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

Cardiac Amyloidosis

A 72 year old male presents to the cardiology clinic with progressive exertional dyspnea, fatigue, and bilateral lower limb edema over several months. He reports a prior history of bilateral carpal tunnel syndrome and lumbar spinal stenosis several years before the onset of cardiac symptoms. Vital signs show blood pressure of 110/70 mm Hg and pulse rate of 78 beats per minute. On examination, there is elevated jugular venous pressure and bilateral pitting edema. Lungs are clear. Electrocardiography shows low or discordant QRS voltage relative to increased wall thickness. Echocardiography reveals concentric left ventricular wall thickening, small left ventricular cavity, biatrial enlargement, restrictive filling pattern, and an apical sparing pattern on global longitudinal strain. Serum and urine testing show no monoclonal protein. Bone scintigraphy with Tc-99m PYP demonstrates Perugini grade 3 myocardial uptake. Diagnosis?

Diagnosis is transthyretin cardiac amyloidosis, most likely wild type ATTR cardiomyopathy.

1. Definition

Cardiac amyloidosis is an infiltrative cardiomyopathy caused by extracellular deposition of misfolded amyloid fibrils in the myocardium, leading to restrictive physiology, heart failure, arrhythmias, and conduction abnormalities.

2. Major Types

1. AL amyloidosis
• Due to immunoglobulin light chains from a plasma cell dyscrasia
• Rapidly progressive with frequent multiorgan involvement
2. ATTR amyloidosis
• Due to misfolded transthyretin protein
• Includes:
1. Wild type ATTR, typically affecting older men
2. Variant ATTR, due to TTR gene mutation, often with neuropathy

3. Why It Is Underdiagnosed

1. Mimics heart failure with preserved ejection fraction
2. Often attributed to hypertensive heart disease or aging myocardium
3. Extracardiac clues may precede cardiac symptoms by 5 to 7 years, especially in ATTR

4. Clinical Red Flags

4.1 Cardiac

1. HFpEF or borderline EF with increased wall thickness
2. Biatrial enlargement and restrictive filling pattern
3. Low or discordant ECG voltage relative to wall thickness
4. Elevated troponin or NT-proBNP out of proportion to symptoms
5. Atrial fibrillation or conduction disease

4.2 Extracardiac

1. Bilateral carpal tunnel syndrome
2. Lumbar spinal stenosis
3. Biceps tendon rupture
4. Peripheral neuropathy
5. Autonomic dysfunction, including orthostatic hypotension or GI dysmotility
6. Proteinuria or nephrotic syndrome, more suggestive of AL amyloidosis
7. Macroglossia, also suggestive of AL amyloidosis

5. Pathophysiology

1. Protein misfolding leads to formation of beta sheet amyloid fibrils
2. Deposition occurs in the extracellular myocardial space
3. Results in:
1. Concentric wall thickening without true hypertrophy
2. Diastolic dysfunction and restrictive physiology
3. Conduction system infiltration
4. Fixed stroke volume, leading to poor tolerance of vasodilators and beta blockers

Extracardiac involvement may affect nerves, tendons, ligaments, gastrointestinal tract, and kidneys

6. Diagnostic Approach

6.1 Step 1: Exclude AL Amyloidosis

This is essential because AL amyloidosis is a medical emergency

1. Serum immunofixation electrophoresis
2. Urine immunofixation electrophoresis
3. Serum free light chain assay

6.2 Echocardiography

1. Concentric LV wall thickening
2. Small LV cavity
3. Biatrial enlargement
4. Restrictive filling pattern
5. Apical sparing on strain imaging

6.3 ECG

1. Low or discordant voltage relative to LV thickness
2. Conduction abnormalities such as AV block or atrial fibrillation

6.4 Cardiac MRI

1. Diffuse subendocardial or transmural late gadolinium enhancement
2. Difficulty nulling the myocardium
3. T1 mapping and extracellular volume quantification for disease assessment

6.5 Nuclear Imaging

1. Tc-99m PYP, DPD, or HMDP scanning
2. Perugini grade 2 or 3 uptake with negative monoclonal protein confirms ATTR noninvasively

6.6 Genetic Testing

Performed after ATTR diagnosis to distinguish:

1. Wild type ATTR
2. Variant ATTR

6.7 Biopsy

Indicated when:

1. AL amyloidosis is suspected
2. Imaging findings are equivocal
3. Presentation is atypical

Endomyocardial biopsy is most sensitive. Congo red staining shows apple green birefringence, and mass spectrometry confirms subtype.

