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ECG Reference · Pericardium, Lungs, Brain and Others

Cardiac sarcoidosis on ECG

Cardiac sarcoidosis

Cardiac sarcoidosis is a granulomatous myocardial involvement in systemic sarcoidosis that disrupts conduction and creates arrhythmogenic substrate foci. The most characteristic manifestation is unexplained high-grade or complete AV block, especially in a patient younger than 60 years; intraventricular conduction disturbances, pathological Q waves, QRS fragmentation, and ventricular arrhythmias are also possible. Their combination increases suspicion but is not mandatory.

7 min readFor medical students and physiciansUpdated 18.10.2026
Prepared by WhiteCoat Pro editorial teamCriteria verified against guidelines by two independent reviewers
Полная АВ-блокада (III степени)P идут своим ритмом (85 в минуту), QRS — своим, реже (35 в минуту); PR всё время разный. Выскальзывающий ритм желудочковый — QRS широкие.IIPPPPPP 0,70 сRR 1,70 с → 35/мин
Complete AV block on ECG is a frequent manifestation of cardiac sarcoidosis. Diagram, 25 mm/s, 10 mm/mV.

ECG criteria

  1. Unexplained Mobitz II second-degree AV block, high-grade or complete AV block, especially at an age under 60 years; isolated PR interval prolongation (first-degree) is less specific
  2. Bundle branch block (most commonly right) or intraventricular block not explained by known structural heart disease
  3. Pathological Q waves without a history of myocardial infarction (pseudoinfarction pattern) in two or more contiguous leads, most commonly in the inferior (II, III, aVF) or anterior (V1–V4) leads; the same thresholds as for ischemic Q are used (duration approximately ≥30 ms and depth ≥1 mm in most leads, with separate duration and morphology criteria for V2–V3), but in sarcoidosis, Q waves often do not fit a typical coronary distribution and require comparison with MRI, clinical presentation, and coronary anatomy — by itself, this does not differentiate sarcoidosis from myocardial infarction
  4. QRS fragmentation (fragmented QRS) with a narrow QRS (<120 ms) — an additional R' wave (RSR') or a notch on the upstroke/downstroke of the R or S wave, not representing a typical bundle branch block, in two contiguous leads of the same anatomical region; with a wide QRS (≥120 ms, including bundle branch blocks), separate modified criteria are applied (multiple notches on R or S waves). This sign is nonspecific, reflects heterogeneous myocardial scarring, and is not an independent diagnostic marker of sarcoidosis
  5. Nonspecific ST-segment and T-wave changes
  6. Frequent ventricular premature beats, nonsustained or sustained ventricular tachycardia (monomorphic or polymorphic) — especially significant in known systemic sarcoidosis or signs of myocardial involvement on MRI/PET
  7. Low QRS voltage — nonspecific, evaluated in the context of possible concomitant pericardial effusion
Heart rate/rhythmcan be anything: from bradycardia in AV block to VT
Where to lookPR interval, QRS (duration and morphology), leads II, III, aVF, V1
Typical findinghigh-grade or complete AV block in a relatively young patient
Dangersudden cardiac death from VT/VF or complete AV block

What it looks like on ECG

Cardiac sarcoidosis does not have a single specific pattern — changes depend on the localization of granulomas in the conduction system and ventricular myocardium.

FindingLeadsWhat it means
High-grade/complete AV block—involvement of the basal interventricular septum and conduction system; the specific level of block cannot be determined from a single ECG
Right/left bundle branch blockV1 (RBBB), V6 (LBBB)involvement of the interventricular septum
Pathological Q waveII, III, aVF, or V1–V4scarring and inflammatory lesion mimics myocardial infarction
QRS fragmentationcontiguous leads of the same wallheterogeneous myocardial scarring, nonspecific
Ventricular extrasystoles, VT—re-entry circuit around the scar/inflammation zone

AV block can progress unpredictably: in some patients, moderate conduction disturbances eventually progress to high-grade or complete block, while in others they remain stable for a long time. The rate of transition from mild degrees to complete block cannot be predicted in advance, which is why suspected sarcoidosis requires monitoring and assessment of structural and inflammatory heart involvement. The combination of bundle branch block and AV conduction disturbance in a patient under 60 years without another clear cause is a reason to suspect sarcoidosis or another infiltrative/granulomatous myocardial disease.

