Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Dissection of the ascending aorta (type A) following later after aortic valve replacement has been described with increasing frequency. This study analyzes the role of aortic valve replacement for the evolution of late dissection. In a series of 80 consecutive patients with type A dissection, a previous aortic valve replacement had been performed in 12 cases (15%). In addition to arterial hypertension (p < 0.001) and Marfan syndrome (p < 0.01), multivariate analysis identified previous aortic valve replacement (p < 0.01) as an independent predisposing factor for type A dissection. Dissection occurred 3 +/- 4 years after aortic valve replacement with a clinical and anatomical profile similar to classic dissection as proven by comparison to a group of 62 patients with classic dissection associated with arterial hypertension or Marfan syndrome. With 75% and 66%, respectively, 30 day and 1 year survival of patients with dissection following later after aortic valve replacement was similar to patients with classic type A dissection. Extensive thinning and/or fragility (p < 0.05) of the aortic wall in the presence of a mildly dilated aorta (45 +/- 5 mm) at the time of aortic valve replacement was associated with a high risk for late dissection; this finding was substantiated by comparison to a control group of 10 consecutive patients with a similarly dilated aortic root but no dissection. Type and diameter of valve prostheses, cross-clamp time, NYHA functional class, and left ventricular ejection fraction were unrelated to late dissection. Previous aortic valve replacement is an independent predisposing factor for a dissection of the ascending aorta later. At the time of aortic valve replacement, prophylactic replacement or wrapping of the ascending aorta should be considered in patients with a thinned/fragile aortic wall even without a markedly dilated aortic root.
 ...
PMID:[Aortic valve replacement as an independent predictive factor for later development of aortic dissection]. 978 93

Most computations of arterial mechanics treat the wall as a mechanically homogeneous body, but there are no data to support or refute this. To evaluate this assumption, experiments were performed that measured the deformation of 4 elastic lamellae located at 4 equidistant points across the thickness of the media. Data were obtained at 25-mm Hg pressure steps between 0 and 200 mm Hg. To satisfy the constraints of incompressibility in an isovolumetric cylinder, the innermost structures must undergo larger deformations than the outermost structures. This manifests as thinning of the wall. Therefore, each experiment was performed twice: once with a vessel segment in its normal cylindrical configuration, and again with a contiguous vessel segment turned inside-out to form an inverted cylinder. The deformations of individual lamellae obtained in normal and inverted vessel segments were averaged to determine their extensions independent of location. Results showed that the extensibilities of the lamellae were equal at all 4 anatomic locations across the media, suggesting equal stiffnesses of the lamellae. Other studies were performed to examine the distribution of the circumferential retractions of the lamellae that occurs when a vessel is extended longitudinally. Results showed that circumferential retraction also was distributed uniformly across the wall. These findings demonstrate that the elastic lamellae behave uniformly in both the circumferential and longitudinal directions at different locations across the wall thickness. Because of the interlocked structure of the elastin, muscle, and collagen in the media, these findings suggest that although the media is histologically heterogeneous, it acts mechanically as a homogeneous material.
Hypertension 1999 Mar
PMID:Distribution of lamellar deformations: implications for properties of the arterial media. 1008 91

Tissue kallikrein is a serine protease thought to be involved in the generation of bioactive peptide kinins in many organs like the kidneys, colon, salivary glands, pancreas, and blood vessels. Low renal synthesis and urinary excretion of tissue kallikrein have been repeatedly linked to hypertension in animals and humans, but the exact role of the protease in cardiovascular function has not been established largely because of the lack of specific inhibitors. This study demonstrates that mice lacking tissue kallikrein are unable to generate significant levels of kinins in most tissues and develop cardiovascular abnormalities early in adulthood despite normal blood pressure. The heart exhibits septum and posterior wall thinning and a tendency to dilatation resulting in reduced left ventricular mass. Cardiac function estimated in vivo and in vitro is decreased both under basal conditions and in response to beta-adrenergic stimulation. Furthermore, flow-induced vasodilatation is impaired in isolated perfused carotid arteries, which express, like the heart, low levels of the protease. These data show that tissue kallikrein is the main kinin-generating enzyme in vivo and that a functional kallikrein-kinin system is necessary for normal cardiac and arterial function in the mouse. They suggest that the kallikrein-kinin system could be involved in the development or progression of cardiovascular diseases.
 ...
PMID:Cardiovascular abnormalities with normal blood pressure in tissue kallikrein-deficient mice. 1122 91

The purpose of the present review was to determine whether exercise training improves cardiac function in patients with prior myocardial infarction. Home exercise programs for patients with myocardial infarction effectively improve their ability to exercise as well as quality of life. A computer-based, automated, telemetry system comprising central and peripheral computers and telephone line was developed. Myocardial infarction patients were evaluated for peak oxygen uptake and anaerobic threshold. Some studies have in fact suggested that using echocardiography, exercise training in patients with reduced left ventricular function after a myocardial infarction leads to further myocardial damage, including wall thinning, infarct and expansion. A more recent analysis by these investigators suggested that training actually has a beneficial effect on the remodeling process. Many factors appear to influence the extent of the remodeling process, including attenuation by Ace inhibition therapy, extent and site of the infarction, hypertension and continued ischemia. Some results suggest early physical training may be safe and improve the autonomic nerve balance and exercise tolerance in patients with acute myocardial infarction.
 ...
PMID:[Rehabilitative intervention after a myocardial infarct]. 1125 12

