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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Measurements of aortic length and circumference in 336 post-mortem specimens confirm earlier, neglected observations on the progressive increase in aortic size which occurs with advancing years. The increase is not related to atherosclerosis , or to hypertension and seems to be part of a true ageing process. The value of measurement of aortic size in body age determination merits exploration by forensic pathologists. Aortic calcification is found in raised and complicated atherosclerotic plaques and its prevalence and severity closely follows the accepted pattern of plaque severity, occurring earlier and more severely in men, in the abdominal aorta and in patients with overt vascular disease in other territories such as patients with cardiac infarcts. No association was found between the amount of calcification and the presence of hypertension, diabetes or neoplasia.
Atherosclerosis 1977 Aug
PMID:Aortic size and aortic calcification. A necropsy Study. 88

Aortic calcification was evaluated preoperatively by computed tomography (CT) in 136 of 275 candidates for coronary artery bypass surgery (age range, 30-80) years (mean 60.2 years), including 110 men and 26 women), from April 1989 to March 1991. Calcification in the mid-ascending aortic wall was detected in 20 (14.7%) cases, calcification in all regions of the aorta was more common in patients older than 60 years (22.5%, n = 71), than younger (6.2%, n = 65) (p less than 0.01). Atherosclerosis of the ascending aorta was identified intraoperatively in 25 (18.3%) cases. Practically, the specificity of CT findings was excellent (98.3%), but the sensitivity was less satisfactory (72.0%) due to the presence of atherosclerosis without calcification. In cases of arteriosclerosis of the ascending aorta, great care was taken to prevent embolism secondary to a dislodged atheromatous plaque. The "aortic no-touch technique", with in situ internal thoracic artery and right gastroepiploic artery anastomosis under ventricular fibrillation, was performed in 6 cases, a single aortic cross-clamp was applied in 19 cases, and conventional methods were employed when the ascending aorta was normal or the "no-touch" or "single-clamp" procedure could not be used (control, 111 cases). No neurologic complications occurred in the "no-touch" group, while 2 cerebral infarctions occurred in the single-clamp group (10.5%) and the control group (1.8%) respectively. These differences between groups was not significant. Patients with a calcified ascending aorta are at higher risk for neurologic complications of coronary bypass. The risk can be decreased by minimizing surgical trauma to the ascending aorta by the use of "no-touch" techniques.
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PMID:[The calcified ascending aorta--preoperative evaluation and intraoperative management]. 140 60

Since aortic calcification is seen on X-rays of the prelumbar region in many patients, its relation with cardiovascular disease (CVD) was investigated in a prospective study in The Netherlands. X-rays were taken of 1359 men and 1598 women, in 1975-78. In the subsequent 9 years, 50 men and 33 women died from CVD. The prevalence of aortic calcification was about 10% in middle-aged subjects and rose with age to a maximum of 45% in men and 75% in women. Aortic calcification was associated with a six-fold increased risk of CVD death in men aged 45 years, independent of major CVD risk factors. For each year of age over 45, risk associated with the presence of aortic calcification declined by 6%. Death rates in middle-aged women were too small for risk analysis. These results suggest that atherosclerosis in other than coronary or cerebral vessels may have predictive relevance for CVD death: its diagnosis indicates intervention on present CVD risk factors.
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PMID:Aortic calcification as a predictor of cardiovascular mortality. 287 72

Eleven of 14 survivors who sustained trauma to the abdominal aorta have been evaluated 16 to 18 years after injury through personal interview, physical examination, and abdominal contrast computerized tomography (CCT). The average age of survivors was 39 years (range, 37-47). All patients had minimal debridement of the aortic injury with lateral arteriorrhaphy. No patients had symptoms of arterial insufficiency. However, five patients had abnormal ankle/brachial indices (ABI). In four patients, ABI was less than 1.00 at rest and a fifth patient's ABI decreased significantly: 0.60 left and 0.65 right from an average of 1.00 bilaterally after standardized exercise treadmill. CCT evaluation revealed aortic calcification in five patients in the area of aortic injury. Aortic calcification occurred only in the patients with abnormal ABI's. This long-term followup identifies no evidence for late compromise in the aorta; however, there is a suggestion that injury and repair may contribute to the accelerated development of atherosclerosis.
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PMID:Long-term followup of penetrating abdominal aortic injuries after 15 years. 341 61

Aortic calcification was demonstrated in experimental animal models of hyperhomocysteinemia. Mild hyperhomocysteinemia was associated with aortic calcification, suggesting a relationship between homocysteine (HCY) and the pathogenesis of aortic calcification. In the present study, the effect of HCY on vascular calcification was examined in calcifying and non-calcifying vascular smooth muscle cells (VSMCs). Cell calcification was induced by incubation of VSMCs with beta-glycerophosphate. Proliferation of VSMCs was studied by cell counting, 3H-thymidine (3H-TdR) and 3H-leucine (3H-Leu) incorporation. 45Ca accumulation, cell calcium content, and alkaline phosphatase (ALP) activity were measured as indices of calcification. The results showed that the proliferation of calcifying VSMCs, which was indicated by cell counting, 3H-TdR and 3H-Leu incorporation in calcifying VSMCs, was enhanced as compared with that of non-calcifying VSMCs. HCY promoted increases in cell number, 3H-TdR and 3H-Leu incorporation in both calcifying and non-calcifying VSMCs, but with more prominent effect in calcifying VSMCs. The stimulating effects of HCY on the three parameters in calcifying VSMCs were antagonized by PD98059, a specific inhibitor of mitogen activated protein kinase kinase (MAPKK). The ALP activity, 45Ca uptake, and calcium deposition in the calcifying VSMCs were greater than those in non-calcifying VSMCs. PD98059 had no effect on ALP activity, 45Ca uptake, and calcium deposition in calcifying VSMCs. HCY caused marked increases in 45Ca uptake and calcium deposition both in calcifying and non-calcifying VSMCs. HCY, however, enhanced ALP activity in the calcified VSMCs but not in the non-calcifying VSMCs. The non-calcifying VSMCs treated with HCY showed the same low ALP activity, as did the control VSMCs. In calcifying VSMCs, the HCY-induced increases in 45Ca uptake, calcium deposition, and ALP activity were also attenuated by PD98059. The results demonstrated that HCY potentiated VSMC calcification probably through the mechanisms by which HCY promotes atherosclerosis.
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PMID:Homocysteine potentiates calcification of cultured rat aortic smooth muscle cells. 1460 23