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

Primary intracerebral haemorrhage (ICH) refers to spontaneous bleeding from intraparenchymal vessels. It accounts for 10-20% of all strokes, with higher incidence rates amongst African and Asian populations. The major risk factors are hypertension and age. In addition to focal neurological findings, patients may present with symptoms of elevated intracranial pressure. The diagnosis of ICH can only be made through neuro-imaging. A CT scan is presently standard, although MRI is increasingly important in the evaluation of acute cerebrovascular disease. A significant proportion of intracerebral haematomas expand in the first hours post-ictus and this is often associated with clinical worsening. There is evidence that the peri-haematomal region is compromised in ICH. This tissue is oedematous, although the precise pathogenesis is controversial. An association between elevated arterial pressure and haematoma expansion has been reported. Although current guidelines recommend conservative management of arterial pressure in ICH, an acute blood pressure lowering trial is overdue. ICH is associated with a high early mortality rate, although a significant number of survivors make a functional recovery. Current medical management is primarily aimed at prevention of complications including pneumonia and peripheral venous thromboembolism. Elevated intracranial pressure may be treated medically or surgically. Although the latter definitively lowers elevated intracranial pressure, the optimal patient selection criteria are not clear. Aggressive treatment of hypertension is essential in the primary and secondary prevention of ICH.
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PMID:Current intracerebral haemorrhage management. 1263 41

Functional outcome at three months was studied in 72 patients with ischemic stroke. The Canadian Neurological Scale was used to assess the severity of stroke at admission and functional outcome at 3 months was assessed using modified Rankin scale. The size and site of the infarct was noted from the initial CT. Risk factors like hypertension, diabetes, and serum cholesterol were analyzed. Initial neurological scoring at admission, and size and site of the infarct were significantly associated with functional recovery at 3 months.
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PMID:Functional recovery in ischemic stroke. 1474 56

Renal artery stenosis (RAS) is a potentially curable cause of renovascular hypertension (RVH) and is caused by either atherosclerosis or fibromuscular dysplasia (FMD) in the vast majority of patients. Although intra-arterial digital subtraction angiography (IA-DSA) is still considered the standard of reference test for the anatomical diagnosis of RAS, noninvasive techniques such as MR angiography, CT angiography, and color-aided duplex ultrasonography are promising alternatives that also allow functional characterization of RAS. We provide an overview of these techniques and discuss their relative merits and shortcomings. Analysis of high-quality studies shows that both MR and CT angiography are significantly more accurate for the diagnosis of at least 50% atherosclerotic RAS than ultrasonographic techniques. The primary strength of ultrasonography at present is its suggested ability to predict functional recovery based on preinterventional resistance index measurements. A still unresolved issue is the detection of FMD. Because missing RVH may have serious consequences the most important requirement for a screening test is that it has high sensitivity.
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PMID:Contemporary imaging techniques for the diagnosis of renal artery stenosis. 1598 76

The purpose of this study was to examine whether exercise training, superimposed on compensated-concentric hypertrophy, could increase myocardial hypoperfusion-reperfusion (H/R) tolerance. Female Wistar-Kyoto rats (WKY) and spontaneously hypertensive rats (SHR) (age: 4 mo; N = 40) were placed into a sedentary (SED) or exercise training (TRD) group (treadmill running; 25 m/min, 1 h/day, 5 days/wk for 16 wk). Four groups were studied: WKY-SED (n = 10), WKY-TRD (n = 10), SHR-SED (n = 10), and SHR-TRD (n = 10). Blood pressure and heart rate were determined, and in vitro isolated heart performance was measured with a retrogradely perfused, Langendorff isovolumic preparation. The H/R protocol consisted of a 75% reduction in coronary flow for 17 min followed by 30 min of reperfusion. Although the rate-pressure product was significantly elevated in SHR relative to WKY, training-induced bradycardia reduced the rate-pressure product in SHR-TRD (P < 0.05) without an attenuation in systolic blood pressure. Heart-to-body weight ratio was greater in both groups of SHR vs. WKY-SED (P < 0.001). Absolute and relative myocardial tolerance to H/R was greater in WKY-TRD and both groups of SHR relative to WKY-SED (P < 0.05). Endurance training superimposed on hypertension-induced compensated hypertrophy conferred no further cardioprotection to H/R. Postreperfusion 72-kDa heat shock protein abundance was enhanced in WKY-TRD and both groups of SHR relative to WKY-SED (P < 0.05) and was highly correlated with absolute left ventricular functional recovery during reperfusion (R2= 0.86, P < 0.0001). These data suggest that both compensated hypertrophy associated with short-term hypertension and endurance training individually improved H/R and that increased postreperfusion 72-kDa heat shock protein abundance was, in part, associated with the cardioprotective phenotype observed in this study.
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PMID:Myocardial hypoperfusion/reperfusion tolerance with exercise training in hypertension. 1622 83

