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

Nineteen planimetric indices of 110 cardiac healthy subjects, 141 patient with left ventricle loading and 136 patients with right ventricle loading are analyzed. On the base of the variation analysis and determination of statistically significant differences, it was established that in right-ventricular loading the following indices deviate from the norm: ASX, AQZ, AQRSX, AQRSz, SAQRSx, SAQRSy, SAQRSz, SAS, SAQRSg, whereas in left-ventricular loading -- ARx, ARz, AQRSx, AQRSz, SAQRx, SAQRSy, SAQRz, SAR, SAQRSg. At a second stage, the sensitivity of the separate indices from the groups with left ventricular and right-ventricular loading was amalyzed, as well as the separate subgroups (pulmonary stenosis, aortic stenosis, mitral stenosis, interauricular defect, arterial hypertension, mitral or aortic insufficiency. The results were compared with those of axial indices, obtained from another investigation of the authors. The planimetric analysis was established to be more complex than the axial and the index SAQRSg to be with the best sensitivity in the cases with hemodynamically lightly loaded musculature.
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PMID:[Planimetric analysis of ventricular depolarization on Frank's corrected orthogonal electrocardiogram in healthy hearts and in patients with ventricular loading]. 52 72

Changes in activity of sympathetic-adrenal and + renin-angiotensin-aldosterone systems (SAS and RAAS), hemodynamics and electrolyte metabolism when correcting sodium balance in consideration of their "salt sensitivity" were studied in 83 hypertension stage I and II patients. In moderate restriction of sodium chloride response of the patients was not uniform. "Salt--sensitive" subjects responded positively with improvement of central and peripheral hemodynamics, electrolyte balance in enhanced activity of SAS and RAAS. In salt nonresponders and in paradoxical sensitivity SAS and RAAS show activation, most distinct in paradoxical sensitivity, and worse central and peripheral hemodynamics, electrolyte imbalance.
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PMID:[Various neurohumoral aspects of hemodynamic changes in patients with hypertension after correction of electrolyte disorders]. 176 49

In 21 patients suffering from severe sleep-apnoea syndrome we measured continuously haemodynamic parameters, blood gases, ECG, EEG, respiratory rate and ultrasonic cardiogram before and under treatment with nasal CPAP-breathing. All patients (male, age 29 to 58 yrs) had normal blood gases, heart-minute-volumes pulmonary artery pressures and left ventricular end-diastolic wedge pressures, when they were awake. During sleep all developed a decrease of pO2 and severe pulmonary artery hypertension with mean pulmonary artery pressures of 64 mmHg. In 10 patients an enlargement of the right ventricular diameter up to 13 mm difference could be seen. Treatment with nasal CPAP-breathing could reduce or even prevent changes in blood gases and in the haemodynamic system. The pulmonary artery pressures normalised in all patients. No right ventricular enlargement could be seen during nasal CPAP-breathing. Treatment with CPAP-breathing could normalise haemodynamic disorders in patients with severe SAS and may perhaps prevent development of cor pulmonale.
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PMID:[Hemodynamic changes with and without CPAP-ventilation in patients with sleep apnea]. 186 12

We compared 8 patients diagnosed with geriatric sleep apnea syndrome (GSAS) with 12 healthy older controls (GCON) matched on age, sex, weight, education, and socioeconomic standing. GSAS was diagnosed if patients had an apnea + hypopnea index (AHI) greater than or equal to 10 and an impairment involving at least two of the following: hypertension, cardiac arrhythmias, or daytime hypersomnolence. In addition to significant differences on selection variables (e.g., AHI, frequency of hypertension, Multiple Sleep Latency Test), GSAS patients had significantly more sleep disturbance, were sleepier on subjective measures, were more depressed, and had lower scores on tests of nonverbal problem solving and nonverbal memory. Thus, GSAS resembles SAS described in middle-aged populations. More research is needed to determine the most efficient diagnostic parameters for identifying pathological levels of SDB in older persons.
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PMID:Geriatric sleep apnea syndrome: a preliminary description. 239 13

