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

The changes induced by transient hypertension upon cardiac geometry (G) are unclear. Pregnancy-induced hypertension (PIH) offers a natural and spontaneous model of this condition. To assess geometric changes according to two-dimensionally guided M-mode echocardiography, we compared patients with PIH with normal pregnant women (NPW). Fifty-five women, aged 28.5 +/- 7.5 years, with PIH (defined as blood pressure >140/90 mm Hg in the third trimester of pregnancy and without a history of hypertension) were compared with 57 NPW aged 30.7 +/- 7.5 years. Left ventricular mass index (LVMI) (Devereux formula) and relative wall thickness (RWT) (Ganau formula) were calculated by means of echocardiography done in the left lateral decubitus 2 to 4 days postpartum. Subjects were considered to have: normal geometry (NG) if both LVMI and RWT fell below the mean +/- 1 SD or 2 SD; concentric hypertrophy (CH) if both were elevated; eccentric hypertrophy (EH) if LVMI was elevated and RWT was normal; and concentric remodeling (CR) if LVMI was normal and RWT was elevated. Comparisons were performed by the Student t test. Patients with PIH had higher LVMI (106 +/- 29.4 v 90.6 +/- 19.8 g/m2; P < .05) and RWT (0.41 +/- 0.07 v 0.38 +/- 0.05; P < .05). Considering the mean +/- 1 SD of NPW as the limit of normality the G pattern was NG in 26 (47%) and abnormal in 29 (53%), of which 14 (25.5%) had EH, 11 (20%) had CR, and four (7%) had CH. If we considered the mean +/- 2 SD, the G pattern was NG in 46 (84%) and abnormal G in nine (16%), EH in four (7%), CR in three (5%), and CH in 2 (4%). According to these data, women with PIH had higher LVMI and RWT compared with NPW. The most frequent abnormal G patterns were EH and CR.
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PMID:Left ventricular geometry in pregnancy-induced hypertension. 1077 25

The purpose of this study was to determine the relationship between the lupus anticoagulant and the proteinuric and non-proteinuric Gestational Hypertension in primigravids without subjacent pathology. Sixty- five patients with a single gestation of twenty or more weeks long were studied. Thirty four patients (Group A) were pregnant women with a normal blood pressure. Hypertensive disease developed during pregnancy (according to Davey and MacGillivray, classification) affected 31 patients (Group B). A test to determine the presence of the lupus anticoagulant was performed on all of them, according to the method of the diluted Russel viper venom. None of the patients developed any other symptomatic subjacent pathology. Fifty-five percent of the Group B patients developed proteinuric gestational hypertension (preeclampsia) and forty-five percent of them non-proteinuric gestational hypertension. The test to determine the lupus anticoagulant was negative in all the patients from both groups. The results suggest that the presence of a lupus anticoagulant is unlikely in the proteinuric and non-proteinuric gestational hypertension in primigravidas without subjacent pathology, therefore it remains as a controversial study issue.
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PMID:[Lupus anticoagulant in preeclampsia and non-proteinuria gestational hypertension in primiparous women]. 1096 Oct 45

Gestational hypertension complicates approximately 5%-7% of pregnancies and it may be deleterious to both maternal and fetal health. Gestational hypertension is a multisystem disorder which always resolves itself after delivery; its primary pathology still remains incompletely clarified. The renin-aldosterone system is a major determinant of sodium balance in pregnancy. To evaluate the changes in renin and aldosterone levels during normal and hypertensive pregnancy we undertook this study. Plasma renin activity and aldosterone levels were measured in 71 pregnant (43 normotensive, 28 hypertensive) and 24 non-pregnant (12 normotensive, 12 hypertensive) women, aged 19-43 years (mean +/- SD 28 +/- 2.8). Women were allocated into the following five groups: Groups 1 and 2 consisted of 12 normotensive and 12 hypertensive non-pregnant women, respectively; group 3 consisted of 20 women (14 normotensive and 6 hypertensive) at 11-19 weeks of gestation; group 4 consisted of 24 women (14 normotensive and 10 hypertensive) at 20-29 weeks of gestation, and group 5 consisted of 27 women (15 normotensive and 12 hypertensive) at 30-37 weeks of gestation. Both plasma renin activity and aldosterone levels progressively increased during normotensive pregnancy and were higher compared to normotensive non-pregnant women. Among hypertensive pregnant women, plasma renin activity levels remained unchanged during the three trimesters of pregnancy and were higher compared to hypertensive non-pregnant women. Only during the third trimester did aldosterone levels significantly increase in hypertensive pregnant women, compared to hypertensive non-pregnant women. Despite stable renin levels, aldosterone levels increased significantly during the third trimester of hypertensive pregnancy. Thus, we conclude that aldosterone biology seems to be directly or indirectly involved in the etiology of gestational hypertension independently of renin levels.
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PMID:The renin-aldosterone system during normal and hypertensive pregnancy. 1120 4

