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Query: UMLS:C0020538 (hypertension)
170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The clinical, roentgenologic and laboratory findings in 124 patients with dissecting aneurysm of the aorta are reported. In 53 patients the dissection occurred in the ascending aorta ("proximal" dissection), and in 71 patients the site of origin was the descending thoracic aorta ("distal" dissection). Certain distinct clinical differences between the groups were apparent. Although hypertension was an important predisposing factor, it was significantly more common in distal dissection, as was atherosclerosis. Back pain and hypertension on hospital presentation characterized patients with distal dissection. Conversely patients with proximal dissection were younger and had a significantly higher incidence of Marfan's syndrome, cystic medial necrosis, anterior chest pain, pulse deficits, neurologic compromise, aortic insufficiency and congestive heart failure. In both groups, syncope appeared to correlate well with the occurrence of cardiac tamponade. Chest roentgenograms almost always showed an abnormal aortic contour. Aortic angiography, when performed, was usually confirmatory of the diagnosis.
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PMID:The clinical recognition of dissecting aortic aneurysm. 102 Jul 50

Data regarding the etiology and subsequent course of 54 patients with an occlusion of the central retinal artery included the following: of 44 patients over 40 years of age at the time of the central retinal artery occlusion, eight (18%) had cerebrovascular accidents, but only two patients (5%) had a stroke clearly related to the vessels involving the affected central retinal artery. Five patients (11%) had occlusive disease of the ipsilateral internal carotid artery; two of these had cerebral involvement later or simultaneously. Ten of the older patients had cardiac valvular disease and presumed embolic occlusion of the central retinal artery. Associated medical disorders were common. Of the ten patients under 40 years of age, six occlusions were secondary to atrial myxoma, mitral insufficiency with Marfan's syndrome, polycythemia, hypercoagluopathy, hypertension, and orbital compression. Four had no apparent etiology at onset and were in good health many years later.
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PMID:Central retinal artery occlusion. 112 94

A family is described in which two brothers (44 and 48 years old) had aortic dissecting aneurysms (the first one died, the other one underwent surgical treatment and is still living) in the absence of clinical features of Marfan syndrome and of systemic hypertension. Two of the six living siblings have aortic dilation on echocardiography. Histologic examination of the aortic wall at autopsy or surgery revealed a loss of elastic fibers, deposition of mucopolysaccaride-like material and medionecrosis. We can postulate a genetically-determined disease of connective tissue usually described as "Marfan's forme fruste".
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PMID:[Familial dissecting aortic aneurysm]. 176 52

A 23-year-old woman with Marfan's syndrome was scheduled for Cesarean section at 31 week gestation because of progressive aortic dissection. Since she had undergone two surgical corrections for scoliosis (Harrington rod instrumentation) 5 and 12 years ago, we selected general anesthesia. She had been taking diltiazem and propranolol for hypertension and tachycardia. Anesthesia was induced with thiopental 75 mg iv followed by O2-N2O-enflurane (4%) by face mask. Following iv administration of vecuronium 4 mg and tracheal injection of 4% lidocaine 120 mg, the trachea was intubated without a significant hemodynamic change. Anesthesia was maintained with O2-N2O-enflurane (0.5-1.5%) before delivery. Following delivery, enflurane was discontinued and small doses of fentanyl iv (total 0.2 mg) were given with iv infusion of nitroglycerin (0.2-0.5 micrograms.kg-1.min-1) during surgery. Bleeding after delivery was controllable by iv infusion of oxytocin. The Apgar score was good (9 at 1 min and 10 at 5 min respectively). Post-operative course was uneventful. Therapeutic abortion or Cesarean section should be performed as soon as possible in a patient with dissecting aortic aneurysm because of increasing risk of aneurysm rupture during pregnancy. During the surgery, minimal hemodynamic changes are required to prevent the rupture.
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PMID:[General anesthesia for cesarean section in a patient with Marfan's syndrome associated with dissecting aortic aneurysm]. 205 91

The authors retrospectively analyzed the prevalence of renal artery stenosis in 63 consecutive patients with aortic dissection who underwent thoracic and abdominal aortography. Ten patients (16%) had renal artery stenosis, five with atherosclerosis and five with fibromuscular lesions. Risk factors for aortic dissection were Marfan disease in nine patients, bicuspid aortic valve in one, and hypertension in 54 (including seven patients with Marfan syndrome). If the patients with Marfan syndrome and the patient with the bicuspid aortic valve are excluded, renal artery stenosis was present in 10 of 53 patients (19%) when the cause of dissection was presumably hypertension. This finding suggests that renovascular hypertension is a greater risk factor for aortic dissection than is essential hypertension. The success of angiotensin converting enzyme inhibitors and percutaneous transluminal renal angioplasty (PTRA) in controlling renovascular hypertension has been proved. In this series, emergent PTRA successfully controlled the hypertension in one patient with a type B dissection, resulting in an excellent clinical outcome. Angiography should be routinely performed on patients with aortic dissections to evaluate for renal artery stenosis.
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PMID:Renal artery stenosis in patients with aortic dissection: increased prevalence. 205 16

