Hereditary and environmental influences on arterial function.
1. With the ageing population and increasing heart failure, arterial function has been shown to contribute to cardiovascular risk because of its adverse effects on ventriculovascular coupling. Population studies have confirmed independent prognostic information of arterial stiffening on cardiovascular survival. 2. The term 'arterial function' encompasses a range of phenotypes, including measures of arterial structure/remodelling, measures of arterial wall mechanics, surrogate measures of stiffness and of wave reflection. There exists significant interaction between these measures and none is truly independent of the others. Added to this complexity is the recognition that, although arterial function has a strong genetic component, quantification requires a range of techniques from twin to family and population studies. 3. The contribution of heritability is often derived from statistical models with input from genomic scanning and candidate gene studies. Studies to date confirm a significant heritable component for the majority of phenotypes examined. However, it has also been recognized that the factors involved in blood pressure maintenance are likely to be separate to those in arterial structural degeneration with ageing. Candidate genes for arterial function go beyond those of the sympathetic and renin-angiotensin systems and include genes involved in signalling pathways and extracellular matrix modulation. 4. The present review examines the evidence for heritability of the major arterial function phenotypes with environmental and ageing modulation. A brief overview of the impact of atherosclerotic risk factors on arterial function is included.
Hayward
C S
CS
Heart Failure and Transplant Unit, Department of Cardiology, St Vincent's Hospital, Sydney, New South Wales, Australia. cshayward@stvincents.com.au
Benetos
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A
D000375:Aging / Q000235:genetics*; D001158:Arteries / Q000473:pathology / Q000503:physiopathology*; D050197:Atherosclerosis / Q000150:complications / Q000235:genetics* / Q000473:pathology / Q000503:physiopathology; D001794:Blood Pressure / Q000235:genetics; D002318:Cardiovascular Diseases / Q000235:genetics* / Q000473:pathology / Q000503:physiopathology; D003187:Compliance; D030541:Databases, Genetic; D005109:Extracellular Matrix / Q000235:genetics; D020022:Genetic Predisposition to Disease; D005828:Genetics, Population; D006801:Humans; D008957:Models, Genetic; D015233:Models, Statistical; D010375:Pedigree; D010641:Phenotype; D011110:Polymorphism, Genetic; D011673:Pulsatile Flow / Q000235:genetics; D040641:Quantitative Trait Loci; D012307:Risk Factors; D015398:Signal Transduction / Q000235:genetics; D018433:Twin Studies as Topic