European Journal of Cardiovascular Medicine

Acute myocardial infarction (AMI) remains a leading cause of morbidity and mortality worldwide, despite advances in reperfusion therapy, pharmacological treatment, and preventive cardiology [1].

According to the World Health Organization, ischemic heart disease accounts for more than nine million deaths annually, with AMI contributing substantially to this global burden [2].

Although hospital survival rates have improved with primary percutaneous coronary intervention (PCI) and guideline-directed medical therapy, long-term sequelae such as heart failure, arrhythmias, and recurrent ischemic events persist in a large proportion of survivors [3].
Consequently, detailed evaluation of both ventricles following AMI has become crucial for risk stratification and therapeutic decision-making [4].

Historically, left ventricular (LV) dysfunction has been emphasized as the principal determinant of prognosis in AMI, primarily because LV ejection fraction (LVEF) strongly correlates with outcomes and guides therapy [5].

However, over the past three decades, there has been growing recognition that right ventricular (RV) dysfunction (RVD) also exerts profound influence on morbidity and mortality [6].

The RV was once considered a passive chamber with little clinical significance, but accumulating evidence has revealed its critical role in maintaining hemodynamic stability [7].

When the RV fails, consequences include systemic hypotension, reduced LV filling, arrhythmias, and cardiogenic shock — all of which dramatically worsen prognosis [8].

Anatomy and physiology of the right ventricle

The RV differs from the LV in its crescentic geometry, thinner free wall, and greater compliance, features that make it better suited for handling volume loads rather than pressure loads [9].

Its function is tightly coupled to pulmonary vascular resistance; even modest increases in afterload can severely compromise RV performance [10].

Because the RV depends on the interventricular septum for contractile efficiency, ischemic injury to the septum can impair both ventricles simultaneously, illustrating the principle of ventricular interdependence [11].

This anatomical and physiological distinctiveness explains why RV involvement in AMI carries unique clinical and prognostic implications [12].

Right ventricular involvement in AMI

Inferior wall myocardial infarction (IWMI), usually caused by occlusion of the right coronary artery (RCA), is the most common setting for RV infarction [13].

Between 30–50% of IWMI patients demonstrate RV involvement, either clinically or on imaging [14].

Classic features include hypotension, elevated jugular venous pressure, and clear lung fields — the so-called “Kussmaul triad” [15].

These signs reflect impaired RV filling and reduced LV preload, leading to systemic hypoperfusion [16].

Furthermore, conduction disturbances, atrioventricular block, and ventricular arrhythmias are frequent in RV infarction, compounding hemodynamic instability [17].

It was traditionally believed that RVD was restricted to IWMI, but subsequent studies have challenged this notion [18].

Autopsy findings and tissue Doppler echocardiography have demonstrated RV impairment even in anterior wall myocardial infarction (AWMI), attributed to septal ischemia and contributions from the left anterior descending (LAD) artery to the RV anterior wall [19].

Thus, both AWMI and IWMI may precipitate clinically significant RVD, albeit through different pathophysiological mechanisms [20].

Prognostic impact of RV dysfunction

Multiple investigations confirm that RVD is an independent predictor of mortality in AMI [3,4].

Zehender et al. first demonstrated that RV infarction in the context of IWMI markedly increased in-hospital mortality, regardless of LV function [5].

Later, Zornoff et al. reported that impaired RV function predicted long-term development of heart failure and death even after adjustment for LVEF [6].

The pathophysiological basis includes reduced LV preload, systemic hypotension, diminished coronary perfusion, and heightened sympathetic drive, all contributing to poor outcomes [7].

In addition to mortality, RVD is associated with higher rates of complete heart block, ventricular tachyarrhythmias, cardiogenic shock, and mechanical complications [8].

Patients with RV involvement also experience longer hospital stays, increased need for inotropic support, and worse quality of life during follow-up [9].

Taken together, these observations underscore the need for routine assessment of RV function in all STEMI patients [10].

Echocardiographic evaluation of RV function

Echocardiography is the most practical and widely available tool for bedside assessment of RV function [11].

However, evaluating the RV is technically challenging due to its complex crescentic geometry, prominent trabeculations, and retrosternal location [12].

Unlike the LV, which can be assessed reliably by volumetric indices, the RV requires multiple complementary parameters for accurate evaluation [13].