Use of the commonly prescribed protease inhibitor Crixivan appears to result in a bizarre adverse effect, despite its desirable effects on T-cell count and viral load. This adverse effect is more common in women than men, and includes the following symptoms: (1) limb wasting, (2) fat gain in the torso, (3) breast enlargement, (4) skin thinning, (4) vein enlargement, (5) irregular periods, (6) high blood pressure and high blood glucose, (6) fatigue, and (7) decreased sex drive. It is believed that 5 to 10 percent of patients taking Crixivan suffer from some of these symptoms, but the percentage would probably be much higher if the number of women alone were studied. Some physicians have been unsupportive about complaints of these symptoms, and have told their patients to exercise or that the changes may be due to aging. One suggestion for dealing with these symptoms is to get body composition measurements prior to starting a protease-containing regimen. Exercise continues to remain important, primarily to prevent wasting. However, dieting is not recommended since it does not reduce the fat deposits and it does contribute to wasting of the limbs. If the symptoms become intolerable, a change in regimen may be needed.
 ...
PMID:The new body of AIDS: Crixivan bellies, legs, and humps. 1136 90

The past decade has witnessed enormous progress in our understanding of the nature of this process. The development of an atherosclerotic plaque is a complex process which begins with endothelial dysfunction, the trigger for which are factors such as hypercholesterolemia, smoking, hypertension, hyperhomocysteinemia and impaired glucose metabolism. This dysfunction includes increased endothelial permeability to lipoproteins and other plasma constituents, which is mediated by NO, PDGF, prostacyclin, angiotensin II and endothelin; up-regulation of endothelial adhesion molecules including VCAM-1, ICAM-1, and selectins and migration of leukocytes and monocytes-macrophages in the subendothelial space mediated by oxidized LDL, MCP-1, PDGF and MCSF. The next step includes smooth-muscle cells migration (stimulated by PDGF and TGF-beta), T-cell activation (mediated by TNF-alpha and IL-2), formation of foam-cells from macrophages (mediated by oxidized LDL, MCSF, TNF-alpha and IL-1) and platelet adherence and aggregation (stimulated by thromboxane A2, tissue factor etc). The smooth muscle cells form a fibrous cap which confers mechanical stability of the plaque and separates the lipid rich thrombogenic core from the lumen and circulating blood. Whether a plaque will remain intact and therefore stable or rupture and lead to thrombosis causing an acute coronary syndrome (MI, unstable angina pectoris) depends upon a number of factors, the most important of which is its composition. Plaque size plays only a minor role in determining risk of an acute coronary syndrome. Rupture of the fibrous cap occurs due to thinning of the cap caused by an influx and activation of macrophages which release metalloproteinases and other proteolytic enzymes (stimulated by inflammatory cells, particularly T-lymphocytes). These enzymes cause degradation of the fibrous tissue of the cap which can result in thrombous formation and occlusion of the artery. Stable plaques have a thick fibrous cap, a small lipid core, and few inflammatory cells. In contrast, vulnerable plaques have a high lipid content, numerous inflammatory cells, and a thin fibrous cap with reduced collagen and vascular smooth muscle cells in it. Although vulnerable plaques are believed to account for only a small number of all coronary atheromas, they are responsible for most acute coronary events.
 ...
PMID:[New information on the pathophysiology of atherosclerosis]. 1137 94

Previous series that described phenotypes in carriers of Alport's syndrome did not distinguish genetically between carriers of X-linked and autosomal recessive disease. In this study, modes of inheritance in unselected families with Alport's syndrome associated with two city and two provincial hospitals were determined using microsatellite markers, and carriers of disease haplotypes were identified within these families. All 47 carriers (100%) from 18 families with X-linked Alport's syndrome had dysmorphic hematuria on phase-contrast microscopy, but few developed renal failure (3 of 40 carriers; 8%), clinical hearing loss (2 of 45 carriers; 4%), retinopathy (1 of 30 carriers; 3%), or lenticonus (0 of 30 carriers; 0%). Eleven of the 14 carriers (79%) from 2 families with autosomal recessive disease had dysmorphic hematuria, but none had renal failure, clinical hearing loss, retinopathy, or lenticonus. Urinary red blood cell counts in carriers of X-linked Alport's syndrome were greater than those in carriers of autosomal recessive disease (P < 0.0001), but the frequency of proteinuria and hypertension and levels of proteinuria were not different. There was more tubulointerstitial damage in carriers of X-linked disease (P = 0.012); however, carriers of autosomal recessive disease had more widespread and more uniform thinning of the glomerular basement membrane (P < 0.0001) and less lamellation (P < 0.04).
 ...
PMID:A comparison of the clinical, histopathologic, and ultrastructural phenotypes in carriers of X-linked and autosomal recessive Alport's syndrome. 1172 53