Pregnancy-induced hypertension (PIH), which includes both gestational hypertension and preeclampsia, is a common and morbid pregnancy complication for which the pathogenesis remains unclear. Emerging evidence suggests that insulin resistance, which has been linked to essential hypertension, may play a role in PIH. Conditions associated with increased insulin resistance, including gestational diabetes, polycystic ovary syndrome, and obesity, may predispose to hypertensive pregnancy. Furthermore, metabolic abnormalities linked to the insulin resistance syndrome are also observed in women with PIH to a greater degree than in normotensive pregnant women: These include glucose intolerance, hyperinsulinemia, hyperlipidemia, and high levels of plasminogen activator inhibitor-1, leptin, and tumor necrosis factor-alpha. These observations suggest the possibility that insulin resistance may be involved in the pathogenesis of PIH and that approaches that improve insulin sensitivity might have benefit in the prevention or treatment of this syndrome, although this requires further study.
Hypertension 2001 Feb
PMID:Brief review: hypertension in pregnancy : a manifestation of the insulin resistance syndrome? 1123 Feb 77

Gestational hypertension during the third trimester reflects an exaggerated maternal inflammatory response to pregnancy. We hypothesized that oxidative stress present even in normal pregnancy becomes uncompensated in hypertensive patients. A glucose-6-phosphate dehydrogenase (G6PD) activity sufficient to meet the increased reductive equivalent need of the cells is indispensable for defense against oxidative stress. The erythrocyte glutathione redox system was studied, where G6PD is the only NADPH source. The glutathione (GSH) redox status was measured both in vivo and after an in vitro oxidative challenge in pregnant women with gestational hypertension (n = 19) vs. normotensive pregnant subjects (n = 18) and controls (n = 20). An erythrocyte GSH depletion with an increase in the oxidized form (GSSG) resulted in an elevated ratio GSSG/GSH (0.305 +/- 0.057; mean +/- SD) in hypertensive pregnant women vs. normotensive pregnant or control subjects (0.154 +/- 0.025; 0.168 +/- 0.073; p <.001). In hypertensive pregnant patients, a "GSH stability" decrease after an in vitro oxidative challenge suggested a reduced GSH recycling capacity resulting from an insufficient NADPH supply. The erythrocyte GSSG/GSH ratio may serve as an early and sensitive parameter of the oxidative imbalance and a relevant target for future clinical trials to control the effects of antioxidant treatment in women at increased risk of the pre-eclampsia syndrome.
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PMID:Blood glutathione redox status in gestational hypertension. 1127 71

The changes induced by transient hypertension on cardiac structure and function are unclear. Pregnancy-induced hypertension offers a natural and spontaneous model of this condition. To assess the potential of echocardiographic Doppler to unmask left ventricular function impairment, we studied 28 women aged 26.4 +/- 7.2 years with pregnancy-induced hypertension defined as blood pressure higher than 140/90 mm Hg in the third trimester of pregnancy without a history of hypertension. Twenty normal pregnant women, aged 27.5 +/- 6.4 years, were the controls. Left ventricular diastolic diameter, fractional shortening, E velocity, A velocity, E/A ratio, isovolumetric relaxation time (IRT), isovolumetric contraction time (ICT), ejection time (ET), and the combined index of myocardial performance (Tei index = IRT + ICT/ET), were calculated by echocardiography Doppler 2 to 4 days postpartum. There were statistically significant differences between groups in the following parameters: E/A ratio: 1.3 +/- 0.3 in pregnancy-induced hypertension v 1.5 +/- 0.3 in normal pregnant women (P < .05), IRT: 104 +/- 14 msec v 84 +/- 7 msec (P < .000), and the Tei index: 0.51 +/- 0.15 v 0.35 +/- 0.04 (P < .00), respectively. According to this data pregnancy-induced hypertension evaluated 2 to 4 days after delivery showed left ventricular dysfunction, mainly diastolic. The IRT and the Tei index are the most useful echocardiographic parameters to unmask left ventricular dysfunction in pregnancy-induced hypertension.
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PMID:Left ventricular function impairment in pregnancy-induced hypertension. 1128 Dec 40

Chronic hypertension induces changes in the structure of the left ventricle, atrium, and aortic root. However, the effects of transient hypertension are unclear. Pregnancy-induced hypertension (PIH) offers a natural and spontaneous model of this condition. Using M-mode echocardiography, we studied 95 consecutive patients with PIH, who were compared with 83 normal pregnant women (NPW). We evaluated diastolic diameter (DD), systolic diameter (SD), septal thickness (ST), posterior wall thickness (PWT), shortening fraction (SF), relative wall thickness (RWT), left ventricular mass index (LVMI), left atrial dimension (LAD), and aortic root dimension (ARD). Patients with PIH had higher ST (9.98 +/- 1.47 mm v 8.96 +/- 1.43 mm, P < .000), PWT (9.28 +/- 1.48 mm v 8.55 +/- 1.35 mm, P < .000), LVMI (107.65 +/- 27.87 g/m2 v 92.38 +/- 17.99 g/m2, P < .000), and RWT (0.406 +/- 0.06 v 0.377 +/- 0.06 mm, P < .002). There were no significant differences in DD, SD, SF, LAD, and ARD. In conclusion, PIH increases the LVMI due to an increase in the ST and PWT. The dimensions of the left ventricle, left atrium, and aortic root do not change.
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PMID:Dimensions of the left ventricle, atrium, and aortic root in pregnancy-induced hypertension. 1133 88