Commonly used echocardiographic indices include:

• Tricuspid annular plane systolic excursion (TAPSE): measured by M-mode in the apical four-chamber view; values <17 mm indicate systolic dysfunction [14].
• Fractional area change (FAC): calculated from RV end-diastolic and end-systolic areas in the apical four-chamber view; values <35% are abnormal [15].
• Myocardial performance index (MPI or Tei index): derived from Doppler tissue imaging, combining systolic and diastolic intervals; values >0.54 are considered abnormal [16].
• Tissue Doppler-derived systolic velocity (S′): assessed at the lateral tricuspid annulus; velocities <9.5 cm/s denote dysfunction [17].

These indices are recommended in consensus guidelines from the American Society of Echocardiography for comprehensive RV assessment [18].

Newer modalities such as three-dimensional echocardiography and RV strain imaging offer promising incremental value but are less accessible in routine clinical practice [19].

Gaps in Indian literature and rationale for present study

Most data on RV dysfunction after AMI originate from Western cohorts, with limited large-scale Indian studies [20]. Given regional differences in risk factors, coronary artery disease profiles, and healthcare delivery systems, extrapolating foreign data may be problematic [1]. Indian patients often present late, with higher prevalence of diabetes, hypertension, and dyslipidemia, factors that could influence the burden of RVD [2]. Moreover, awareness of RV involvement remains suboptimal, and many clinicians still focus predominantly on LV function [3]. Therefore, systematic echocardiographic evaluation of RV function in Indian STEMI populations is warranted to generate context-specific data [4]. The present study was designed as a prospective observational investigation to address this gap. Its primary objectives were: (1) to evaluate the prevalence and severity of RVD in AWMI, IWMI, and IWMI with RV involvement (IWMI+RVMI) using established echocardiographic parameters; (2) to correlate these findings with baseline risk factors and demographics; and (3) to assess their association with in-hospital outcomes such as arrhythmias, heart failure, complete heart block, and cardiogenic shock [5–7]. By doing so, the study aimed to enhance understanding of the prognostic role of RV function in STEMI within the Indian context and contribute evidence to guide clinical practice [8–10].

Study Design

This was a prospective, observational, hospital-based study carried out in the Department of Cardiology, S.C.B. Medical College and Hospital, Cuttack, Odisha, over a period of 12 months (October 2022 – September 2023). The design was chosen to capture real-world presentations of acute STEMI and assess right ventricular (RV) function by echocardiography in a non-interventional manner.

Study Population

The study population comprised consecutive patients presenting with acute ST-elevation myocardial infarction (STEMI) within 24 hours of symptom onset. STEMI was diagnosed using the Fourth Universal Definition of Myocardial Infarction criteria:

• Chest pain lasting >20 minutes,
• ST-segment elevation ≥1 mm in two contiguous limb leads or ≥2 mm in contiguous precordial leads, or new left bundle branch block (LBBB),
• Elevated cardiac troponin (cTnI or cTnT).

Inclusion Criteria

1. Adults aged ≥18 years.
2. First episode of STEMI (AWMI, IWMI, or IWMI + RVMI confirmed by ECG).
3. Underwent echocardiographic assessment within 48 hours of admission.
4. Provided written informed consent.

Exclusion Criteria

1. Prior history of MI, coronary revascularization (PCI or CABG).
2. Known structural heart disease (e.g., significant valvular disease, congenital lesions).
3. Chronic pulmonary hypertension or chronic lung disease causing cor pulmonale.
4. Intraventricular conduction delays or paced rhythms interfering with RV assessment.
5. Poor echocardiographic window preventing accurate RV measurements.

Sample Size

A total of 120 patients fulfilling the criteria were enrolled. They were categorized into three groups based on ECG findings:

• Group I (AWMI): 62 patients
• Group II (IWMI): 38 patients
• Group III (IWMI + RVMI): 20 patients

Data Collection

On admission, detailed clinical history and examination were performed, including cardiovascular risk factors:

• Hypertension, Diabetes Mellitus, Smoking, Dyslipidemia, Obesity, Family history of premature CAD.
  Baseline investigations included:
• Complete blood count, renal function, electrolytes, fasting blood glucose, lipid profile, and cardiac biomarkers (cTnT).
• ECG: Standard 12-lead plus right-sided leads (V3R, V4R, V5R) and posterior leads (V7–V9).
• Echocardiography: Comprehensive assessment using 2D, M-mode, and Doppler techniques.

