Skip to main content

Echo Measurement (Jenni Criteria)



Here’s how to measure the non-compacted : compacted (NC:C) ratio on echocardiography for diagnosing LV non-compaction (LVNC)

πŸ«€ Step-by-Step Echo Measurement (Jenni Criteria)


1. View:

Use the parasternal short-axis or apical 4-chamber view — where trabeculations are most prominent (usually at the apex, mid-lateral, or inferior wall).


2. Timing:

Measure at end-systole (when the myocardium is thickest and best defined).


3. Zoom in:

Magnify the region of interest — typically the apical segments.


4. Identify layers:


Non-compacted (NC) layer: the thick, spongy, trabeculated part (inner layer).


Compacted (C) layer: the thin, dense, outer myocardial layer (toward the epicardium).



5. Measure thickness:

At a perpendicular angle to the myocardial wall:


Measure the NC thickness (from endocardial border to the trough of recesses).


Measure the C thickness (from trough of recesses to epicardial surface).



6. Calculate ratio:


In this example c/b 

Where is b is the width of non compaction

Diagnostic threshold:

➡️ NC:C > 2:1 in end-systole is diagnostic (Jenni et al. criteria).


🧭 Tips


Always measure at the same site in the same cardiac cycle phase.


Color Doppler can confirm deep recesses filled with blood from the LV cavity (not coronary flow).


Compare with adjacent normal segments — non-compacted myocardium appears spongy and bilayered.

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.