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ECG Predictors of Sudden Cardiac

Death in Cardiomyopathies
Yoga Yuniadi
Indonesian Heart Rhythm Society
The Spectrum of Epidemiology
Underlying SCD
Classification of Cardiomyopathy

Richardson et al. Circulation. 1996; 93: 841-2
Multiple ECG risk markers
for SCD risk assessment

Narayanan, et al. Europace. 2015
Electrocardiographic markers linked to SCD risk
in the general population

Narayanan, et al. Europace. 2015
Hypertrophic Cardiomypathy (HCM)

Hypertrophic obstructive cardiomyopathy (HOCM)
Idiopathic hypertrophic subaortic stenosis (IHSS)
Pathomechanisms of SCD in HCM
 Abnormal intramural
coronary arteries with
thickened walls and
narrowed lumens
 Chaotic, disorganised left
ventricular architecture
(“cellular disarray”)
predisposing to abnormal
transmission of electrical
impulses and thus
serving as a substrate for
Distribution of cardiovascular causes of
sudden death in 1435 young competitive

Maron et al. Circulation. 2007;115:1643-1655
Dagger-like Q waves of HCM
ECG Features of HCM
• LVH : precordial voltages and non-specific ST segment and T-wave
• Asymmetrical septal hypertrophy: deep, narrow (“dagger-like”) Q
waves in the lateral (V5-6, I, aVL) and inferior (II, III, aVF) leads.
These may mimic prior myocardial infarction, although the Q-wave
morphology is different: infarction Q waves are typically > 40 ms
duration while septal Q waves in HCM are < 40 ms. Lateral Q waves
are more common than inferior Q waves in HCM.
• Left ventricular diastolic dysfunction may lead to compensatory left
atrial hypertrophy, with signs of left atrial enlargement (“P mitrale”)
on the ECG.
• Atrial fibrillation and supraventricular tachycardias are common.
Ventricular dysrhythmias (e.g. VT) also occur and may be a cause of
sudden death.
‘Pathological’ Q-waves
(the 2017 International criteria)
A. Examples of ‘non-
pathological’ Q wave: A 5
mm deep nonpathological Q-
wave. Note that it is <25% of
the following R-wave and
<40 ms in duration.

B. A 5 mm deep pathological Q-
wave. Note that it is ≥25% of
the following R-wave.

C. A 1.5 mm deep pathological
Q-wave. Note that it is ≥4 ms
in duration
Giant T wave inversion of Apical HCM
Long-short-long Induction
Predictors of Arrhythmia Events

Halliday, et al. Circulation. 2017;136:215–231
Different morphologies of the
fragmented QRS

Das, et al. Heart Rhythm. 2007;4(11):1385-92
Dilated Cardiomyopathy
Annual Rate of the Arrhythmic Endpoint
According to LGE Status in DCM Patients

Di Marco, et al. J Am Coll Cardiol HF 2017;5:28–38
Fragmented QRS in DCM:
Arrhythmic Events

Das MK et al. Heart Rhythm 2010;7:74–80
(microvolt) T Waves Alternans
• TWA positive:
– sustained alternans voltage ≥1.9μV during
exercise with an onset heart rate ≤110beats/min,
or 1.0μV at rest for a period of at least 1min,
provided that the alternans ratio was ≥3.

Adachi, et al. Jpn Circ J 2001; 65: 76 –80
Prospective studies on TWA

Verrier, et al. J Am Coll Cardiol 2011;58:1309–24
Summary of TWA
• Overall, it is reasonable to consider TWA
evaluation whenever there is suspicion of
vulnerability to lethal cardiac arrhythmias.
However, there is as yet no definitive evidence
from interventional trials that it can guide
Definition - Mechanisms
• Diabetic CM is defned as
the cardiovascular
damage present in
diabetes patients
• characterized by
myocardial dilatation and
hypertrophy, decrease in
the systolic and diastolic
• independent of the
coexistence of ischemic
heart disease or
Arrhythmogenic Right Ventricle
Cardiomyopathy (ARVC)
• An inherited myocardial
disease associated with
paroxysmal ventricular
arrhythmias and
sudden cardiac death.
• Characterized
pathologically by fibro-
fatty replacement of the
right ventricular
ECG Features
• Epsilon wave (most specific finding, seen in
30% of patients)
• T wave inversions in V1-3 (85% of patients)
• Prolonged S-wave upstroke of 55ms in V1-3
(95% of patients)
• Localised QRS widening of 110ms in V1-3
• Paroxysmal episodes of ventricular tachycardia
with LBBB morphology (e.g. right ventricular
• Some ECG characteristics are pathognomonic
to cardiomyopathies
• ECG predictors can be used to stratify patients
highr risk to arrhythmic events
• ECG predictors can not solely been used to
decide treatment
• ECG predictors of SCD warrant further
examination by means of imaging and invasive
EP study.