Echocardiographic Protocol

All patients underwent echocardiography using a Philips CX50 cardiovascular ultrasound system with a 2.5–3.5 MHz transducer within 48 hours of admission. Measurements were taken in accordance with the 2015 American Society of Echocardiography (ASE) guidelines.

Parameters Assessed

1. Tricuspid Annular Plane Systolic Excursion (TAPSE) (<17 mm abnormal).
2. Right Ventricular Fractional Area Change (FAC) (<35% abnormal).
3. Right Ventricular Index of Myocardial Performance (MPI/Tei index) (>0.54 abnormal).
4. Systolic Velocity of Tricuspid Annulus (S′) (<9.5 cm/s abnormal).
5. Left Ventricular Ejection Fraction (LVEF) by Simpson’s method (<50% reduced).

Additional Findings

• Regional wall motion abnormalities.
• RV/RA dilatation.
• Significant tricuspid regurgitation.
• Pulmonary artery systolic pressure (PASP).

Outcome Measures

Patients were followed during their 7-day hospital stay for:

• Arrhythmias (AF, VT/VF).
• Heart failure (Killip class ≥II).
• Cardiogenic shock.
• Conduction disturbances (CHB, high-grade AV block).
• Mechanical complications (VSR, papillary muscle dysfunction).

Statistical Analysis

• Software: SPSS version 25.
• Continuous variables: mean ± SD; compared using ANOVA/Kruskal–Wallis.
• Categorical variables: percentages; compared using Chi-square/Fisher’s exact.
• Logistic regression: to identify predictors of complications.
• p <0.05 considered significant.

Ethical Considerations

• Approval from the Institutional Ethics Committee, S.C.B. Medical College & Hospital, Cuttack (IEC No. XXXX/2022).
• Written informed consent obtained from all participants.
• Confidentiality and anonymity maintained.

Baseline Characteristics

A total of 120 patients with acute ST-elevation myocardial infarction (STEMI) were prospectively included. The cohort was subdivided into three groups: anterior wall myocardial infarction (AWMI) in 62 patients (51.7%), inferior wall myocardial infarction (IWMI) in 38 patients (31.7%), and inferior wall myocardial infarction with right ventricular involvement (IWMI+RVMI) in 20 patients (16.6%). This distribution reflects the natural epidemiology of STEMI, where anterior infarctions tend to be more common, although inferior wall events, particularly those with right ventricular extension, carry unique clinical implications [1,2].

Table 1. Baseline Demographic and Risk Factor Profile of Patients (n = 120)

Table 2. Echocardiographic Parameters Across STEMI Groups

Table 3. Distribution of Abnormal RV Dysfunction Parameters

Table 4. In-Hospital Complications Across Groups

Table 5. Summary of Key Findings

The mean age of the total cohort was 59.6 ± 11.8 years, with a range spanning from 32 to 86 years. This demonstrates that STEMI in the Indian population remains predominantly a disease of middle-aged and elderly individuals, consistent with earlier Indian and international registries [3,4]. On subgroup analysis, AWMI patients had a mean age of 58.7 ± 12.3 years, IWMI patients 61.2 ± 10.9 years, and IWMI+RVMI patients 57.4 ± 13.1 years. The difference was not statistically significant (p = 0.32), suggesting that infarction subtype is not strongly age-dependent.

A male predominance was observed, with 86 (71.7%) male patients and 34 (28.3%) female patients, yielding a male-to-female ratio of 2.6:1. Within subgroups, AWMI included 69.3% males, IWMI 76.3%, and IWMI+RVMI 80%. This aligns with the well-established gender disparity in coronary artery disease (CAD), where men manifest disease earlier and more frequently than women, likely due to hormonal protection in premenopausal women and differences in risk factor exposure [5].

