Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004153 (atherosclerosis)
77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Reports documented a higher frequency of apolipoprotein E (apoE) allele epsilon 4 among mothers of children diagnosed with Down syndrome. We studied the prevalence of apoE alleles among 56 conceptuses with trisomy 13, trisomy 18, or trisomy 21. The presence of the 3 most common apoE alleles (epsilon 2, epsilon 3, epsilon 4) was determined by polymerase chain reaction-restriction fragment length polymorphism, and trisomy status was detected by fluorescent polymerase chain reaction followed by DNA fragment analysis and by conventional cytologic methods. We found no significant difference in the distribution of apoE alleles in the group of trisomy 21 fetuses compared with samples from healthy blood donors. The odds of having trisomy 18 for the apoE epsilon 4 group was 3-fold as high as for apoE epsilon 3 allele compared with the healthy control group. Furthermore, a statistically significant association was found for those with trisomy 18 and apoE epsilon 4, while for those with trisomy 13 and apoE epsilon 4, the test showed no significant association. The observed apoE allele epsilon 3 frequencies among patients with Down syndrome and healthy control subjects may help explain and support previous work that did not find high rates of atherosclerosis among these persons. The role of apoE alleles in the development of trisomies needs further study.
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PMID:Apolipoprotein E allele distribution in trisomy 13, 18, and 21 conceptuses in a Hungarian population. 1076 55

A saccular aneurysm in the right-sided aortic arch with aberrant left subclavian artery is an uncommon disease, and surgical treatment is complicated. Three patients with Edwards type III-B right aortic arch and enlargement of the Kommerell's diverticulum underwent operations. Right thoracotomy was the preferred approach for this lesion and partial cardiopulmonary bypass is a safe and simple procedure when the aortic arch has mild atherosclerosis.
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PMID:Surgical treatment of an aneurysm in the right aortic arch with aberrant left subclavian artery. 1138 41

This study investigated the previously uncertain relationship of embolic load captured during coronary artery bypass grafting and the extent of ascending aortic atherosclerosis as measured by wall thickness. Patients (n=113) underwent isolated arrested heart coronary artery bypass grafting. Ascending aortic wall thickness measures were obtained by epiaortic ultrasound. Aortic segmental values (distal, mid, proximal) were determined by the summation of measures (anterior lateral, posterior, medial) at each segment. An intraaortic filter (EMBOL-X) System, Edwards Lifesciences, Irvine, CA) was placed into the arterial cannula, distal to the aortic measurements, just before releasing the aortic cross-clamp. Particulate debris was found in 96% (109/113) of filters. Mean number of particles was 6.8+/-4.8 (range 0-23) and mean particle surface area was 5.5+/-7.0 mm(2) (range 0-51 mm(2)). Total aortic wall thickness, distal third, mid third, and proximal third thicknesses were 27.4+/-4.4 mm, 9.5+/-2.0 mm, 9.0+/-1.9 mm, and 8.8+/-1.4 mm, respectively. There was no significant correlation between the number of particles or surface area and any of the aortic wall thickness measures. These results suggest that during on-pump, arrested heart coronary artery bypass grafting, embolic load from the ascending aorta is independent of the extent of ascending aortic atherosclerosis in patients with low or moderate risk aortic pathology.
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PMID:Do particulate emboli from the ascending aorta in coronary bypass grafting correlate with aortic wall thickness? 1767 Jun 92