One hundred eleven autopsy cases of dissecting aneurysm were collected from western Japan. The ratio of males to females was 3:2 and the sixth and seventh decades of life were most frequently affected. All 11 cases of Marfan's syndrome were in patients under 40 years of age. DeBakey's type III dissections showed a male predilection and more severe atherosclerosis than in control cases. Many patients with types I and II dissections died of hemorrhage in the acute phase, while many patients with type III dissection died in the subacute or chronic phase, and half of the patients died of diseases other than hemorrhage. Hypertension was recognized in 73.7% of the 95 cases which showed no other obvious risk factors. Histologic examinations suggested that cystic medial necrosis was related to the pathogenesis of the disease in Marfan's syndrome, but was not so apparent in non-Marfan's syndrome. Laminar medial necrosis was found in many cases, but was considered to be a secondary ischemic change following dissection, as supported by other investigators. There were only a few cases in which dissection seemed to be directly caused by atherosclerosis.
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PMID:Dissecting aneurysm: a clinicopathologic and histopathologic study of 111 autopsied cases. 231 7

Between 1974 and July 1989 110 operations for thoracic aortic aneurysms in 107 patients (69 males, 38 females) were performed, whose ages ranged from 14 to 74. 37 patients had an aortic valvular disease, 15 had Marfan's syndrome, 28 of these patients had a history of thoracic trauma or of previous aortic or cardiac surgery (14 posttraumatic aneurysms, 9 aneurysms after cardiac surgery, 5 after repair of aortic coarctation), 29 patients had hypertension. 63 patients underwent repair of dissecting aneurysms, 47 of non-dissecting (saccular or fusiform) thoracic aortic aneurysms. 67 repairs were emergency and 43 elective. The hospital mortality for the entire series was 34.5%. The analysis of multiple preoperative and intraoperative variables showed that mortality following thoracic aortic aneurysm repair is higher with increasing age (65.7% mortality for operations between the 60th and 70th year of age, 100% mortality beyond the 70th year of age) and emergency surgery (hospital mortality 52.2% compared with 6.9% for elective operations). A significant increase in mortality was noted related to the aneurysm type (poorer prognosis in DeBakey type I and II), to history of hypertension, to preoperative shock or to perforation of the aneurysm, including haemopericardium or haemothorax.
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PMID:Results of surgical repair for 110 thoracic aortic aneurysms. 237 34

A family is described in which nine members over two generations had an aortic dissecting aneurysm or aortic or arterial dilation at a young age. The family has been followed up since 1977 after the death of a second teenager from a kindred of 11. None of the patients had the Marfan syndrome or a history of systemic hypertension. Three members died of ruptured aortic dissecting aneurysm and acute hemopericardium at 14, 18 and 24 years of age, respectively; a fourth member died suddenly at age 48 years, a few years after aortic repair for aneurysmal dilation. One member underwent surgical repair of an ascending aortic dissecting aneurysm at age 18 years and is still alive. Four members are currently under close medical observation for aortic or arterial dilation. Histologic examination of the aortic wall at autopsy or surgery in three patients revealed a loss of elastic fibers, deposition of mucopolysaccharide-like material in the media and cystic medial changes. Types I and III collagen from cultured fibroblasts appeared normal on gel electrophoresis. Results of indirect immunofluorescent studies of the elastin-associated microfibrillar fiber array in skin and fibroblast culture from multiple family members were also normal. This dramatic familial cluster of aortic dissecting aneurysm and aortic or arterial dilation suggests a genetically determined disease of autosomal dominant inheritance although the basic defect remains unknown.
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PMID:Familial aortic dissecting aneurysm. 264 12

Acute dissection of the aorta is a rare disease which, when left untreated, has a disastrous prognosis. Two aetiological factors are essential: acquired or congenital fragility of the aortic elastic tissue, and arterial hypertension. The condition must be diagnosed as early as possible to avoid a fatal outcome: it is a surgical emergency. The clinical diagnosis rests on a history of migrating pain and on the presence of signs of ischaemia in a vascular territory. It is confirmed by complementary investigations, chiefly angiography. Acute dissection of the ascending aorta is treated by surgery: the ascending segment is resected, the distal cylindres are recoupled to close the portal of entry, and the aortic regurgitation is treated by valvuloplasty or aortic valve replacement. The introduction of the GRF biological glue has considerably improved the per-operative prognosis and lowered the hospital mortality to 10%. Long-term post-operative follow-up of the patient is crucial, since iterative dissection and formation of aneurysms are not exceptional, especially in patients with Marfan's syndrome.
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PMID:[Acute dissection of the aorta in 1986. Proposal for a new anatomopathological classification]. 294 2

To determine the feasibility of detecting cardiovascular disease in a large group of young competitive athletes, a prospective screening evaluation of intercollegiate student athletes was undertaken at the University of Maryland. Initial clinical screening (including personal and family history, physical examination and 12 lead electrocardiogram) was performed in 501 athletes. Ninety of these subjects had positive findings on one or more of the three studies and agreed to further cardiologic evaluation. The vast majority (75 [84%] of 90) had no definitive evidence of cardiovascular disease, although 1 athlete had mild systemic hypertension and 14 (15%) had echocardiographic evidence of relatively mild mitral valve prolapse that had not been previously suspected. In three athletes with relatively mild ventricular septal hypertrophy (14 to 15 mm), it was not possible to discern with absolute certainty whether the wall thickening was a manifestation of hypertrophic cardiomyopathy or secondary to athletic conditioning ("athlete heart"). Therefore, this screening protocol identified no athletes with definite evidence of hypertrophic cardiomyopathy, Marfan's syndrome or other cardiovascular diseases that convey a significant potential risk for sudden death or disease progression during athletic activity. This failure to identify such diseases could have been due to a lack of sensitivity of the screening tests or to the low frequency with which these diseases occur in youthful healthy athletes. A systematic preparticipation screening program (such as the present one) does not appear to be an efficient means of detecting clinically important cardiovascular disease in young athletes.
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PMID:Results of screening a large group of intercollegiate competitive athletes for cardiovascular disease. 296 Jul 27


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