Coronary calcification with no flow limiting lesions: A potential cause for ischaemic dysfunction in syndrome X patients

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.