ST T Changes: Ischemia, Strain, Secondary or Memory ?

Dr. Darshan Jhala,

M.D., D.M.(Card.),

Lilavati Hospital,

Nanavati Super Speciality Hospital,

BSES MG Hospital,

Mumbai.

‘To A Man With A Hammer, Every Problem Is A Nail.’ • Mark Twain

• So

To A Cardiologist, Is Every ST Shift Ischemia/MI ?

Why Is ST Segment Isoelectric and T Upright ? Phase 2 = ST Segment Phase 3 = T Wave

Endo. Endo. Depolarization Repolarization

Epi. Epi.

Causes of ST Segment shift :

• Specific patterns of ST-T wave changes may be seen in association with various disease states.

• Ischemia

• Myocardial Injury

• Pericarditis

• LVH

• Intraventricular conduction Delays (RBBB, LBBB)’

• Aneurysm

• Persistent Juvenile t-wave pattern

• Early Repolarization

• ‘Memory’ Phenomenon

• Electrolyte abnormalities

• Post-cardiac surgical state

• Anemia

• Fever

• Acidosis or alkalosis

• Catecholamines

• Drugs

• Acute abdominal process

• Endocrine abnormalities

• Metabolic changes

• Cerebrovascular accidents

What Is This ?

Cardiac ‘Memory’ Effect (CM) :

• Cardiac memory (CM)

• refers to a specialized form of remodeling. It is characterized by an altered T wave on electrocardiogram (ECG) or

• vectorcardiogram recorded during sinus rhythm (or any

• rhythm with normal ventricular activation) and induced by

• a preceding period of altered electrical activation.

• CM has been described following stimuli such as

• electrical pacing, intermittent left bundle branch block, paroxysmal tachycardia, and preexcitation

Mechanism:

• Changes in AP configuration

• Ion Channel remodeling

Clinical Implications Of CM :

• can confound the diagnosis of cardiac ischemia • (1) positive TaVL, • (2) positive or isoelectric TI • (3) maximal precordial TWI > TWI(III)

(92% sensitive and 100% specific for CM)

• ventricular pacing, long thought to be a “neutral” intervention with regard to cellular and subcellular function, in fact is a potent modulator of cellular processes.

Why is a Normal ECG being shown over here ?

ERS : ‘J’ Wave Syndrome :

• The ERS is commonly seen in athletes, cocaine users, HOCM,VSDs

• Prevalence varies between 3%

and 24% in the general population

• Young males, especially those predisposed to vagotonia,African Americans, and athletes are subpopulations known to have a higher prevalence of ERS

ERS : Electrophysiologic Mechanism :

ERS : ECG Diagnosis :

• The electrocardiographic hallmark of ERS is elevation (> 1 mm above baseline) of the QRS - ST junction

• Manifested as either QRS slurring or notching, ST segment elevation with upper concavity,

• ProminentT-waves in two or more contiguous inferior and/or lateral leads

Types :

• 1: ER in the lateral precordial leads that is • healthy male athletes and has the • lowest risk of malignant arrhythmias

• 2: ER in the inferior and inferolateral leads • greater risk of malignant arrhythmias;

• 3: ER pattern in all ECG leads • highest risk of malignant arrhythmias

and electrical storms.

: ERS : Benign V/S Malignant :

Benign

• Rapidly ascending ST segment elevation) following J-point elevation

Malignant

• Horizontal or descending ST segment elevation

• Slurred or notched J-point elevation ≥ 2 mm

• ER pattern in inferior or inferolateral leads

• Persistent ER during exercise

• Extension of ER into a BrS pattern.

ER : ECGs :

• Benign

• Malignant

ER Pattern :

• 13 % of general population

• 75 % in Men

• Arrhythmia after 55 yrs • SCD 11/100000 with J waves

• 30/100000 with Horiz.ST elev.

• Due to ↓ Na/Ca current or↑ K current

• PMVT/Torsade

‘J’Wave syndromes:

• ERS

• Brugada Syndrome

• Osborne Waves

• Increased Vagal tone

• Neural Injury

• Hypercalcemia

ARVD :

LBBB, RBBB and LVH

• Discordance between the QRS complex and the ST-T abnormalities, • The ST segment and T wave are both abnormal and deviate in the same

direction, • The ST and T abnormalities are not dynamic. Exceptions : • Left ventricular hypertrophy may be associated with symmetric T-wave

inversion without ST-segment depression : HCM

Concordant = MI, Disconcordant = BBB but does not exclude MI

PR/PQ Segment Depression : Pseudo ST Elev.

Liu’s criteria for diagnosing atrial ischaemia / infarction : • PR elevation >0.5 mm in V5 & V6 with reciprocal PR depression in V1 &

V2

• PR elevation >0.5 mm in lead I with reciprocal PR depression in leads II & III

• PR depression >1.5 mm in the precordial leads

• PR depression >1.2 mm in leads I, II, & III

• Abnormal P wave morphology: M-shaped,W-shaped,irregular,or notched (minor criteria)

Another Normal ECG : Pericarditis :

Pericarditis • Diffuse pericarditis involves not only the subepicardial

layer of the ventricular wall, which is responsible for the ST-segment elevation, but also the subepicardial layer of the atrial wall, which causes an atrial injury pattern.

ER V/s Pericarditis :

• The ratio of the T wave amplitude to the ST elevation should be > 4 if early repolarization is present. In other words, the T wave in early repolarization is usually 4 times the amplitude of the ST elevation. Another way to describe this would be that the ST elevation is less than 25% of the T wave amplitude in early repolarization.

• PQ Segment depression.

• The ST elevation in early repolarization resolves when the person exercises.

• Early repolarization, unlike pericarditis, should not be associated with any symptoms

Hyperkalemia • Even though the pseudoinfarction pattern of

hyperkalemia is well known, the ST-segment elevation is so striking at times that one cannot help agonizing over

the possibility of coexistent acute infarction.

Conclusions :

• All ST T abnormalities are not ischemic,

• Clinical data is a must for interpreting a given ECG,

• Comparing previous and subsequent ECGs very important,

• Know the metabolic milieu during the ECG recording,

• Remember channelopathies, specific Genetic syndromes.

Thank You