Outcomes from 197 pregnancies in 141 female kidney transplant recipients were analyzed from data collected via questionnaires, hospital records, and phone interviews. All recipients were maintained on cyclosporine (CsA) before and during pregnancy. Of the livebirths, 54% were premature (< 37 wk) and 50% were low-birthweight (LBW) (< 2500 g). The incidence of recipient drug-treated hypertension (HTN) was 56%; preeclampsia, 29%; infections and complications 22%; and rejection during pregnancy and up to 3 mo. post delivery (rej.), 11%. Graft loss within 2 years of delivery occurred in 9% of recipients (GrL < 2). No recipients reported a pregnancy after a postpregnancy graft loss. Mean serum creatinine was reported before, during, and after pregnancy. Mean cyclosporine doses were similar in recipients during and after pregnancy. Data were analyzed by logistic regression using SAS. Outcomes included prematurity, LBW, rej., and GrL < 2. In a case-controlled study comparing a recipient group with graft dysfunction during pregnancy vs. a group with good graft function, there was a trend toward lower mean prepregnancy CsA doses (in mg/kg) in the graft dysfunction group. A decline in recipient graft function during pregnancy is associated with lower newborn birthweights and lower maternal graft survival in cyclosporine treated female kidney recipients. Pregnancy-related infections and complications are associated with rejection and graft loss in this population. Close monitoring of CsA dosing and serum creatinine levels during pregnancy and immediately postpartum is recommended as CsA dosage adjustment may be required.
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PMID:Variables affecting birthweight and graft survival in 197 pregnancies in cyclosporine-treated female kidney transplant recipients. 787 49

Maternal cigarette smoking during pregnancy as a risk factor for having a child with cleft lip/palate has been suggested by several epidemiologic studies. However, most of these studies contained small sample sizes, and a clear association between these two factors could not be established. The U.S. Natality database from 1996 and a case-control study design were used to investigate the association between maternal smoking during pregnancy and having a child with cleft lip/palate. The records of 3,891,494 live births from the 1996 U.S. Natality database were extracted to obtain cleft lip/palate cases and random controls. The National Center for Health Statistics collects maternal and newborn demographic and medical data from the birth certificates of all 50 states. New York (excluding New York City), California, Indiana, and South Dakota did not collect smoking data, and the data from these states were excluded from the analysis. A total of 2207 live births with cleft lip/palate cases were identified, and 4414 controls (1:2 ratio) were randomly selected (using the SAS program) from live births with no congenital defects. Odds ratios and 95 percent confidence intervals were determined from logistic regression models, adjusting for confounding variables, including maternal demographic and medical risk factors. A significant association was found between any amount of maternal cigarette use during pregnancy and having a child with cleft lip/palate [unadjusted odds ratio 1.55 (1.36, 1.76), p < 0.001]. Univariate analysis showed that maternal education level, age, race, and maternal medical conditions (diabetes and pregnancy-associated hypertension) were potential confounders. After adjusting for these confounders, the odds ratio remained significant [Mantel-Haenszel odds ratio 1.34 (1.16, 1.54), p < 0.001]. To determine the dose response of cigarette smoking during pregnancy, the cigarette consumption per day was divided into four groups: none, 1 to 10, 11 to 20, and 21 or more. A dose-response relationship was found when comparing each smoking category with the no smoking reference group: 1.50 (1.28, 1.76), 1.55 (1.23, 1.95), and 1.78 (1.22, 2.59), respectively. This means that increased cigarette smoking during pregnancy resulted in increased odds of having a child with cleft lip/palate. This is the largest study to date to test the association between maternal cigarette smoking during pregnancy and having a newborn with cleft lip/palate. The significant trend in the dose-response relationship strongly suggests the association of smoking tobacco and this common congenital deformity. These results emphasize the public health risks associated with smoking during pregnancy. To prevent this devastating craniofacial anomaly, educational initiatives should be considered that will alert expectant mothers to the association between smoking during pregnancy and the occurrence of cleft lip/palate.
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PMID:Maternal cigarette smoking during pregnancy and the risk of having a child with cleft lip/palate. 1069 50

Several epidemiological studies have suggested that sleep-disordered breathing is a risk factor for cardiovascular disease, particularly hypertension, stroke and IHD. The relative risk for IHD among obstructive SAS(OSAS) patients is 1.2 to 6.9 higher compared with the general population. The prevalence of SAS with an apnea-hypopnea index(AHI) of 10 and over was 35 to 40% in IHD, while 23.8% of SAS patients had IHD. These evidence suggests that IHD is an important prognostic factor in SAS patients. Characteristic pathophysiological conditions such as sleep apnea-induced hypoxemia and sympathetic activation may play an important role in the genesis of nocturnal angina pectoris. Most patients with OSAS are obese, and the complication of non-insulin dependent diabetes mellitus is quite a few. Insulin resistance is also attracting great attention as a cause of the cardiovascular complication of SAS.
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PMID:[Sleep apnea syndrome (SAS) and ischemic heart disease (IHD)]. 1094 39

