Three Dimensional Carotid and Femoral Ultrasound is not Superior to Two Dimensional Ultrasound as a Predictor of Coronary Atherosclerosis Among Men With Intermediate Cardiovascular Risk.

BACKGROUND: Current cardiovascular disease (CVD) risk stratification scales, drawn up from traditional risk factors, have important limitations. The detection of subclinical atherosclerosis, by a non-invasive technique such as peripheral arteries ultrasound (US) may improve cardiovascular risk (CVR) stratification, especially in intermediate risk population. Our aim was to compare the predictive power of atherosclerotic plaques detected in carotid and femoral arteries by 2-dimensional (2D) vs. 3-dimensional (3D) US for positive coronary artery calcium score (CACS), used as a proxy for CVD, in a middle-aged sample with intermediate 10-year CVR (7.5-20%). METHODS: To detect atherosclerotic plaques by 2D vs. 3D US scan of carotid and femoral arteries and comparison of their association with CACS obtained by computed tomography (CT) of subjects with intermediate CVR belonging to the Aragon Workers' Health Study. RESULTS: 120 men were included, with a 10.4% average 10 years CVR. Forty-one (34.2%) participants had CACS ≥ 1. 90 participants (75%) had at least one plaque detected by 2D scan while 85 participants (70.8%) had at least a plaque detected by 3D US. Conventional CVR estimates c-statistic for CACS was .590. Although the variables most predicted of CACS ≥ 1 were those measured by 3D US (total plaque volume and mean of plaque density, c-statistics: .743 and .750 respectively), their predictive capacity was not statistically significantly different from the number of territories with plaque, measured either by 2D and 3D US (c-statistics .728 to .740 respectively). CONCLUSION: Subclinical atherosclerosis measured by 2D and 3D US were better predictors of CACS ≥ 1 than CVR estimated by conventional guidelines. In our sample, 3D US did not show any significant advantages with respect to 2D US for the prediction of coronary atherosclerosis.

Aortic Valvular Disease in Elderly Subjects with Heterozygous Familial Hypercholesterolemia: Impact of Lipid-Lowering Therapy.

Hypercholesterolemia and statins are risk factors for aortic stenosis (AS) and vascular calcification, respectively. Whether heterozygous subjects with familial hypercholesterolemia (HeFH) treated with statins are at risk of AS is unknown. We study the prevalence of AS, aortic valve calcification (AoVC), and aortic sclerosis (ASc) in elderly subjects with HeFH in a prolonged statin treatment. Case-control study, cases were adults ≥65 years of age with a genetic diagnosis of HeFH, LDLc >220 mg/dl, and statin treatment ≥5 years. Controls were relatives of HeFH patients, with LDLc <190 mg/dl. Participants underwent a cardiac ultrasound for aortic valve analysis. We studied 205 subjects, 112 HeFH and 93 controls, with mean age 71.8(6.5) years and 70.0(7.3) years, respectively. HeHF, with respect to controls, presented greater gradients of aortic transvalvular pressure, 7.4(7.3) mmHg versus 5.0(2.8) mmHg, and maximum aortic velocity, 1.7(0.7) m/s versus 1.5(0.4) m/s, and lower aortic valve opening area, 2.0(0.7) cm2 versus 2.4(0.6) cm2 (all p < 0.05). AoVC and ASc were also more prevalent in HeFH (p < 0.05 between groups). Moderate/severe AS prevalence was higher among HeFH: 7.1% versus 1.1% (age- and sex-adjusted odds ratio (OR) 8.33, p = 0.03). Independent risk factors for aortic valve disease in HeFH were age and LDLc before treatment. The number of years under statin treatment was not associated with any aortic valve measurement. Subjects ≥65 years with HeFH in prolonged statin treatment show more aortic valvular disease and higher frequency of AS than controls. Life-long elevated LDLc exposure, rather than time of exposure to statins, explains this higher risk.

La lipoproteína(a) se asocia a la presencia de arteriosclerosis en pacientes con hipercolesterolemia primaria / Lipoprotein(a) is associated to atherosclerosis in primary hypercholesterolemia