Stroke is the third leading cause of death in the United States after heart disease and cancer; it has an incidence of approximately 750,000 cases per year, and it is a leading cause of disability in adults. The factors predicting a poor outcome from stroke include severe initial neurological dysfunction, hypertension, cardiac arrhythmias, myocardial infarction, hypercholesterolemia, and diabetes mellitus. The armamentarium available for improvement of neurological function after stroke is currently limited to placement in specialized stroke units, optimal therapy for medical complications, and intense physical, occupational and speech rehabilitation. Despite many trials, no pharmacological intervention has been shown convincingly to improve neurological outcome. This review was undertaken to determine the appropriate time for new approaches to the therapy of stroke such as the infusion of stem cells into the central nervous system. The literature shows in large case series that functional recovery from stroke reaches a maximum level by 3-6 months after onset, and no further recovery occurs beyond this time. Nevertheless, about 80% of these patients reach their maximum function for activities of daily living within 6 weeks from onset. Initiation of a clinical trial of stem cell therapy would require demonstration of optimal clinical improvement by neurological evaluations, with no change over at least 4 weeks of observation. Accordingly, in subjects with first-ever ischemic stroke who remained neurologically unchanged from the second until the third month after the acute event, implementation of stem cell therapy would be appropriate at approximately 3 months after the stroke.
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PMID:Time course and outcome of recovery from stroke: relevance to stem cell treatment. 1642 47

One consequence of elevated afterload pressure is the activation of the angiotensin II type 1 receptor and nonspecific cation channels with subsequent Ca2+ accumulation via the Na+/H(+)-Na+/Ca2+ exchanger combination and the T-type or L-type Ca2+ channels. Intracellular Ca2+ overload is cytotoxic, in part, by inducing the mitochondrial permeability transition (MPT) pore. Therefore, we tested the hypotheses that: (1) increased afterload pressure worsens myocardial ischemia-reperfusion injury in healthy heart, (2) the Na+/H(+)-Na+/Ca2+ exchanger combination and both the T-type and L-type Ca2+ channels are involved in the exacerbating impact of high afterload pressure on infarct size, and (3) elevated afterload enhances infarct size in part via the MPT pore. Accordingly, the effect of candesartan (angiotensin II type 1 receptor antagonist), cariporide (inhibitor of the Na+/H+ exchanger), mibefradil (T-type Ca2+ channel blocker), diltiazem (L-type Ca2+ channel blocker), or cyclosporine A (inhibitor of MPT pore) were examined. The elevation in afterload pressure from 80 to 160 cmH2O increased baseline myocardial performance but caused larger infarcts and worsened recovery of mechanical function after ischemia reperfusion. Whereas mibefradil abrogated the effect of high afterload pressure on infarct size, the other agents reduced infarct size at both afterload pressures. Hearts exposed to mibefradil, diltiazem, or cariporide displayed greater functional recovery than those exposed to candesartan or cyclosporine A, revealing that an uncoupling exists between reduced cell death and recovery of mechanical function of the viable portions of the myocardium. The data also uncovered an important link between pressure-mediated exacerbation of infarct size and T-type Ca2+ channel activity.
Hypertension 2006 May
PMID:Mechanisms underlying afterload-induced exacerbation of myocardial infarct size: role of T-type Ca2+ channel. 1650 94

There is no specific treatment to improve the functional recovery in the chronic stage of ischemic stroke. To provide the new therapeutic options, we examined the effect of overexpression of hepatocyte growth factor (HGF) in the chronic stage of cerebral infarction by transferring the HGF gene into the brain using hemagglutinating virus of Japan envelope vector. Sixty rats were exposed to permanent middle cerebral artery occlusion (day 1). Based on the sensorimotor deficits at day 7, the rats were divided equally into control vector or HGF-treated rats. At day 56, rats transfected with the HGF gene showed a significant recovery of learning and memory in Morris water maze tests (control vector 50+/-4 s; HGF 33+/-5 s; P<0.05) and passive avoidance task (control vector 132.4+/-37.5 s; HGF 214.8+/-26.5 s; P<0.05). Although the total volume of cerebral infarction was not related to the outcome, immunohistochemical analysis for Cdc42 and synaptophysin in the peri-infarct region revealed that HGF enhanced the neurite extension and increased synapses. Immunohistochemistry for glial fibriary acidic protein revealed that the formation of glial scar was also prevented by HGF gene treatment. Additionally, the number of the arteries was increased in the HGF group at day 56. These data demonstrated that HGF has a pivotal role for the functional recovery after cerebral infarction through neuritogenesis, improved microcirculation, and the prevention of gliosis. Our results also provide evidence for the feasibility of gene therapy in the chronic stage of cerebral infarction.
Hypertension 2006 Apr
PMID:Gene transfer of hepatocyte growth factor gene improves learning and memory in the chronic stage of cerebral infarction. 1650 98