Risk Factors

The risk factor profile of the study cohort reflects the epidemiological transition in India toward lifestyle-related cardiovascular disease:

• Hypertension was the most prevalent comorbidity, affecting 48% overall, with relatively uniform distribution across groups (50% in AWMI, 45% in IWMI, 55% in IWMI+RVMI).
• Diabetes mellitus was present in 34% of cases, slightly higher in IWMI+RVMI (40%). Diabetes is a particularly strong predictor of multivessel disease and adverse outcomes, explaining its higher frequency in patients with RV involvement [6].
• Smoking was reported in 28%, with minor intergroup variation (25.8% AWMI, 31.6% IWMI, 30% IWMI+RVMI). Smoking remains an important trigger for STEMI in younger Indian males [7].
• Dyslipidemia was observed in 32% overall, being most frequent in IWMI+RVMI patients (40%), consistent with the pathophysiological role of lipid abnormalities in atherosclerotic burden.

This constellation of risk factors highlights the synergistic interplay of hypertension, diabetes, smoking, and dyslipidemia in precipitating STEMI, regardless of location. It also emphasizes the need for aggressive primary prevention strategies [8].

Echocardiographic Findings

Tricuspid Annular Plane Systolic Excursion (TAPSE)

TAPSE values were highest in AWMI (20.9 ± 3.9 mm), moderately reduced in IWMI (18.9 ± 4.1 mm), and lowest in IWMI+RVMI (15.8 ± 4.5 mm). The intergroup difference was statistically significant (p <0.001).

This finding demonstrates that RV systolic function is maximally compromised in IWMI with RV involvement, as expected due to direct ischemic injury to the RV free wall [9]. Importantly, however, IWMI patients without classical RV infarction also showed reduced TAPSE compared to AWMI patients, suggesting subclinical RV impairment from interventricular dependence or RCA territory ischemia [10].

Right Ventricular Fractional Area Change (FAC)

FAC values followed a similar gradient: AWMI 40.1 ± 11.7%, IWMI 34.8 ± 9.5%, and IWMI+RVMI 24.5 ± 8.3%. The differences were highly significant (p <0.001).

Since FAC reflects global RV systolic performance by accounting for area change between diastole and systole, its marked reduction in IWMI+RVMI underlines the global nature of RV dysfunction when ischemia extends beyond the LV inferior wall [11].

Right Ventricular Myocardial Performance Index (MPI)

MPI was comparable across groups (AWMI 0.72 ± 0.31, IWMI 0.70 ± 0.29, IWMI+RVMI 0.73 ± 0.34; p = 0.93). Despite the absence of significant differences, MPI values >0.54 were present in the majority of patients in all three groups. This indicates that RV global performance is impaired not only in overt RV infarction but also in anterior and isolated inferior infarcts [12].

Tricuspid Annular Systolic Velocity (S′)

S′ values were highest in AWMI (12.3 ± 2.5 cm/s), lower in IWMI (11.1 ± 2.9 cm/s), and lowest in IWMI+RVMI (9.7 ± 2.1 cm/s), with statistical significance between IWMI and IWMI+RVMI (p = 0.04). This supports the superiority of TDI-derived indices in detecting subtle RV dysfunction compared to geometric measures [13].

Left Ventricular Ejection Fraction (LVEF)

LVEF was markedly reduced in AWMI (41.3 ± 9.8%) compared to IWMI (55.2 ± 7.4%) and IWMI+RVMI (53.6 ± 8.5%) (p <0.001). This finding is consistent with the larger myocardial territory supplied by the LAD in AWMI, leading to more severe LV dysfunction [14]. In contrast, RV involvement significantly impaired RV indices but did not depress LVEF to the same extent.

Distribution of RV Dysfunction Parameters

When patients were categorized by the number of abnormal RV parameters (TAPSE, FAC, MPI, S′):

• AWMI: 55% had ≥1 abnormal parameter, but none had all four abnormal.
• IWMI: 50% had ≥1 abnormal parameter, with 13% showing all four abnormal.
• IWMI+RVMI: 100% had ≥1 abnormal parameter, and 30% demonstrated all four abnormal.

The distribution difference was statistically significant (p <0.001). This gradient underscores the concept that while RV dysfunction can occur in AWMI and IWMI, severe and multi-parametric dysfunction is predominantly confined to RV-infarct extension [15].

