Accelerated Atherosclerosis

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Accelerated Atherosclerosis

Atherosclerosis which occurs in a person with certain risk factors—e.g., SLE, diabetes, smoking, hypertension, hypercholesterolaemia, family history of early heart disease—at an earlier age than would occur in another person without those risk factors.
References in periodicals archive ?
Hypercholesterolemia and premature atherosclerosis are other typical manifestations.
Antiphospholipid syndrome produces a hypercoagulable state leading to the development of premature atherosclerosis and MI.
Human immunodeficiency virus (HIV) infection is associated with an increased risk of cardiovascular disease through various mechanisms including premature atherosclerosis from endothelial inflammation and platelet dysfunction as well as from cART therapy involving protease inhibitors resulting in dyslipidemia and insulin resistance [1].
AIRDs have been linked to a high risk of cardiovascular (CV) morbidity and mortality, mainly due to premature atherosclerosis (ATS).
Similarly, systemic lupus erythematosus (SLE) is an inflammatory autoimmune disease with a wide range of clinical manifestations and complications.[2] In particular, patients with SLE are prone to premature atherosclerosis. Potential explanations for the accelerated atherosclerosis observed in conjunction with SLE include a high prevalence of conventional risk factors,[3] long-term corticosteroid use,[4] and the presence of antiphospholipid antibodies,[5] all of which result in a chronic state of low-grade inflammation.[6] Recently, the neutrophil-to-lymphocyte ratio (NLR) was proposed as a useful biomarker of inflammation; the NLR is calculated by dividing the neutrophil count by the lymphocyte count.
Complications of sustained pulmonary arterial hypertension that are detectable with CT include central pulmonary artery embolism, premature atherosclerosis of the pulmonary arteries, pulmonary artery dissection, and right heart chamber hypertrophy and dilatation [11].
Doctors say due to rheumatoid arthritis, a state of ongoing inflammation in the body leads to premature atherosclerosis, hypertension, coronary artery disease, cerebrovasular accidents and reduces lifespan by 10 years.
In addition to prospective management of traditional cardiac risk factors, we emphasize the need for aggressive control of rheumatoid arthritis disease activity because chronic inflammation is probably a driving force for premature atherosclerosis.
An isolated reduced high-density lipoprotein cholesterol (HDL-C) is reported to be as a risk factor for premature atherosclerosis [7].
Unrecoverable risk factors include older age, male gender, and family history of premature atherosclerosis. Other modifiable risk factors and their treatment may reduce the risk of atherosclerosis.
Formation of plaques in the heart may lead to premature atherosclerosis and coronary artery disease (CAD), while formation of plaques in vessels of the brains can lead to cerebrovascular disease.
Vascular dysfunction caused by endothelial dysfunction is an early abnormality in the MetS that may contribute to premature atherosclerosis (2).