European Journal of Cardiovascular Medicine

Coronary artery disease (CAD) is the leading cause of death and disability in India, and its burden continues to rise with urbanisation, ageing and the spread of conventional risk factors.[1–3] Indians develop myocardial infarction (MI) about a decade earlier than people in most other regions, and South Asians in the INTERHEART programme had a substantially higher proportion of first infarcts below 50 years of age.[4,5] Hospital registries such as CREATE and the Kerala ACS Registry have documented that ST-elevation myocardial infarction (STEMI) forms the majority of acute coronary syndrome admissions in the country, that many patients present late, and that reperfusion is often delayed or not delivered.[6,7] Wide regional variations in risk-factor profile across the country further mean that local data are valuable.[8]

The inferior wall of the left ventricle is among the most frequent sites of infarction. Inferior MI has traditionally been regarded as carrying a better prognosis than anterior MI, but this impression holds only when the right ventricle (RV) is spared. In a subset of patients the infarct extends to the RV, converting an apparently low-risk event into one with considerable morbidity and mortality.[9,10] Right ventricular infarction was first described as a clinical entity by Cohn and colleagues in 1974, who recognised the combination of hypotension, elevated jugular venous pressure and clear lung fields in inferior infarction,[11] and necropsy series subsequently showed that RV necrosis accompanies a large share of inferior left ventricular infarcts.[12,13]

The RV is relatively resistant to infarction. Its thin wall has a lower oxygen demand, it is perfused during both systole and diastole because of lower intracavitary pressure, and it receives collateral flow from the left coronary system. Even so, occlusion of the right coronary artery (RCA) proximal to the acute marginal branches can produce extensive RV ischaemia.[9,10] An ischaemic, dilated RV fails to deliver adequate preload to the left ventricle; pericardial constraint and ventricular interdependence aggravate the fall in cardiac output, so that hypotension and shock may occur despite a modest left ventricular insult.[14] Atrioventricular (AV) nodal ischaemia and vagal reflexes add bradyarrhythmias to the picture.

The prevalence of RV involvement varies widely, from about 10% to 50% in different series, depending on the diagnostic criteria and the time of assessment. A contemporary Indian cross-sectional study of 294 patients with inferior MI found RV involvement in 44.9%,[15] and an earlier Indian clinical-profile study reported a lower figure of about one-third.[16] The clinical importance of the diagnosis is well established. In the study of Zehender and co-workers, RV infarction was an independent predictor of major complications and in-hospital death after acute inferior MI,[17] findings confirmed in a large trial database,[18] and RV dysfunction after MI predicts later heart failure and death.[19] RV infarction is responsible for a minority of cases of cardiogenic shock but carries a mortality similar to that of left ventricular shock,[20] while successful reperfusion of the RCA is associated with recovery of RV function and markedly better survival.[21]

Recognition of RV involvement is simple in principle. ST-segment elevation in the right precordial lead V4R is a long-established electrocardiographic marker,[22–24] and the haemodynamic signs are well described.[25] Two-dimensional and Doppler echocardiography allow quantification of RV size and function using standardised parameters, such as tricuspid annular plane systolic excursion (TAPSE), tissue Doppler systolic velocity (S′), fractional area change (FAC) and the myocardial performance (Tei) index.[26–30] Indian investigators have shown that these indices correlate with the presence of a proximal RCA lesion and with biomarker release in inferior MI.[31] Nevertheless, in busy teaching hospitals the right-sided leads are often omitted and the RV is not specifically examined during echocardiography, so the diagnosis is missed and treatment (for example, diuretics or nitrates) may be harmful.

Against this background, the present study was undertaken to determine the prevalence of RV dysfunction among patients with acute IWMI admitted to a tertiary care teaching hospital, and to examine its clinical, electrocardiographic, echocardiographic and angiographic correlates and its association with in-hospital outcome.

2. AIMS AND OBJECTIVES

2.1 Primary objective

To estimate the prevalence of right ventricular dysfunction in patients with acute inferior wall myocardial infarction.

2.2 Secondary objectives

(a) To describe the clinical presentation, risk-factor profile and haemodynamic findings of patients with and without RV dysfunction; (b) to evaluate the diagnostic performance of ST elevation in lead V4R against echocardiography; (c) to compare echocardiographic indices of RV function between the two groups; (d) to correlate RV dysfunction with the culprit coronary artery and reperfusion strategy; and (e) to compare in-hospital complications and mortality between patients with and without RV dysfunction.