After reviewing the general characteristics of lipids (LDL-C, VLDL-C, HDL-C) and atherothrombosis, including the I-VIII degrees of its histopathological arterial lesions (with contributions of J. E. Edwards and R. Virmani), the authors described the P. Libby's data on lipoprotein-associated phospholipaseA2 (Lp-PLA2) and its two inflammatory mediators: lysophosphatidylcholine and oxidized nonesterified fatty acids. They are involved in plaque progression and vulnerability. Lp-PLA2 is an emerging proinflammatory marker. The new drug darapladib inhibits Lp-PLA2 and acts against inflammation. LDL-C is present in the atherosclerotic plaque from the circulating blood in arterial lumen (through the dysfunctional endothelium) and vasa vasorum as well as after the decomposition of foam cells (monocytes-phagocytes, smooth muscle and dendritic cells) and outpoured erythrocytes (its membranes) after hemorrhage. The blood from the arterial lumen can also enter the atherosclerotic plaque through the lesions in its fibrous cap (erosion, fissure, rupture). Atherosclerosis as a disease or as an inevitable accompaniment of aging ("the senescence hypothesis"). The familial hypercholesterolemia is usually due to mutation of just one gene--a defective LDL-C receptor gene on chromosome 19. The accelerated and severe atherosclerosis very resistant to therapy occurs. The patients with homozygous familial hypercholesterolemia can die of myocardial infarction in early childhood. Therapeutic decrease of LDL-C and increase of HDL-C slows down the evolution of atherosclerosis, stabilizes the atherosclerotic plaques, and even brings about their partial regression. Statins, niacin, ezetimibe, LDL-C apheresis, and surgery: shunt between the portal and inferior caval veins, liver transplantation, and partial ileal bypass. The elevated LDL-C is the most established risk factor for atherosclerosis with impact on coronary heart disease mortality of 26%, and it should be the primary target of preventive and therapeutic efforts.
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PMID:Low and high density lipoprotein--cholesterol and coronary atherothrombosis. 1970 10

Anomalous origin of the right coronary artery is a rare congenital anomaly that was first described in 1948 by White and Edwards. It is well established that an anomalous origin of the right coronary artery can lead to angina pectoris, myocardial infarction, or sudden death, in the absence of atherosclerosis. Thus from the literature data it has been also suggested that the abnormal origin and course of anomalous coronary arteries could make them more prone to atherosclerosis due to altered flow patterns. We report our experience involving one patient who had significant atherosclerotic disease and was successfully treated with percutaneous coronary intervention (PCI) and stent implantation in an anomalous right coronary artery arising from the left coronary artery.
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PMID:Percutaneous coronary intervention of an anomalous right coronary artery originating from the left coronary artery. 2067 83

Catheter-based valve implantation techniques are becoming a viable option in various clinical situations to replace difficult redo open heart surgical procedures. This is a report of a first, to our knowledge, successful valve-in-valve (VinV) transcatheter aortic valve implantation (TAVI) into a homograft through the transaortic (TAo) access route using an Edwards SAPIEN valve prosthesis (Edwards Lifesciences, LLC, Irvine, CA) in a patient with poor left ventricular function and generalized severe atherosclerosis.
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PMID:Transaortic valve-in-valve implantation after previous aortic root homograft. 2309 52

An 84-year-old man with severe aortic valve stenosis underwent transcatheter aortic valve implantation (TAVI). We selected a transapical approach TAVI because he had a 48-mm abdominal aortic aneurysm and his descending aorta was covered with severe atherosclerosis, a so-called "shaggy aorta". A 26-mm Sapien XT prosthesis (Edwards Lifesciences, Irvine, CA, USA) was successfully implanted, and TAVI was performed using cardiopulmonary bypass. His postoperative clinical course was unremarkable on the first day. On postoperative day 3, however, his systemic circulation suddenly collapsed due to cardiac tamponade. We performed an emergency re-thoracotomy. This operation improved his systemic circulation, but he had no movement in either leg. Magnetic resonance imaging showed spinal cord ischemia around the T10 level and acute multifocal micro cerebral infarctions. The cause of his neurological symptoms was thought to be spinal cord ischemia brought about by the shaggy aorta and low blood pressure due to cardiac tamponade after TAVI. <Learning objective: Postoperative spinal cord injury is caused by hypotension embolisms, and aortic dissection particularly in patients with severe aortic arteriosclerosis. Spinal cord ischemia is a rare complication after transcatheter aortic valve implantation because the descending aorta is not operated upon. However, it is necessary to keep in mind that postoperative hemodynamic instability can cause spinal cord ischemia in patients with a shaggy aorta.>.
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PMID:Postoperative paraplegia after transapical transcatheter aortic valve implantation. 3132 Sep 49