Our aim was to determine the frequency of hypertension in the Hungarian stroke population, and to compare it with the data of other stroke registries. We attempted to find characteristic cluster-like associations between hypertension and another nine risk factors in different stroke subtypes and to ascertain the role of hypertension in leukoaraiosis, in early mortality, in stroke recurrence and in the case fatality rate up to 10 years. Risk factor profile of 500 unselected acute stroke cases of the Budapest Stroke Data Bank were analysed. We compared data of hypertensive stroke patients to those of unaffected ones. LIFEREG procedure of the SAS software package, cluster analysis, logistic regression, Pearson's correlation coefficient and Student's t-test were used as statistical methods. Hypertension was documented in 75% of the patients. The largest clusters were formed by the following groups: atherosclerotic stroke, hypertension with ischaemic heart disease; lacunar stroke and haemorrhage, hypertension with elevated serum cholesterol, cardiogenic embolism, ischaemic heart disease with atrial fibrillation. The case fatality rate was significantly higher in the group of hypertensive patients with ischaemic heart disease relative to those without it during the 10 years follow-up period. In the leukoaraiosis-group, systolic blood pressure was significantly higher than in the non-leukoaraiosis group. The rate of hypertension was higher than in other stroke registries. Hypertension appears to be the most frequent risk factor in stroke patients but case fatality rate is determined by presence or absence of ischaemic heart disease.
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PMID:Hypertension and clusters of risk factors in different stroke subtypes (an analysis of Hungarian patients via Budapest Stroke Data Bank). 1208 Apr 34

Four basic control mechanisms of breathing (brainstem respiratory centre, peripheral and central chemoreceptors, intero- and exteroceptive reflexes and suprapontine influences), as well as their sleep-related disorders are analysed. A decrease in central chemoreceptor sensitivity to CO2 and an increase in upper airway resistance during sleep result in hypoventilation and mild hypoxaemia already in physiological conditions. Compensatory increase in ventilatory effort with synchronous inhibition of pharyngeal dilators during sleep reduces the upper airway lumen manifesting with snoring, upper airway resistance syndrome, and OSA. The resulting hypoxaemia may cause marked cardiovascular, neuro-psychic, endocrine-metabolic and behavioural disorders. The augmented ventilatory effort and hypoxaemia evoke reflex dilation of airways and arousal from sleep, stimulating the sympatho-adrenal system, which provokes autoresuscitation by gasping preventing fatal asphyxia. Failure of this autoresuscitation mechanism seems to cause SIDS. Elimination of voluntary breathing by sleep either in Ondine's curse induced by lesions of respiratory centre, or in congenital central hypoventilation syndrome caused by insufficient central chemoreceptors result in respiratory failure and death. Nocturnal attacks of bronchial and cardiac asthma, lung oedema and other consequences of pulmonary congestion are also discussed. The pathomechanism of extreme daytime sleepiness, chronic fatigue, and disorders of memory, cognitive and other brain functions, are also analysed. Severe cardiovascular consequences of SAS may manifest acutely as angina pectoris, myocardial infarction. dysrhythmias, transient ischaemic attacks and even stroke or sudden cardiac death. OSAS may result also in development of hypertension, central obesity, diabetes mellitus, erectile dysfunction, depression, and various behavioural disorders.
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PMID:[Regulation of respiration and its sleep-related disorders]. 1244 39

Metabolic syndrome, indicated by insulin resistance/hyperinsulinemia, obesity, central obesity, atherogenic dyslipidemia, and hypertension, contributes to atherosclerotic cardiovascular disease. However, it is controversial whether the indicators of metabolic syndrome are related to subclinical atherosclerosis collectively or individually. Whether there is any gender-based difference in the mechanisms of metabolic syndrome-induced atherosclerosis progression is also unknown. Two models were compared in this study. Model 1 assumes that a latent factor, metabolic syndrome per se, impacts subclinical atherosclerosis (collective effects model); Model 2 assumes the effect of the syndrome is mediated through its indicators (individual effects model). Data were obtained from the Los Angeles Atherosclerosis Study. The cohort consists of 573 adults (age, 40-60 years) who were asymptomatic for cardiovascular disease. Subclinical atherosclerosis was assessed by measuring common carotid artery intima-media thickness (CCA-IMT) using B-mode ultrasound. Three examinations were completed at 1.5-year intervals from 1995-1999. The analyses were performed with SAS 8.2 and AMOS 4.0. The results showed that atherogenic effects of metabolic syndrome were mediated through its indicators; there were gender-based differences in the mechanisms of metabolic syndrome-induced atherosclerosis. Central obesity was significantly associated with the baseline IMT for men only, whereas triglycerides were significantly associated with the progression of IMT for women only. Systolic blood pressure was significantly associated with the baseline and progression for both men and women. However, fasting insulin was not found to be significantly associated with the baseline and progression of IMT in the multivariate model, although it was significantly associated with other components of metabolic syndrome.
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PMID:Metabolic syndrome and progression of atherosclerosis among middle-aged US adults. 1650 91


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