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

The association between coagulation abnormalities and pregnancy outcome was investigated in a case-control study conducted at Lady Hardings Medical College and Associated Hospitals in New Delhi, India, in 1991-92. Enrolled were 30 neonates born to mothers with pregnancy-induced hypertension (PIH) and 30 infants of normotensive mothers. Compared with control infants, infants of mothers with PIH had significantly elevated levels of prothrombin time (PT), partial thromboplastin time with kaolin (PTTK), thrombin time (TT), and fibrinogen and fibrinogen degradation products (FDP) and significantly reduced platelet counts and fibrinogen. PTTK and TT were significantly higher in neonates born to mothers with hypertension of more than 1 month's duration, but the difference in PT, fibrinogen, and platelet count was not significant. Also observed was a significant correlation between decreasing gestational age and derangement in all coagulation parameters and between decreasing birth weight and an increase in FDP level. The incidence of disseminated intravascular coagulation was higher in preterm than term neonates. 43.3% of neonates required admission to the neonatal intensive care unit and the perinatal mortality rate was 3.3%.
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PMID:Correlation of coagulation abnormalities with clinical outcome in neonates of mothers with pregnancy induced hypertension. 983 64

We report the results of a feasibility study using intravenous magnesium sulphate for deliberate hypotension in 16 ASA 1 patients undergoing major oral and maxillofacial surgery. All the patients received a standard nitrous oxide, oxygen, isoflurane, opioid and muscle relaxant anaesthetic. Magnesium sulphate was infused at 40 g/h until the mean arterial pressure reached 55 +/- 5 mmHg, followed by a maintenance dose of 5 g/h until 30 minutes prior to the end of surgery. The mean arterial pressure was significantly (P < 0.01) reduced by the magnesium sulphate when compared to baseline values. Control of the mean arterial pressure was satisfactory. No patient had reflex tachycardia, cardiac arrhythmia or rebound hypertension. In 14 patients the surgeons thought that the blood loss was less than when using other hypotensive anaesthetic techniques. In 2 patients the surgeons thought the blood loss was excessive. In another 2 patients, the surgeons thought that there was excessive facial swelling on completion of surgery. Postoperative muscle weakness and sedation were not problems clinically. Fourteen patients were extubated immediately after surgery and another 2 patients an hour later in the recovery room. Intraoperative urine output was well maintained. On completion of surgery, the prothrombin time was significantly increased (P < 0.05), and the partial thromboplastin time significantly decreased (P < 0.05) in all the patients (when compared to preoperative values); the clinical significance of this is unclear. The use of intravenous magnesium sulphate for deliberate hypotension is feasible in ASA 1 patients using a standard nitrous oxide, oxygen, isoflurane, opioid and muscle relaxant technique. This study forms the basis for a larger controlled study where the issues of postoperative sedation and weakness and coagulopathy can be dealt with in greater detail.
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PMID:Is it feasible to use magnesium sulphate as a hypotensive agent in oral and maxillofacial surgery? 1010 49

Gestational hypertension with or without proteinuria is a multifactorial disease in which the presence of a hypercoagulable state has been suggested. The prothrombin G20210A, the Factor V (FV) Leiden mutations, and the C677T 5-10 methylenetethrahydrofolate reductase (MTHFR) polymorphism were investigated in 140 women with gestational hypertension and in 216 normotensive women from Southern Italy. Nine controls (4.1%) and 16 cases (11.4%; OR: 2.96, 95% CI: 1.27-6.91) carried the prothrombin A20210 allele. FV Leiden mutation was observed in 4 controls (1.8%) and 11 cases (7.9%; OR: 4.53, 95% CI: 1.41-14.53). The TT MTHFR genotype was found in 36 controls (16.6%) and 34 cases (24.4%: OR: 1.61, 95% CI: 0.96-2.74). The impact of potential confounding variables was evaluated using a logistic regression analysis. Nulliparity, Factor V Leiden and prothrombin A20210 carrier status resulted to be independent risk factors of having gestational hypertension with or without proteinuria. Imbalance of haemostasis, through prothrombotic genetic factors, may predispose to the occurrence of gestational hypertension.
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PMID:Prothrombotic genetic risk factors and the occurrence of gestational hypertension with or without proteinuria. 1010 58

