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At least 469 records · Page 26Linked to original sources
PubMed1996

Lung transplantation in children with pulmonary hypertension and congenital heart disease.

Pulmonary vascular disease with or without associated congenital heart disease is the indication for lung transplantation in 30% of all children requiring this procedure. Although many of these children will have primary pulmonary hypertension, a substantial number are children whose pulmonary vascular disease is either associated with a congenital heart lesion or secondary to it. Heart-lung transplantation has been performed in these children in the past, but because of the scarcity of availability of donor heart-lung blocks, lung transplantation with repair of associated congenital cardiac lesions has of necessity been performed more frequently. As one might expect, the operative and postoperative management of these patients is a good deal more complex than pulmonary transplantation for primary lung diseases. The early mortality is correspondingly higher as well, although survival beyond that time is quite similar to that of lung transplantation for other diseases. Factors that increase the early mortality include previous thoracic procedures and the complexity of the underlying cardiac diagnosis. Although the overall experience with this complex group of patients is small, the results seem similar to the prior experience with heart-lung transplantation. Thus, we remain optimistic that this will continue to be a viable form of therapy for children with pulmonary vascular disease associated with congenital heart lesions. The quality of life of the surviving patients is excellent and limited only by those factors impacting upon lung transplantation in general, such as rejection, infection, and the development of bronchiolitis obliterans.

Adolescent↗
PubMed1996

Stent redilation in canine models of congenital heart disease: pulmonary artery stenosis and coarctation of the aorta.

In a canine puppy model, pulmonary artery stenosis was created by banding the left pulmonary artery to 30-40% of its original diameter. Animals underwent right heart catheterization and angiography 1-2 mo later, and Palmaz P308 stents were implanted. Stent redilation was performed 3-5 mo later. One mo postredilation, the animals were restudied and sacrificed. Coarctations of the aorta were created by transverse aortic incision and longitudinal repair. P308 stent implantation was performed 2-3 mo later. Stent redilation was performed after 6-10 mo, and the animals were restudied and sacrificed 1-2 mo later. Stent implantation was performed in 6 puppies with pulmonary artery stenosis, as 2 animals developed postoperative pulmonary arterial hypoplasia, precluding stenting. The stenosis diameter increased from 4.8 +/- 0.5 mm to 7.4 +/- 0.6 mm (mean +/- SE) following stenting (P = 0.005), and increased further to 9.2 +/- 0.7 mm following redilation (P < 0.001). There were no significant vessel tears or ruptures. Coarctation stenting was performed in 8 animals. The coarctation was dilated from 5.8 +/- 0.9 mm to 9.8 +/- 0.6 mm (P < 0.001), and to 13.5 +/- 0.5 mm at redilation (P = 0.002). Redilation could not be performed in 1 animal. Aortic rupture and death occurred in 2 of 7 animals at redilation. Stent implantation and redilation in experimental pulmonary artery stenosis appears safe and effective. Though stent implantation for coarctation of the aorta appears safe, there was a 28% aortic rupture rate at stent redilation in this model.

Angioplasty, Balloon↗
PubMed1994

[Race and left ventricle hypertrophy without hypertension and pulmonary heart disease].

PURPOSE: To analyze the association between black people and left ventricular hypertrophy (LVH) in the absence of hypertension and/or other cardiopulmonar disease. METHODS: Data were collected from necropsies carried out in the Anatomopathologic Service (APS). Hospital Edgard Santos from 1970 to 1986, Salvador. It were included only subjects at ages > or = 20 years and free of hypertension and any cardiopulmonar disease. A LV wall > 1.6cm was considered as LVH (standardized criteria of the APS). Controls variables were age, sex, and absence of the mentioned diseases. It was used a case-control epidemiological study design and the association measured by "odds ratio" (OR) for no matched case-control study. RESULTS: From the 208 subjects studied, 48 (23.1%) had LVH. There was no difference in the frequency of right ventricular hypertrophy between cases and controls (p > 0.05). The mean of heart weight was higher for LVH cases (p < 0.001), but there was no evidence of association between blacks and LVH (OR = 1.05, p > 0.05 and confidence interval at 95% = 0.8, 1.31. The highest odds possible for the association in this study (assuming that all 3 LVH losses were black subjects) would be 1.5, also no statistically significant. CONCLUSION: In the absence of hypertension and other cardiopulmonar diseases, LHV is common in necropsies in Salvador, Brazil, with similar frequencies in blacks, whites and mullatos and seems not be a risk factor for hypertension in black people.

Adult↗
PubMed1995

Lung cancer among workers exposed to silica dust in Chinese refractory plants.