After myocardial infarction (MI), the left ventricle (LV) undergoes ventricular remodeling characterized by progressive global dilation, infarct expansion, and compensatory hypertrophy of the noninfarcted myocardium. Little attention has been given to the response of remodeling myocardium to additional hemodynamic overload. Studies have indicated that gender may influence remodeling and the response to both MI and hemodynamic overload. We therefore determined 1) structural and function consequences of superimposing hemodynamic overload (systemic hypertension) on remodeling myocardium after a MI and 2) the potential influence of gender on this remodeling response. Male and female Dahl salt-sensitive and salt-resistant rats underwent coronary ligation, resulting in similar degrees of MI. One week post-MI, all rats were placed on a high-salt diet. Four groups were then studied 4 wk after initiation of high-salt feeding: MI female, MI female + hypertension, MI male, and MI male + hypertension. Hypertension-induced pressure overload resulted in additional comparable degrees of myocardial hypertrophy in both females and males. In females, hypertension post-MI resulted in concentric hypertrophy with no additional cavity dilation and no measurable scar thinning. In contrast, in males, hypertension post-MI resulted in eccentric hypertrophy, further LV cavity dilation, and scar thinning. Physiologically, concentric hypertrophy in post-MI hypertensive females resulted in elevated contractile function, whereas eccentrically hypertrophied males had no such increase. Female gender influences favorably the remodeling and physiological response to hemodynamic overload after large MI.
 ...
PMID:Influence of gender on the response to hemodynamic overload after myocardial infarction. 1238 28

Stercoral perforation of the colon is a rare phenomenon with fewer than 90 cases reported in the literature to date. The pathogenesis of stercoral ulceration is thought to result from ischemic pressure necrosis of the bowel wall caused by a stercoraceous mass. Stercoral perforation in more than 90 per cent of cases involves the sigmoid or rectosigmoid colon with associated fecal mass causing localized mucosal ulceration and bowel wall thinning due to localized pressure effect. We report the case of a 45-year-old woman who presented with a 12-hour history of epigastric pain. Significant comorbidities included systemic lupus erythematosus, sarcoidosis, hypertension, and previous history of congestive heart failure. The patient was also on prednisone and a nonsteroidal anti-inflammatory drug for joint pains. On physical examination the patient had signs of generalized peritonitis. Chest X-ray showed significant free air under the diaphragm. Emergency laparotomy revealed localized perforation over the antimesenteric border of the sigmoid colon with associated stercoral mass at the site of perforation. A segmental resection of the sigmoid colon with end colostomy (Hartmann's procedure) was performed. The patient made an uneventful recovery. Stercoral perforation is often a consequence of chronic constipation; however, there are other predisposing factors as the condition is rare compared with the frequency of severe constipation. One of the hypotheses includes the association of nonsteroidal anti-inflammatory drugs (NSAIDs) with stercoral perforation of the colon. Our case report lends support to this association with NSAID use; thus there need to be greater awareness and caution when using NSAIDs in chronically constipated patients.
 ...
PMID:Stercoral perforation of the sigmoid colon: report of a rare case and its possible association with nonsteroidal anti-inflammatory drugs. 1246 20

It is uncertain whether chronic beta-adrenoreceptor (beta-AR)-activation in hypertension could initiate the progression from compensated left ventricular (LV) hypertrophy to pump dysfunction. It is also uncertain if this effect is through adverse LV remodeling (chamber dilatation with wall thinning and pump dysfunction) or intrinsic myocardial contractile dysfunction. We evaluated the effect of 5 months of isoprenaline (0.02 mg x kg(-1) x d(-1)) on hemodynamics, LV wall thickness, cavity size, and interstitial characteristics in spontaneously hypertensive rats (SHR) with compensated LV hypertrophy. In the absence of myocyte necrosis, changes in volume preload, pressure afterload, and heart rate or decreases in baseline systolic myocardial elastance (load independent measure of intrinsic myocardial contractility), ISO produced a right shift in LV diastolic pressure-volume (P-V) relations (chamber dilatation), a decrease in LV wall thickness despite a further increase in LV weight in SHR, LV pump dysfunction (right shift in LV systolic P-V relations), and deleterious interstitial remodeling (increments in total and noncrosslinked myocardial collagen concentrations). The isoprenaline-induced LV geometric, chamber performance, and interstitial changes were similar to alterations noted during decompensation in older SHR. In summary, in the absence of tissue necrosis and baseline intrinsic myocardial contractile dysfunction, chronic beta-AR activation induces interstitial and chamber remodeling and, hence, pump dysfunction. These data suggest that chronic sympathetic activation initiates the progression from compensated concentric LV hypertrophy in hypertension to cardiac dysfunction primarily through deleterious cardiac remodeling rather than intrinsic myocardial contractile dysfunction.
Hypertension 2003 Mar
PMID:Beta-adrenergic activation initiates chamber dilatation in concentric hypertrophy. 1262 50


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>