7. Management

7.1 AL Amyloidosis

1. Urgent hematology referral
2. Plasma cell directed chemotherapy
3. Autologous stem cell transplantation in selected patients
4. Supportive cardiac care

7.2 ATTR Amyloidosis

1. Tafamidis
• First line therapy for ATTR cardiomyopathy
• Stabilizes transthyretin
• Improves survival and reduces hospitalizations
2. Gene silencing therapies
• Patisiran and inotersen, mainly for variant ATTR with neuropathy
• Vutrisiran, given subcutaneously every 12 weeks, with emerging evidence for cardiovascular benefit
3. Supportive therapy
• Loop diuretics, carefully titrated

8. Important Management Principles

1. Avoid or use extreme caution with digoxin
2. Avoid non-dihydropyridine calcium channel blockers
3. Beta blockers are often poorly tolerated
4. Avoid aggressive vasodilators if poorly tolerated
5. Anticoagulate all patients with atrial fibrillation
6. Pacemaker may be required for conduction disease
7. CRT if standard indications are met
8. ICD is not routinely indicated unless clear arrhythmic risk is present

9. Monitoring and Follow Up

1. Serial NT-proBNP and troponin levels
2. Echocardiography with strain imaging
3. Cardiac MRI or nuclear imaging for disease progression
4. Functional assessment with 6 minute walk test and quality of life measures

10. Key Clinical Insight

Heart failure with preserved ejection fraction, increased wall thickness without hypertension, low or discordant ECG voltage, apical sparing on strain imaging, and extracardiac features such as bilateral carpal tunnel syndrome strongly suggest cardiac amyloidosis, particularly ATTR

11. Exam Level Pearls

1. Low voltage ECG with thick myocardium is a classic clue
2. Always exclude AL amyloidosis first
3. Perugini grade 2 to 3 uptake confirms ATTR if monoclonal proteins are absent
4. Apical sparing pattern is highly suggestive
5. Extracardiac features may precede cardiac symptoms by years
6. Tafamidis is first line therapy for ATTR cardiomyopathy
7. AL amyloidosis is a medical emergency requiring urgent treatment

Cardiogenic Shock

A 72-year-old male presents to the emergency department with severe chest pain and progressive shortness of breath for 4 hours. The pain is sudden in onset, substernal, crushing, radiates to the left arm and jaw, and is associated with diaphoresis, nausea, and vomiting. He has a history of hypertension, type 2 diabetes mellitus, ischemic heart disease, and heart failure with reduced ejection fraction, and is a current smoker with a 40 pack-year history. On examination, he appears pale, anxious, and diaphoretic, with a blood pressure of 80/55 mmHg, heart rate of 118/min, respiratory rate of 30/min, and oxygen saturation of 88 percent on room air. His extremities are cold and clammy with delayed capillary refill. Jugular venous distension is present, and lung auscultation reveals bilateral basal crackles. Cardiac examination demonstrates an S3 gallop, and urine output is markedly reduced. Electrocardiography shows ST-segment elevation in leads V1 to V4. Laboratory evaluation reveals elevated troponin and a serum lactate of 5.2 mmol/L. Bedside echocardiography demonstrates severe left ventricular systolic dysfunction with an ejection fraction of approximately 25 percent and anterior wall hypokinesis. Right heart catheterization shows a cardiac index of 1.7 L/min/m² and a pulmonary capillary wedge pressure of 24 mmHg. Diagnosis?

Diagnosis is Acute Myocardial Infarction Related Cardiogenic Shock (AMI-CS).