Mechanism

Non-caseating granulomas infiltrate the myocardium in patches, with a predilection for the basal interventricular septum, the left ventricular free wall, and the conduction system area. A granuloma near the AV node or the bundle of His disrupts AV conduction. As granulomas heal, fibrosis forms — this slows and fragments impulse propagation through the ventricular myocardium, creating zones of slow conduction around the scar. These zones become the substrate for re-entry ventricular tachycardia. Pseudoinfarction Q waves can occur both as a result of active inflammation altering the vector of excitation and as a result of an established scar; they are interpreted together with clinical presentation, coronary anatomy, and late gadolinium enhancement (LGE) patterns on MRI. The presence of sarcoidosis does not rule out concomitant coronary artery disease — it must be ruled out according to indications.

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Causes

  • Systemic sarcoidosis with cardiac involvement (cardiac sarcoidosis is detected clinically in a fraction of patients, and subclinically more often at autopsy and by MRI/PET)
  • Isolated cardiac sarcoidosis (without overt pulmonary and lymph node involvement) — a rare but documented variant
  • Factors increasing the likelihood of cardiac involvement: young or middle age, unexplained high-grade AV block, or VT without established coronary artery disease

Differential diagnosis

  • True prior myocardial infarction: the absence of an ACS history and typical coronary distribution of Q waves does not reliably rule out infarction. Differentiation relies on clinical presentation, serial ECGs, echocardiography, MRI with LGE pattern, and evaluation of coronary arteries (CT coronary angiography or invasive coronary angiography as indicated); FDG-PET assesses active inflammation rather than atherosclerosis
  • Idiopathic degenerative AV block of the elderly (Lenègre–Lev disease): sarcoidosis should be suspected specifically in young and middle-aged patients with conduction disturbances without another clear cause
  • Arrhythmogenic right ventricular cardiomyopathy: similar in VT substrate and QRS fragmentation, differentiated by imaging data and predominant localization of involvement (RV in ARVC vs. diffuse/septal in sarcoidosis)
  • Other infiltrative cardiomyopathies (amyloidosis): amyloidosis is more typically characterized by low voltage with pseudoinfarction Q waves and diastolic dysfunction, but the ECG picture can overlap — imaging and, if necessary, biopsy resolve this
  • Myocarditis: acute clinical presentation, elevation of injury biomarkers, but granulomatous myocarditis in sarcoidosis can present similarly to infectious myocarditis

Clinical significance and management

Unexplained high-grade AV block or bundle branch block in a patient with known or suspected sarcoidosis is an indication for extended cardiac evaluation: echocardiography, contrast-enhanced cardiac MRI, FDG-PET, Holter monitoring. Detecting cardiac sarcoidosis changes prognosis and management: it is one of the few potentially reversible causes of AV block and VT where immunosuppressive therapy may help.

In high-grade or complete AV block, permanent cardiac pacing is indicated. In cardiac sarcoidosis, the very need for permanent pacing is usually a reason to consider implantable cardioverter-defibrillator (ICD) therapy with pacing capabilities rather than a conventional pacemaker, due to the high background risk of ventricular arrhythmias. Separately, indications for ICD (outside the context of an isolated pacing requirement) are determined by: a history of cardiac arrest or sustained VT; reduced ejection fraction ≤35% despite optimal medical therapy; for an EF of 36–50%, the decision is individualized taking into account extensive LGE on MRI, inducible VT during electrophysiological testing, and other high-risk features — these factors are assessed on par with EF rather than as secondary.

In systemic sarcoidosis, symptoms, ECG, and usually echocardiography are evaluated at the initial diagnosis stage; in case of abnormalities or clinical suspicion of heart involvement, Holter monitoring and imaging are performed. The scope and frequency of follow-up are individualized.

