across studies.

The diagnostic performance of PDW was further supported by ROC curve analysis. PDW showed AUC values of 0.743 at 0 hours and 0.797 at 6 hours (p = 0.0001), indicating fair diagnostic accuracy. At a cut-off of 16.250 fl, PDW had a sensitivity of 94.6% and a specificity of 45% at 0 hours; at 6 hours, a cut-off of 16.150 fl yielded a sensitivity of 97.2% and a specificity of 52.2%. These high sensitivities suggest PDW is a valuable early marker, though its modest specificity limits its use as a standalone test.

Compared to Alvitigala et al. [24], who reported a lower AUC for PDW (0.620), our results suggest better diagnostic utility. Similarly, Pervin S [26] et al showed an AUC of 0.846 with 94.3% sensitivity and 52.8% specificity, echoing our findings. Differences in AUC, cut-offs, and diagnostic accuracy across studies may reflect variations in methodology, sample size, and patient profiles.

In conclusion, PDW is significantly elevated in ACS and may serve as a helpful adjunct to Troponin I, especially in resource-limited settings. Though not a replacement for Troponin I, its high sensitivity and ease of access through routine CBC testing make it a promising addition to the diagnostic toolkit. Further large-scale studies are warranted to validate these findings and to explore the role of PDW in clinical decision-making.

PDW is significantly elevated in ACS and demonstrates high sensitivity as an adjunct diagnostic marker. It may be valuable in early ACS assessment, especially where Troponin I testing is limited.

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