Montreal-FH-SCORE Predicts Coronary Artery Calcium Score in Patients With Familial Hypercholesterolemia

Béland-Bonenfant, Sarah; Paquette, Martine; Fantino, Manon; Bourque, Lucienne; Saint-Pierre, Nathalie; Baass, Alexis; Bernard, Sophie

doi:10.1016/j.cjco.2020.09.007

Cited by 5 publications

(4 citation statements)

References 32 publications

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“…In line with previous investigations [15,24,25], asymptomatic FH patients included in the present a cohort showed high prevalence and wide extension of CAD, reaffirming the notion that FH must be considered a high-risk group for premature atherosclerotic vascular damage.…”

Section: Discussionsupporting

confidence: 91%

“…Indeed, AS doesn't take into account the presence of soft plaques, and even if several studies [24,25] suggested that it may be useful in ASCVD risk stratification, it cannot exclude reliably the presence of obstructive CAD. In this regard, in our population soft plaques were significantly more represented in the group with obstructive CAD and were the cause of complete vessel obstruction in two patients.…”

Section: Discussionmentioning

confidence: 99%

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Effectiveness of clinical scores in predicting coronary artery disease in familial hypercholesterolemia: a coronary computed tomography angiography study

et al. 2023

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Purpose One of the major challenges in the management of familial hypercholesterolemia (FH) is the stratification of cardiovascular risk in asymptomatic subjects. Our purpose is to investigate the performance of clinical scoring systems, Montreal-FH-score (MFHS), SAFEHEART risk (SAFEHEART-RE) and FH risk score (FHRS) equations and Dutch Lipid Clinic Network (DLCN) diagnostic score, in predicting extent and severity of CAD at coronary computed tomography angiography (CCTA) in asymptomatic FH. Material and methods One-hundred and thirty-nine asymptomatic FH subjects were prospectively enrolled to perform CCTA. MFHS, FHRS, SAFEHEART-RE and DLCN were assessed for each patient. Atherosclerotic burden scores at CCTA (Agatston score [AS], segment stenosis score [SSS]) and CAD-RADS score were calculated and compared to clinical indices. Results Non-obstructive CAD was found in 109 patients, while 30 patients had a CAD-RADS ≥ 3. Classifying the two groups according to AS, values varied significantly for MFHS (p < 0.001), FHRS (p < 0.001) and SAFEHEART-RE (p = 0.047), while according to SSS only MFHS and FHRS showed significant differences (p < 0.001). MFHS, FHRS and SAFEHEART-RE, but not DLCN, showed significant differences between the two CAD-RADS groups (p < .001). MFHS proved to have the best discriminatory power (AUC = 0.819; 0.703–0.937, p < 0.001) at ROC analysis, followed by FHRS (AUC = 0.795; 0.715–0.875, p < .0001) and SAFEHEART-RE (AUC = .725; .61–.843, p < .001). Conclusions Greater values of MFHS, FHRS and SAFEHEART-RE are associated to higher risk of obstructive CAD and might help to select asymptomatic patients that should be referred to CCTA for secondary prevention.

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Section: Discussionsupporting

confidence: 91%

Section: Discussionmentioning

confidence: 99%

Effectiveness of clinical scores in predicting coronary artery disease in familial hypercholesterolemia: a coronary computed tomography angiography study

et al. 2023

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“…In our study of asymptomatic patients with FH, we found a significant number of zero calcium scores (45% of CCS, 48% of TCSasc, and 75% of TCSdsc). We found no similar studies on TCS in FH patients, but the CCS results are comparable to percentages reported by other authors [32]. However, interpreting TCSdsc results requires caution, as they may not adequately reflect the difference in the severity of atherosclerotic burden between both groups, owing to the high percentage of zero calcium scores.…”

Section: Limitations Of the Studysupporting

confidence: 58%

Aortic Wall Thickness as a Surrogate for Subclinical Atherosclerosis in Familial and Nonfamilial Hypercholesterolemia: Quantitative 3D Magnetic Resonance Imaging Study and Interrelations with Computed Tomography Calcium Scores, and Carotid Ultrasonography