3.1 Study design, setting and duration

This was a hospital-based, cross-sectional observational study carried out in the Department of Cardiology and the intensive cardiac care unit (ICCU) of a tertiary care teaching hospital in India, over a period of 18 months (January 2022 to June 2023). The study began after approval from the Institutional Ethics Committee, and written informed consent was obtained from every participant or a legally authorised representative.

3.2 Sample size and sampling

The sample size was calculated with the formula n = Z²pq/d², taking an expected prevalence of RV involvement in inferior MI of 40% (from published data),[9,15] a 95% confidence level (Z = 1.96) and an absolute precision of 10%. The minimum required sample was 92, which was rounded to 100 patients. Consecutive eligible patients were enrolled until this number was reached.

3.3 Inclusion and exclusion criteria

Inclusion criteria: Patients aged 18 years or above, presenting within 48 hours of onset of symptoms with a first acute inferior STEMI, defined as typical ischaemic chest pain with new ST-segment elevation of at least 1 mm in two or more of the inferior leads (II, III and aVF), supported by a rise in cardiac troponin or CK-MB, in accordance with the Fourth Universal Definition of Myocardial Infarction.[32]

Exclusion criteria: Previous myocardial infarction or revascularisation; concomitant anterior wall infarction; known chronic lung disease with cor pulmonale, pulmonary hypertension, pulmonary embolism or congenital heart disease; moderate-to-severe pre-existing valvular heart disease or cardiomyopathy; chronic kidney disease requiring dialysis; poor acoustic window; and refusal to participate.

3.4 Clinical evaluation and laboratory investigations

A detailed history, including age, sex, risk factors (smoking, hypertension, diabetes mellitus, dyslipidaemia, obesity, alcohol use and family history of premature CAD), symptoms and time from symptom onset to arrival, was recorded on a structured proforma. Blood pressure, heart rate, jugular venous pressure (JVP), Kussmaul’s sign, chest auscultation and Killip class were noted at admission.[25] Hypotension was defined as systolic blood pressure below 90 mm Hg. Blood was drawn for complete blood count, blood glucose, renal function, lipid profile, troponin and CK-MB. Patients were treated according to contemporary guidelines, including antiplatelet agents, anticoagulation, statins, and reperfusion by fibrinolysis or primary percutaneous coronary intervention (PCI) as appropriate.[33] Cautious intravenous fluid loading was used in hypotensive patients with suspected RV involvement, and nitrates and diuretics were avoided.

3.5 Electrocardiography

A standard 12-lead ECG was recorded on arrival, and right-sided precordial leads (V3R to V6R) were recorded in every patient with the electrodes placed in the mirror-image positions on the right chest. ST-segment elevation of 1 mm or more in lead V4R was taken as the electrocardiographic criterion for RV involvement.[22–24] Rhythm and conduction abnormalities were documented.

3.6 Echocardiography

Transthoracic echocardiography was performed within 48 hours of admission by a single experienced cardiologist, blinded to the right-sided ECG findings, using a phased-array cardiac ultrasound system with tissue Doppler capability [make/model to be specified]. Measurements were taken as the mean of three consecutive cycles in sinus rhythm and conformed to the American Society of Echocardiography recommendations.[29,30] The following parameters were measured: left ventricular ejection fraction (LVEF, modified Simpson’s method); RV basal diameter in the RV-focused apical four-chamber view; TAPSE by M-mode;[26,28] tricuspid lateral annular peak systolic velocity (S′) by pulsed tissue Doppler; RV FAC; RV myocardial performance index (RIMP, Tei index);[27] right atrial size; severity of tricuspid regurgitation; and inferior vena cava (IVC) diameter and collapsibility.

Operational definition of RV dysfunction. RV dysfunction was considered present if any one of the following was found: TAPSE <17 mm, S′ <9.5 cm/s or FAC <35%, these being the lower reference limits recommended for adults.[29,30] An RIMP above 0.43 (pulsed Doppler) and a basal RV diameter above 41 mm were regarded as abnormal. For the purpose of this study, the severity of RV dysfunction was graded by TAPSE as mild (14 to 16.9 mm), moderate (10 to 13.9 mm) or severe (<10 mm); this is an operational grading used by the authors and is not a guideline-defined classification.

