Arterial Abnormalities in the Offspring of Patients with Premature Myocardial Infarction

Gaeta, Giovanni Battista; Michele, Mario De; Cuomo, Sergio; Guarini, Pasquale; Foglia, M; Bond, M. Gene; Trevisan, Maurizio

doi:10.1056/nejm200009213431203

Cited by 174 publications

(116 citation statements)

References 32 publications

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“…Our findings are compatible with animal studies demonstrating that higher-frequency pulsatile flow was associated with increased NO release. 28 A genetic contribution to endothelial function has been supported by earlier studies demonstrating that young individuals with a family history of CVD have diminished endothelial function 29,30 and that genetic polymorphisms may influence endothelial function. 31,32 Heritability estimates the portion of the variability accounted for by genetic factors after adjusting for the clinical correlates retained in the model.…”

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confidence: 91%

Clinical Correlates and Heritability of Flow-Mediated Dilation in the Community

et al. 2004

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Background-Studies in selected samples have linked impaired endothelial function with cardiovascular disease and its risk factors. The clinical correlates and heritability of endothelial function in the community have not been described. Methods and Results-We examined a measure of endothelial function, brachial artery flow-mediated dilation (FMD), expressed as both percent (FMD%) and actual dilation by ultrasound with the occlusion cuff below the elbow in 2883 Framingham Study participants (52.9% women; mean age, 61 years). A subset of 1096 participants performed a 6-minute walk test before FMD determination. Mean FMD% was 3.3Ϯ3.0% in women and 2.4Ϯ2.4% in men. In stepwise multivariable linear regression models, FMD% was inversely related to age, systolic blood pressure, body mass index (BMI), lipid-lowering medication, and smoking, whereas it was positively related to female gender, heart rate, and prior walk test. The estimated heritability of FMD% was 0.14. FMD actual dilation findings were similar, except that female sex and BMI were not significantly associated. Conclusions-Increasing age, systolic blood pressure, BMI, and smoking were associated with lower FMD% in our community-based sample, whereas prior exercise and increasing heart rate were associated with higher FMD%. The estimated heritability of FMD was modest. Future research will permit more complete characterization of the genetic and environmental determinants of endothelial function and its prognostic value in the community. Key Words: endothelium Ⅲ epidemiology Ⅲ risk factors Ⅲ genetics B rachial artery flow-mediated dilation (FMD) serves as a measure of endothelial vasodilator function in humans. 1 Experimental and clinical studies suggest that development of endothelial dysfunction, including reduced NO bioavailability, contributes to the atherosclerosis and pathogenesis of cardiovascular disease (CVD) events. 2 Human studies demonstrate that endothelial dysfunction precedes the development of clinically apparent atherosclerosis in individuals with CVD risk factors such as smoking, 3 hypertension, 4 hyperlipidemia, 5 diabetes mellitus, 5 and obesity. 6 Furthermore, effective treatment of risk factors may reverse endothelial dysfunction. 7 Finally, studies in individuals with risk factors or prevalent CVD have demonstrated that endothelial dysfunction identifies patients at risk for future CVD events. 2,8 Previous investigations relating risk factors to endothelial dysfunction largely were limited to small, highly selected samples. Our objective was to assess the independent correlates of endothelial function in a large community-based sample. MethodsThe Framingham Offspring Study design has been described elsewhere. 9 Participants in the seventh examination (1998 to 2001) were eligible for the present investigation (nϭ3539). Exclusion criteria were residence in a nursing home (nϭ205), mastectomy (nϭ34), Raynaud disease (nϭ9), subject refusal (nϭ83), equipment malfunction/miscellaneous (nϭ15), predigital capture (nϭ177), or technically inade...

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confidence: 91%

Clinical Correlates and Heritability of Flow-Mediated Dilation in the Community

et al. 2004

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“…The vessels in the offspring or relatives of patients with premature CAD show structural and functional changes more commonly, even before clinically manifestations start [50]. Therefore, individual differences in endothelial function are susceptible to later atherosclerosis, might relate not only to different levels of exposure to risk factors, but also to inter-individual differences in the carriage of risk alleles of genes expressed in the vascular endothelium.…”

Section: Genetics Of Endothelial Dysfunctionmentioning

confidence: 99%

Endothelial Dysfunction in Type 2 Diabetes Mellitus

et al. 2015

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Endothelial dysfunction is an imbalance in the production of vasodilator factors and when this balance is disrupted, it predisposes the vasculature towards prothrombotic and pro-atherogenic effects. This results in vasoconstriction, leukocyte adherence, platelet activation, mitogenesis, pro-oxidation, impaired coagulation and nitric oxide production, vascular inflammation, atherosclerosis and thrombosis. Endothelial dysfunction is focussed as it is a potential contributor to the pathogenesis of vascular disease in diabetes mellitus. Under physiological conditions, there is a balanced release of endothelial-derived relaxing and contracting factors, but this delicate balance is altered in diabetes mellitus and atherosclerosis, thereby contributing to further progression of vascular and endorgan damage. This review focuses on endothelial dysfunction in atherosclerosis, insulin resistance, metabolic syndrome, oxidative stress associated with diabetes mellitus, markers and genetics that are implicated in endothelial dysfunction.

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“…In particular, acute reactions to infectious agents are associated with an increased risk of both arterial ischaemic events and VTE and are accompanied by both arterial and venous endothelial dysfunction (40,43,44); increased circulating levels of some biomarkers of endothelial dysfunction, like endothelial microparticles or P-selectin, are associated with both an enhanced risk of cardiovascular events and of VTE (45)(46)(47); recent data have shown in patients with VTE an increase of circulating fibronectin, an endothelium-released plasma factor previously shown to correlate with arterial endothelial dysfunction (48,49); several other clinical conditions characterised by an impaired arterial endothelial function, like airpollution, chronic HIV infection, a family history of myocardial infarction, the metabolic syndrome, rheumatoid arthritis and microalbuminuria, have been reported to be associated not only with an increased risk of arterial events but also of venous thrombosis (12,14,16,19,21,22,(50)(51)(52).…”

Section: (ǡTable 2)mentioning

confidence: 99%

Endothelium, venous thromboembolism and ischaemic cardiovascular events

Gresele

Momi

Migliacci³

2010

Thromb Haemost

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SummaryThe association between venous thromboembolism and arterial thrombosis has emerged as consistent clinical observation in the last few years. While several experimental, epidemiological and pharmacologic studies support this association, the initial pathophysiological mechanism linking these two clinical conditions remains to be established. This review discusses the pathophysiological bases and a number of ex- perimental and clinical observations suggesting that the common link between venous thromboembolism and arterial thrombosis is represented by a dysfunctional endothelium.

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Arterial Abnormalities in the Offspring of Patients with Premature Myocardial Infarction

Abstract: Structural and functional changes are present at an early age in the arteries of persons with a parental history of premature myocardial infarction.

Cited by 174 publications

References 32 publications

Clinical Correlates and Heritability of Flow-Mediated Dilation in the Community

Clinical Correlates and Heritability of Flow-Mediated Dilation in the Community

Endothelial Dysfunction in Type 2 Diabetes Mellitus

Endothelium, venous thromboembolism and ischaemic cardiovascular events

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