PURPOSE: To evaluate the relationship between coronary artery calcium (CAC) and coronary vasodilator function. METHODS: We evaluated 136 patients without known coronary artery disease (CAD) undergoing vasodilator stress (82)Rb PET/CT and CAC scoring who showed normal myocardial perfusion. The CAC score, resting and hyperemic myocardial blood flow (MBF), coronary flow reserve (CFR) and coronary vascular resistance were analyzed. RESULTS: Global and regional CAC scores showed significant but weak inverse correlations with hyperemic MBF (r=-0.31 and r=-0.26, p< or =0.0002 respectively) and CFR (r=-0.28 and r=-0.2, p< or =0.001 respectively). With increasing CAC score, there was a modest stepwise decline in CFR on a per-patient basis (1.8+/-0.5 vs 1.7+/-0.5 vs 1.5+/-0.4, p=0.048, with total CAC=0, 1-400 and >400, respectively) and on a per-vessel basis. In multivariable modeling only body mass index and CAC score were predictive of CFR. CONCLUSION: In patients with an intermediate likelihood of, but without overt, CAD, there is a statistically significant but weak inverse correlation between CAC content and coronary vasodilator function. The strength of this association weakens after adjusting CAC scores for age, gender and coronary risk factors. This suggests that CAC and coronary vasodilator function provide biologically different information regarding atherosclerosis.
PURPOSE: To evaluate the relationship between coronary artery calcium (CAC) and coronary vasodilator function. METHODS: We evaluated 136 patients without known coronary artery disease (CAD) undergoing vasodilator stress (82)Rb PET/CT and CAC scoring who showed normal myocardial perfusion. The CAC score, resting and hyperemic myocardial blood flow (MBF), coronary flow reserve (CFR) and coronary vascular resistance were analyzed. RESULTS: Global and regional CAC scores showed significant but weak inverse correlations with hyperemic MBF (r=-0.31 and r=-0.26, p< or =0.0002 respectively) and CFR (r=-0.28 and r=-0.2, p< or =0.001 respectively). With increasing CAC score, there was a modest stepwise decline in CFR on a per-patient basis (1.8+/-0.5 vs 1.7+/-0.5 vs 1.5+/-0.4, p=0.048, with total CAC=0, 1-400 and >400, respectively) and on a per-vessel basis. In multivariable modeling only body mass index and CAC score were predictive of CFR. CONCLUSION: In patients with an intermediate likelihood of, but without overt, CAD, there is a statistically significant but weak inverse correlation between CAC content and coronary vasodilator function. The strength of this association weakens after adjusting CAC scores for age, gender and coronary risk factors. This suggests that CAC and coronary vasodilator function provide biologically different information regarding atherosclerosis.
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