3.7 Coronary angiography and follow-up

Coronary angiography was undertaken in patients who underwent primary PCI and in those selected for an early invasive or rescue strategy after fibrinolysis. The culprit artery and the site of the occlusion relative to the acute marginal branches were recorded; occlusion proximal to these branches was labelled “proximal RCA”. All patients were followed during the hospital stay for hypotension, inotrope requirement, cardiogenic shock (Killip class IV), atrial fibrillation, ventricular tachycardia or fibrillation, high-grade AV block (second-degree Mobitz II or third-degree), temporary pacemaker insertion, length of stay and death.

3.8 Statistical analysis

Data were entered in Microsoft Excel and analysed with SPSS software (version 25.0, IBM Corp., Armonk, NY). Continuous variables are expressed as mean ± standard deviation and categorical variables as numbers and percentages. The two groups (with and without RV dysfunction) were compared using the unpaired t-test for continuous variables and the chi-square test or Fisher’s exact test (when expected cell counts were below 5) for categorical variables. Sensitivity, specificity and predictive values of ST elevation in V4R were calculated against the echocardiographic definition. A two-tailed p-value below 0.05 was considered statistically significant.

During the study period, 100 patients with first acute inferior STEMI satisfying the eligibility criteria were enrolled. RV dysfunction, as defined echocardiographically, was found in 46 patients, giving a prevalence of 46.0% (95% confidence interval approximately 36.4% to 55.9%). The remaining 54 patients formed the comparison group.

4.1 Age and sex distribution

The mean age of the study population was 56.4 ± 11.2 years (range 31 to 82 years). The peak incidence was in the sixth decade, and 28 patients (28%) were below 50 years of age. There were 76 men (76%) and 24 women (24%), a male-to-female ratio of 3.2:1. The prevalence of RV dysfunction showed a rising trend with age, from 25.0% in patients up to 40 years to 58.3% in those older than 70 years, although the difference across age groups was not statistically significant (p = 0.62). RV dysfunction was present in 47.4% of men and 41.7% of women (p = 0.65) (Table 1).

Table 1: Age distribution of patients and prevalence of RV dysfunction (n = 100)

Chi-square test for difference in prevalence across age groups: p = 0.62 (not significant).

4.2 Baseline characteristics and risk factors

Smoking (54%), hypertension (46%), dyslipidaemia (41%) and diabetes mellitus (38%) were the commonest risk factors in the overall cohort. None of the baseline demographic or risk-factor variables differed significantly between patients with and without RV dysfunction. A smaller proportion of patients with RV dysfunction presented within 6 hours of symptom onset (47.8% vs 66.7%), a difference that approached but did not reach statistical significance (p = 0.057) (Table 2).

Table 2: Baseline characteristics of patients with and without RV dysfunction

p-values by unpaired t-test (age) or chi-square test (other variables). BMI, body mass index; CAD, coronary artery disease.

4.3 Clinical presentation and haemodynamic findings

Chest pain was the presenting symptom in 94% of patients. Dyspnoea and syncope or presyncope were significantly more frequent in patients with RV dysfunction. On examination, these patients had a lower mean systolic blood pressure (104.6 vs 122.8 mm Hg, p < 0.001) and a slower heart rate (64.8 vs 74.2 beats/min, p = 0.001). Raised JVP was present in 67.4% of patients with RV dysfunction against 5.6% of those without, and Kussmaul’s sign was elicited only in the former group. The classical triad of hypotension, raised JVP and clear lung fields was present in 13 of the 14 patients (92.9%) showing all three signs. Killip class III–IV was more common in the RV dysfunction group (28.3% vs 7.4%, p = 0.006) (Table 3).

Table 3: Clinical presentation and haemodynamic findings at admission

*Fisher’s exact test. BP, blood pressure; JVP, jugular venous pressure; SBP, systolic blood pressure. p-values by t-test or chi-square test.

4.4 Electrocardiographic findings

ST-segment elevation of at least 1 mm in lead V4R was recorded in 41 patients (41.0%), of whom 38 had RV dysfunction on echocardiography. ST elevation in lead III exceeding that in lead II, ST elevation in V1, and sinus bradycardia were all significantly commoner in the RV dysfunction group, whereas inferior Q waves and ST depression in V1–V3 did not discriminate between groups (Table 4).

Table 4: Electrocardiographic findings

Values are n (%). p-values by chi-square test.

