European Journal of Cardiovascular Medicine

Acute myocardial infarction is characterized by loss of contractile tissue and geometric remodeling, producing substantial impairment of both RV and LV systolic and diastolic functions [1]. Acute left ventricular myocardial infarction (LVMI) initiates a cascade of hemodynamic and mechanical changes that can compromise right ventricular (RV) performance even when the RV coronary territory is not directly infarct-related. The RV is a pyramidal chamber composed of the free wall and interventricular septum; its systolic function relies on longitudinal shortening of the RV free wall in a peristaltic wave from apex to outflow tract, with additional contribution from septal contraction [2]. Compared with the left ventricle (LV), the RV free wall is thinner, generates lower pressures, and has more favorable oxygen supply–demand characteristics owing to rich collateralization from the left coronary system and perfusion that extends into both systole and diastole in the absence of hypertrophy. These features render the RV relatively resistant to ischemia compared with the LV, so overt RV infarction during isolated left coronary occlusion is less common; nonetheless, clinically meaningful RV dysfunction can still occur in the setting of LVMI through multiple indirect mechanisms [3].

A central mechanism is ventricular interdependence: the two ventricles share circumferential myocardial fibers, a common septum, and a constraining pericardium, such that alterations in LV geometry, loading conditions, or septal mechanics are transmitted to the RV [4,5]. Consistent with this, RV dysfunction may be primary (intrinsic RV myocardial abnormality) or secondary to LV dysfunction as a consequence of ventricular interdependence [6]. In acute LVMI, elevated LV filling pressures, ischemic or stunned septal segments, and pericardial constraint can shift the septum toward the RV, increase RV afterload via secondary pulmonary hypertension, and blunt RV longitudinal shortening—all culminating in impaired RV systolic and diastolic function [7]. RV involvement after acute LV MI is associated with higher morbidity and mortality [3]. Moreover, RV function is a significant predictor of clinical outcomes in LV AMI, and RV involvement may occur in a subset of anterior wall MI (AWMI) patients, increasing in-hospital mortality [8].

Echocardiography remains the first-line modality for bedside assessment of RV function in the acute setting because it is widely available, repeatable, and provides complementary geometric and tissue-level information despite the RV’s complex, asymmetric shape [9]. In particular, two-dimensional echocardiography is an essential component of clinical assessment across cardiac disorders, including AMI [5]. A pragmatic multiparametric approach combines conventional and tissue Doppler indices—such as RV end-diastolic diameter (RVEDD), tricuspid annular plane systolic excursion (TAPSE), fractional area change (FAC), tricuspid annular systolic velocity (S′), RV E/E′ for filling pressures, and the myocardial performance index (MPI/Tei index)—to profile RV systolic–diastolic performance and global function.

Notwithstanding available recommendations, there remains a knowledge–practice gap between guideline statements and real-world RV assessment. Therefore, we aimed to conduct a hospital-based observational study evaluating RV function in acute LV MI using echocardiography. Within this context, the present study focuses specifically on patients with acute LVMI and seeks to delineate the prevalence, severity, and clinical correlates of RV dysfunction using echocardiography, leveraging the pathophysiological framework of ventricular interdependence and its prognostic implications in acute infarction.

After approval from institutional ethical committee, this observational, cross-sectional study was conducted in the Department of General Medicine at Sri Aurobindo Medical College and Post-Graduate Institute (SAIMS), Indore. 50 Consecutive patients of either sex presenting for the first time with acute ST-elevation myocardial infarction (STEMI) were screened in the General Medicine services. Patients who met eligibility criteria were approached, the study purpose and procedures were explained in a language they understood, and written informed consent was obtained.

Inclusion criteria: First presentation of acute STEMI with willingness to provide informed consent.

Exclusion criteria: Evidence of any associated right ventricular (RV) infarction on electrocardiogram (ECG) and echocardiography; atrial fibrillation or flutter, bundle branch block, or other intraventricular conduction delays; prior myocardial infarction; or prior coronary artery bypass graft (CABG) surgery.

Sample size

A total of 50 patients were included. The a priori minimum sample size was derived assuming a mean RV end-diastolic dimension index of 12.7 with a standard deviation of 7 (from prior literature), using a one-sample t-test framework (effect size 0.39), 80% power, and two-sided α = 0.05 in G*Power. This yielded 43 subjects; allowing for anticipated non-participation, a target enrollment of ~50 was set.