Introducción: Diferentes estudios epidemiológicos han sugerido que la Lp(a) puede ser un factor de riesgo especialmente en pacientes con hipercolesterolemia. Métodos: Un total de 909 sujetos fueron seleccionados para este estudio, de los cuales 307 fueron diagnosticados de hipercolesterolemia familiar dependiente del LDLR o APOB (HF+), 291 de hiperlipidemia familiar combinada (HFC) y 311 de hipercolesterolemias primarias no dependientes del LDLR ni APOB (HF-). Se estudiaron los principales factores de riesgo, consumo de estatinas, lípidos plasmáticos, Lp(a), HbA1c y proteína C reactiva (PCR). En todos ellos medimos el grosor íntima-media (GIM) de la carótida común y bulbo en ambos lados. Resultados: Los valores de Lp(a) fueron de 21,9 mg/dl (9,24-50,5) en sujetos HF+, 22,4 mg/dl (6,56-51,6) en sujetos con HFC y 32,7 mg/dl (14,6-71,5) en sujetos con HF- (p < 0,001). El análisis de regresión mostró que la concentración de Lp(a) se asoció de forma independiente con el GIM únicamente en los sujetos del grupo HF-. La enfermedad cardiovascular fue más frecuente en sujetos con Lp(a) > 50 mg/dl (17,7%) que en los sujetos con concentraciones < 15 mg/dl (9,6%) y entre 15-50 mg/dl (10,1%), y se concentró fundamentalmente en el grupo de sujetos HF- (6,7, 11,3, y 23,4% para los grupos de Lp[a] < 15 mg/dl, 15-50 mg/dl, y > 50 mg/dl, respectivamente). Conclusiones: La Lp(a) se asocia al desarrollo de arteriosclerosis especialmente en sujetos con HF- (no dependientes del LDLR ni APOB) y concentraciones de Lp(a) > 50 mg/dl

Introduction: Several studies have suggested that Lp(a) could be a risk factor mainly in hypercholesterolemic patients. Methods: A total of 909 individuals were selected for this study. 307 were diagnosed of familiar hypercholesterolemia with a pathogenic mutation in LDLR or APOB genes (FH+), 291 of familiar combined hyperlipidemia (FCH) and 311 of familial hypercholesterolemia without a pathogenic mutation in LDLR nor APOB genes (FH-). Main risk factor were studied, included statin treatment. Plasma lipids, Lp(a), HbA1c and C-reactive protein. Intima-media thickness (IMT) of common and bulb carotid in both sides were measured in all subjects. Results: Lp(a) values (median, interquartile range) were 21.9 mg/dL (9.24-50.5) in FH+, 22.4 mg/dL (6.56-51.6) in FCH and 32.7 (14.6-71.5) in FH- (P < .001). Regression analysis including age, gender, HDL cholesterol, LDL cholesterol corrected for Lp(a), Lp(a), C-reactive protein, packs of cigarettes/day per year, systolic blood pressure and glucose as independent variables, demonstrate that Lp(a) was associated with carotid IMT in FH- subjects. Cardiovascular disease was more frequent in subjects with Lp(a) >50mg/dL (17.9%) than in subjects with Lp(a) < 15 mg/dL (9.6%), and between 15-50mg/dL (10.1%), and it was concentrated mostly in FH-group (6.7, 11.3, and 23.4% for the groups of Lp(a) < 15 mg/dL 15-50 mg/dL, and > 50 mg/dL, respectively). Conclusions: Our results indicate that Lp(a) is associated with atherosclerosis burden especially in subjects with FH- and concentrations of Lp(a) > 50 mg/dL

[Lipoprotein(a) is associated to atherosclerosis in primary hypercholesterolemia]. / La lipoproteína(a) se asocia a la presencia de arteriosclerosis en pacientes con hipercolesterolemia primaria.

INTRODUCTION: Several studies have suggested that Lp(a) could be a risk factor mainly in hypercholesterolemic patients. METHODS: A total of 909 individuals were selected for this study. 307 were diagnosed of familiar hypercholesterolemia with a pathogenic mutation in LDLR or APOB genes (FH+), 291 of familiar combined hyperlipidemia (FCH) and 311 of familial hypercholesterolemia without a pathogenic mutation in LDLR nor APOB genes (FH-). Main risk factor were studied, included statin treatment. Plasma lipids, Lp(a), HbA1c and C-reactive protein. Intima-media thickness (IMT) of common and bulb carotid in both sides were measured in all subjects. RESULTS: Lp(a) values (median, interquartile range) were 21.9mg/dL (9.24-50.5) in FH+, 22.4mg/dL (6.56-51.6) in FCH and 32.7 (14.6-71.5) in FH- (P<.001). Regression analysis including age, gender, HDL cholesterol, LDL cholesterol corrected for Lp(a), Lp(a), C-reactive protein, packs of cigarettes/day per year, systolic blood pressure and glucose as independent variables, demonstrate that Lp(a) was associated with carotid IMT in FH- subjects. Cardiovascular disease was more frequent in subjects with Lp(a) >50mg/dL (17.9%) than in subjects with Lp(a) <15mg/dL (9.6%), and between 15-50mg/dL (10.1%), and it was concentrated mostly in FH-group (6.7, 11.3, and 23.4% for the groups of Lp(a) <15mg/dL 15-50mg/dL, and >50mg/dL, respectively). CONCLUSIONS: Our results indicate that Lp(a) is associated with atherosclerosis burden especially in subjects with FH- and concentrations of Lp(a)>50mg/dL.