Common interpretation errors

  • Interpreting pseudoinfarction Q waves as a consequence of a true myocardial infarction and failing to continue searching for the cause in a patient without CAD risk factors
  • Dismissing an AV conduction disturbance in a young patient as a "normal variant" or vagotonia without dynamic monitoring
  • Failing to associate bundle branch block with the systemic diagnosis of sarcoidosis if it is already known from the history
  • Ignoring high-grade ventricular premature beats in a patient with pulmonary sarcoidosis, considering them an incidental finding
  • Limiting evaluation to a single resting ECG: paroxysmal AV block and nonsustained VT in sarcoidosis may not be captured without Holter monitoring
Test yourselfThree exam- and accreditation-level questions with detailed explanations.

1. Which ECG finding in a 35-year-old patient with systemic sarcoidosis requires the most urgent further cardiac evaluation?

Mobitz II and high-grade AV block in a young patient without another clear cause are potentially life-threatening manifestations of cardiac sarcoidosis requiring urgent assessment.

2. Why can pathological Q waves appear in cardiac sarcoidosis without prior myocardial infarction?

Non-caseating granulomas and subsequent fibrosis create local areas of altered excitation resembling a post-infarction scar, regardless of the condition of the coronary arteries.

3. Which method is key for further evaluation following an ECG finding suspicious for cardiac sarcoidosis?

The ECG only points in the direction of the search; LGE-MRI is usually the first imaging modality, revealing scar-fibrotic lesions, while FDG-PET additionally assesses active inflammation or is used when MRI is contraindicated.

Frequently asked questions

Which ECG feature is most characteristic of cardiac sarcoidosis?

The most characteristic finding is unexplained high-grade or complete AV block, especially in a patient younger than 60 years without another obvious cause. Bundle branch block, pathological Q waves, and ventricular arrhythmias are also possible, but a strict combination of signs is not required.

Can a diagnosis of cardiac sarcoidosis be made from a single ECG?

No, the ECG only raises suspicion. The key imaging modality is usually contrast-enhanced cardiac MRI (assessing LGE for scars and fibrosis), while FDG-PET is used additionally to assess inflammation activity or when MRI is contraindicated or inconclusive. The diagnosis is established based on a combination of clinical and imaging criteria; histological confirmation is desirable and preferably obtained from an accessible extracardiac site rather than endomyocardial biopsy, but it is not mandatory in all cases.

Is cardiac sarcoidosis dangerous?

Yes, it is dangerous due to sudden cardiac death from ventricular tachycardia, ventricular fibrillation, or progressive complete AV block. Cardiac involvement is one of the leading causes of death in systemic sarcoidosis, making early detection of heart involvement crucial.

How does a pseudo-infarction Q wave in sarcoidosis differ from a true infarction Q wave?

Reliable differentiation requires correlating clinical presentation, serial ECGs, coronary anatomy as indicated, and cardiac MRI: sarcoidosis more often reveals a non-ischemic, patchy pattern of late gadolinium enhancement (LGE), whereas myocardial infarction shows subendocardial or transmural enhancement within the territory of a single coronary artery. The absence of CAD risk factors does not rule out infarction by itself, as sarcoidosis and CAD can coexist.

Is a pacemaker or defibrillator required in cardiac sarcoidosis?

In high-grade or complete AV block, permanent cardiac pacing is indicated. In cardiac sarcoidosis, the need for permanent pacing usually tips the scale toward an implantable cardioverter-defibrillator (ICD) with pacing capabilities due to the risk of ventricular arrhythmias. Specific indications for an ICD depend on a history of sustained VT or cardiac arrest, an ejection fraction ≤35%, or 36–50% combined with extensive LGE or inducible VT and other risk factors.

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Related terms

More in the section "Pericardium, Lungs, Brain and Others"

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Sources

  • Surawicz B., Knilans T. Chou's Electrocardiography in Clinical Practice
  • Goldberger A. Clinical Electrocardiography: A Simplified Approach
  • AHA/ACCF/HRS Recommendations for the Standardization and Interpretation of the Electrocardiogram, 2009

Educational material for medical students and physicians. Does not replace clinical guidelines and physical examination; the ECG must always be interpreted in conjunction with the clinical picture.