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

The incidence of congenital valvular heart disease has not significantly altered in recent decades. Major factors contributing to altered profiles of acquired valvular heart disease in the past few decades include an increased elderly segment of the population and increasing recognition of nonrheumatic forms of valvular heart disease. Mitral valve prolapse, and similar involvement of other valves, together with senile calcific aortic stenosis have emerged as the most common forms of valvular heart disease in developed countries. Body leanness and hypertension are additional etiological factors for senile calcific aortic stenosis. Severe calcification of a congenital bicuspid aortic valve continues to be an important cause of aortic stenosis in the elderly. Idiopathic degeneration of the aortic and mitral valves, apparently a different condition than mitral valve prolapse, has also become recognized. Despite a recent increase in the incidence of acute rheumatic fever in North America, rheumatic heart disease remains an infrequent cause of valvular heart disease in developed nations. Its incidence has diminished in the Middle East, but it is still frequent in underdeveloped countries. Intravenous drug abuse is increasing in importance as a cause of valvular heart disease in urban centers in the United States. Syphilitic heart disease is very rare.
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PMID:Etiology of valvular heart disease. 873 80

Nineteen consecutive patients with Turner's syndrome and different karyotypes underwent full cardiological evaluation (physical examination, electrocardiogram, chest X-ray and echocardiogram). Congenital heart disease was found in 26%. Other cardiovascular pathologies (long QT syndrome or systemic hypertension) were found in two patients. When compared with the general population, a higher incidence was present for all types of congenital heart diseases observed. Among cardiac anomalies in Turner's patients, aortic malformations (aortic coarctation and bicuspid aorta) were the most frequent, followed by patent ductus arterious and pulmonary valve stenosis. We have observed that the most severe malformations were preferably found with the 45,X karyotype. Pulmonary valve stenosis was found in a mosaicism 45,X/46,XX case. No anomaly was found in patients with X isochromosome. The ring pattern was not found in our series.
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PMID:[The Turner syndrome and cardiovascular changes]. 883 May 99

Venous valves are more frequent in distal veins and venulae, providing a protecting action against blood skin reflux. Structurally simple, collagen and endothelium, they allow a cavity to be formed by distension, when occlusion occurs. Venous angioscopy can distinguish bicuspid floating valves, reinforced, reinforcing valves with free edges and seat valves as well as the presence of apertures of small collateral vessels in the sinus, of which they play a role in the filling up. Valves are inefficient in supine and in standing among 20% of the adult population. Sinuses allow vortices to be created, low recirculating zones, where blood flow move slowly in niches, at a low shear rate, independently from the main stream. A deep vortex is located in sinus, usually empty, but likely to receive red cell aggregates and leukocytes in the condition of stasis and hyperviscosity. Such a vortex is hypoxic, cause of endothelial activation. In such areas fibrin-leucocytic nidus are created, histologically recognized, of which sub-endothelium has become thick and thrombogenic. Two stages characterized its progression: stage I: a few alteration in the valves, little thrombin generation, taken over by the coagulation inhibitors: AT III, APC and TFPI. Stage II: damaged valves, local consumption of the inhibitors and extended generation of thrombin over the platelets, through factor IXa. Hereditary inhibitor deficits increase the risk (frequent factor Leyden V). When the coagulation cascade is considered, VIIa-tissue factor complex appears to be the thrombotic pathway, leading first to wall linked thrombin, uneasily reached by AT III and facteur IXa non inhibited by TFPI, therefore explaining the platelet extension. Monocytes, which can bear tissue factor, may be "lodged" inside the niches. Besides this important role in deep venous thrombosis, incompetent venous valves are responsible for the skin venous hypertension, a subsequent ground for ulcers. Their role in chronic venous insufficiency is uncertain. In the near future, venous angioscopy will bring about new findings about the pathophysiology of venous valves.
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PMID:[Venous valves in the legs: hemodynamic and biological problems and relationship to physiopathology]. 948 Mar 31

