RESUMO
Accurate identification of individuals at high coronary risk would reduce acute coronary syndrome incidence and morbi-mortality. We analyzed the effect on coronary risk prediction of adding coronary artery calcification (CAC) and Segment Involvement Score (SIS) to cardiovascular risk factors. This was a prospective cohort study of asymptomatic patients recruited between 2013-2017. All participants underwent a coronary computed tomography angiography to determine CAC and SIS. The cohort was followed-up for a composite endpoint of myocardial infarction, coronary angiography and/or revascularization (median = five years). Discrimination and reclassification of the REGICOR function with CAC/SIS were examined with the Sommer's D index and with the Net reclassification index (NRI). Nine of the 251 individuals included had an event. Of the included participants, 94 had a CAC = 0 and 85 a SIS = 0, none of them had an event. The addition of SIS or of SIS and CAC to the REGICOR risk function significantly increased the discrimination capacity from 0.74 to 0.89. Reclassification improved significantly when SIS or both scores were included. CAC and SIS were associated with five-year coronary event incidence, independently of cardiovascular risk factors. Discrimination and reclassification of the REGICOR risk function were significantly improved by both indexes, but SIS overrode the effect of CAC.
RESUMO
Heterozygous familial hypercholesterolemia (HeFH) can be associated with early coronary artery disease (CAD) in asymptomatic patients. The objectives of the present study were to assess the prevalence and magnitude of subclinical CAD in patients with HeFH using coronary computed tomographic angiography (CCTA) and to determine the clinical and genetic profile of those at the greatest risk of CAD. The study included 50 consecutive patients with HeFH diagnosed according to the Dutch Lipid Clinic Network criteria and a control group of 70 healthy subjects. The findings from CCTA for the patients with HeFH were compared with those from the control group, who had been referred for CCTA as a part of a preventive medical examination. In 82% of the patients with HeFH, genetic DNA was screened for low-density lipoprotein receptor (LDLR) gene mutations using a microarray. CCTA revealed a significantly greater Agatston calcium score in the study group than in the control group (260 vs 46; p = 0.002). The prevalence of CAD in the patients with HeFH was 48%. It was significant in 26%, involving mainly the proximal segments of the coronary arteries. In the control group, the prevalence of CAD was 33% and was significant in 5% (p <0.05 for prevalence and severity of CAD compared to patients with HeFH). In those with HeFH, increased age, null allele LDLR mutations, and low high-density lipoprotein blood levels at diagnosis showed a statistically significant association with CAD (p <0.05). In conclusion, patients with HeFH present with a greater prevalence, extension, and severity of subclinical CAD than the general population. Increased age, low high-density lipoprotein levels, and LDLR null allele mutations are related to the occurrence of CAD. CCTA has emerged as a useful technique for the screening of subclinical CAD in patients with HeFH.