Procedures

Demographic details (age, sex) and comorbidities (hypertension, diabetes mellitus, smoking status, and obesity) were recorded. All enrolled patients underwent a 12-lead ECG, measurement of cardiac biomarkers (Troponin I/T and CK-MB), and transthoracic echocardiography at presentation. Echocardiography was used to assess RV structure and function. The following parameters were measured: right atrial (RA) size; right ventricular (RV) size; tricuspid annular plane systolic excursion (TAPSE) as a marker of RV systolic function; presence and grade of tricuspid regurgitation (TR); indices of pulmonary artery hypertension (PAH) derived from TR velocity where applicable; and inferior vena cava (IVC) diameter and collapsibility.

Statistical analysis

Clinical and echocardiographic data were captured prospectively on a structured proforma, and master charts were prepared in Microsoft Excel. Statistical analyses were performed using SPSS version 25.0. Descriptive statistics summarized baseline characteristics (mean ± SD or median [range] for continuous variables; counts and percentages for categorical variables). Normality of continuous variables was assessed before inferential testing. Between-group comparisons used Student’s t-test for normally distributed data; associations between categorical variables used Chi-square or Fisher’s exact tests as appropriate. Correlations between continuous variables were examined using correlation coefficients. Two-sided p < 0.05 was considered statistically significant.

A total of 50 consecutive, first-presentation STEMI patients were enrolled. The mean age was 56.0 ± 12.7 years (range 19–84), with the largest proportion in the 51–60-year band (30%). Males comprised 62%, yielding a male:female ratio of ~1.6:1; men outnumbered women in both age strata (<50 and ≥50 years), reflecting the known male predominance in premature and established coronary disease. Chest pain was the commonest presenting symptom (68%), followed by breathlessness (28%) and diaphoresis (24%). Cardiometabolic risk was substantial: dyslipidemia (68%) and diabetes (62%) were most frequent, with nearly half having hypertension (48%); Obesity (46%); History of CAD (44%); tobacco (42%) and alcohol use (32%) were also prevalent. On examination, tachycardia (40%) and systolic hypotension <100 mmHg (32%) were the most common abnormal signs, consistent with heightened sympathetic drive and hemodynamic compromise in acute infarction.

Table 1. Baseline and demographic characteristics (N = 50)

* BP: blood pressure; JVP: jugular venous pressure.

ECG territory and biomarkers: Electrocardiography localized the infarct to the left-coronary (anterior/anteroseptal/high-lateral/anterolateral/extensive anterior) territory in 34 patients (68%), constituting the primary acute LVMI cohort for this study’s objective, while 16 patients (32%) had isolated inferior-wall MI (IWMI) and were analyzed secondarily for context. Within the LVMI cohort, distribution favored anteroseptal and anterolateral patterns, in keeping with proximal LAD involvement that is classically associated with larger ischemic burden and septal dysfunction. Cardiac biomarkers were obtained in all; Troponin-T was positive in 60% (30/50), and mean CPK 104 (lab units) with higher values in AWMI than IWMI.

Echocardiographic assessment focused on right-sided structure and systolic performance. Across the entire cohort, TAPSE values were widely distributed; within the LVMI cohort, the mean TAPSE was 17.8 ± 4.6 mm, and 41.2% met the a-priori criterion for RV systolic dysfunction (TAPSE ≤ 18 mm). Clinically, this indicates that four in ten patients with acute left-territory MI exhibited measurable impairment of RV longitudinal shortening at presentation—supporting the concept of ventricular interdependence, whereby septal injury, altered LV geometry, raised left-sided filling pressures, and pericardial constraint propagate dysfunction to the RV. [Table 2]

Table 2. ECG territory and RV systolic function distribution (N = 50)

*TAPSE: tricuspid annular plane systolic excursion.

Echocardiography at presentation and discharge: Right-sided indices showed a high burden of dysfunction at presentation with partial recovery by discharge (mean hospital stay ~±5 days). At presentation, TAPSE <17 mm in 58%, FAC <35% in 42%, E/E′ >6 in 54%, RV-MPI >0.55 in 60%, and LVEF <50% in 78%. At discharge, abnormalities persisted in a sizable minority. [Table 3]

Table 3. Echocardiographic parameters at presentation and discharge (N=50)

*RVEDD: RV end-diastolic diameter; TAPSE: tricuspid annular plane systolic excursion; FAC: fractional area change; RV-MPI: RV myocardial performance index; LVEF: LV ejection fraction.