Cardiovascular abnormalities are frequently encountered in patients with Turner's syndrome. These include coarctation of the aorta, aortic root dilatation, bicuspid aortic valve, atrial and ventricular septal defects. Aortic dissection is a rare but devastating complication of Turner's syndrome that usually occurs in adulthood. We report a case of Turner's syndrome with coarctation of the aorta and chronic aortic dissection, and review the relevant literature. There have been 21 prior reported cases of aortic dissection in patients with Turner's syndrome. Possible etiologic factors contributing to the occurrence of aortic dissection in this syndrome are protean. They include the presence of cystic medial necrosis, coarctation of the aorta, bicuspid aortic valve, aortic root dilatation, and hypertension, although cases of aortic dissection and Turner's syndrome have been described in patients without any risk factors. As our knowledge of the natural history of congenital heart defects and risk factors for aortic dissection in Turner's syndrome is limited, periodic cardiac evaluation of these patients may be warranted. Early recognition and treatment of this potentially lethal complication of Turner's syndrome is essential.
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PMID:Aortic dissection and Turner's syndrome: case report and review of the literature. 969 76

The patient was an 18-year-old man who had been diagnosed as having a bicuspid aortic valve and dilatation of the ascending aorta six years previously. As he grew up, aneurysmal change of the ascending aorta and hypertension in the upper body gradually progressed. Preoperative evaluation showed annulo-aortic ectasia and the following congenital abnormalities: bicuspid aortic valve, hypoplastic aortic arch, and coarctation of the aorta. Composite graft replacement and extended total aortic arch replacement were carried out.
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PMID:A single-stage operation for bicuspid aortic valve, annulo-aortic ectasia, hypoplastic aortic arch, and coarctation of the aorta: A case report. 1041 70

Aortic dissection is a catastrophic event that is commonly associated with severe pain, massive hemorrhage, and high mortality. In this report, we present the case of a 31-year-old man who presented with painless, hemorrhagic left pleural effusion. Further investigation revealed a 9-cm dissecting ascending aortic aneurysm that was thought to be due to a congenitally bicuspid aortic valve. We suggest that ascending aortic aneurysm be included in the differential diagnosis of hemorrhagic pleural effusion, even in the absence of the classic features of aortic dissection, such as chest pain, advanced age, or history of hypertension.
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PMID:Painless left hemorrhagic pleural effusion: An unusual presentation of dissecting ascending aortic aneurysm. 1098 24

A 65-year-old man with chronic hypertension developed dyspnea, a cough, and a new diastolic murmur. Two-dimensional echocardiography showed severe aortic regurgitation. No valvular vegetations were identified and blood cultures were negative. Surgical intervention was recommended, but the patient died of an acute intracranial hemorrhage two weeks later. At autopsy, the posterior aortic cusp was flail, due to rupture of the residual cord above two large fenestrations. There was no acute or healed endocarditis. To our knowledge, this is the eighth reported case of aortic valve incompetence due to spontaneous rupture of a fenestrated cusp. Patients ranged in age from 31-67 years (mean, 54), and 4 (50%) were older than 60 years. Seven (88%) of the 8 were men, and 4 (57%) of 7 had chronic hypertension. Analogously, in another four reported cases, aortic insufficiency developed following spontaneous rupture of the fenestrated raphe of an atypical congenitally bicuspid aortic valve. Noninfective and nontraumatic rupture of cord-like aortic valve structures may result in severe acute aortic regurgitation, particularly in men with chronic hypertension.
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PMID:Acute aortic regurgitation due to spontaneous rupture of a fenestrated cusp: report in a 65-year-old man and review of seven additional cases. 1072 25