1. Definition

Cardiogenic shock is a clinical syndrome of end-organ hypoperfusion due to primary cardiac pump failure, typically characterized by:

1. Hypotension (SBP <90 mmHg or MAP <65 mmHg)
2. Evidence of hypoperfusion:
1. Oliguria
2. Altered mental status
3. Lactate >2 mmol/L
3. Hemodynamic evidence:
1. Cardiac index <2.2 L/min/m²
2. Elevated PCWP >18 mmHg (LV dominant shock)

Cardiogenic shock may occur without overt hypotension.

2. Etiology

2.1 Primary

1. Acute myocardial infarction
2. Acute decompensated heart failure

2.2 Mechanical Complications (Must Not Be Missed)

1. Papillary muscle rupture leading to acute mitral regurgitation
2. Ventricular septal rupture
3. Free wall rupture

2.3 Electrical

1. Ventricular tachyarrhythmias
2. Complete heart block

2.4 Other

1. Myocarditis
2. Severe valvular disease
3. Right ventricular infarction

3. Pathophysiology

3.1 Core Mechanism

1. Decreased contractility
2. Decreased cardiac output
3. Hypotension
4. Hypoperfusion

3.2 Compensatory Mechanisms

1. Sympathetic activation → vasoconstriction → increased afterload
2. RAAS activation → fluid retention → increased preload

3.3 Vicious Cycle

1. Increased LVEDP → pulmonary edema
2. Reduced coronary perfusion → worsening ischemia
3. Lactic acidosis
4. Multiorgan failure

4. Hemodynamic Profile

1. Decreased cardiac index
2. Increased PCWP (LV dominant shock)
3. Increased right atrial pressure
4. Increased systemic vascular resistance

PCWP may be normal or low in RV shock

5. Classification

5.1 SCAI Shock Staging

1. Stage A: At risk
2. Stage B: Beginning shock
3. Stage C: Classic shock
4. Stage D: Deteriorating
5. Stage E: Extremis

First 24 hours are critical

5.2 Phenotypes

1. LV dominant congested phenotype
2. RV shock
3. Biventricular cardiometabolic phenotype

6. Clinical Features

6.1 Core Features

1. Hypotension
2. Cold, clammy extremities
3. Oliguria
4. Altered mental status
5. Elevated lactate

6.2 Cardiac Findings

1. S3 gallop
2. Elevated JVP
3. Pulmonary crackles

7. Diagnosis

7.1 Laboratory

1. Lactate >2 mmol/L
2. Elevated troponin

7.2 ECG

1. ST elevation
2. Arrhythmias

7.3 Echocardiography

1. Reduced LVEF
2. Regional wall motion abnormalities
3. Mechanical complications

7.4 Hemodynamic Monitoring

1. Cardiac index <2.2
2. Elevated PCWP

7.5 Key Prognostic Parameter

CPO = (MAP × CO) / 451

1. Strong predictor of mortality
2. CPO <0.6 W indicates severe shock

8. Management

8.2 Hemodynamic Support

Vasopressor

1. Norepinephrine (first line)

Inotropes

1. Dobutamine
2. Milrinone (risk of hypotension)

8.3 Definitive Therapy

AMI-CS

1. Immediate PCI (life-saving)

8.4 Mechanical Support

Impella

1. LV unloading
2. Improves cardiac output
3. Mortality benefit in selected patients (DanGer Shock)

IABP

1. No routine mortality benefit

VA ECMO

1. Refractory shock
2. Biventricular failure

10. Key Clinical Insight

1. Acute MI + hypotension + hypoperfusion = cardiogenic shock
2. Low CI + high PCWP = LV shock
3. Requires:
1. Immediate recognition
2. Urgent PCI
3. Norepinephrine ± inotrope
4. Early mechanical support

11. Exam Level Pearls

1. Cold and wet patient = cardiogenic shock
2. Lactate >2 mmol/L = hypoperfusion
3. Norepinephrine > dopamine
4. PCI improves survival
5. Mechanical complications must not be missed