Introduction

Acute myocardial infarction (AMI) remains one of the leading causes of morbidity and mortality worldwide, despite considerable advances in diagnosis and reperfusion therapy [1].  Among all forms of AMI, anterior myocardial infarction occupies a unique and grave position due to its extensive myocardial involvement and higher risk of fatal arrhythmias, heart failure, and cardiogenic shock.

The anterior wall is primarily supplied by the left anterior descending (LAD) artery, and obstruction of this artery especially proximal occlusions often results in large infarct size with significant left ventricular dysfunction. Consequently, early risk stratification and the identification of reliable prognostic indicators are essential for optimizing clinical management and improving outcomes [2].

Electrocardiography (ECG) remains the cornerstone of initial assessment in patients presenting with chest pain. Despite the availability of advanced imaging modalities such as coronary angiography, echocardiography, cardiac MRI, and computed tomography, ECG maintains its irreplaceable role as a rapid, non‑invasive, and cost‑effective tool that provides immediate insight into ischemic burden and electrophysiological alterations [3]. Traditionally, ST‑segment elevation has served as the hallmark for diagnosing acute transmural ischemia, whereas other ECG parameters including Q waves, T‑wave inversion, and various conduction times offer valuable prognostic information. In recent years, attention has increasingly turned to the P‑wave, representing atrial depolarization, as a subtle yet clinically meaningful reflection of cardiovascular health. Alterations in P‑wave morphology and duration can mirror underlying atrial electrical remodeling influenced by ventricular dysfunction, ischemia, or autonomic imbalance [4].

The P‑wave peak time (PWPT) defined as the interval from the onset of the P‑wave to its peak amplitude has emerged as a sensitive measure of intra‑atrial conduction. It reflects both the integrity of atrial tissue and the downstream effects of ventricular pathology on atrial electrical activation. Prolonged P‑wave peak time has been associated with left atrial enlargement, increased atrial pressure, and delayed inter‑atrial conduction, conditions frequently encountered in patients with coronary artery disease and left ventricular systolic dysfunction [5]. In the context of acute anterior myocardial infarction, where left ventricular impairment and ischemic stress are prominent, PWPT may serve as a surrogate indicator of hemodynamic burden and the extent of myocardial damage. Because atrial and ventricular electrical activities are interlinked via mechanical and neurohumoral pathways, changes in PWPT could parallel the severity of coronary involvement [6].

Coronary artery disease (CAD) typically progresses through a complex sequence of endothelial injury, lipid accumulation, and inflammatory infiltration, ultimately leading to luminal narrowing and plaque rupture. The number of occluded or significantly stenotic vessels provides a direct measure of disease severity. Patients with multivessel involvement experience higher rates of adverse clinical events, including recurrent ischemia, arrhythmia, and mortality, compared to those with single‑vessel disease [7]. Understanding the relationship between electrocardiographic markers and angiographic findings, therefore, remains crucial for both prognostication and treatment planning. Several studies have proposed ECG‑based indices such as fragmented QRS, QT dispersion, and signal‑averaged P‑wave duration to indirectly reflect coronary severity. However, differences in P‑wave peak time across ECG leads, particularly in anterior infarction, have not yet been fully explored as an indicator of multivessel disease burden [8].

Mechanistically, anterior infarction can induce regional left atrial strain and changes in conduction velocity. Ischemic dysfunction of the interventricular septum, which contributes to both atrial and ventricular depolarization pathways, may prolong PWPT by delaying the electrical impulse propagation through remodeled atrial fibers. Furthermore, sympathetic activation and elevated afterload secondary to ventricular dysfunction increase atrial wall tension and slow conduction, resulting in more pronounced PWPT differences between leads representing right and left atrial activation (e.g., leads I, II, V1) [9]. This suggests that P‑wave peak time difference defined as the maximal variation in PWPT among different leads may serve as a global reflection of cardiovascular stress induced by severe coronary involvement.

