Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

Voluntary end-expiratory apnoea in a 23-year-old asymptomatic mild hypertensive patient consistently elicited bradyarrhythmias (complete heart block and sinus pause) and sympathetic activation to muscle blood vessels, indicating simultaneous sympathetic and parasympathetic activation during apnoea. The sympathetic bradyarrhythmic response to apnoea was potentiated by hypoxia and eliminated by atropine. Baroreflex activation also attenuated the bradycardic response to apnoea. A 43-year-old hypertensive patient with sleep apnoea also exhibited bradyarrhythmias (sinus arrest for up to 10 s) and a fall in perfusion pressure to less than 50 mmHg during episodes of sleep apnoea. These cardiovascular changes were associated with a reduction in oxygen saturation to levels as low as 35%. Neither patient was on any medication. Simultaneous sympathetic and parasympathetic activation during episodes of apnoea may predispose to cardiovascular catastrophe. These chemoreflex mediated autonomic changes are inhibited by baroreflex activation. We propose that patients with impaired baroreflexes (patients with hypertension or heart failure and premature infants) may be especially susceptible to excessive autonomic responses to chemoreflex stimulation during periods of apnoea. In these patient groups, bradyarrhythmias, hypoxia, hypoperfusion and sympathetic activation during apnoea may predispose to sudden death.
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PMID:Parasympathetic hyperresponsiveness and bradyarrhythmias during apnoea in hypertension. 149 63

The cyclical changes in heart rate and systemic blood pressure that accompany apneic events are predominantly mediated by fluctuations in the activity of the autonomic nervous system. Increased vagal efferent parasympathetic activity is responsible for the cyclical reductions in heart rate during apnea. In contrast, the cyclical elevations in systemic blood pressure are believed to result from recurrent peripheral vasoconstriction mediated by repetitive activation of the sympathetic nervous system. Maximal activation and pressures coincide with apnea termination and brief arousal from sleep. These cyclical elevations in systemic pressure during sleep increase ventricular workload and, thereby, may contribute to the development of ventricular hypertrophy. Systemic hypertension is present during wakefulness in approximately 50% of patients with OSA. Although age and obesity are the predominant risk factors for diurnal hypertension, OSA probably makes an independent contribution in younger obese men. Sinus bradycardia, Mobitz type 1 second-degree heart block, and prolonged sinus arrest have all been documented in association with the apneic events. Increased ventricular ectopy has been observed with oxyhemoglobin desaturations below 60%. Myocardial ischemia, infarction, sudden death, and stroke all demonstrate similar circadian variations in time of onset. Peak frequencies occur between 6 AM and noon, generally within several hours of awakening. Although sleep is associated with decreased frequencies of these adverse cardiovascular events in the general population, evidence exists linking REM sleep to an increased risk of myocardial ischemia. In men who habitually snore, epidemiologic data have detected an increased risk for ischemic heart disease and stroke. Habitual snoring has also been associated with an increased risk of sudden death during sleep. In patients with clinically significant OSA, there is reasonable information indicating excessive mortality in the absence of treatment. This mortality is predominantly cardiovascular and tends to occur during sleep.
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PMID:Hypertension, cardiac arrhythmias, myocardial infarction, and stroke in relation to obstructive sleep apnea. 152 12

To evaluate the spectrum of coronary artery disease (CAD) in cocaine users, coronary angiograms obtained from 33 patients (26 men [79%] and 7 women [21%], mean age 37 years) with history of cocaine use and cardiac symptoms were retrospectively reviewed. Clinical indications for coronary angiograms included chest pain (n = 28), congestive failure (n = 4) and complete heart block (n = 1). Coronary angiograms were reviewed independently by 2 angiographers unaware of patient's clinical status. Thirteen patients (40%) had normal coronary angiograms, and 20 (60%) had CAD; 7 (21%) had mild CAD (less than or equal to 70% diameter stenosis), and 13 (40%) had significant CAD (greater than 70% diameter stenosis). Of 13 patients with significant CAD, 7 had 1-vessel, 4 had 2-vessel and 2 had 3-vessel CAD. There was enzymatic evidence of myocardial infarction in 12 of 33 patients (36%); all 12 had CAD (10 with significant and 2 with mild CAD). Mean age and number of risk factors (serum total cholesterol, cigarette smoking, systemic hypertension, diabetes mellitus, family history of CAD, and obesity) in patients with CAD (mild or significant) and with normal coronary angiograms were not statistically different. Left ventricular ejection fraction was normal in 15 patients (45%) and depressed in 18 (55%). All patients with CAD and low ejection fractions (n = 12) had regional wall motion abnormalities, whereas all those with normal coronary arteries and low ejection fraction (n = 6) had global hypokinesia.
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PMID:Frequency of coronary artery disease and left ventricle dysfunction in cocaine users. 159 68

