Atherosclerosis and Cardiovascular Disease
Atherosclerosis is a specific form of arteriosclerosis in which an artery wall thickens as a result of invasion and accumulation of white blood cells (termed "fatty streaks" early on because of appearance being similar to that of marbled steak) and containing both living active WBCs (called inflammation) and remnants of dead cells, including cholesterol and triglycerides, eventually calcium and other crystallized materials, within the outer-most and oldest plaque. These changes reduce the elasticity of the artery walls but do not affect blood flow for decades because the artery muscular wall enlarges at the locations of plaque. However, the wall stiffening may eventually increase pulse pressure; widened pulse pressure is one possible result of advanced disease within the major arteries. It is a syndrome affecting arterial blood vessels, a chronic inflammatory response, i.e. white blood cells, in the walls of arteries, largely involving the accumulation of macrophages and white blood cells and promoted by low-density lipoproteins (LDL, plasma proteins that carry cholesterol and triglycerides) without adequate removal of fats and cholesterol from the macrophages by functional high-density lipoproteins (HDL) (see apoA-1 Milano). It is commonly referred to as a "hardening" or furring of the arteries. It is caused by the formation of multiple atheromatous plaques within the arteries.
Cardiovascular disease refers to any disease that affects the cardiovascular system, principally cardiac disease, vascular diseases of the brain and kidney, and peripheral arterial disease. The causes of cardiovascular disease are diverse but atherosclerosis and/or hypertension are the most common. In addition, with aging come a number of physiological and morphological changes that alter cardiovascular function and lead to increased risk of cardiovascular disease, even in healthy asymptomatic individuals.
Cardiovascular disease is the leading cause of deaths worldwide, though, since the 1970s, cardiovascular mortality rates have declined in many high-income countries. At the same time, cardiovascular deaths and disease have increased at a fast rate in low- and middle-income countries. Although cardiovascular disease usually affects older adults, the antecedents of cardiovascular disease, notably atherosclerosis, begin in early life, making primary prevention efforts necessary from childhood. There is therefore increased emphasis on preventing atherosclerosis by modifying risk factors, for example by healthy eating, exercise, and avoidance of smoking tobacco.
Population-based studies show that atherosclerosis, the major precursor of cardiovascular disease, begins in childhood. The Pathobiological Determinants of Atherosclerosis in Youth Study demonstrated that intimal lesions appear in all the aortas and more than half of the right coronary arteries of youths aged 7–9 years.
This is extremely important considering that 1 in 3 people will die from complications attributable to atherosclerosis. In order to stem the tide, education and awareness that cardiovascular disease poses the greatest threat, and measures to prevent or reverse this disease must be taken.
A fairly recent emphasis is on the link between low-grade inflammation that hallmarks atherosclerosis and its possible interventions. C-reactive protein (CRP) is a common inflammatory marker that has been found to be present in increased levels in patients who are at risk for cardiovascular disease. Also osteoprotegerin, which is involved with regulation of a key inflammatory transcription factor called NF-κB, has been found to be a risk factor of cardiovascular disease and mortality.
An indication of the role of HDL on atherosclerosis has been with the rare Apo-A1 Milano human genetic variant of this HDL protein. A small short-term trial using bacterial synthetized human Apo-A1 Milano HDL in people with unstable angina produced fairly dramatic reduction in measured coronary plaque volume in only six weeks vs. the usual increase in plaque volume in those randomized to placebo. The trial was published in JAMA in early 2006. Ongoing work starting in the 1990s may lead to human clinical trials—probably by about 2008. These may use synthesized Apo-A1 Milano HDL directly, or they may use gene-transfer methods to pass the ability to synthesize the Apo-A1 Milano HDLipoprotein.
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