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

In preterm infants, closure of the ductus arteriosus (DA) is often delayed, especially in those with respiratory distress syndrome (RDS). However, it has been suggested that functional closure of the DA may occur as early as 24 hours of age in some preterm infants exposed to intrauterine stress, and this is usually associated with decreased incidence of RDS. This suggests that accelerated maturation of the DA as well as of the lungs occurs in utero. Accordingly, histologic evidence of accelerated maturation of the DA was sought in a prospective autopsy study of 55 preterm infants ranging in gestational age from 19 to 32 weeks. There were four infants with clinically closed DA which showed histologic evidence of closure. The birth weight of these four infants ranged from 750--1,100 gm, the gestational age ranged from 24--32 weeks, and age of death was 39 hours to 6 days. The immediate causes of death were intracerebral hemorrhage or intrapulmonary hemorrhage, or both. Obstetric complications included chronic second trimester vaginal bleeding, abruptio placenta, malnutrition, diabetes, pulmonic stenosis of moderate degree, and chronic hypertension. These findings support the hypothesis that in some preterm infants exposed to chronic intrauterine stress, maturation of the DA is accelerated. This may result clinically in effective postnatal closure of the DA.
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PMID:Morphologic evidence of accelerated closure of the ductus arteriosus in preterm infants. 736 32

A 20-year-old woman with cyanotic congenital heart disease composed of corrected transposition of the great vessels, severe pulmonic stenosis, atresia of the left pulmonary artery and a large ventricular septal defect, had a successful pregnancy following a pulmonary-systemic shunt (Blalock-Taussig). The hemoglobin decreased from 21 to 16 g/dL following the operation. The antepartum course was complicated by intrauterine growth retardation and pregnancy-induced hypertension. A normal fetal nonstress test and biophysical profile permitted continuation of the pregnancy until 38 weeks' gestation, with delivery of a healthy infant.
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PMID:Successful pregnancy in a woman with cyanotic congenital heart disease after a palliative pulmonary-systemic shunt. A case report. 752 54

Four patients with suprarenal coarctation of the abdominal aorta were managed from 1978 to 1993 (mean follow-up 8.75 years). Ages at the time of diagnosis were 2 months, 8 months, 4.5 years, and 15 years, respectively. Three children presented with severe hypertension, two of whom were in congestive heart failure, and the fourth child presented with a cold, ischemic leg. The 8-month-old patient had Williams syndrome (supravalvular aortic and pulmonic stenosis, bilateral renal artery stenosis and celiac artery occlusion, "elfin" facies, and mental retardation) and was treated nonoperatively. After 12 years of follow-up, he was given five medications to control hypertension, cardiac arrhythmias, and heart failure. Three patients with abdominal aortic coarctation were treated operatively and none died. Two patients underwent bypass grafting from the supraceliac aorta to the infrarenal aorta, with bilateral renal artery reconstruction in one. Postoperative arteriograms obtained 1 year or more after operation were normal in both cases. The 2-month-old patient underwent patch aortoplasty, with subsequent reoperation 1.5 years later for recurrent hypertension and heart failure with a bypass graft to the left kidney and removal of an infarcted right kidney. In all three patients, operative repair of the suprarenal aortic coarctation has resulted in long-term control of blood pressure and cardiac and renal function.
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PMID:Coarctation of the abdominal aorta. 852 35

Nineteen consecutive patients with Turner's syndrome and different karyotypes underwent full cardiological evaluation (physical examination, electrocardiogram, chest X-ray and echocardiogram). Congenital heart disease was found in 26%. Other cardiovascular pathologies (long QT syndrome or systemic hypertension) were found in two patients. When compared with the general population, a higher incidence was present for all types of congenital heart diseases observed. Among cardiac anomalies in Turner's patients, aortic malformations (aortic coarctation and bicuspid aorta) were the most frequent, followed by patent ductus arterious and pulmonary valve stenosis. We have observed that the most severe malformations were preferably found with the 45,X karyotype. Pulmonary valve stenosis was found in a mosaicism 45,X/46,XX case. No anomaly was found in patients with X isochromosome. The ring pattern was not found in our series.
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PMID:[The Turner syndrome and cardiovascular changes]. 883 May 99