Pregnancy induced hypertension remains the most frequent reason of maternal and fetal complications. Recent studies of the entire pathophysiology of the abnormal implantation proved association between the impaired placental performance and the reduced uteroplacental circulation. Therefore the Doppler examination of uterine and umbilical blood flow may provide the early recognition of high-risk pregnancies complicated by maternal hypertension and fetal intrauterine growth retardation. The authors endeavor to describe the details and characteristics of uteroplacental haemodynamic changes during the course of physiologic and defective implantation. On the basis of the currently available scientific publications they summarize the role of the uterine and umbilical artery Doppler velocimetry as a screening tool in the detection of the consequences of the impaired uteroplacental perfusion. They conclude that abnormal velocity waveforms obtained from the uterine and umbilical arteries may help to improve the efficacy of the prenatal care and the perinatal outcome as well. The clinical benefits of this screening method will be precisely defined on the basis of further multicenter studies in Hungary.
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PMID:[The role of uterine and umbilical artery Doppler velocimetry for the early detection of pathologic pregnancy]. 1134 Nov 67

The objective of this study was to evaluate diastolic parameters and left ventricular geometry in gestational hypertension. Twenty-one consecutive pregnant women with gestational hypertension and 21 normotensive women matched for age and gestational age were enrolled in the third trimester of gestation. Echocardiographic and uterine color Doppler evaluations were performed. Systolic, diastolic, and mean blood pressure, total vascular resistance (TVR), and uterine resistance index were higher in hypertensive women than in control subjects (P<0.01). Left atrial function and cardiac output were significantly lower in gestational hypertension (P<0.01). Patients with gestational hypertension had longer left ventricular isovolumetric relaxation time (IVRT) (P<0.0001); lower velocity-time integral of the A wave (P<0.05) and of the diastolic pulmonary vein flow (P<0.05); and higher velocity-time integral of the reverse pulmonary vein flow (P<0.05). Systolic fraction of the pulmonary vein flow was higher in women with gestational hypertension than in control subjects (P<0.01); the difference in duration of pulmonary vein flow and A wave was closer to 0 in gestational hypertension (P<0.0001). Altered left ventricular geometry was found in 100% of hypertensive patients and in 19.05% of normotensive patients (P<0.001). IVRT, left ventricular end-systolic volume, atrial function, and uterine resistance index were directly related to TVR (P<0.01); deceleration time of the E wave showed a quadratic correlation with TVR (P<0.01). Gestational hypertension is characterized by an altered cardiac geometric pattern of concentric hypertrophy. The altered geometric pattern assessed during gestational hypertension is associated, in our study, with depressed systolic function, high TVR, altered diastolic function, and left atrial dysfunction. Deceleration time of the E wave, IVRT, and left atrial fractional area change, found in concomitance with the highest TVR, may be useful in the evaluation of cardiac function and hemodynamics present in pregnancy-induced hypertension.
Hypertension 2001 May
PMID:Maternal diastolic dysfunction and left ventricular geometry in gestational hypertension. 1135 30

Pregnancy-induced hypertension (PIH) is estimated to affect 7% to 10% of all pregnancies in the United States. Despite being the leading cause of maternal death and a major contributor of maternal and perinatal morbidity, the mechanisms responsible for the pathogenesis of PIH have not yet been fully elucidated. Studies during the past decade, however, have provided a better understanding of the potential mechanisms responsible for the pathogenesis of PIH. The initiating event in PIH appears to be reduced uteroplacental perfusion as a result of abnormal cytotrophoblast invasion of spiral arterioles. Placental ischemia is thought to lead to widespread activation/dysfunction of the maternal vascular endothelium that results in enhanced formation of endothelin and thromboxane, increased vascular sensitivity to angiotensin II, and decreased formation of vasodilators such as nitric oxide and prostacyclin. The quantitative importance of the various endothelial and humoral factors in mediating the reduction in renal hemodynamic and excretory function and elevation in arterial pressure during PIH is still unclear. Investigators are also attempting to elucidate the placental factors that are responsible for mediating activation/dysfunction of the maternal vascular endothelium. Microarray analysis of genes within the ischemic placenta should provide new insights into the link between placental ischemia and hypertension. More effective strategies for the prevention of preeclampsia should be forthcoming once the underlying pathophysiologic mechanisms that are involved in PIH are completely understood.
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PMID:Pathophysiology of pregnancy-induced hypertension. 1141 54


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