Turner's syndrome is associated with congenital heart disease in a third of cases. Several reports of aortic dilatation and of death by dissection or rupture of the aorta have been published. The authors undertook a prospective study to assess the incidence of cardiac malformations and aortic dilatation in genetically confirmed Turner's syndrome. Twenty-six out of 34 patients recalled (76%), aged 7 to 30 years (average 17 +/- 6 years) accepted their inclusion in this study and underwent clinical examination, ECG, chest X-ray and echocardiography. Thirteen patients had a monosomy 45X and 13 a mosaic or structural abnormality. Six had a history of cardiovascular disease (operated coarctation: 2 cases, kinking: 2 cases, Hypertension: 2 cases). Eight patients (30%) had one or several anatomical cardiovascular abnormalities: bicuspid aortic valve (19.2%), abnormalities of the aortic isthmus (kinking or coarctation) (15.4%), aortic regurgitation (7.7%), mitral stenosis (3.8%), partial anomalous venous drainage (3.8%), patent ductus arteriosus (3.8%) and left superior vena cava (11.5%). Systematic evaluation of the aorta resulted in the diagnosis of dilatation of the ascending aorta in 1 case and dilatation of the sinus of Valsalva in 2 other cases. The authors conclude that echocardiographic evaluation is essential after the diagnosis of Turner's syndrome. It should be repeated regularly to detect dilatation of the aorta which carries the risk of serious complications, such as rupture or dissection of the aorta.
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PMID:[Heart malformations and vascular complications associated with Turner's syndrome. Prospective study of 26 patients]. 1085 54

Women with Turner's syndrome (TS) have a threefold increase in mortality, primarily as a result of their cardiovascular complications. Recently, the risk of fatal aortic dissection has come to light as a major cause of mortality in women with TS. The aim of this study was to assess the prevalence of aortic root dilatation in a group of women with TS and to investigate the factors contributing to its development. Thirty-eight women with TS attending a dedicated adult Turner clinic were examined clinically and by M-mode and two-dimensional echocardiography on at least one occasion. Aortic root dilatation was defined as an aortic root diameter greater than the 95th centile for body surface area. Fasting serum lipid concentrations were measured in all women. Additionally, 18 subjects underwent noninvasive assessment of central arterial stiffness using applanation tonometry. Fifty percent of subjects were hypertensive and a similar number had an abnormal echocardiogram. A bicuspid aortic valve was present in 33% of subjects, 16 women (42%) had ascending aortic root dilatation. This was associated with a bicuspid aortic valve in four women and hypertension in 11. Two women had isolated aortic root dilatation. Aortic root diameter was significantly associated with systolic blood pressure (r = 0.5, P = 0.003) and left ventricular thickness (r = 0.5, P = 0.02). There was no association with serum lipids or arterial compliance. Structural cardiac abnormalities are present in up to 50% of women with Turner's syndrome. Aortic root dilatation is a significant risk in women with Turner's syndrome and is closely dependent on blood pressure. Aortic root dilatation does not appear to be related to atherosclerosis and is more likely to be due to a mesenchymal defect. Regular surveillance of the aortic root diameter is essential in all women with Turner's syndrome and hypertension should be treated aggressively when present in order to minimize the risk of potentially fatal aortic dissection.
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PMID:Hypertension is a major risk factor for aortic root dilatation in women with Turner's syndrome. 1120 27

The authors studied the risk factors for dilatation of the ascending aorta in patients operated for coarctation of the aorta. A prospective study of the diameters of the ascending aorta by magnetic resonance imaging was undertaken in 46 patients with an average age of 30 months (range 6 days to 11 years) at surgery, and 10 years of age (6 months to 31 years) at the time of the investigation. The diameters were measured at the level of the sinus of Valsalva, at the sino-tubular junction, and compared with reference tables with respect to body surface area. Twenty six per cent of patients had dilatation of the ascending aorta. The predisposing factors were investigated. Age, type of surgery, postoperative hypertension. Doppler gradient in the isthmic region, anatomical appearances of the repair observed by MRI were not predictive of this complication. On the other hand, age of patients at MRI and bicuspid aortic valves (present in 66% of cases) (p < 0.05) were significant risk factors. These results indicate that regular follow-up by echocardiography or MRI of the diameter of the ascending aorta is necessary in patients operated for coarctation of the aorta and with bicuspid aortic valves.
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PMID:[Magnetic resonance imaging of dilatation of the ascending aorta after repair of coarctation of the aorta]. 1143 7


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