ECG Changes Associated With Prior Myocardial Infarction
(In the Absence of LVH and LBBB)
Myocardial infarction (MI) results in irreversible myocardial necrosis followed by healing with fibrotic scar formation. This scar tissue is electrically inactive and alters normal cardiac depolarization and repolarization, producing characteristic electrocardiographic (ECG) changes that may persist for life. Recognition of these ECG patterns is essential for diagnosing prior (old) MI, particularly in asymptomatic patients or those presenting later with heart failure, arrhythmias, or ischemic symptoms.
Pathophysiological Basis
Following MI, necrotic myocardium is replaced by fibrosis. Because scar tissue does not conduct electrical impulses normally, the direction and timing of ventricular activation change. These alterations lead to abnormal Q waves, QS complexes, fragmented QRS patterns, and abnormal R-wave progression. The ECG therefore becomes a surrogate marker of myocardial scar.
Pathological Q Waves
Q waves represent initial ventricular depolarization moving away from electrically silent myocardium.
Diagnostic criteria include: Any Q wave ≥ 20 ms or QS complex in leads V2 and V3
Q wave ≥ 30 ms in duration and ≥ 1 small square (≥ 1 mm) deep
QS complex in any two contiguous leads
Contiguous lead groupings: Lateral leads: I, aVL
Anterior leads: V1–V6
Inferior leads: II, III, aVF
Clinical significance: Pathological Q waves are highly specific for prior transmural MI. Persistence of Q waves beyond the acute phase strongly suggests myocardial scarring. However, interpretation should be cautious in young individuals, athletes, and in certain normal variants.
Abnormal R-Wave Progression
Normally, R-wave amplitude gradually increases from V1 to V6.
ECG features suggestive of prior MI: R wave ≥ 1 small square
R/S ratio ≥ 1 in V1 or V2
Concordant (upright) T waves
Absence of conduction defects
Clinical relevance: This pattern often suggests posterior or high lateral myocardial infarction and reflects loss of opposing electrical forces due to scarred myocardium.
Fragmented QRS Complex (fQRS)
Fragmented QRS represents non-homogeneous ventricular activation caused by myocardial fibrosis.
Typical ECG patterns: Notched R wave
Notched S wave
RSR′ or RSR′ with ST elevation
rSr pattern
Key characteristics: QRS duration usually < 120 ms
Present in two or more contiguous leads in a coronary territory
Clinical importance: Fragmented QRS is a sensitive marker of prior MI, even in the absence of pathological Q waves. It correlates with myocardial scar burden and is associated with increased risk of ventricular arrhythmias and adverse cardiac outcomes.
QS Complexes
A QS complex reflects complete absence of initial positive ventricular depolarization.
Important points: Commonly seen in extensive anterior MI
More specific than isolated Q waves
Indicates large transmural myocardial scar
Conditions to Exclude Before Diagnosis
Before attributing ECG changes to prior MI, the following must be excluded: Left ventricular hypertrophy
Left bundle branch block
Ventricular pacing
Pre-excitation syndromes (e.g., WPW)
Certain cardiomyopathies
These conditions can mimic Q waves or abnormal R-wave progression.
Clinical Applications
Detection of prior MI on ECG is clinically important for: Risk stratification
Guiding secondary prevention strategies
Explaining reduced left ventricular systolic function
Evaluating unexplained heart failure or ventricular arrhythmias
Pre-operative cardiovascular assessment
ECG findings should always be interpreted in conjunction with clinical history and imaging modalities such as echocardiography. Cardiac MRI remains the gold standard for detecting myocardial scar.
Key Takeaway
In patients without LVH or LBBB, prior myocardial infarction is suggested by: Pathological Q waves or QS complexes in contiguous leads
Abnormal R-wave progression with R/S ≥ 1 in V1–V2
Fragmented QRS complexes indicating myocardial scar
A structured ECG approach allows reliable identification of old MI and plays a vital role in long-term cardiovascular management.
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