Increased levels of hemostatic factors and genetic mutations of proteins involved in coagulation may play a role in the pathogenesis of coronary artery disease. We investigated clotting activity of factors II (FII:C), V (FV:C), VII (FVII:C), and X (FX:C), the prothrombin gene 20210G-->A transition, and the factor V Leiden mutation in 200 survivors of myocardial infarction and in 100 healthy controls. FV:C (P<0.0001) and FVII:C (P<0.0001) were found to be independent risk factors for myocardial infarction. High FV:C or high FVII:C combined with smoking or arterial hypertension increased the relative risk for myocardial infarction up to 50-fold. One of 177 patients (0.6%) and 4 of 89 controls (4.5%) had the prothrombin 20210 AG genotype. Eleven of 177 patients (6.2%) and 6 of 89 controls (6.7%) were heterozygous for the factor V Leiden mutation. No homozygous carrier for these mutations was found. Neither the prothrombin gene 20210G-->A transition (odds ratio [OR], 0.1; 95% confidence interval [CI], 0.01 to 1.1) nor the factor V Leiden mutation (OR, 1.0; 95% CI, 0.4 to 2.8) were associated with an increased relative risk for myocardial infarction. In conclusion, our data indicate that neither the prothrombin gene 20210G-->A transition nor the factor V Leiden mutation are risk factors for myocardial infarction. High FVII:C was confirmed to be an independent risk factor for myocardial infarction. Moreover, we describe for the first time that high FV:C is an independent risk factor for myocardial infarction.
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PMID:Coagulation factors II, V, VII, and X, prothrombin gene 20210G-->A transition, and factor V Leiden in coronary artery disease: high factor V clotting activity is an independent risk factor for myocardial infarction. 1019 31

The antithrombotic potential of oral anticoagulants is undisputed as the frequency of recurrent thrombosis is high unless anticoagulant therapy is continued after hospital discharge. However, the relationship between potency and/or changes in anticoagulant therapy and frequency of complications remains unclear. Optimizing the clinical management of oral anticoagulation information obtained by databases may be advantageous in addition to meeting safety criteria, as described in the "Saarland Model." The Phoenix-database implicates an association between bleeding complications and the hypertensive elderly. From 1968 to 1993 most reports about cerebral/intraspinal bleedings occurred at prothrombin (PT)-values below 20% in the elder patients (>60 years of age) (12%; 367 reports). In the Saarland Model, 60 patients were followed from our department during a 3-year period. Our findings suggest neither a correlation of the range of PT values and the bleeding events nor an association with age or hypertension. It became obvious that "stable phases" of International Normalized Ratio (INR) [+/-15% change of 4 serial controls using nearly constant weekly oral anticoagulant dosages (+/-15%)] might be considered as a valid criterion of safety. At least the individual risk profile determines the patient's fate.
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PMID:Analysis and occurrence of adverse events with oral anticoagulant therapy. 1032 23