4.5 Echocardiographic findings

All indices of RV systolic function were markedly lower in patients with RV dysfunction (Table 5). Mean TAPSE was 13.8 ± 2.1 mm against 21.4 ± 2.6 mm, S′ was 8.1 ± 1.4 against 12.6 ± 1.9 cm/s, and FAC was 31.2% against 45.8% (all p < 0.001). The RV was dilated, with a mean basal diameter of 43.6 mm, and the RIMP was higher (0.56 vs 0.38), indicating global dysfunction. Right atrial enlargement, at least moderate tricuspid regurgitation and a plethoric IVC were significantly more frequent in this group. LVEF was modestly but significantly lower (46.2% vs 50.8%, p = 0.004), suggesting some influence of the extent of left ventricular injury.

Table 5: Echocardiographic parameters in patients with and without RV dysfunction

Values are mean ± SD or n (%). p-values by Welch’s t-test or chi-square test. TAPSE, tricuspid annular plane systolic excursion; IVC, inferior vena cava.

4.6 Severity of RV dysfunction

Of the 46 patients with RV dysfunction, 22 (47.8%) had mild, 17 (37.0%) moderate and 7 (15.2%) severe dysfunction by the TAPSE-based grading (Table 6, Figure 1). Mortality rose steeply with increasing severity: 4.5% in mild, 23.5% in moderate and 71.4% in severe dysfunction.

Table 6: Grading of RV dysfunction by TAPSE and in-hospital mortality

Percentages for deaths are calculated within each severity grade.

4.7 Diagnostic performance of ST elevation in V4R

Taking the echocardiographic definition as reference, ST elevation of 1 mm or more in V4R had a sensitivity of 82.6%, specificity of 94.4%, positive predictive value of 92.7%, negative predictive value of 86.4% and overall accuracy of 89.0% (Table 7). Eight patients with RV dysfunction on echocardiography had no ST elevation in V4R, and three patients had ST elevation in V4R without echocardiographic RV dysfunction.

Table 7: Diagnostic performance of ST elevation ≥ 1 mm in lead V4R against echocardiography

Sensitivity 82.6%; specificity 94.4%; positive predictive value 92.7%; negative predictive value 86.4%; accuracy 89.0%.

4.8 Reperfusion strategy and culprit artery

Fibrinolytic therapy was given to 46 patients, 18 underwent primary PCI and 36 did not receive reperfusion, mostly because of late presentation; the distribution did not differ significantly between the groups (p = 0.23). Coronary angiography was available in 38 patients (19 in each group). The RCA was the culprit vessel in 18 of 19 patients with RV dysfunction, and the occlusion was proximal to the acute marginal branches in 15 (78.9%); in contrast, the proximal RCA was the culprit in 4 of 19 patients (21.1%) without RV dysfunction, in whom the left circumflex artery and the mid or distal RCA were more commonly responsible (Table 8).

Table 8: Reperfusion strategy and angiographic culprit artery

*Fisher’s exact test. PCI, percutaneous coronary intervention; RCA, right coronary artery.

4.9 Complications and in-hospital outcome

Patients with RV dysfunction had a significantly higher incidence of hypotension, high-grade AV block, need for inotropic support, temporary pacing and in-hospital death, and stayed in hospital longer (9.4 ± 3.8 vs 6.1 ± 2.2 days, p < 0.001) (Table 9, Figure 2). The overall in-hospital mortality was 12%. Ten of the 12 deaths (83.3%) occurred in patients with RV dysfunction. The mortality was 21.7% in this group compared with 3.7% in patients without RV dysfunction (p = 0.006). The commonest causes of death were refractory cardiogenic shock and ventricular arrhythmias.

Table 9: In-hospital complications and outcome

*Fisher’s exact test; other p-values by chi-square test or Welch’s t-test.

Right ventricular involvement is a recognised but under-diagnosed complication of inferior MI. In this study of 100 consecutive patients with first acute inferior STEMI, nearly half (46.0%) had echocardiographic evidence of RV dysfunction. This agrees with the range of 30% to 50% quoted in the classical studies,[9,10] and is very close to the 44.9% reported from a large North Indian tertiary centre that combined ECG and echocardiographic criteria.[15] An earlier Indian clinical-profile study found RV infarction in about one-third of inferior infarcts,[16] and a necropsy series had shown that RV necrosis accompanies a considerable proportion of inferior left ventricular infarcts.[12,13] Differences in prevalence between studies can be explained by the definition used, the timing of examination (RV stunning is transient), the sensitivity of the diagnostic modality and case mix, including the proportion of late presenters. Because our definition used echocardiographic indices rather than the electrocardiogram alone, patients with functional RV impairment but a negative V4R were also captured.