The effect of beta-adrenergic blockade (propranolol) on exercise performance was studied in 15 patients (12 men and 3 women, mean age 70 years) with complete heart block treated with a ventricular-inhibited pacemaker (VVI). In a double-blind procedure, the patients were randomly given either 0.1 mg/kg of propranolol or saline solution i.v. before a first exercise test and vice versa before a second test. The interval between the tests was 24 hours. Nine patients were in sinus rhythm, 4 patients had atrial flutter, and 2 others had atrial fibrillation. The exercise capacity was on an average 11% lower with propranolol than with placebo (p less than 0.001). The most marked reductions (20 and 33%) were found in the two patients with atrial fibrillation. The atrial rate in patients with sinus rhythm was significantly lower with propranolol than placebo both at rest (68 vs. 83 beats/min, p less than 0.001) and at maximal work load (91 vs. 141 beats/min, p less than 0.001). The present findings show that beta blockade has negative effects on exercise capacity in patients with complete heart block treated with VVI pacemakers. This finding should be considered in the selection of drug treatment in patients with fixed rate pacing and concomitant hypertension and/or ischemic heart disease.
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PMID:Exercise performance and beta-adrenergic blockade in patients with complete heart block treated with ventricular inhibited pacing. 174 9

Fifteen cases of chronic heart block were studied. Eight of them could be designated as idiopathic or primary heart block; the others were associated with hypertension, diabetes and ischaemic heart disease, either singly or in various combinations. In six cases, the whole heart was available for histopathological study of the conduction system. In the other 9 cases, only a portion of the heart muscle was available for examination. A V nodal fibrosis extending upto the proximal bundle of His was seen in all the six whole heart autopsy materials. Fibrosis of the adjacent myocardium was seen in five cases. In three cases, conducting system fibrosis was associated with atherosclerotic (1 case) or diabetic changes (3 cases) of the intramural vessels. In the 9 partial autopsy studies, myocardial fibrosis was seen in two cases, diabetic microangiopathy in one and atherosclerotic changes in two including an old thrombus in one. Thus, diabetic microangiopathy was seen in total four cases. These changes may be responsible for the cardiomegaly and cardiac failure associated with conduction defects observed in diabetes. In the idiopathic group also, heart block could be considered as a significant facet of a primary myocardial degenerative process.
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PMID:Cardiac changes implicated in chronic heart block. 181 5

We analysed the outcome of pregnancy in patients with pre-existing lupus nephritis, seen in a tertiary referral centre for nephrology. Fifty-three pregnancies in 25 patients who already had clinical and histological evidence of lupus nephritis were recorded between January 1970 and June 1989, and data were analysed retrospectively. All 53 pregnancies occurred in patients with more or less stable disease, while three pregnancies during which lupus first presented were excluded. Six pregnancies were ended by therapeutic abortions (four for social reasons), and in eight spontaneous abortion occurred. Thus, 39 deliveries occurred, 28 at 36 weeks or more, while 11 were delivered prematurely, of which one was a stillbirth. After allowance was made for therapeutic abortions, the fetal loss rate (9/47) was 19%. Seventeen Caesarian sections were performed in the 39 completed pregnancies (44%), 11 as emergencies. Although the overall fetal loss, incidence of premature births and Caesarian section rate were all higher than expected for a population of normal women, neither initial histology, treated hypertension, the presence of proteinuria or a nephrotic syndrome showed statistically significant relationships with the outcome of completed pregnancies. In no case was maternal renal function affected irreversibly, although proteinuria increased substantially during pregnancy in six patients, and creatinine clearance fell during pregnancy, also in six patients. No 'flares' in systemic disease were seen, but all patients save five were treated with a brief period of high-dose oral corticosteroids or intravenous methylprednisolone in the postpartum period. No case of neonatal lupus or congenital heart block was observed.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The outcome of pregnancy in women with lupus nephritis. 184 58

Systemic lupus erythematosus (SLE) is a collagen vascular disease that may have a tremendous impact on pregnancy. The pregnant patient with SLE is at increased risk for fetal wastage, intrauterine growth retardation (IUGR), intrauterine fetal demise (IUFD), pregnancy-induced hypertension (PIH), and exacerbations of the lupus process. SLE is an autoimmune disease with tremendous implications for pregnancy. The diagnosis of SLE is based on criteria developed by The American Rheumatism Association. The recent identification of circulating antibodies associated with women who have lupus has led to some confusion. The circulating antibodies are associated with an increased risk of fetal wastage. However, those antibodies have been documented in women who do not have lupus. The diagnosis of SLE and pregnancy requires intensive obstetrical care. SLE may also affect the neonate, from skin lesions to complete heart block. This article describes the effects of SLE on the mother, pregnancy, and the neonate.
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PMID:Systemic lupus erythematosus: obstetric and neonatal implications. 220 68