Clinically, identifying a robust ECG parameter that correlates with angiographic severity could provide significant advantages. Coronary angiography remains the gold standard for evaluating vessel involvement; however, it is invasive, costly, and not suitable for immediate risk stratification in all settings, particularly in resource‑limited environments. If PWPT difference reliably reflects multivessel disease, clinicians could potentially use it as a rapid screening tool to estimate coronary burden and predict adverse outcomes even before angiographic confirmation [10]. This approach aligns with the current trend toward integrating simple bedside indices such as the Modified Shock Index, QT dispersion, and P‑wave parameters into early prognostic algorithms for acute coronary syndromes.

Previous investigations examining atrial conduction parameters in AMI patients have provided valuable context. Several studies have linked increased P‑wave dispersion and prolonged total P‑wave duration with poor left ventricular function, higher Killip class, and long‑term arrhythmic complications, particularly atrial fibrillation [11]. Nevertheless, few have focused on the P‑wave peak time difference as a quantitative measure directly associated with the anatomical extent of coronary artery involvement. Given that the anterior wall infarction poses a distinct pattern of ischemic stress on both the left ventricle and adjacent atrial myocardium, this subset of patients constitutes an ideal model for investigating electro‑mechanical coupling between atrial conduction and coronary pathology [12].

Moreover, the P‑wave physiology offers unique insight into how electrical conduction interacts with vascular pathology. Ischemia modulates ion channel activity, intracellular calcium handling, and autonomic tone all of which influence atrial depolarization timing. In the acute phase of myocardial infarction, neurohumoral activation through catecholamines and inflammatory cytokines can alter atrial refractoriness and variability of PWPT across leads. Multivessel disease, by expanding the ischemic territory, further intensifies these electrophysiological changes, suggesting a potential dose–response relationship between coronary burden and PWPT variation [13]. This hypothesis aligns with clinical observations associating extensive CAD with more profound ECG alterations not only in the ST segment or QRS complex but also within atrial conduction parameters.

From a pathophysiological standpoint, one can surmise that the atrial electrical delay seen in patients with multivessel disease derives from a combination of structural and functional disturbances. Structural remodeling, including myocyte degeneration and interstitial fibrosis secondary to ischemic hemodynamic stress, directly impedes conduction velocity. Functional contributors, such as elevated left atrial pressure and reduced coronary perfusion reserve, further exacerbate the delay, manifesting as increased PWPT difference between leads. These processes reflect a systemic continuation of ischemic heart disease rather than isolated ventricular pathology, reinforcing the conceptual view that the atrium operates as an early mirror of global cardiac function [14].

Assessing the diagnostic and prognostic value of PWPT difference, therefore, carries both practical and theoretical implications. Practically, it promises an easily obtainable ECG‑based metric that could complement existing clinical scores. Theoretically, it underscores the interconnected nature of atrial‑ventricular electrophysiology and broadens the scope of electrocardiographic interpretation beyond traditional ST and QRS parameters. In the modern era of personalized cardiovascular medicine, integrated indices such as PWPT difference may support rapid triage, guide therapeutic urgency, and even predict long‑term outcomes if validated in larger cohorts [15].

Despite such promise, empirical evidence remains limited, and systematic investigations focusing precisely on anterior myocardial infarction are scarce. Previous literature often grouped various infarct localizations together, potentially obscuring subtle differences in conduction behavior specific to the anterior wall. Moreover, few studies have stratified CAD severity by the number of affected vessels while directly correlating these angiographic findings with quantitative ECG measures. Hence, there is a clear need for focused analysis that isolates anterior infarction and explores how PWPT difference corresponds to multivessel involvement [16].

In this context, the present study aims to fill that knowledge gap by examining the relationship between P‑wave peak time difference and the extent of coronary artery involvement defined according to the number of diseased vessels in patients experiencing their first episode of acute anterior myocardial infarction. By integrating electrocardiographic observation with angiographic data, the study seeks to determine whether PWPT difference may serve as a reliable, non‑invasive indicator of coronary severity. The findings could enhance clinical characterization of anterior AMI, refine risk stratification protocols, and encourage a more comprehensive view of ECG interpretation encompassing both ventricular and atrial domains. Ultimately, such insights may contribute to more timely and individualized interventions in patients undergoing primary percutaneous coronary intervention (PPCI), fostering improved short‑ and long‑term cardiovascular outcomes.