A retrospective cohort mortality study was conducted for lung cancer among silica and clay brick workers at 11 refractory plants in China. The cohort included 6266 male workers employed before 1962 and followed between 1963 and 1985. The standardized rate ratios (SRR) were obtained by comparing the mortality rates of the silica-exposed cohort with those of a population of 11 470 male steel workers. As expected, significant excesses were observed for all deaths, all cancers, lung cancer, cardiorespiratory diseases, pulmonary heart diseases, and pulmonary tuberculosis. The lung cancer SRR was 1.49 (P < 0.01) for the total cohort. The increased lung cancer risk was attributed to the silicotics (SRR 2.10; P < 0.01) in the cohort. Higher lung cancer risk was found with increasing latency and severity of silicosis; this finding suggests that the excess was possibly related to occupational exposure to silica dust. Among the silicotics, there was a twofold excess of lung cancer risk among both the nonsmokers and the smokers.

China↗
PubMed1978

The pulmonary circulation in congenital heart disease. II. Pulmonary hypertension.

In young children with congenital heart disease the pulmonary circulation is exposed to abnormal haemodynamic conditions before it is fully developed. In the newborn infant the persistence or development of pulmonary hypertension rapidly leads to structural change. The speed with which an increase in muscularity can develop has hitherto been underestimated. In most children dying in early infancy with congenital heart disease and pulmonary hypertension the presence of thick walled small arteries is due not to persistence of the high wall thickness of foetal life, but to a rapid postnatal response of the pulmonary circulation to pulmonary hypertension. In older patients with a ventricular septal defect, aged between 3 months and 4 years, the presence of pulmonary hypertension has been shown to interfere with the growth and development of the pulmonary circulation, judging this by reduction in size and multiplication of intra-acinar arteries and an increase in muscularity of both pre and intra-acinar arteries and veins. In these patients elevation of pulmonary vascular resistance was associated with failure of the intra-acinar pulmonary circulation to develop normally and not with obliterative pulmonary vascular disease. Recent studies indicate that growth and development of the peripheral pulmonary circulation can be quantitated in lung biopsies taken from infants and young children with congenital heart disease. It should therefore be possibe to correlate structure and function at a critical period of lung development, before the changes of obliterative pulmonary vascular disease are established.

Aortic Coarctation↗
PubMedDate not supplied

Nebulized nitroglycerin in children with pulmonary hypertension secondary to congenital heart disease.

Pulmonary hypertension continues to be a major cause of morbidity and mortality, despite new treatments. Since inhaled nitric oxide has been reported to be effective in some cases, we investigated using nebulized nitroglycerine to treat pulmonary hypertension in children with congenital heart disease. Four children (ages 6-72 months) with severe pulmonary hypertension secondary to congenital heart disease (all with membranous ventricular septal defect, undergoing cardiac catheterization) were given 3 cc of nebulized normal saline over 10 min as placebo control, followed by nebulized nitroglycerine (20 micrograms/Kg in 3 cc normal saline). Normal saline administration did not elicit any change, but nitroglycerine administration resulted in the following changes (mean +/- SE, paired statistics): systolic pulmonary artery pressure from 68 +/- 8 to 53 +/- 6 at 10 min into treatment (P 0.006), mean pulmonary artery pressure 47 +/- 4 to 38 +/- 4 (P 0.005), heart rate 131 +/- 8 to 127 +/- 7 (P 0.13), systolic blood pressure 85 +/- 8 to 88 +/- 3 (P 0.7), mean blood pressure 59 +/- 6 to 63 +/- 4 (P 0.5). These results indicate that nebulized nitroglycerine may be an effective, easy to administer, inexpensive, and safe alternative for treatment of severe pulmonary hypertension in children with congenital heart disease, especially in areas where other treatments such as extracorporeal membrane oxygenation or inhaled nitric oxide are inaccessible.

Aerosols↗
PubMed1984

Pulmonary wedge angiography for the evaluation of the pulmonary vascular bed in congenital heart disease.

Pulmonary wedge angiograms (PWA) were analyzed qualitatively and quantitatively to evaluate the pulmonary vascular bed in 40 patients with congenital heart disease. The patients were divided into four groups: group 1, normal pulmonary hemodynamics; group 2, increased pulmonary blood flow; group 3, pulmonary hypertension (PH); and group 4, PH with elevated pulmonary vascular resistance. The PWA were analyzed for tapering, pulmonary circulation time (PCT) index, and vascular image. The tapering was normal in groups 1 and 2 and was more rapid in groups 3 and 4. The PCT index was slightly lower in groups 3 and 4 than in groups 1 and 2. With 100% oxygen, the tapering became less severe and the PCT index increased in group 3. However in group 4, these parameters did not improve with 100% oxygen, suggesting that more advanced vascular changes had developed. These studies confirm the usefulness of the PWA in evaluating the pulmonary vascular bed of patients with congenital heart disease and PH.

Angiography↗
PubMed1976

Pulmonary arteriography in congenital heart disease.

