Introduction

The struggle in differentiating between conduction and structural heart disease can be daunting, and can lead to inaccurate diagnoses and inappropriate treatment plans. This difficulty is often encountered when using only electrocardiography results to differentiate between left posterior fascicular block (LPFB) and right ventricular hypertrophy (RVH).

LFPB is a result of electrical conduction disturbances, while RVH consists of structural changes happening in the right ventricle. Appropriate diagnosis and differentiation are achieved through proper clerking, taking notes on aetiology and clinical presentation, and utilising appropriate diagnostic tools. 

Definition & pathophysiology

Left Posterior Fascicular Block (LPFB)

To make LPFB easy to understand, imagine the human heart as a house with beautiful, bright lights, and to turn on these lights, several wires are used to send messages (electricity) through the house. In a situation where this wire is blocked, inhibiting message (electricity) transmission in the house, thus resulting in poor or improper electrical transmission.

Just as these wires energise the lights in a house, in the human heart, they ensure it beats correctly and in the proper rhythm. This wire is called the left posterior fascicle. When this wire is blocked, the human heart still functions, but messages (signals, impulses) are sent abnormally and through irregular pathways and thus resulting in left posterior fascicle block.

In more scientific terms, Surawicz B, et al defined LPFB as a blocked or delayed electrical impulse in the left posterior fascicle of the heart, which results in an abnormal dissemination (spread) of impulses through the left anterior (front) fascicle. This is a type of intraventricular delay of the left posterior (back) fascicle of the left branch of the Purkinje system, which is important for spreading electrical signals around the heart.¹

The abnormal dissemination of impulses through the anterior fascicles further results in an altered ventricular activation sequence.² Left posterior fascicular block does not affect the cardiovascular integrity, but is often associated with myocardial ischaemia, altering the anterior fascicle supplied by the left anterior descending artery.¹

Right ventricular hypertrophy

The right ventricle of the human heart is responsible for pumping blood to the lungs through the pulmonary artery. In conditions such as pulmonary hypertension, valve stenosis, or chronic lung disease (such as COPD), the right ventricle is forced to work harder, leading to enlargement and thickening of the muscle wall of the right ventricle.³ Think of it like a bodybuilder who becomes more muscular and thick from working hard.⁴

Right ventricular hypertrophy can be further defined as a structural response of the right ventricular muscular walls due to increased pressure or workload, thereby making the walls thicken.⁵ However, the adaptive thickening mechanism predisposes the heart to right heart failure because the heart can no longer stretch and fill with enough blood to pump around the body.⁶ Compared to LPFB, RVH illustrates the changes in the heart muscle structures that can affect the entire human body.

Aetiological differences between LPFB and RVH

Causes of LPFB:

• Ischaemic heart disease with more involvement in the anterior septal region
• An idiopathic degenerative fibrosis that is mostly seen in elderly people
• Complications from surgeries such as valve repair and coronary artery bypass grafting
• Iatrogenic (caused by medical intervention) injury or trauma from invasive cardiac procedures
• Toxicity from drugs and metabolic imbalance
  

LPFB is usually asymptomatic, but it only manifests in conjunction with other conduction disturbances or underlying cardiac diseases.⁷

Causes of RVH

RVH is caused by thickening of the ventricular walls and congenital (present at birth) diseases. Other causes include the following:

• Chronic obstructive pulmonary disease (COPD)
• Pulmonary hypertension, which can be a result of thromboembolic origins or sometimes idiopathic (no known cause or disease)^8,9
• Congenital heart diseases like atrial septal defect, ventricular septal defect and tetralogy of Fallot
• Obstructive sleep apnoea occurs in longstanding, untreated or mismanaged cases

These conditions predispose the right ventricle to pressure and thus result in hypertrophy.

