Key result
Severe focal myocardial calcification in dialysis patients mimics MI on ECG via pathological Q waves.
Why the study?
Whether myocardial calcification can lead to pathological Q waves on electrocardiogram remains uncertain.
Case Report (n=1)
No
Myocardial calcification should be considered in the differential diagnosis for pathological Q waves on ECG in patients with chronic kidney disease and abnormal calcium-phosphate metabolism.
Alerts clinicians to rare ECG mimic in CKD; single case leaves open need for validation before diagnostic change.
Background: Myocardial infarction is the most common cause of pathological Q waves on electrocardiogram (ECG), but other conditions that cause myocardial injury or abnormal conduction (such as cardiomyopathy, myocarditis, cardiac tumors or amyloidosis, WPW, etc.) can also produce pathological Q waves. Whether myocardial calcification can lead to pathological Q waves remains uncertain. Case summary: A 24-year-old man with a solitary kidney and multiple childhood abdominal surgeries had been on maintenance hemodialysis since 2017 (three times weekly), with a dialysis vintage of approximately 8 years. He was admitted for left upper-limb swelling of 2 months' duration. On admission his temperature was 36.6°C, blood pressure 93/75 mmHg, and heart rate 95 bpm. ECG showed complete left bundle branch block (cLBBB) and pathological Q waves in leads I, aVL, V5 and V6, without significant ST-T elevation. Transthoracic echocardiography(TTE) revealed global cardiac enlargement with marked systolic and diastolic dysfunction (LVEF ≈ 22%, LVEDD 80 mm), and an irregular hyperechoic mass at the cardiac apex measuring approximately 3.0 × 4.0 cm. Contrast chest CT confirmed focal calcifications in the high lateral wall and a hemispherical calcified lesion at the apex. Laboratory tests showed severe renal impairment (serum creatinine 827 µmol/L), markedly elevated NT-proBNP (32,961 pg/ml), mildly elevated troponin I (0.216 ng/ml) and myoglobin >1,000 ng/ml. Prior records documented severe disturbances of mineral metabolism: serum calcium 1.88 mmol/L, serum phosphorus 3.27 mmol/L, 25-OH vitamin D 13.05 ng/ml, and iPTH up to 2,000 pg/ml. Management and outcome: The patient underwent diagnostic evaluation, vascular access revision, and continued dialysis; his symptoms improved and he was discharged. He continues regular outpatient hemodialysis and is under follow-up. Conclusion: We report a rare case of focal myocardial calcification with pathological Q waves in a maintenance dialysis patient. Chronic kidney disease (CKD)-related disturbances of calcium-phosphate metabolism can cause metastatic myocardial calcification. Severe focal calcification may produce mechanical compression and cell necrosis, disrupt electrical coupling, create electrically silent zones, and result in pathological Q waves. In CKD patients with abnormal ECG findings, myocardial calcification should be included in the differential diagnosis and evaluated using imaging and metabolic data.
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Li et al. (2026) conducted a case report in Myocardial calcification and chronic kidney disease (n=1). Myocardial calcification was evaluated on Pathological Q waves on ECG. Severe focal myocardial calcification in a maintenance dialysis patient can produce localized electrical silence and pathological Q waves on electrocardiogram, mimicking myocardial infarction.
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