To determine the usefulness of systemic venous flow patterns in patients with mild/moderate right ventricular hypertension, 17 patients with isolated mild/moderate pulmonic stenosis and 17 age-matched normal children were evaluated with pulsed Doppler echocardiography. Tricuspid valve, superior vena caval, and hepatic vein pulsed Doppler recordings were obtained with simultaneous respirometry and electrocardiography. Peak velocities and velocity-time integrals were measured for Doppler signals corresponding with ventricular systole, ventricular diastole, ventricular end systole, and atrial systole. The groups were similar in weight, heart rate, tricuspid inflow Doppler echocardiograms, and cardiac indexes. Compared with normal subjects, patients showed changes in respiratory variation for some superior vena caval and hepatic vein indexes. In addition, hepatic vein measurements made at ventricular end systole were significantly lower and measurements made at atrial systole were significantly higher in patients than in normal subjects. These changes in systemic venous flow patterns may provide a sensitive indicator of early right-sided heart dysfunction.
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PMID:Doppler systemic venous flow patterns: changes in children with mild/moderate pulmonic stenosis. 894 40

Ventriculo-coronary arterial connections are frequently observed in pulmonary atresia with intact interventricular septum. Sustained right ventricular hypertension during cardiac morphogenesis is thought to be responsible for persistence of myocardial sinusoidal-coronary artery connections. Considering an unusual observation of ventriculo-coronary arterial connections in a patient with critical pulmonary valve stenosis, we speculate that sinusoidal connections in pulmonary atresia with intact ventricular septum occur not only because it is the only exit for blood from the blind right ventricle, but also because of intrinsic altered morphogenesis of the right ventricle myocardium.
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PMID:Right ventricular myocardial sinusoidal-coronary artery connections in critical pulmonary valve stenosis. 956 30

Thirty patients with complete atrioventricular septal defect were operated upon between 1989 and 1996 at our institute. Their ages ranged from two months to 24 years (mean age 2.81 years). All patients had severe pulmonary arterial hypertension except one who had associated pulmonic stenosis. Four patients had severe atrioventricular valve regurgitation and another six had moderate regurgitation. Five patients had Down's syndrome. The cleft in the left atrioventricular valve was closed in all but seven patients. There were five (16.66%) in-hospital deaths which included two patients in whom the cleft was left open. Follow-up ranged from three months to eight years. All patients were evaluated by 2D echocardiography in the immediate post-operative period and three to six monthly subsequently. One patient progressed to moderate and another to severe left atrioventricular valve regurgitation during follow-up. In both the patients the cleft had been left open. All other patients continue to have stable left atrioventricular valve status, that is, none or trivial to mild regurgitation. In view of late deterioration of the left atrioventricular valve regurgitation only in those patients where the cleft was left open, we suggest complete closure of the cleft in all complete atrioventricular canal defects.
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PMID:Routine cleft closure in repair of complete atrioventricular septal defects. 1005 78

Left ventricular (LV) deformation with ventricular septal shift is one of the most distinctive echocardiographic observations in patients with chronic right ventricular (RV) pressure overload (PO). However, little is known about the effects of RVPO on LV performance and regional synchrony. Accordingly, our objective was to test the hypothesis that chronic RVPO affects regional wall motion, synchronicity, and global LV function using a novel speckle-tracking approach to quantify and characterize regional LV wall motion dyssynchrony. Displacement and strain imaging echocardiographic studies were performed in 20 patients with RVPO from pulmonary arterial hypertension or pulmonic stenosis (mean age 53 +/- 16 years, New York Heart Association class 2.6 +/- 0.7, and peak RV systolic pressure 73 +/- 28 mm Hg) and 20 age-matched normal subjects (mean age 47 +/- 16 years). Segmental signals from 6 segments around the mid-LV short axis were defined as dyssynchronous if their changes were opposite to that of the global LV signal at each time frame, and overall LV dyssynchrony was calculated as the percentage of dyssynchrony in all 6 segments within the specified time interval from onset of QRS to the end of isovolumic relaxation. RVPO was associated with a large degree of regional dyssynchrony with paradoxical ventricular septal motion observed by displacement imaging (21 +/- 6%, p <0.05 vs control group), which was closely associated with LV eccentricity index (r = 0.79, p <0.05) and LV myocardial performance index with linear regression (r = 0.76, p <0.05). In contrast, strain imaging showed uniform segmental radial thickening in the RVPO group, which was similar to the control group, and suggests that there was no intrinsic LV contractile dyssynchrony. In conclusion, LV wall motion dyssynchrony assessed by displacement imaging, not intrinsic contractile dyssynchrony by strain imaging, coexists with LV chamber deformation with ventricular septal shift and is closely associated with impairment of LV performance.
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PMID:Role of radial strain and displacement imaging to quantify wall motion dyssynchrony in patients with left ventricular mechanical dyssynchrony and chronic right ventricular pressure overload. 1839 60

