OBJECTIVE: Presence of coronary artery calcium (CAC) is associated with a high risk of adverse cardiovascular outcomes. Nevertheless, although CAC is a marker of atherosclerosis it is still uncertain whether CAC is a marker of plaque vulnerability. Therefore, the aim of this study was to verify if calcification identifies a vulnerable patient rather than the vulnerable plaque. METHODS: A morphologic and morphometric study on 960 coronary segments (CS) of 2 groups of patients was performed: (i) 17 patients who died from AMI (510 CS); (ii) 15 age-matched control patients without cardiac history (CTRL, 450 CS). RESULTS: Calcification was found in 47% CS of AMI and in 24.5% CS of CTRL. The area of calcification was significantly higher in AMI compared to CTRL (p = 0.001). An inverse correlation was found between the extension of calcification and cap inflammation (r(2) = 0.017; p = 0.003). Multivariate regression analysis demonstrated that the calcification was not correlated with the presence of unstable plaques (p = 0.65). Similarly, the distance of calcification from the lumen did not represent an instability factor (p = 0.68). CONCLUSION: The present study suggests that CAC score evaluation represents a valid method to define the generic risk of acute coronary events in a population, but it is not useful to identify the vulnerable plaque that need to be treated in order to prevent an acute event.
OBJECTIVE: Presence of coronary artery calcium (CAC) is associated with a high risk of adverse cardiovascular outcomes. Nevertheless, although CAC is a marker of atherosclerosis it is still uncertain whether CAC is a marker of plaque vulnerability. Therefore, the aim of this study was to verify if calcification identifies a vulnerable patient rather than the vulnerable plaque. METHODS: A morphologic and morphometric study on 960 coronary segments (CS) of 2 groups of patients was performed: (i) 17 patients who died from AMI (510 CS); (ii) 15 age-matched control patients without cardiac history (CTRL, 450 CS). RESULTS:Calcification was found in 47% CS of AMI and in 24.5% CS of CTRL. The area of calcification was significantly higher in AMI compared to CTRL (p = 0.001). An inverse correlation was found between the extension of calcification and cap inflammation (r(2) = 0.017; p = 0.003). Multivariate regression analysis demonstrated that the calcification was not correlated with the presence of unstable plaques (p = 0.65). Similarly, the distance of calcification from the lumen did not represent an instability factor (p = 0.68). CONCLUSION: The present study suggests that CAC score evaluation represents a valid method to define the generic risk of acute coronary events in a population, but it is not useful to identify the vulnerable plaque that need to be treated in order to prevent an acute event.
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