At a young age, ischemic stroke is an uncommon event in which prothrombotic factors are likely to play an important role. In 202 referred cases, 105 men and 97 women, median age 39 years (range, 3 to 50), with a history of ischemic stroke and in 1036 age frequency-matched apparently healthy individuals from the same ethnic background, we have investigated whether inherited prothrombotic conditions increase the risk of ischemic stroke. Neither abnormal plasma levels of natural anticoagulants and fibrinogen nor significant increase of the prothrombin A20210 allele was found in stroke cases compared with controls. Hypertension (odds ratio [OR], 22.61), male sex (OR, 2.30), smoking (OR, 2.78) and alcohol habits (OR, 0.14), a personal history of venous thromboembolism (OR, 4.53), a family history of stroke (OR, 1.93), high circulating levels of fibrinogen (P=0.0190), and total cholesterol (P=0.101) were all independently associated with ischemic stroke. Compared with noncarriers, carriers of the factor V (FV) Leiden mutation (OR, 2.56), and to a lesser extent, of the methylenetetrahydrofolate reductase (MTHFR) TT genotype (OR, 1.60), had an independent higher estimated risk of having a history of ischemic stroke. The relationship with the FV Leiden mutation was greater in women (OR, 3.95). Thus, in addition to established determinants, FV Leiden mutation is independently associated with the occurrence of ischemic stroke in this setting. The greater association in women suggests the possibility of an interaction of this genotype with female hormones.
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PMID:Inherited prothrombotic conditions and premature ischemic stroke: sex difference in the association with factor V Leiden. 1039 94

Thrombophilia is now considered a multicausal disease, with an interplay of acquired and genetic risk factors. Recent studies have shown that patients with the 20210 A prothrombin mutation display remarkably similar characteristics compared with patients with Factor V Leiden mutation. It is evident that neither the Factor V Leiden mutation nor the 20210 A prothrombin mutation is a major risk factor for myocardial infarction or stroke, unless accompanied by other classical risk factors, including diabetes mellitus, hypertension and smoking. Finally, the homozygous form of the thermolabile methylenetetrahydrofolate reductase gene, although leading to elevated homocysteine levels, seems not to represent a genetic risk factor for venous thrombosis.
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PMID:Thrombophilia. 1046 43

Evidence suggests that isolated intracranial hypertension (iIH) is often associated with cerebral venous thrombosis (CVT). In eight patients referred to our Institution for iIH who were later shown to harbor CVT we have performed a comprehensive coagulation work-up, including genetic tests for inherited predisposition to thrombophilia, to clarify the etiology of sinus venous thrombosis. All subjects were women. All but one were overweight. There were high plasma concentrations of D dimer, thrombin-anti-thrombin complexes or prothrombin fragments 1 and 2, further supporting the neuroimaging diagnosis of CVT. Importantly, seven of eight cases had a raised level of plasminogen activator inhibitor 1, a well known inhibitor of fibrinolysis related to obesity. Tissue plasminogen activator levels were elevated accordingly. Factor V gene mutation was present in one subject, and the 20,210 prothrombin gene mutation was found in another individual. Three patients had elevated plasmatic levels of homocysteine. In conclusion, the present study provides solid evidence that impaired fibrinolysis probably related to overweight, acting in concert with other prothrombotic abnormalities, is involved in the pathogenesis of CVT presenting as iIH.
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PMID:A hypofibrinolytic state in overweight patients with cerebral venous thrombosis and isolated intracranial hypertension. 1063 43

