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Updated: Jul 16, 2025

Identifying Coronary Artery Calcification on Non-gated Computed Tomography Scans
Published on: August 28, 2018
Transient left bundle branch block associated with very high coronary artery calcium: a case report
Alexander C Razavi1, Sindhu Prabakaran2, Mariem Sawan3
1Department of Medicine, Division of Cardiology, Emory University School of Medicine, Atlanta, GA, USA.
Insights
Coronary artery calcium (CAC) scoring, a measure of atherosclerosis, may be linked to transient left bundle branch block (LBBB) in patients with chest pain. High CAC burden can guide intensified cardiovascular preventive therapy beyond obstructive disease detection.
Area of Science:
- Cardiology
- Radiology
- Preventive Medicine
Background:
- Coronary artery calcium (CAC) quantifies subclinical atherosclerosis and predicts atherosclerotic cardiovascular disease (ASCVD) risk.
- CAC is underutilized in inpatient chest pain evaluation.
- High CAC burden is strongly associated with ASCVD risk.
Observation:
- A 64-year-old woman with hypertension, type 2 diabetes, and hyperlipidemia presented with dyspnea and elevated troponin.
- Initial ECG showed T-wave inversions; subsequent ECG revealed a new left bundle branch block (LBBB).
- Coronary computed tomography angiography (CCTA) revealed extensive CAC (1262 Agatston score) with nonobstructive disease.
Findings:
- Pharmacologic stress testing noted extensive CAC but no definite ischemia.
- The patient experienced a transient LBBB during the diagnostic workup.
- A CAC score >= 1000 was incidentally associated with LBBB.
Implications:
- CAC measurement can aid in managing chest pain and guiding ASCVD preventive pharmacotherapy.
- Integrating CAC burden into functional testing may optimize statin and other preventive therapies.
- This case highlights the potential association between very high CAC and transient LBBB.
Abstract:
Coronary artery calcium (CAC) is the measure of subclinical coronary artery atherosclerosis most strongly associated with atherosclerotic cardiovascular disease (ASCVD) risk. However, CAC is rarely reported in the inpatient setting to guide chest pain management. We present a case of very high CAC in a 64-year-old woman with hypertension, type 2 diabetes, and hyperlipidemia presenting with dyspnea. Initial electrocardiogram (ECG) demonstrated normal conduction with a heart rate of 76 beats/min, but new T-wave inversions in V1-V4 and a high-sensitivity troponin-I (hsTnI) value of 6 ng/L (normal < 6 ng/L). Repeat ECG in the emergency department showed normal sinus rhythm (heart rate of 80 beats/min); however, it subsequently demonstrated a left bundle branch block (LBBB) with a repeat hsTnI of 7 ng/L. Stress testing with pharmacologic single-photon emission computerized tomography did not show scintigraphic evidence of ischemia but noted extensive CAC and a concern for balanced ischemia. Subsequent coronary computed tomography angiography (CCTA) showed nonobstructive disease and a total Agatston CAC score of 1262. Invasive evaluation with left heart catheterization was deferred given the patient's unchanged symptoms and CCTA findings. Statin therapy was intensified and aspirin, metoprolol succinate, and antihypertension therapies were continued. Initiation of glucose-lowering therapy and lipoprotein(a) testing was strongly recommended on follow-up. Our case suggests that CAC ⩾ 1000 may be incidentally associated with transient LBBB during the workup of coronary artery disease. Here, we specifically show that functional testing that incorporates measurement of CAC burden can help to improve ASCVD-preventive pharmacotherapy initiation and intensification beyond the identification of obstructive disease alone.
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