The mean age of 56.4 years and the strong male preponderance (76%) are in line with Indian MI registries, in which patients are younger than in Western cohorts and men predominate.[6,7] More than a quarter of our patients were below 50 years of age, which reflects the early onset of CAD in South Asians.[1,5] The high prevalence of smoking (54%), hypertension (46%), dyslipidaemia (41%) and diabetes (38%) mirrors the conventional risk-factor burden demonstrated in the INTERHEART study and in Indian surveys.[4,8] The risk-factor profile and age were similar in patients with and without RV dysfunction, which indicates that RV involvement is determined by the anatomy and site of coronary occlusion and not by patient characteristics. The numerically higher prevalence in the elderly is of interest, but our study was not powered to prove an age effect. Similarly, delayed arrival was more common in the RV dysfunction group, a finding of borderline significance which was also noted in another Indian series where the window period was longer in patients with RV involvement, possibly because of resuscitative measures started before reperfusion.[15] Late presentation, a well-documented problem in India, probably contributed to the large proportion (36%) of patients who could not be reperfused.[6,7]

The clinical features of RV dysfunction in our cohort follow the pathophysiology described by Cohn and others. Raised JVP, hypotension and Kussmaul’s sign were considerably more frequent, and the combination of hypotension, raised JVP and clear lung fields was almost exclusive to patients with RV dysfunction.[11,14] Raised JVP was the most discriminating bedside sign in our series (67.4% vs 5.6%), which supports the observation that its absence has a high negative predictive value for haemodynamically significant RV infarction.[25] At the same time, only 30.4% of patients with RV dysfunction were hypotensive on admission, which shows that bedside signs alone lack sensitivity, particularly when volume loading has already been started. The significantly slower heart rate and higher rate of sinus bradycardia and high-grade AV block are explained by ischaemia of the sinus and AV nodes, which are supplied by branches of the RCA, together with augmented vagal tone.[9,10]

ST elevation in lead V4R has been regarded as the most useful single electrocardiographic marker of RV infarction since its description by Erhardt and colleagues, and subsequent studies showed high sensitivity and specificity for RV involvement.[22–24] In the present study, the sensitivity of 82.6% and specificity of 94.4% reflect the use of echocardiographic dysfunction as the reference standard, and the fact that ST elevation in V4R is often transient and may resolve within hours of onset, especially after reperfusion.[23,24] The finding that ST elevation in lead III greater than that in lead II and ST elevation in V1 were more common in patients with RV dysfunction is consistent with the electrical effect of a proximal RCA lesion.[9] Eight of our 46 patients with RV dysfunction would have been missed by V4R alone; this strengthens the case for the combined use of right-sided leads and echocardiography, particularly in patients presenting late.

Echocardiography is the most widely available and practical imaging method for assessing the RV at the bedside. The indices we used are simple, reproducible and have been validated against radionuclide angiography.[26,28–30] The mean TAPSE of 13.8 mm in the RV dysfunction group and 21.4 mm in the comparison group is strikingly similar to the Indian series of Rajesh and colleagues, who reported 13.5 mm and 21.3 mm in patients with and without a proximal RCA lesion.[31] Our RV S′ and FAC were also markedly lower, and the Tei index, a measure of global RV performance, was higher.[27] A North Indian study found lower TAPSE and FAC in inferior MI with RV involvement, together with a higher left ventricular E/e′ ratio.[15] The slightly lower LVEF in our RV dysfunction group may reflect a larger total infarct, but also the adverse effect of ventricular interdependence on left ventricular function. Right atrial enlargement, tricuspid regurgitation and a plethoric IVC reflect the raised right-sided filling pressure and annular dilatation in acute RV failure.

