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Updated: Feb 25, 2026
Identifying Coronary Artery Calcification on Non-gated Computed Tomography Scans
Published on: August 28, 2018
Coronary calcification with no flow limiting lesions: A potential cause for ischaemic dysfunction in syndrome X
Elisabetta Palmerini1, Henrik Antti2, Dmitry Shungin3,4
1E. Malan Heart Centre, Department of Cardiovascular Diseases, IRCCS San Donato Hospital, Milan, Italy.
Insights
Coronary artery calcification (CAC) is linked to exertional angina in patients without obstructive coronary lesions. Higher CAC scores correlate with impaired ventricular function and reduced blood flow reserve, suggesting CAC causes stiffness and ischemia.
Area of Science:
- Cardiology
- Medical Imaging
- Physiology
Background:
- Exertional angina without obstructive coronary lesions is a diagnostic challenge.
- Coronary artery calcification (CAC) may play a role in these symptoms.
Purpose of the Study:
- To assess CAC extent and its relationship with ventricular wall motion using stress echocardiography.
- To investigate the link between CAC and exertional angina in patients with non-obstructive coronary artery disease.
Main Methods:
- Compared CT coronary calcium score (CACS) and dobutamine stress echocardiography in 55 patients.
- Divided patients into groups based on CACS (<100 vs. >100).
- Utilized multiple linear regression to analyze echocardiographic parameters against CACS and patient groups.
Main Results:
- Patients with higher CACS (>100) showed reduced resting left ventricular (LV) long axis function and increased left atrial (LA) volume.
- Stress echocardiography revealed worsening LV function and increased wall motion score index in the higher CACS group.
- Multivariate analysis confirmed correlations between ischemic LV disturbances, reduced long axis function, and CAC score.
Conclusions:
- Symptomatic patients with non-obstructive coronary lesions and significant CAC exhibit stress-induced LV dysfunction.
- CAC severity correlates with these functional changes, suggesting it contributes to coronary wall stiffness and limited flow reserve.
- CAC may be a key mechanism underlying exertional ischemia in this patient population.
Aim:
Exertional angina in patients with no coronary flow limiting lesions remains a clinical puzzle. We aimed to assess the extent of coronary artery calcification (CAC) and its relationship to ventricular wall motion function using stress echocardiography in a group of patients limited by exertional angina, but no obstructive lesions.
Methods:
We compared CT coronary calcium score (CACS) and dobutamine stress echocardiography in 55 patients (age 64.7 ± 7.7 years), divided into Group 1 (CACS ≤ 100) and Group 2 (CACS > 100). No patient had LV ejection fraction-EF < 55%, pulmonary hypertension, arrhythmia, renal failure or parathyroid disease. Multiple linear regression analysis was used to test the association between gender-standardized continuous echocardiographic parameters and patient groups adjusted for age, body surface area, osteoporosis and CV risk factors and CACS.
Results:
At rest, LV long axis 'subendocardial' function was reduced (amplitude: β - 1.11 SD, p < 0.05, R2 0.6 and systolic velocity: β - 1.08 SD, p < 0.05, R2 0.44), left atrial (LA) indexed volume was raised (β 1.06 SD, p < 0.05, R2 0.37) and its systolic velocity decreased (β - 1.05 SD, p < 0.05, R2 0.35) in Group 2. With stress, wall motion score index increased (p < 0.05) and long axis disturbances worsened only in the same group. Multivariate analysis demonstrated clear relationship between ischaemic LV disturbances, reduced long axis amplitude, global longitudinal systolic strain and early diastolic strain rate. Resting and stress RV lengthening velocity also correlated with CAC score.
Conclusion:
In symptomatic patients with no obstructive coronary lesions and with more than mild CAC, long axis disturbances and wall motion score index rise occur with stress, at the time of symptom development and correlate with severity of arterial calcification. These findings suggest CAC as a potential mechanism for coronary wall stiffness and consequently exertional ischaemic changes as a result of limited flow reserve.
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