Skip to main content

PVCs arising from Inferoapical Left Ventricle

 

Watch the above video for ECG example explained.

Premature Ventricular Complexes (PVCs) Arising from the Inferoapical Left Ventricle

Premature ventricular complexes (PVCs) originating from the inferoapical left ventricle (LV) represent a less common subset of idiopathic ventricular ectopy. Unlike the more frequent right ventricular outflow tract (RVOT) PVCs, inferoapical LV PVCs arise from the distal inferior wall or apical segments of the LV and have distinct electrocardiographic and mapping characteristics.


Recognition of their ECG pattern is essential for:


Accurate localization


Differentiation from fascicular or papillary muscle PVCs


Planning catheter ablation




---


Anatomical Substrate


The inferoapical LV corresponds to:


Distal inferior wall


True apex (inferior portion)


Region supplied mainly by the posterior descending artery (RCA or LCx depending on dominance)



Potential arrhythmogenic substrates:


Idiopathic focal automaticity


Triggered activity


Small areas of fibrosis (post-myocarditis or subclinical ischemia)


Post-infarct scar (if structural disease present)




---


ECG Characteristics


Localization relies heavily on 12-lead ECG morphology.


1. Bundle Branch Pattern


Most inferoapical LV PVCs demonstrate:


Right bundle branch block (RBBB) morphology


Because activation spreads from LV to RV



Dominant R wave in V1



This differentiates them from RVOT PVCs (which show LBBB pattern).



---


2. Frontal Plane Axis


Axis depends on exact origin:


Superior axis (negative QRS in inferior leads)

→ Suggests origin from inferior LV wall


May show:


Negative QRS in II, III, aVF


Positive in I and aVL




If origin is more apical-inferior:


Inferior leads often deeply negative


Marked superior axis deviation




---


3. Precordial Transition


Late precordial transition (after V4–V5)


Dominant S waves in early precordial leads


Broad QRS (>140 ms typical in LV origin)




---


Typical ECG Summary Pattern


Inferoapical LV PVC:


RBBB morphology


Superior axis


Late transition


Broad QRS


Often monomorphic




---


Differentiation from Other LV PVC Sites


1. Fascicular PVCs


Narrower QRS


RBBB + superior axis (posterior fascicle VT)


Often responsive to verapamil


Usually re-entrant rather than purely focal



2. Papillary Muscle PVCs


Variable axis


Multiple morphologies


Often difficult ablation due to mobility



3. LV Outflow Tract PVCs


Inferior axis (positive II, III, aVF)


Early transition



Inferoapical PVCs typically have a superior axis, helping distinction.



---


Clinical Presentation


Patients may present with:


Palpitations


Missed beats


Exercise-induced ectopy


High PVC burden (>10–15%) leading to PVC-induced cardiomyopathy



In structurally normal hearts → Often benign

In structural heart disease → Requires detailed evaluation



---


Diagnostic Workup


1. 12-Lead ECG


Morphology analysis


Axis determination


QRS width



2. Holter Monitoring


PVC burden


Monomorphic vs polymorphic


Coupling interval



3. Echocardiography


LV function


Regional wall motion abnormality


LV dilation (PVC cardiomyopathy)



4. Cardiac MRI


Indicated if:


Reduced EF


Suspicion of scar


Atypical morphology



Detects:


Inferior wall fibrosis


Apical scar




---


Mechanism


Most idiopathic inferoapical PVCs are due to:


Focal automaticity


Triggered activity



Less commonly:


Scar-related reentry


Ischemic substrate




---


Management


1. Conservative


Reassurance if asymptomatic


Monitor LV function




---


2. Medical Therapy


Beta blockers


Non-dihydropyridine CCB (if focal)


Class IC agents (in structurally normal heart)


Amiodarone (if structural disease)




---


3. Catheter Ablation


Indications:


Symptomatic PVCs


PVC burden >10–15%


LV dysfunction suspected due to PVCs


Drug intolerance



Mapping features:


