Inferior Wall STEMI

A 50 year old male presents to the emergency department with acute onset substernal chest pain, diaphoresis, and vomiting for the past 30 minutes. He has a history of hypertension, diabetes mellitus, and hyperlipidemia, and is noncompliant with medications. He is an active smoker. On examination, blood pressure is 90/60 mm Hg, pulse rate is 58 beats per minute, and respiratory rate is 18 breaths per minute. Jugular venous pressure is elevated. Electrocardiography shows sinus bradycardia with ST-segment elevation in leads II, III, and aVF, with reciprocal ST depression in leads I and aVL. Cardiac troponins are elevated, although treatment should not be delayed while awaiting results. Echocardiography shows inferior wall hypokinesis. Diagnosis?

Diagnosis is Inferior Wall ST Elevation Myocardial Infarction (STEMI), most likely due to right coronary artery occlusion, with suspected right ventricular infarction.

1. Definition

Inferior wall myocardial infarction is an acute ischemic injury involving the inferior wall of the left ventricle, most commonly due to right coronary artery occlusion in right-dominant circulation, and less commonly due to left circumflex artery occlusion in left-dominant anatomy.

2. Epidemiology and Risk Factors

2.1 Epidemiology

1. Accounts for 40 to 50 percent of all myocardial infarctions
2. Generally has a better prognosis than anterior MI
3. Right ventricular involvement occurs in up to 40 percent of cases and worsens outcomes

2.2 Risk Factors

1. Hypertension
2. Diabetes mellitus
3. Hyperlipidemia
4. Smoking
5. Obesity and sedentary lifestyle
6. Advanced age and family history

3. Pathophysiology

3.1 Core Mechanism

1. Atherosclerotic plaque rupture leads to platelet activation and thrombus formation
2. Results in acute coronary occlusion, causing myocardial ischemia and necrosis

3.2 Coronary Anatomy

1. Right coronary artery supplies the inferior wall, right ventricle, and often the SA and AV nodes
2. In left-dominant circulation, the LCx supplies the inferior wall

3.3 Conduction Abnormalities

1. Sinus bradycardia is common in early inferior MI
2. AV nodal block, especially Mobitz type I, is frequent
3. High-grade AV block may occur and requires urgent management

3.4 Bezold–Jarisch Reflex

1. Causes bradycardia, hypotension, and vasodilation
2. Triggered by inferior wall ischemia and vagal activation

4. Clinical Features

4.1 Core Symptoms

1. Chest pain, often radiating to arm or jaw
2. Diaphoresis
3. Nausea and vomiting

4.2 Inferior MI Specific Features

1. Bradycardia due to vagal tone and nodal ischemia
2. Hypotension with elevated JVP, suggesting right ventricular infarction
3. Relative absence of pulmonary edema in isolated RV infarction

5. ECG Findings

1. ST-segment elevation in leads II, III, and aVF
2. Reciprocal ST depression in leads I and aVL
3. ST elevation in lead III greater than lead II suggests RCA involvement
4. Right-sided leads (V4R) should be obtained to evaluate for right ventricular infarction

6. Diagnostic Evaluation

6.1 Electrocardiography

1. Initial test of choice
2. Should be performed immediately

6.2 Cardiac Biomarkers

1. Troponins are elevated
2. Diagnosis of STEMI is ECG-based, and treatment should not be delayed

6.3 Echocardiography

1. Shows inferior wall motion abnormalities
2. Helps detect right ventricular involvement and complications

6.4 Coronary Angiography

1. Confirms the culprit vessel
2. Enables primary PCI, the definitive therapy

6.5 Laboratory Studies

1. CBC, metabolic panel, and coagulation profile prior to intervention

7. Key Clinical Insight

Inferior STEMI with hypotension, elevated JVP, and bradycardia strongly suggests right ventricular infarction due to proximal RCA occlusion.

8. Management

8.1 Reperfusion Therapy

1. Primary PCI within 90 minutes is preferred
2. Thrombolysis if PCI cannot be performed within 120 minutes

8.2 Antithrombotic Therapy

1. Aspirin 162 to 325 mg
2. P2Y12 inhibitor such as clopidogrel or prasugrel
3. Anticoagulation with unfractionated heparin or alternatives

8.3 Hemodynamic Management

1. Intravenous crystalloids for hypotension due to RV infarction
2. Avoid nitrates and diuretics in RV infarction due to preload dependence
3. Norepinephrine is the preferred vasopressor if hypotension persists

8.4 Bradyarrhythmia Management

1. Atropine for symptomatic bradycardia
2. Temporary transvenous pacing if high-grade AV block persists

8.5 Adjunct Therapy

1. High-intensity statins
2. ACE inhibitors or ARBs
3. Beta blockers only if no hypotension, bradycardia, AV block, or RV infarction

8.6 Secondary Prevention

1. Smoking cessation
2. Control of blood pressure, lipids, and glucose
3. Cardiac rehabilitation

9. Complications

1. Bradyarrhythmias and AV nodal block
2. Right ventricular failure
3. Cardiogenic shock
4. Ventricular tachycardia or ventricular fibrillation

10. Prognosis

1. Better prognosis than anterior MI
2. Mortality approximately 2 to 9 percent
3. Worse outcomes with right ventricular involvement, delayed reperfusion, or conduction abnormalities

11. Exam Level Pearls

1. ST elevation in II, III, and aVF indicates inferior MI
2. ST elevation in lead III greater than lead II suggests RCA occlusion
3. Hypotension with elevated JVP indicates right ventricular infarction
4. Avoid nitrates in RV infarction
5. Inferior MI commonly causes bradycardia and AV block
6. Obtain right-sided ECG leads when RV infarction is suspected