Territory-wise RV function (AWMI vs IWMI): Across indices, AWMI patients had more frequent RV abnormalities both at presentation and at discharge. [Table 4]

Table 4. Echo abnormalities by territory, presentation vs discharge (AWMI n=34; IWMI n=16)

Haemodynamics, TAPSE distribution, and length-of-stay by territory: Hemodynamics and utilization differed by infarct territory. LVMI (AWMI) patients were more often tachycardic, had lower mean TAPSE, and experienced a longer hospital stay than IWMI (LVMI 9.5 ± 4.7 vs IWMI 6.6 ± 4.7 days). These differences were statistically and clinically meaningful, suggesting larger ischemic burden, septal dysfunction, and diminished RV reserve in anterior events [Table 5].

Table 5. Heart rate, TAPSE, and hospital stay by infarct location

AWMI: anterior-wall MI (LVMI); IWMI: inferior-wall MI.

Treatment strategies and angiography: Definitive revascularization predominated: thrombolysis → PCI (54%) and primary PCI (24%); thrombolysis-only (18%) and CABG (4%) were less common. Patients discharged after thrombolysis-only showed the least improvement in RV indices at discharge. [Table 6]

Table 6. Treatment strategy (N=50)

Angiography showed LAD predominance in AWMI and RCA predominance in IWMI; multivessel disease was frequent. [Table 7]

Table 7. Coronary angiography summary (N=50)

LAD: left anterior descending; RCA: right coronary artery; LCX: left circumflex; DVD: double-vessel disease; TVD: triple-vessel disease.

In-hospital outcomes: Adverse outcomes underscored the prognostic value of RV function in acute LVMI. Within LVMI, MACE occurred in ~29%, heart failure in ~24%, and all-cause mortality in ~18%. Stratification by RV systolic function across the entire cohort revealed a clear gradient: TAPSE ≤ 18 mm tracked with higher mortality and MACE, as well as more heart-failure and recurrent MI events, identifying a readily obtainable bedside marker for high-risk phenotype in acute LVMI [Tables 8-9]

Table 8. Adverse events by infarct location (LVMI vs IWMI)

*MI: myocardial infarction; MACE: major adverse cardiac events. Multiple events could occur in the same patient.

Table 9. Adverse events by RV systolic function (entire cohort, N = 50)

*Abbreviations: LVMI, left-ventricular myocardial infarction; AWMI, anterior-wall MI; IWMI, inferior-wall MI; TAPSE, tricuspid annular plane systolic excursion; BP, blood pressure; JVP, jugular venous pressure; ECG, electrocardiography

In this single-centre cohort of first-presentation STEMI, we specifically evaluated right-ventricular (RV) function in the context of acute left-ventricular myocardial infarction (LVMI) and found that RV systolic impairment is both common and clinically meaningful. Among patients with LV territory infarction, the mean TAPSE was 17.8 ± 4.6 mm, and ~41% met the a-priori threshold for RV systolic dysfunction (TAPSE ≤18 mm). Clinically, this indicates that nearly four in ten patients with acute LVMI exhibit impaired RV longitudinal mechanics at presentation—supporting the paradigm of ventricular interdependence in which septal injury, altered LV geometry and loading, and pericardial constraint can propagate dysfunction to the RV.

Baseline demographics mirrored the Indian AMI phenotype. The mean age was 56 years, with the largest proportion in the 51–60-year band, and men comprised 62% of the cohort. This age–sex distribution, together with the high prevalence of dyslipidaemia and diabetes, aligns with prior Indian data showing earlier CAD onset and a heavier cardiometabolic burden [2,10,11]. Lifestyle factors (tobacco, alcohol) likely contribute to the excess risk in men <50 years, while hormonal protection may partially account for lower event rates among premenopausal women.

Comprehensive echocardiography showed a high burden of RV abnormality at presentation—TAPSE < 17 mm in 58%, FAC < 35% in 42%, E/E′ > 6 in 54%, RV-MPI > 0.55 in 60%, alongside LVEF < 50% in 78%. By discharge (mean ~5 days), indices improved but remained abnormal in a sizable minority: TAPSE < 17 mm in 44%, FAC < 35% in 40%, E/E′ > 6 in 38%, RV-MPI > 0.55 in 52%, and LVEF < 50% in 64%. The pattern suggests early, partial recovery of both RV systolic (TAPSE/FAC) and diastolic (E/E′) function, while global RV performance (MPI) lagged—plausibly reflecting persistent afterload and ongoing septal stunning in the early convalescent phase.