Pulmonary outflow tract obstruction may occur at subvalve, valve, or pulmonary artery level. Selective ventriculography will usually define the intracardiac obstruction (whether valve, subvalve, or both) and may define pulmonary arterial abnormalities. Increasing experience in the surgical management of patients with tetralogy of Fallot and other conotruncal abnormalities characterized by significant pulmonary outflow tract obstruction suggests that preoperative recognition of pulmonary arterial stenosis is essential to the successful operative management of these patients (1-4). Because of the anatomicospacial relationships of the pulmonary arteries in "simple" (tetralogy of Fallot) and complex conotruncal malformations, selective ventriculography may not invariably provide sufficient detail about the morphologic state of the pulmonary arteries. Similarly, even selective pulmonary arteriography in the standard anterioposterior, lateral, and oblique views may not always allow accurate anatomic assessment of these vessels. Therefore, we wish to document a maneuver that has proved valuable in the assessment of pulmonary arteries during selective pulmonary arteriography. This maneuver was originally suggested to Peter M. Olley by Dr. L. M. Bargeron, Jr., and the surgical valve obtained from this angiographic view was stressed by Dr. John Kirklin in his John Keith lecture at the Canadian Cardiovascular Society (5). Although it is being used at some cardiovascular centers, we feel its application warrants this report.

Child, Preschool↗
PubMed2003

Vascular remodeling process in reversibility of pulmonary arterial hypertension secondary to congenital heart disease.

Pulmonary vascular remodeling process was analyzed using morphometry in lung biopsy specimens taken from 26 children, aged 6 to 160 months, who had congenital heart disease and significant pulmonary arterial hypertension. Reparative surgery was performed in 22 patients and palliative surgery was performed in four patients. One patient expired postoperatively and four others after hospital discharge. Vascular remodeling examination revealed a characteristic pathological picture: pronounced medial thickening with increased collagen content (fibrosis), without significant arterial intimal proliferation. At a mean follow-up of 44 months, 72% of the survivors were asymptomatic with no medication. Diagnosed by echocardiogram, 22% of these patients were shown to have pulmonary arterial hypertension. The characteristic pathological features described above occurred in 38% of the patients who either expired or had pulmonary hypertension postoperatively. These findings were an aid to identifying a high risk group in which the outcome does not meet expectations for the classical grade I and II changes. We concluded that the presence of isolated medial thickening does not ensure either survival or a normal postoperative pulmonary arterial pressure at late follow-up and that the collagen content can be a better reference for good outcome. Early intracardiac repair is recommended before the development of significant medial fibrosis.

Adolescent↗
PubMed1992

Stress failure of pulmonary capillaries: role in lung and heart disease.

Pulmonary capillaries have extremely thin walls to allow rapid exchange of respiratory gases across them. Recently it has been shown that the wall stresses become very large when the capillary pressure is raised, and in anaesthetised rabbits, ultrastructural damage to the walls is seen at pressures of 40 mm Hg and above. The changes include breaks in the capillary endothelial layer, alveolar epithelial layer, and sometimes all layers of the wall. The strength of the thin part of the capillary wall can be attributed to the type IV collagen in the extracellular matrix. Stress failure of pulmonary capillaries results in a high-permeability form of oedema, or even frank haemorrhage, and is apparently the mechanism of neurogenic pulmonary oedema and high-altitude pulmonary oedema. It also explains the exercise-induced pulmonary haemorrhage that occurs in all racehorses. Several features of mitral stenosis are consistent with stress failure. Overinflation of the lung also leads to stress failure, a common cause of increased capillary permeability in the intensive care environment. Stress failure also occurs if the type IV collagen of the capillary wall is weakened by autoantibodies as in Goodpasture's syndrome. Neutrophil elastase degrades type IV collagen and this may be the starting point of the breakdown of alveolar walls that is characteristic of emphysema. Stress failure of pulmonary capillaries is a hitherto overlooked and potentially important factor in lung and heart disease.

Animals↗
PubMed2002

Pulmonary arterial hypertension in congenital heart disease.

Pulmonary arterial hypertension (PAH) is a recognized complication of congenital systemic to pulmonary arterial cardiac shunts. The prognosis of PAH in this situation is better than primary or other secondary forms of PAH. Our knowledge of the pathophysiology of PAH complicating congenital heart disease has evolved over the past decade. Despite differences in etiology and pathobiology, therapies that have proven successful for primary PAH may benefit this group of patients.

Eisenmenger Complex↗
PubMed2005

[Pulmonary arterial hypertension in adults with congenital heart disease].

Pulmonary arterial hypertension is a chronic, persistent elevation in pulmonary artery pressure without evidence of left heart failure. Pulmonary hypertension is common in patients with adult congenital heart disease and is usually the result of an increase of pulmonary blood flow through a large left to right shunt. This condition is progressive and patients are symptomatic and usually die between the third and fifth decades of life. To date, there is no standardized treatment for this condition and a general policy of non-intervention to avoid destabilization of the balanced physiology is recommended. Intravenous prostanoids have been shown to have an effect but they are invasive and associated with major side effects. Lung and combined heart and lung transplantation might be a therapeutic option for selected patients. However, donor shortage is a major issue. Oral advanced therapies have been recently shown to improve haemodynamics and survival in idiopathic pulmonary hypertension or in pulmonary hypertension related to scleroderma and may have a role in patients with pulmonary hypertension secondary to congenital heart disease.

Eisenmenger Complex↗