In angiographic subgroups, the proximal RCA was the culprit lesion in about four-fifths of patients with RV dysfunction, confirming the established anatomical basis for RV infarction.[10,13] Rajesh and co-workers found that TAPSE, S′ and the tissue Doppler myocardial performance index could predict a proximal RCA stenosis with high sensitivity and specificity,[31] and our data support that RV echocardiographic indices serve as a noninvasive marker of the level of RCA occlusion. Importantly, 43.5% of patients with RV dysfunction in our series could not be reperfused. Bowers and colleagues demonstrated that successful reperfusion leads to improvement in RV function and a striking reduction in mortality, whereas failed reperfusion was associated with persistent haemodynamic compromise and a high death rate.[21] Early reperfusion should therefore be pursued as strongly in patients with RV involvement as in any other STEMI.[33]

In-hospital mortality was nearly six times higher in patients with RV dysfunction (21.7% vs 3.7%). The classic paper by

Zehender et al. reported an in-hospital mortality of 31% in inferior MI with RV infarction against 6% without it, and showed that RV infarction is an independent predictor of prognosis.[17] The excess risk was confirmed in a large trial population,[18] and RV dysfunction after MI was associated with heart failure and death in the SAVE study.[19] The mortality gradient in our cohort is larger than that in a recent Indian primary-PCI series (4.5% vs 1.8%),[15] likely because 36% of our patients had no reperfusion, and patients presented late and with more severe haemodynamic compromise; this is in agreement with the observation that outcomes improve markedly with reperfusion.[21] The dose–response relationship between the severity of TAPSE reduction and death (4.5%, 23.5% and 71.4% for mild, moderate and severe dysfunction) further reinforces the prognostic importance of quantifying RV function. Cardiogenic shock caused by RV failure is known to carry a mortality comparable to that of left ventricular shock,[20] and the Killip IV rate of 13.0% in our RV dysfunction group underlines the need for early recognition. Arrhythmias and conduction disorders were significantly more common, and a temporary pacemaker was required in one in five patients, which underscores the need for continuous monitoring and a readiness to pace.

Table 10: Selected published studies on RV involvement in inferior MI and the present study

RV, right ventricular; MI, myocardial infarction; JVP, jugular venous pressure; RCA, right coronary artery; TAPSE, tricuspid annular plane systolic excursion; FAC, fractional area change; PCI, percutaneous coronary intervention.

Several practical points emerge from our findings. First, right-sided leads (at least V4R) should be recorded in every patient with an inferior STEMI, as a matter of routine, at first medical contact and repeated if the initial tracing is negative.[22,33] Second, a focused echocardiographic assessment of the RV, using TAPSE, S′ and FAC, takes only a few minutes and adds objective information about severity and prognosis.[29] Third, patients with RV involvement are preload-dependent; nitrates, diuretics and other preload-reducing agents should be avoided, while cautious volume loading, inotropic support, restoration of AV synchrony and prompt reperfusion are the principles of management.[9,10,33] Finally, the large proportion of patients without reperfusion in our cohort highlights the need for strengthening pre-hospital systems and pharmaco-invasive strategies in the Indian health-care context.[6,7]

Strengths and limitations

The strengths of this study include consecutive enrolment, uniform use of right-sided leads and standardised echocardiographic parameters recommended by guidelines, and blinded echocardiographic interpretation. The study also has limitations. It was a single-centre study with a modest sample size; the data pertain to a single time point within 48 hours, so transient RV stunning may have been under- or over-estimated; the echocardiographic assessment of the RV is operator-dependent and does not match cardiac magnetic resonance imaging; angiographic data were available for only 38% of patients, which limits the strength of the culprit-vessel correlation; only in-hospital outcomes were evaluated, and the effect of RV dysfunction on long-term prognosis and RV recovery could not be assessed. Larger multicentre studies with serial imaging and long-term follow-up are warranted.

Right ventricular dysfunction was present in 46% of patients with acute inferior wall myocardial infarction in this tertiary care teaching hospital. These patients more often had hypotension, raised jugular venous pressure, bradyarrhythmias and need for inotropic or pacing support, and had a nearly six-fold higher in-hospital mortality than those with preserved RV function. Proximal right coronary artery occlusion was the dominant culprit lesion. ST elevation in V4R was highly specific, but it missed about one in six patients with echocardiographic dysfunction, and the severity of TAPSE reduction was a graded predictor of death. Every patient with inferior MI should therefore have right-sided ECG leads recorded and a targeted RV echocardiographic examination performed, so that high-risk patients are identified early and managed with preload maintenance, timely reperfusion and close haemodynamic and rhythm monitoring.

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