A 70-year-old patient with a history of hypertension and hypercholesterolemia was referred for evaluation of necrotic toes. The patient had a history of several cerebrovascular accidents during the previous month. Initially, she developed sudden-onset left upper extremity weakness which, over the ensuing 4 days, progressed to complete left-sided weakness. This was followed by the development of acute dysarthria. A transesophageal echocardiogram revealed moderate left ventricular hypertrophy, several vegetations on her tri-leaflet aortic valve associated with moderate aortic regurgitation, and a large right atrial thrombus with a mobile component. Bubble studies failed to reveal any septal defects. The patient's electrocardiogram was nonspecific. As serial blood cultures were negative despite fevers of up to 39.8 degrees C, the patient was treated with a 6-week course of intravenous ceftriaxone, ampicillin, gentamicin, and ciprofloxacin for a presumed diagnosis of culture-negative endocarditis. Fungal cultures of the blood were negative. The patient, however, progressed and developed several necrotic toes. Physical examination was significant for ischemic changes of the left first, second, third, and fifth toes, as well as the right first and second toes. Diffuse subungual splinter hemorrhages in the toenails, numerous 2-4-mm palpable purpuric papules on the lower extremities, and nontender hemorrhagic lesions of the soles were also noted. Peripheral and carotid pulses were intact and no carotid bruits were heard. Cardiopulmonary and abdominal examinations were unremarkable. Neurologic examination revealed a disoriented, dysarthric patient with left central facial nerve paralysis, as well as spasticity, hyperactive reflexes, and diminished strength and sensation in the left upper and lower extremities. A left visual field defect and left hemineglect were also present. The patient's last brain computerized tomogram revealed areas of low attenuation consistent with cerebral infarctions in three distinct areas of the brain. These included the left occipitotemporal area, the right parieto-occipital area, and the right posterior frontal region. The regions affected were in the distribution of both the anterior and posterior circulation. No evidence of hemorrhage was noted. The patient subsequently complained of abdominal discomfort. A computerized tomogram of the abdomen with oral and intravenous contrast revealed a 4-cm x 3-cm irregular mass in the tail of the pancreas with several low-attenuation lesions throughout the liver which were consistent with infarctions or metastases. Several splenic infarctions were also present. A biopsy of the tumor revealed pancreatic adenocarcinoma. The patient's carcinoembryonic antigen level was 18. 4 ng/mL (0-3) and the CA 19-9 antigen level was 207,000 U/mL (0-36). The alpha-fetoprotein level was normal. Other significant laboratory findings included a prothrombin time of 16.7 (international normalized ratio, 1.4), an activated partial thromboplastin time of 32 (ratio, 1.3), and a platelet count of 85,000/mm3. The Russell viper venom time, sedimentation rate, and C3 levels were normal, and the patient was negative for antinuclear antibodies, anticardiolipin antibodies, and antibodies to extractable nuclear antigens. Of note, the patient was not receiving any anticoagulation. Blood cultures for mycobacteria and fungi, human immunodeficiency virus serology, and urinalysis and culture were negative. The patient subsequently developed an inferior wall myocardial infarction and was transferred to the coronary care unit. In line with the family's request, aggressive care was ceased and the patient expired. The patient's family refused an autopsy.
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PMID:Cutaneous manifestations of marantic endocarditis. 1080 80

We report 5 patients with intracerebral hemorrhage after orthotopic liver transplantation (OLT) and identify the possible risk factors. Between November 1991 and April 1999, 75 adult patients received 77 orthotopic liver transplants at Queen Mary Hospital, Hong Kong. Five patients (6.5%) developed intracerebral hemorrhage postoperatively. Clinical and laboratory data were reviewed, and potential risk factors were analyzed. The 5 patients developed intracerebral hemorrhage within 40 days (range, 1 to 37 days; median, 4 days) after OLT. The mortality rate was 80% (4 of 5 patients). The intraoperative blood transfusion volume (median, 17,200 mL; range, 15,750 to 30,360 mL) administered to patients who developed intracerebral hemorrhage postoperatively was significantly greater than that (median, 6,990 mL; range, 1,840 to 22,680 mL) for patients without the complication (P =.0008). Massive intraoperative transfusion (>15,000 mL) was required in all 5 patients (100%) with intracerebral hemorrhage but only 9 of 72 patients (12.5%) in the other group (P =.0001). Four of 5 patients (80%) with intracerebral hemorrhage had intraoperative hypotension compared with 7 of 72 patients (9.7%) in the other group (P =.001). No significant difference was found in age, prothrombin time (PT), activated partial thromboplastin time (APTT), incidence of hypertension, bleeding at extracerebral sites, cyclosporine A neurotoxicity, thrombocytopenia, hemodialysis, and sepsis between the patients with and without intracerebral bleeding. However, the median cumulative score of coagulation parameters (PT, APTT, platelet count) was significantly greater in the group with than without intracerebral bleeding (median score, 3 v 1; P =.023). Intracerebral hemorrhage is 1 of the most disastrous complications after OLT. Intraoperative hypotension, massive intraoperative transfusion, and coagulopathy may be correlated with this complication.
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PMID:Intracerebral hemorrhage after liver transplantation. 1082 37


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