Gałąska,

Kulawiak-Gałąska,

Dorniak

et al. 2023

JCM

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We aimed to compare the extent of subclinical atherosclerosis in the ascending and descending aortas by measuring wall area and thickness using 3D cardiovascular magnetic resonance imaging (aAWAI and dAWAI) in patients with asymptomatic familial hypercholesterolemia (FH) and nonfamilial hypercholesterolemia (NFH). We also aimed to establish the interrelations of CMR parameters with other subclinical atherosclerosis measurements, such as calcium scores, obtained using computed tomography in coronary arteries (CCS) and ascending and descending aorta (TCSasc and TCSdsc), as well as the carotid intima-media thicknesses (cIMT) using ultrasonography. A total of 60 patients with FH (29 men and 31 women), with a mean age of 52.3 ± 9.6 years, were analyzed. A subclinical atherosclerosis assessment was also performed on a group consisting of 30 age- and gender-matched patients with NFH, with a mean age of 52.5 ± 7.9 years. We found the ascending and descending aortic wall areas and thicknesses in the FH group to be significantly increased than those of the NFH group. A multivariate logistic regression analysis showed that a positive FH mutation value was a strong predictor of high aAWAI and dAWAI independent of the LDL cholesterol level. Correlations across CMR atherosclerotic parameters, calcium scores, and cIMT in the FH and NFH groups, were significant but low. Most of the atherosclerosis tests with high results belonged to the FH group. We found that patients with documented heterozygous FH had a higher atherosclerosis burden in the aorta compared to patients with severe hypercholesterolemia without FH gene mutation. Atherosclerosis is not severe in asymptomatic patients with FH, but is more pronounced and also more diffuse than in patients with NFH. The etiology of hypercholesterolemia, and not just cholesterol levels, plays a significant role in determining the degree of subclinical atherosclerosis.

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“…Furthermore, the MFHS can effectively identify patients who are currently receiving statin therapy but may require additional treatment to manage their cardiovascular risk. This can assist clinicians in identifying patients who require more intensive treatment 32,33 . The latest Canadian Cardiovascular Society Position Statement recommends the use of MFHS in the FH population 34 …”

Section: Familial Hypercholesterolemiamentioning

confidence: 99%

Genetic backgrounds and diagnosis of familial hypercholesterolemia

Rogozik,

Główczyńska,

Grabowski

2023

Clinical Genetics

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Lipid disorders play a critical role in the intricate development of atherosclerosis and its clinical consequences, such as coronary heart disease and stroke. These disorders are responsible for a significant number of deaths in many adult populations worldwide. Familial hypercholesterolemia (FH) is a genetic disorder that causes extremely high levels of LDL cholesterol. The most common mutations occur in genes responsible for low‐density lipoprotein receptor (LDLR), apolipoprotein B (APOB), or proprotein convertase subtilisin/kexin type 9 (PCSK9). While genetic testing is a dependable method for diagnosing the disease, it may not detect primary mutations in 20%–40% of FH cases.

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Montreal-FH-SCORE Predicts Coronary Artery Calcium Score in Patients With Familial Hypercholesterolemia

Cited by 5 publications

References 32 publications

Effectiveness of clinical scores in predicting coronary artery disease in familial hypercholesterolemia: a coronary computed tomography angiography study

Effectiveness of clinical scores in predicting coronary artery disease in familial hypercholesterolemia: a coronary computed tomography angiography study

Aortic Wall Thickness as a Surrogate for Subclinical Atherosclerosis in Familial and Nonfamilial Hypercholesterolemia: Quantitative 3D Magnetic Resonance Imaging Study and Interrelations with Computed Tomography Calcium Scores, and Carotid Ultrasonography

Genetic backgrounds and diagnosis of familial hypercholesterolemia

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