Earliest activation at inferoapical LV


Pace mapping match ≥11/12 leads


Often requires retrograde aortic or transseptal LV access



Success rates:


80–90% in experienced centers


Lower if scar-related




---


Prognosis


Excellent in idiopathic cases


Reversible LV dysfunction if PVC-induced cardiomyopathy


Higher risk if associated with structural heart disease




---


Key Takeaways


Inferoapical LV PVCs show RBBB morphology + superior axis


Late precordial transition


Broad QRS


Important to distinguish from fascicular VT


Ablation highly effective when symptomatic or high burden


Thanks

Subscribe @ECGLogic for detailed description of real ECG Cases


Comments

Popular posts from this blog

Brugada ECG vs Incomplete Right Bundle Branch Block (iRBBB)

Brugada ECG vs Incomplete Right Bundle Branch Block (iRBBB) Why this differentiation matters Brugada pattern is a malignant channelopathy associated with sudden cardiac death, while incomplete RBBB is usually a benign conduction variant. Mislabeling Brugada as iRBBB can be fatal; overcalling iRBBB as Brugada can lead to unnecessary anxiety and ICD implantation. --- 1. Basic Definitions Brugada ECG Pattern Primary repolarization abnormality Genetic sodium-channel disorder Characteristic ST-segment elevation in V1–V3 Risk of ventricular fibrillation and sudden death Incomplete RBBB (iRBBB) Depolarization abnormality Delay in right ventricular conduction Common in healthy individuals Usually asymptomatic and benign --- 2. ECG Morphology: Side-by-Side Comparison QRS Duration Brugada: QRS usually <120 ms iRBBB: QRS <120 ms, but with RBBB morphology --- V1–V2 Pattern (Key Differentiator) Brugada Pseudo-RBBB appearance ST elevation ≥2 mm ST segment is coved or saddleback Terminal QRS bl...

Acute Treatment of Hyperkalemia

Acute Treatment of Hyperkalemia – A Practical, Bedside-Oriented Guide Hyperkalemia is a potentially life-threatening electrolyte abnormality that demands prompt recognition and decisive management. The danger lies not only in the absolute potassium value but in its effects on cardiac conduction, which can rapidly progress to fatal arrhythmias. Acute treatment focuses on three parallel goals: stabilizing the cardiac membrane, shifting potassium into cells, and removing excess potassium from the body. Understanding this stepwise approach helps clinicians act quickly and rationally in emergency settings. Why Hyperkalemia Is Dangerous Potassium plays a key role in maintaining the resting membrane potential of cardiac myocytes. Elevated serum potassium reduces the transmembrane gradient, leading to slowed conduction, ECG changes, ventricular arrhythmias, and asystole. Importantly, ECG changes do not always correlate with potassium levels, so treatment decisions should be based on clinical c...

π˜Όπ™£π™©π™žπ™˜π™€π™–π™œπ™ͺπ™‘π™–π™©π™žπ™€π™£ π˜Όπ™›π™©π™šπ™§ π™Žπ™©π™§π™€π™ π™š

 π˜Όπ™£π™©π™žπ™˜π™€π™–π™œπ™ͺπ™‘π™–π™©π™žπ™€π™£ π˜Όπ™›π™©π™šπ™§ π™Žπ™©π™§π™€π™ π™š in  Patient with AF and acute IS/TIA European Heart Association Guideline recommends: • 1 days after TIA • 3 days after mild stroke • 6 days after moderate stroke • 12 days after severe stroke Early anticoagulation can decrease a risk of recurrent stroke and embolic events but may increase a risk of secondary hemorrhagic transformation of brain infarcts.  The 1-3-6-12-day rule is a known consensus with graded increase in delay of anticoagulation between 1 and 12 days after onset of ischemic stroke or transient ischemic attack(TIA), according to neurological severity based on European expert opinions. However, this rule might be somewhat later than currently used in a real-world practical setting.