We used data from the National Birth Defects Prevention Study, a population-based, case-control study, to examine whether previously reported associations between antihypertensive medications and cardiovascular malformations could be confirmed and to explore whether new associations might be identified. Cases (n=5021) were ascertained through birth defects surveillance systems from 1997 through 2003 in 10 US states. Controls (n=4796) were live births without birth defects selected randomly from birth certificates or hospital discharge listings in the same geographic regions. Logistic regression was used to examine the relationship between antihypertensive medication treatment and the occurrence of cardiovascular malformations while controlling for confounding variables. First-trimester treatment with antihypertensive medication was associated with pulmonary valve stenosis (odds ratio [OR]: 2.6; 95% CI: 1.3 to 5.4), Ebstein malformation (crude OR: 11.4; exact 95% CI: 2.8 to 34.1), coarctation of the aorta (OR: 3.0; 95% CI: 1.3 to 6.6), and secundum atrial septal defects (OR: 2.4; 95% CI: 1.3 to 4.4). Treatment initiated after the first trimester was associated with pulmonary valve stenosis (OR: 2.4; 95% CI: 1.1 to 5.4), perimembranous ventricular septal defects (OR: 2.3; 95% CI: 1.2 to 4.6), and secundum atrial septal defects (OR: 2.4; 95% CI: 1.3 to 4.4). Untreated hypertension was associated with Ebstein malformation (OR: 2.1; 95% CI: 1.0 to 4.3) and secundum atrial septal defects (OR: 1.3; 95% CI: 1.0 to 1.6). Antihypertensive medication use and/or the underlying hypertension might increase the risk of having an infant with specific left and right obstructive and septal defects. Additional studies with adequate power will be needed to confirm these findings.
Hypertension 2009 Jul
PMID:Antihypertensive medication use during pregnancy and the risk of cardiovascular malformations. 1943 79

Right ventricular hypertrophy (RVH) and RV failure contribute to morbidity and mortality in pulmonary arterial hypertension (PAH). The cause of RV dysfunction and the feasibility of therapeutically targeting the RV are uncertain. We hypothesized that RV dysfunction and electrical remodeling in RVH result, in part, from a glycolytic shift in the myocyte, caused by activation of pyruvate dehydrogenase kinase (PDK). We studied two complementary rat models: RVH + PAH (induced by monocrotaline) and RVH + without PAH (induced by pulmonary artery banding (PAB)). Monocrotaline RVH reduced RV O(2)-consumption and enhanced glycolysis. RV 2-fluoro-2-deoxy-glucose uptake, Glut-1 expression, and pyruvate dehydrogenase phosphorylation increased in monocrotaline RVH. The RV monophasic action potential duration and QT(c) interval were prolonged due to decreased expression of repolarizing voltage-gated K(+) channels (Kv1.5, Kv4.2). In the RV working heart model, the PDK inhibitor, dichloroacetate, acutely increased glucose oxidation and cardiac work in monocrotaline RVH. Chronic dichloroacetate therapy improved RV repolarization and RV function in vivo and in the RV Langendorff model. In PAB-induced RVH, a similar reduction in cardiac output and glycolytic shift occurred and it too improved with dichloroacetate. In PAB-RVH, the benefit of dichloroacetate on cardiac output was approximately 1/3 that in monocrotaline RVH. The larger effects in monocrotaline RVH likely reflect dichloroacetate's dual metabolic benefits in that model: regression of vascular disease and direct effects on the RV. Reduction in RV function and electrical remodeling in two models of RVH relevant to human disease (PAH and pulmonic stenosis) result, in part, from a PDK-mediated glycolytic shift in the RV. PDK inhibition partially restores RV function and regresses RVH by restoring RV repolarization and enhancing glucose oxidation. Recognition that a PDK-mediated metabolic shift contributes to contractile and ionic dysfunction in RVH offers insight into the pathophysiology and treatment of RVH.
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PMID:The inhibition of pyruvate dehydrogenase kinase improves impaired cardiac function and electrical remodeling in two models of right ventricular hypertrophy: resuscitating the hibernating right ventricle. 1994 38


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