Material and methods

Study Design and Setting: This descriptive cross‑sectional study was conducted at Shahid Madani Heart Hospital, a tertiary cardiovascular referral center affiliated with Tabriz University of Medical Sciences, Tabriz, Iran. Patient enrollment and data collection were carried out over a one‑year period, from the beginning to the end of the 2024. The study was designed to evaluate electrocardiographic characteristics in relation to coronary angiographic findings among patients presenting with acute anterior myocardial infarction.

Sampling: A census sampling strategy was applied, whereby all eligible patients meeting the predefined criteria during the study period were consecutively enrolled. Using this approach, a total of 82 patients were included in the final analysis. This method was chosen to minimize selection bias and to ensure comprehensive representation of the target population within the defined timeframe.

  Inclusion and Exclusion Criteria

Patients were eligible for inclusion if they were diagnosed with a first episode of acute anterior myocardial infarction, confirmed by typical clinical symptoms, characteristic electrocardiographic changes, and elevated cardiac biomarkers, and if they underwent primary percutaneous coronary intervention (PPCI) during the index hospitalization. Additional inclusion criteria were age ≥18 years, availability of a standard 12‑lead electrocardiogram recorded at admission prior to PPCI, and complete coronary angiographic data. Patients were excluded if they had a prior history of myocardial infarction, previous coronary revascularization (PCI or CABG), known atrial fibrillation or other sustained atrial arrhythmias, bundle branch block or significant intraventricular conduction delay, pacemaker rhythm, moderate to severe valvular heart disease, congenital heart disease, cardiomyopathy, electrolyte disturbances affecting ECG interpretation, or poor‑quality electrocardiographic recordings that precluded accurate P‑wave analysis.

Study Procedure: Upon admission, all patients underwent a comprehensive clinical evaluation including detailed medical history, physical examination, and assessment of cardiovascular risk factors. Standard 12‑lead electrocardiograms were recorded at rest using a uniform recording speed and calibration prior to coronary intervention. Electrocardiograms were analyzed offline by trained investigators blinded to angiographic findings, with particular attention to P‑wave morphology. The P‑wave peak time was defined as the interval from the onset of the P‑wave to its maximal amplitude, and the P‑wave peak time difference was calculated as the difference between the maximum and minimum values measured across selected leads.

Coronary angiography was performed according to standard institutional protocols via the femoral or radial approach. Angiographic images were reviewed by experienced interventional cardiologists who were blinded to electrocardiographic measurements. The severity of coronary artery disease was determined based on the number of major epicardial coronary arteries exhibiting significant luminal stenosis. Patients were subsequently categorized according to single‑vessel, two‑vessel, or three‑vessel coronary artery involvement.

All collected data, including demographic characteristics, clinical variables, ECG parameters, and angiographic findings, were systematically recorded using a structured data collection form. Data integrity was ensured through double‑checking of entries and cross‑validation with hospital medical records.

Statistical Analysis: Statistical analyses were performed using SPSS software (version XX). Continuous variables were assessed for normality and expressed as mean ± standard deviation or median with interquartile range, as appropriate, while categorical variables were presented as frequencies and percentages. Comparisons between groups based on the number of involved coronary vessels were conducted using appropriate parametric or non‑parametric tests. Correlation analyses were applied to evaluate the relationship between P‑wave peak time difference and the extent of coronary artery involvement. A p‑value <0.05 was considered statistically significant.

Ethical Considerations: The study protocol was reviewed and approved by the Ethics Committee of Tabriz University of Medical Sciences (Ethics Code: IR.TABRIZ.REC.1402.092). The study represents the first specific objective of an approved medical thesis (Thesis Number: 71463). All procedures were conducted in accordance with the principles of the Declaration of Helsinki. Written informed consent was obtained from all participants prior to enrollment, and patient confidentiality was strictly maintained throughout the study.