Autoimmune disorders such as SLE and ITP occur more commonly in young women and are the most common complications in pregnancy. There is considerable controversy concerning the risk to the mother and fetus, and the optimal prepartum management for minimizing that risk. 1. SLE is an autoimmune disorder in which IgG antibodies such as anti dsDNA-IgG, anticardiolipin IgG, and anti SS-A/Ro IgG are produced. Lupus nephropathy accompanied by diminished serum complement (CH50) and a rise in antibodies against dsDNA is a frequent clinical problem during pregnancy, which represents the adverse effect of hypertension or superimposed toxemia and causes fetal death or intrauterine fetal growth retardation. Habitual abortion or fetal death is common in a case with high anticardiolipin IgG titre. Anti SS-A antibodies are often found in the infants of antibody-positive mothers, and the deposition of antibodies in the perinodal region cause congenital heart block. IgG or immune complexes crossing the placenta directly injures the cardiac conduction system. In these cases which have high titre crossing the placenta directly injuries the cardiac conduction system. In these cases which have high titre of autoimmune antibodies, corticosteroid therapy should be started. 2. Management of ITP in pregnancy involves the consideration of three issues: 1) treatment of maternal thrombocytopenia, 2) prediction of fetal thrombocytopenia, 3) obstetrical management. ITP increases the risk for postpartum bleeding of sufficient severity to require blood transfusion. In most of these cases, maternal platelet counts are found to be less than 30,000/mm3. Women who have symptomatic severe steroid-unresponsive ITP may benefit from intravenous IgG(IvIgG) given as elective treatment.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Pregnancy complicated with autoimmune diseases]. 223 Apr 13

We prospectively evaluated infusion-related toxicities in 82 recipients of autologous bone marrow grafts. The grafts were cryopreserved in 10% dimethylsulfoxide and stored in liquid nitrogen. All grafts were concentrated and buffy-coat cells were collected. Forty-seven grafts were treated ex vivo with 4-hydroperoxycyclophosphamide (4-HC) at 100 micrograms/mL; 26 grafts were further processed using density-gradient separation and treated with 4-HC at 60 micrograms/mL. Nine buffy-coat concentrates were frozen without drug treatment. Before infusion, patients were medicated with mannitol, hydrocortisone, and diphenhydramine. Grafts were rapidly thawed and immediately infused without further manipulation. During the infusions, 33 (70%) recipients of treated buffy-coat, 5 (56%) recipients of untreated buffy-coat, and 6 (23%) recipients of density-gradient separated grafts experienced varying symptoms including nausea, abdominal cramping, and flushing. Forced vital capacities for 83% of the recipients of treated buffy-coat concentrates decreased after the graft infusion; six of these patients complained of dyspnea and one patient experienced an acute episode of respiratory decompensation. Decreased heart rates were observed in 98% of the recipients of treated buffy-coat cells with asymptomatic bradycardia occurring in 45%. Forty-five patients (96%) in this group experienced transient hypertension, with 18 (38%) requiring additional medications within 6 hours after the infusion for control of blood pressure. Similar cardiovascular changes were observed in the recipients of untreated buffy-coat concentrates. One recipient of an untreated buffy-coat concentrate had 2 degrees heart block after the graft infusion. Twenty-three (88%) recipients of density-gradient separated grafts had decreased heart rates and 21 (81%) had increased blood pressure. However, the degrees of change were less than those experienced by the recipients of treated buffy-coat cells (P less than .01). Forced vital capacities were not affected by the infusion of the density-gradient separated grafts. No renal failure or obvious hemolytic episodes occurred for any patient group. Minor to moderate toxicities were associated with cryopreserved graft infusions. Recipients of buffy-coat separated grafts, both treated and untreated, experienced more complications than the recipients of density-gradient separated grafts. These toxicities may relate to the volumes of cryoprotectant and cell lysis products infused, which were less for the more highly purified density-gradient separated grafts.
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PMID:Clinical toxicity of cryopreserved bone marrow graft infusion. 229 78

The objective of the study was to evaluate the acute effect of intravenous celiprolol on the electrophysiologic properties of the cardiac conduction system in man and to assess potential problems in terms of its causing heart block or sinus bradycardia. Eight patients with controlled coronary artery disease and hypertension but without conduction system disease were studied. All cardiac drugs e.g., digoxin, sympathomimetics and other beta blockers were discontinued prior to entering the study. Surface ECG leads I, AVF, and Vi were applied to each patient, and the ECG was continuously displayed on an oscilloscope. A quadripolar stimulating electrode (7F) was inserted percutaneously and positioned in the high right atrium and a tripolar or bipolar His bundle recording catheter was positioned cross the tricuspid valve. The atrial and His bundle electrograms were recorded on a direct writing recorder. After completion of the baseline electrophysiologic (EP) measurements, in an open fashion, celiprolol (0.1 mg/kg) was administered intravenously at the rate of 1 mg/min into each of the five patients. The complete battery of the EP measurements were repeated immediately following completion of the infusion. Preliminary data in eight patients demonstrated no significant effect of celiprolol on the cardiac conduction system.
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PMID:Clinical cardiac electrophysiologic study of celiprolol. 242 39


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