Early Cardiovascular Disease (early + cardiovascular_disease)

Distribution by Scientific Domains


Selected Abstracts


Identifying Early Cardiovascular Disease to Target Candidates for Treatment

JOURNAL OF CLINICAL HYPERTENSION, Issue 3 2008
Daniel A. Duprez MD
Most attempts to identify individuals at risk for cardiovascular morbid events have involved screening for risk factors. These traditional risk factors do not identify the underlying atherosclerotic disease nor assess the severity of disease in individual patients. The goal for identifying a marker or markers for early cardiovascular disease that could serve as a surrogate for disease progression and ultimate morbid events is to improve the precision for early detection and treatment. The authors utilize a variety of techniques, which consist of 7 vascular tests (large and small artery elasticity, resting blood pressure and exercise blood pressure response, optic fundus photography, carotid intimal-media thickness, and microalbuminuria) and 3 cardiac tests (electrocardiography, [N-terminal pro-] B-type natriuretic peptide, and left ventricular ultrasonography). Each test is individually scored, and the total disease score is the sum of all the test scores. A study is ongoing to compare the new disease score vs the classical Framingham risk estimate in the prediction of cardiovascular events. [source]


Impact of genetic defects on coronary atherosclerosis in patients suspected of having familial hypercholesterolaemia

EUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 1 2003
O. S. Descamps
Abstract Background In the present study we assessed whether the presence of genetic mutations typical of familial hypercholesterolaemia (FH) was associated with greater atherosclerosis in the coronary vessels in patients with severe hypercholesterolaemia and a family history of early cardiovascular disease. Materials and methods Two hundred and thirty-five patients selected for having severe hypercholesterolaemia and a family history of cardiovascular disease were classified as FH (57 men and 38 women) or non-FH (84 men and 56 women) according to a genetic analysis of the LDL-R or ApoB genes. Coronary atherosclerosis was evaluated by performing a thoracic CT scan and exercise stress testing. Results Familial hypercholesterolaemia individuals had a significantly higher prevalence of coronary calcification than the non-FH patients from among both the men (OR = 3·90; 95% CI 1·86,8·19; P < 0·001) and the women (OR = 2·34; 95% CI 1·01,5·48; P = 0·05). In exercise stress testing, ECG abnormalities suggestive of cardiac ischaemia were found with a higher prevalence in the FH patients than the non-FH patients from among both the men (OR 6·15; 95% CI 2·16,17·5; P < 0·001) and the women (OR 4·76; 95% CI 0·91,24·6; P = 0·06). All differences were statistically significant after adjusting for age and cholesterol and for most classical risk factors that differed between the FH and non-FH groups. Conclusion Among patients with severe hypercholesterolaemia and a family history of early cardiovascular disease, the presence of a genetically ascertained FH is associated with a higher prevalence of coronary artery calcifications and a positive exercise stress test. These results suggest that despite a similar phenotype, patients carrying mutations suggestive of FH may have a greater cardiovascular risk than patients without these mutations. [source]


Identifying Early Cardiovascular Disease to Target Candidates for Treatment

JOURNAL OF CLINICAL HYPERTENSION, Issue 3 2008
Daniel A. Duprez MD
Most attempts to identify individuals at risk for cardiovascular morbid events have involved screening for risk factors. These traditional risk factors do not identify the underlying atherosclerotic disease nor assess the severity of disease in individual patients. The goal for identifying a marker or markers for early cardiovascular disease that could serve as a surrogate for disease progression and ultimate morbid events is to improve the precision for early detection and treatment. The authors utilize a variety of techniques, which consist of 7 vascular tests (large and small artery elasticity, resting blood pressure and exercise blood pressure response, optic fundus photography, carotid intimal-media thickness, and microalbuminuria) and 3 cardiac tests (electrocardiography, [N-terminal pro-] B-type natriuretic peptide, and left ventricular ultrasonography). Each test is individually scored, and the total disease score is the sum of all the test scores. A study is ongoing to compare the new disease score vs the classical Framingham risk estimate in the prediction of cardiovascular events. [source]


Elevated Lp(a) with a small apo(a) isoform in children: risk factor for the development of premature coronary artery disease

ACTA PAEDIATRICA, Issue 12 2008
Albert Dirisamer
Background: levels of Lp(a) and low-molecular-weight apolipoprotein(a) isoform are strongly associated with the development of early cardiovascular disease. Certain types of apo(a) isoforms in combination with elevated levels of Lp(a) may be important in the determining of premature coronary artery disease. Therefore, we investigated the association of familial history of premature coronary artery disease and apo(a) size and Lp(a) levels in children and adolescents with hypercholesterolemia using a novel method determining apo(a) isoforms. Methods and results: Isoforms were classified in six phenotype patterns: S1,S4, B, F and according to their K-IV repeats. Apo(a) isoforms were divided into two groups: low-molecular- and high-molecular apo(a) isoforms. In subjects with double-banded apo(a) isoforms containing a small- and a large-isoform Lp(a) each contribution was based on the intensity of staining of the two bands. The percentage of patients with elevated levels of Lp(a) and a small apo(a) isoform (i.e. elevated small-isoform Lp(a)) was 46% in the risk group and 20% in the control group, p < 0.05. The percentage number of children and adolescents with elevated Lp(a) levels was higher in the risk group, reaching statistical significance (p < 0.05). Conclusion: Elevated levels of small-isoform Lp(a) might be a strong and independent risk factor for the development of premature coronary artery disease in children and adolescents with hypercholesterolemia. [source]