Symptoms 

LPFB symptoms

LPFB, when isolated, is usually asymptomatic and can only be identified during routine cardiac assessment. In situations where symptoms are present, they include the following:

• Chest pain as a result of ischaemic heart disease
• Palpitations or syncopes (fainting) when they manifest with other pathologies
• Associated fatigue or light-headedness in more complex cases
  

It is important to note that LPFB does not manifest with physical signs of heart failure or any systemic venous congestion.²

RVH Symptoms

RVH are usually symptomatic, and the patients usually present with right-sided cardiac dysfunction symptoms, which include the following:

• Dyspnoea (shortness of breath), especially on exertion
• Venous congestion (blood pooling in legs), which leads to peripheral oedema
• lower cardiac output, resulting in fatigue
• In more advanced cases, the following are seen: jugular venous distention, hepatomegaly (enlarged liver), and ascites
• Congenital or late-stage pulmonary conditions are usually associated with cyanosis (blue/grey skin or lips)or clubbing (softened swelling at ends of fingers and toes)⁹

It is important to note that RVH is a progressive cardiac remodelling process with overt clinical signs.

Other diagnostics

ECG plays an important role in the diagnosis and differentials between LPFB and RVH, but still, other diagnostic tools can make it a lot more distinctive. They include the following:

• Imaging
• Echocardiography
• Cardiac MRI
• Chest Radiography
• Functional and Laboratory Studies
• Pulmonary Function Tests
• Biomarkers
• Exercise Stress Testing
  

Echocardiography

In LPFB, echocardiography reveals the normal cardiac structure and any anomalies present. In RHV, it indicates the thickened right ventricular walls (>5 mm), dilated right ventricle, and flattened interventricular septum in severe cases.⁶

Cardiac MRI

Cardiac MRI allows high-resolution visualisation of the ventricular mass and fibrosis. LPFB, in some situations, shows localised fibrosis with the absence of hypertrophy.

RVH: Quantifies right ventricular mass, making chamber dilation and fibrotic remodelling evident.¹⁰

Chest radiography

In LPFB, this indicates an overview of a normal chest silhouette. While RHV indicates the right heart border, enlarged pulmonary arteries, as well as an elevated cardiac apex.⁹

Pulmonary function tests

Helpful in evaluating chronic lung disease contributing to RVH. However, in patients with LPFB, their pulmonary function is within normal limits.⁸

Biomarkers

BNP or NT-proBNP are usually elevated in RVH as a result of myocardial wall exertion and stress. In LPFB, these biomarkers are not often elevated unless associated with heart failure. In some cases, troponins are mildly elevated in LPFB associated with ischaemia.²

Exercise stress testing

In LPFB patients with systemic coronary artery disease, this might trigger ischaemia, while revealing stress-induced hypoxia or right ventricular dysfunction.⁶

Differentials in clinical presentation

This includes comparison across patient history, signs and symptoms, imaging, biomarkers, and biomarkers.

Management options

When LPFB occurs in isolation, no specific management is followed through. However, it is essential to monitor for progression and treat underlying ischaemia if present.⁷ It is important to schedule regular appointments for geriatric or post-cardiac surgery patients. 

In situations with a symptomatic patient with a higher chance of increased grade AV block, it is important to consider implantable pacemakers.

The management options of RVH are usually aetiology-oriented. Patients with pulmonary hypertension are managed with the use of vasodilators, oxygen therapy and anticoagulants in thromboembolic scenarios.⁸

When chronic obstructive pulmonary disease happens in association with RVH, pulmonary care is optimised first; other management options include bronchodilators and oxygen therapy.⁹

In congenital cases, surgery or long-term follow-up is ideal. RVH cases are usually progressive, and early intervention and detection are important to help reduce progression or reverse right ventricular remodelling.⁶ Lastly, the use of diuretics comes in handy as they assist in controlling volume overload; ACE inhibitors or beta-blockers can be used as well.

Can both situations co-exist?

Yes, but it is uncommon. However, it can happen in geriatric patients. When LPFB and RVH co-exist, the patient might present with an ischaemic heart disease and chronic obstructive pulmonary disease, and this can lead to both conduction delay and right ventricular remodelling. When this happens, the patient is sent for comprehensive imaging and functional testing, and management by a cardiologist and pulmonologist is advised. In this scenario, treatment of underlying diseases results in a better prognosis.

Summary

The diagnosis and differentiation of LPFB and RVH can be tricky. Recognising the different aetiologies, clinical presentations, biomarkers, and imaging ensures a proper diagnosis and treatment plan. With advances in cardiology, the ability to differentiate between these two diseases will aid effective care.