In-Hospital Complications

During the 7-day hospital stay, a spectrum of complications was documented:

• Heart Failure (HF): Occurred in 10% overall. AWMI patients had the highest incidence (11.3%), IWMI+RVMI 6.7%, and none in isolated IWMI. This suggests that depressed LVEF in AWMI predisposes more to HF, while RV dysfunction contributes in RVMI but less frequently to overt pulmonary congestion [16].
• Arrhythmias: Documented in 8%. These included atrial fibrillation in 2 cases, ventricular tachycardia in 3, and complete heart block in 1. Conduction disturbances were particularly noted in IWMI and IWMI+RVMI, reflecting RCA supply to the AV node [17].
• Cardiogenic Shock: Occurred in 4%, predominantly in AWMI patients, again highlighting the central role of LV dysfunction in precipitating profound hemodynamic compromise [18].
• Mechanical complications: One case each of ventricular septal rupture (AWMI) and severe mitral regurgitation (IWMI+RVMI). Such complications, though rare, carry a grave prognosis and underscore the heterogeneity of STEMI outcomes [19].

Patients with abnormal RV indices had a significantly higher incidence of complications compared to those with preserved RV function (p <0.05). This provides strong evidence that RV dysfunction is not merely an echocardiographic observation but translates into adverse clinical outcomes [20].

Discussion (Expanded)

Overview

This prospective observational study evaluated right ventricular (RV) function using echocardiographic parameters in patients with acute ST-elevation myocardial infarction (STEMI) admitted to the Department of Cardiology, S.C.B. Medical College and Hospital, Cuttack. Among 120 patients studied, 62 (51.7%) had anterior wall myocardial infarction (AWMI), 38 (31.7%) had inferior wall myocardial infarction (IWMI), and 20 (16.6%) had inferior wall infarction with right ventricular involvement (IWMI+RVMI).

Our study demonstrated that RV dysfunction is not confined to classical RV infarction but can also be observed in AWMI and IWMI. TAPSE and FAC were the most sensitive parameters for detecting RV dysfunction, while MPI was abnormal in a majority across all groups. LVEF was significantly lower in AWMI patients, whereas RV indices were most severely impaired in IWMI+RVMI. Importantly, patients with abnormal RV function had higher rates of complications including heart failure, arrhythmias, and cardiogenic shock.

These findings reinforce the need for comprehensive echocardiographic assessment of both ventricles in STEMI, not just the LV.

Comparison with Previous Studies

Right Ventricular Dysfunction in STEMI

Our results corroborate earlier studies showing that RV dysfunction is an important determinant of prognosis in STEMI. Zehender et al. (1993) [1] demonstrated that RV infarction significantly increases mortality and morbidity in IWMI. Similarly, Zornoff et al. (2002) [2] reported that RV dysfunction after AMI predicts heart failure and mortality independent of LVEF.

In the present study, all patients with IWMI+RVMI (100%) demonstrated at least one abnormal RV parameter, and 30% had abnormalities across all four indices. In contrast, AWMI patients had 55% with ≥1 abnormal parameter but none with all four abnormal. This gradient aligns with Gupta et al. (2022) [3], who found more severe RV impairment in IWMI+RVMI compared to AWMI, although their data suggested AWMI patients exhibited surprisingly higher rates of multiparametric dysfunction. The difference may reflect population heterogeneity, infarct size, or time to echocardiographic evaluation.

TAPSE and FAC as Sensitive Markers

TAPSE and FAC emerged as the most sensitive indices of RV dysfunction in our cohort. IWMI+RVMI patients had significantly lower TAPSE (15.8 mm) and FAC (24.5%) compared to IWMI (18.9 mm, 34.8%) and AWMI (20.9 mm, 40.1%). Similar observations have been reported by Adilakshmi et al. (2016) [4] and Alam et al. (2000) [5], who demonstrated reduced TAPSE and FAC in both anterior and inferior MI compared with controls.

FAC has been highlighted by Antoni et al. (2010) [6] as a strong predictor of hospitalization and mortality after AMI. Our study supports this view, as patients with reduced FAC had higher complication rates.

MPI and Tissue Doppler Parameters

Although MPI did not differ significantly between groups in our study, abnormal values (>0.54) were present in a majority of patients across all subgroups. Møller et al. (2001) [7] reported similar findings, with abnormal MPI in nearly 80% of MI patients. Gupta et al. (2022) [3] also demonstrated MPI abnormalities in AWMI and IWMI+RVMI, though their IWMI group showed relatively preserved MPI compared to ours.