We studied clinical characteristics and prognosis in acute stoke patients with diabetes mellitus registered on the Japanese Standard Stroke Registry database. A total of 16,630 acute stroke patients admitted to 56 hospitals in Japan. They were examined as to their stroke types, risk factors, their severity of stroke according to the NIH Stroke Scale (NIHSS) and Japan Stroke Scale (JSS), and outcomes by the modified Rankin Scale (m-RS). The incidence of subarachnoid hemorrhage was relatively high in the group of patients who had neither hypertension nor diabetes, and the incidence of brain hemorrhage was higher in the group of patients who had hypertension without diabetes. The frequencies of lacunar infarct and atherothrombotic infarct were also higher in the group of patients who had both hypertension and diabetes. In the diabetic group without hypertension, there were less numbers of hemorrhagic stroke. The ratio of good prognosis (m-RS 0-1) was significantly smaller in the diabetic patients with lacunar infarction, cardioembolic infarction, and subarachnoid hemorrhage. Additionally, there was significantly more stroke recurrence in the diabetic patients (33.0% vs. 26.9%, p<0.0001). The diabetic patients who received insulin therapy (-0.8 +/- 7.4), diet therapy (-0.4 +/- 9.4), or oral medicine (-0.9 +/- 7.2), showed significantly less improvements in the NIHSS compared to the non-diabetic patients (-1.6 +/- 8.2), respectively. Moreover, the poor-management diabetic patients showed significantly less improvements in the JSS compared to non diabetic patients (3.8 +/- 7.7 vs. 4.8 +/- 8.6, p<0.005). In conclusions, stroke patients with diabetes mellitus showed more stroke recurrence and resulted in poorer functional recovery compared to patients without diabetes.
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PMID:[Clinical characteristics and prognosis in stroke patients with diabetes mellitus: retrospective evaluation using the Japanese Standard Stroke Registry database (JSSRS)]. 1651 9

Kidney transplantation is now recognized as the treatment of choice for patients with chronic renal failure. Despite the extension of indications to patients suffering severe hypertension, ischemic heart disease, and chronic heart failure, the worldwide results are superb. However, perioperative cardiac complications occur in 6% to 10% of transplanted patients. Aggressive intraoperative volume expansion is still recommended to maximize graft functional recovery (up to 30 mL/kg/h, central venous pressure [CVP] > 15 mm Hg), but patients with preexistent cardiac disease or poor myocardial function are exposed to the risk of fluid overload, acute respiratory failure, and prolonged ventilation. Among the last 90 cases performed at our institution, good functional recovery of the graft was present in 94% of the patients within 2 weeks, despite a much more conservative intraoperative hydration policy (crystalloids 2400 +/- 1000 mL, 15 mL/kg/h, CVP 7-9 mm Hg). Graft failure which occurred in 5 patients was significantly correlated only with donor age, while perioperative cardiovascular complications had been present in 9 cases (10%) who were coronary artery disease patients (55%). Age above 50 years was the only significant risk factor. Supranormal volume loading is probably not always warranted in kidney transplantation.
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PMID:Perioperative fluid management in kidney transplantation: is volume overload still mandatory for graft function? 1664 77

Adrenalectomy continues to play an important role in the management of Cushing's syndrome (CS). Untreated CS causes considerable physical and mental morbidity and mortality. However, little information is available on the effect of adrenalectomy in ameliorating functional disabilities in CS patients. Our study assesses the long-term outcome of adrenalectomy in patients with CS. This is a retrospective analysis of CS patients managed during 1990-2005 at a tertiary care center. We analyzed the clinical presentation, endocrine evaluation, and surgical management preoperatively and following adrenalectomy. The subjects were 37 patients with CS (age 24.5 +/- 15 years, range 1-60 years; male:female 1.0:1.2). There were various etiologies--unilateral adrenocortical adenoma (n = 11), adrenocortical carcinoma (n = 13), pituitary ACTH-secreting adenoma with failed transsphenoidal surgery (n = 4), ectopic unidentified ACTH source (n = 7), bilateral adrenal macronodular hyperplasia (n = 1), primary pigmented nodular adrenal hyperplasia (n = 1) --for which the patients underwent adrenalectomy: unilateral (n = 22), bilateral (n = 13), or adrenonephrectomy (n = 2). Two patients died during the perioperative period owing to chest infection and sepsis. At the median follow-up of 60 months (range 6-144 months), the patients exhibit significant persistence of obesity (41%), proximal muscle weakness (44%), menstrual irregularity (8%), hypertension (31%), and insulin-dependent diabetes (29%). Hirsutism and psychological abnormalities persisted to a lesser extent. All patients had biochemical cure of CS following surgery evidenced by the 8 a.m. basal cortisol < or = 5 microg/dl. The hypothalamic-pituitary-adrenal axis recovered as shown by normalization of the short synacthen-stimulated cortisol level (peak level > or = 20 microg/dl) after a median follow-up of 9 months (range 6-18 months). Incomplete clinical recovery following adrenalectomy emphasizes the need of early recognition and prompt treatment of CS. Surgery for adrenocortical adenoma is safe and effective; however, survival of patients with CS due to adrenocortical carcinoma remains poor. Bilateral adrenalectomy provides early control of hypercortisolism in selected cases of unlocalized ectopic ACTH syndrome or failed transsphenoidal surgery. Even though functional recovery is incomplete after adrenalectomy, quality of life improves considerably.
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PMID:Outcome of adrenalectomy for Cushing's syndrome: experience from a tertiary care center. 1753 56


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