Results from Cardiovascular Examination Do Not Predict Cerebrovascular Macroangiopathy: Data from a Prospective, Bicentric Cohort Study

Background: There is a large overlap in the risk profiles and pathophysiologies of coronary artery disease (CAD) and cerebrovascular macroangiopathy. Therefore, this study aimed to analyse whether findings in CAD examination by coronary angiography or cardio-computer tomography (cardio-CT) are predictive of cerebrovascular macroangiopathy. Methods: Our study was a prospective, bicentric, cross-sectional cohort study. A total of 191 patients without earlier CAD diagnosis who underwent a cardio-CT scan or coronary angiography for the screening of CAD during clinical routine were serially included. Two groups were formed based on the criterion of CAD (yes/no), and both were subsequently examined using sonography of the carotids. The CAD scores Syntax score I, Agatston equivalent score, and CAD-RADS score as well as AHA classification were determined. In cerebrovascular examinations, plaques and stenoses of the internal carotid artery (ICA) and the intima-media thickness (IMT) of the common carotid artery were analysed. Demographic and medical data such as the presence of arterial hypertension, diabetes mellitus, obesity, nicotine abuse, and dyslipidaemia were documented. The primary endpoint was the nominal association between CAD and ICA stenosis controlled for age and gender; secondary endpoints were correlations between ICA stenoses and CAD scores. Results: Of the 191 serially recruited patients (58% male, 65 ± 11 yrs.), 101 fulfilled CAD criteria; 90 did not. Of all patients, 137 had ICA plaques, and 11 thereof had an ICA stenosis ≥ 50%. No association was found between CAD and ICA stenosis (Wald = 0.24; p = 0.624). Accordingly, there was no association between IMT and Syntax score I (Wald = 0.38; p = 0.706), Agatston equivalent score (Wald = 0.89; p = 0.380), CAD-RADS score (Wald = 0.90; p = 0.377), or AHA classification (Wald = 0.21; p = 0.837). Common cardiovascular risk factors, i.e., arterial hypertension (Wald = 4.47; p = 0.034), diabetes mellitus (Wald = 7.61; p = 0.006), and nicotine abuse (Wald = 0.83; p = 0.028), were associated with newly diagnosed CAD but not with ICA plaques, stenosis, or increased IMT. Conclusions: In our cohort, newly diagnosed CAD was associated with typical risk factors. However, neither CAD nor these risk factors were associated with cerebrovascular disease. This suggests that in patients without prior CAD diagnosis, findings from CAD examinations might not be reliably predictive of cerebrovascular disease.