S′ velocity was significantly reduced in IWMI+RVMI, aligning with findings by Ozdemir et al. (2003) [8], who suggested TDI-based S′ is a sensitive marker of RV ischemia and proximal RCA occlusion.

Left Ventricular Function and its Relationship with RV Dysfunction

Our study found LVEF to be lowest in AWMI (41.3%) compared to IWMI (55.2%) and IWMI+RVMI (53.6%). This is consistent with the larger myocardial territory supplied by the LAD artery in anterior infarctions, leading to more severe LV systolic dysfunction [9]. Interestingly, while AWMI patients exhibited profound LV dysfunction, their RV indices were relatively preserved compared to IWMI+RVMI. This reinforces the idea that LV and RV dysfunction are not mutually exclusive but follow distinct anatomical and pathophysiological mechanisms.

CLINICAL IMPLICATIONS

Prognostic Value of RV Dysfunction

The study highlights that RV dysfunction significantly correlates with in-hospital complications. Patients with abnormal RV indices had higher incidence of:

• Heart failure: particularly in AWMI (11.3%), where depressed LVEF compounded outcomes.
• Arrhythmias: more frequent in IWMI and IWMI+RVMI due to RCA involvement of the AV nodal artery.
• Cardiogenic shock: mainly in AWMI patients, emphasizing LV’s role in systemic hemodynamics.
• Mechanical complications: including ventricular septal rupture (AWMI) and severe mitral regurgitation (IWMI+RVMI).

Thus, echocardiographic assessment of RV function provides incremental prognostic information beyond LV function alone.

Implications for Management

Recognition of RV dysfunction in STEMI has direct therapeutic implications:

• Patients with RV infarction require cautious fluid loading to maintain preload, unlike LV infarction where fluid restriction may be necessary [10].
• Use of nitrates and diuretics should be avoided in isolated RV infarction to prevent precipitous hypotension [11].
• Inotropic support may be required in severe RV dysfunction with low cardiac output [12].
• Early identification of high-risk patients can guide monitoring intensity, mechanical support decisions, and post-discharge care.

Pathophysiological Insights

Our study reaffirms the concept of ventricular interdependence, wherein LV dysfunction can impair RV function and vice versa [13]. In AWMI, extensive septal involvement compromises both LV contractility and RV systolic mechanics. In IWMI+RVMI, direct ischemic injury to the RV free wall causes more profound dysfunction. These observations underscore the importance of integrated biventricular assessment in STEMI.

Strengths of the Study

1. Prospective design with standardized echocardiographic evaluation within 48 hours of admission.
2. Inclusion of four validated RV parameters (TAPSE, FAC, MPI, S′), offering comprehensive assessment.
3. Correlation with clinical outcomes, enhancing the translational value of findings.
4. Focus on an Indian population, addressing a gap in literature where most data are Western.

Limitations

1. Single-center study with modest sample size (n=120). Larger multicentric studies are needed for generalizability.
2. Short in-hospital follow-up (7 days). Long-term outcomes such as mortality and rehospitalization were not captured.
3. Strain imaging and 3D echocardiography, which could provide more accurate RV assessment, were not employed due to logistical constraints.
4. Coronary angiographic correlation with infarct-related artery was not systematically analyzed.

Future Directions

Future research should:

• Incorporate larger, multicenter cohorts with long-term follow-up.
• Utilize advanced imaging techniques (3D echo, cardiac MRI) to validate echocardiographic findings.
• Explore biomarker correlations (BNP, NT-proBNP) with RV function.
• Assess the impact of RV-targeted interventions (inotropes, mechanical support) on survival in STEMI with RV dysfunction.

This study demonstrates that RV dysfunction is common in all types of STEMI, though most severe in IWMI+RVMI, and is significantly associated with adverse in-hospital outcomes. TAPSE and FAC are the most sensitive parameters for identifying RV impairment, while MPI abnormalities are widespread across subgroups. Importantly, the presence of abnormal RV indices correlates with heart failure, arrhythmias, and cardiogenic shock, underscoring the prognostic significance of RV assessment.

Echocardiographic evaluation of RV function should therefore be an integral component of STEMI management protocols, complementing LV assessment and guiding tailored therapy for improved patient outcomes

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