Territorial patterns were informative. Anterior/LV territory MI (AWMI) constituted 68% of presentations and was associated with lower TAPSE and longer hospitalizations than inferior-wall MI (IWMI) (mean 9.5 vs 6.6 days). The greater RV impairment in AWMI—traditionally less emphasized than RV dysfunction in IWMI—likely reflects septal involvement, adverse LV–RV interactions, and secondary increases in RV afterload. Our observation that RV dysfunction was more frequent and more severe in AWMI echoes Aher et al. [12], whereas Abdelsabour et al. reported higher RV impairment with IWMI—differences plausibly explained by inclusion of concomitant RV infarction in some series [13].

Revascularization was achieved in most patients (thrombolysis→PCI 54%, primary PCI 24%, CABG 4%). Those discharged after thrombolysis-only (18%) exhibited the least improvement in RV indices, consistent with the concept that definitive reperfusion facilitates early RV recovery via improved septal mechanics and reduced RV afterload. Angiographically, LAD predominated in AWMI and RCA in IWMI; multivessel disease was frequent—findings that parallel the greater residual RV-MPI abnormality and longer hospitalization seen in the cohort.

Prognostically, lower TAPSE identified a high-risk phenotype across the full cohort. Patients with TAPSE ≤18 mm experienced higher all-cause mortality (27.8% vs 6.3%) and greater MACE (38.9% vs 12.5%) than those with TAPSE >18 mm, with parallel excesses in heart failure and recurrent MI. Within the LVMI subset, adverse events were also frequent (MACE ~29%; mortality ~18%), and numerically higher than in IWMI. These gradients are consistent with prior reports linking depressed TAPSE to worse outcomes in AMI (e.g., Schmid et al.) and with data showing poorer short-term prognosis in AWMI compared with IWMI (Stone et al., Aher et al.) [14,15,12]. Importantly, TAPSE is rapid, reproducible, and bedside-available, making it a practical anchor for risk stratification when more advanced techniques are not immediately accessible.

From a systems perspective, resource utilization tracked with RV function: patients with reduced TAPSE were disproportionately represented among those staying >10 days, whereas most with preserved TAPSE were discharged within 10 days. This convergence of physiology, outcomes, and utilization supports routine incorporation of RV assessment—at minimum TAPSE, and where feasible tissue Doppler indices or RV strain—into the acute LVMI echo protocol to refine triage, monitoring intensity, and early post-AMI planning.

Our study has limitations. It was cross-sectional, single-centre, and modest in size (N=50), which may limit power for subgroup analyses and inflates imprecision around some estimates. RV function was indexed primarily by TAPSE; while robust for longitudinal systolic motion, it does not fully capture complex RV geometry or diastolic performance. We did not include systematic tissue Doppler/strain or cardiac MRI—the reference standard for RV volumes and ejection fraction. Finally, we lacked longitudinal follow-up to assess rehospitalization and longer-term mortality. Future multicentre studies with larger samples, comprehensive RV phenotyping (TDI/strain/MRI), standardized reperfusion details, and prospective follow-up are warranted.

Clinical takeaway In acute LVMI, RV dysfunction is frequent at presentation, only partially resolves by discharge, and powerfully stratifies in-hospital risk. Incorporating a multiparametric RV echo bundle (TAPSE, FAC, E/E′, RV-MPI) into the acute LVMI protocol yields actionable, bedside risk information that can guide revascularization urgency, level of care, and discharge planning.

In this single-centre cohort of first-presentation ST-elevation myocardial infarction centred on acute left-ventricular infarction, right-ventricular dysfunction was prevalent at admission and only partly reversible by discharge. A multiparametric echocardiographic approach demonstrated impairment of longitudinal systolic mechanics, global performance, and diastolic filling, with residual abnormalities despite clinical stabilisation. Anterior (left-territory) infarction predominated and was associated with more pronounced right-ventricular dysfunction and longer hospitalisation than inferior infarction, consistent with septal involvement and adverse LV–RV interaction. Reduced tricuspid annular plane systolic excursion delineated a clinically high-risk phenotype and provides a rapid, reproducible anchor for bedside risk stratification when advanced imaging is unavailable. Definitive revascularisation appeared to favour early recovery of right-ventricular indices, whereas thrombolysis alone yielded minimal improvement. These findings support routine, early, and repeated right-ventricular assessment in acute left-ventricular infarction to guide triage, monitoring intensity, revascularisation strategy, and post-discharge follow-up.

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