 Results

In this cohort of 82 patients, 52 were classified in the reflow group and 30 in the no‑reflow group. Comparison of baseline demographic, anthropometric, and hemodynamic characteristics demonstrated no statistically significant differences between the two groups with respect to age, body weight, height, body mass index, systolic and diastolic blood pressure, heart rate, or metabolic and laboratory parameters, including fasting blood glucose, serum creatinine, white blood cell count, hemoglobin, platelet count, lipid profile, and cardiac troponin I levels (all P> 0.05). Similarly, door‑to‑balloon time was comparable between groups, indicating a similar quality and timeliness of reperfusion therapy. In contrast, total ischemic time was significantly longer in patients who developed the no‑reflow phenomenon compared with those who achieved successful reflow, suggesting a greater duration of myocardial ischemia prior to intervention.

Assessment of left ventricular systolic function revealed a markedly lower left ventricular ejection fraction in the no‑reflow group than in the reflow group, highlighting a more severe degree of myocardial injury and impaired cardiac performance in these patients. Analysis of categorical variables showed no significant differences between groups in terms of sex distribution, prevalence of diabetes mellitus, smoking status, or positive family history of cardiovascular disease. Although a higher proportion of patients in the no‑reflow group had a history of hypertension, this difference did not reach statistical significance. Overall, these findings indicate that prolonged ischemic time and reduced left ventricular ejection fraction are the principal distinguishing features associated with the no‑reflow phenomenon, whereas most baseline clinical and laboratory characteristics appear to have limited discriminatory value.

Analysis of covariance demonstrated a statistically significant difference in P‑wave peak time difference between the reflow and no‑reflow groups after adjustment for baseline values. Although both groups exhibited a modest reduction in P‑wave peak time difference following intervention, patients who developed the no‑reflow phenomenon consistently showed higher values both before and after the procedure. The significant ANCOVA result (p = 0.045) indicates that the observed between‑group difference cannot be attributed solely to baseline variation, suggesting an independent association between prolonged P‑wave peak time difference and the occurrence of no‑reflow. These findings imply that atrial conduction delay, as reflected by increased P‑wave peak time difference, may be linked to microvascular dysfunction and impaired myocardial reperfusion in this patient population (table 1 and figure 1).

  Table 1. Assessment of the Association Between P‑Wave Peak Time Difference and the No‑Reflow Phenomenon Using Analysis of Covariance (ANCOVA)

Figure 1. Comparison of the Mean P‑Wave Peak Time Difference Between the Reflow and No‑Reflow Groups

This table summarizes the descriptive statistics of P‑wave peak time difference according to the extent of coronary artery involvement and the predefined PWPTD categories before and after intervention. In patients with single‑vessel disease, mean PWPTD values were comparable between categories at baseline, whereas a more pronounced reduction was observed after intervention in the higher PWPTD category. In contrast, patients with multivessel disease demonstrated relatively similar baseline PWPTD values across categories, with a tendency toward higher post‑intervention values, particularly in those with lower baseline PWPTD. Overall, these findings suggest that changes in atrial conduction timing following intervention may differ according to the extent of coronary involvement, with more favorable reductions observed in single‑vessel disease compared with multivessel disease, reflecting potential differences in myocardial and microvascular recovery (table 2).

 Table 2. Descriptive Statistics of P‑Wave Peak Time Difference in the Two Groups Before and After Intervention

Analysis of covariance demonstrated a statistically significant overall model, indicating that P‑wave peak time difference was meaningfully associated with ST‑segment resolution greater than 50%. Baseline P‑wave peak time difference emerged as a strong independent contributor to the model, accounting for a substantial proportion of the variance, as reflected by a large effect size. Importantly, ST‑segment resolution greater than 50% also showed a significant independent association with P‑wave peak time difference after adjustment for baseline values, albeit with a modest effect size. These findings suggest that improved electrical reperfusion, as evidenced by adequate ST‑segment resolution, is associated with more favorable atrial conduction characteristics, supporting a link between myocardial reperfusion quality and atrial electrical remodeling in this patient population (table 3, figure 2).

 Table 3. Association Between P‑Wave Peak Time Difference and ST‑Segment Resolution >50% in Patients

Figure 2. Comparison of the Mean P‑Wave Peak Time Difference Between Patients with Incomplete ST‑Segment Resolution (STR <50%) and Those with Complete ST‑Segment Resolution (STR ≥50%)

 Discussion