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PubMed2004

Surgical reconstruction of occluded pulmonary arteries in patients with congenital heart disease: effects on pulmonary artery growth.

BACKGROUND: This study was undertaken to determine outcomes and best strategies for treatment of occluded pulmonary arteries in patients with congenital heart disease. METHODS AND RESULTS: Between 1998 and 2002, occlusion of a previously patent pulmonary artery was established in 23 patients. Data were obtained retrospectively. Diagnoses were pulmonary atresia and ventricular septal defect in 11, tetralogy of Fallot in 6, and other forms of pulmonary stenosis or atresia in 6. Median age and weight at diagnosis were 9 years (range, 6 days to 43 years) and 24 kg (range, 2.6 to 60 kg). Fourteen patients had had a previous surgery. The occluded pulmonary artery was visualized at angiography by wedge injection or injection into the collateral circulation. The left pulmonary artery was occluded in 20 patients and the right pulmonary artery in 3. Criteria for reconstruction were estimated duration of occlusion <6 months and ratio of occluded to contralateral artery >0.2. Twelve patients fulfilled these criteria and underwent pulmonary artery reconstruction at a mean interval of 2 months (range, 6 days to 6 months) from evidence of occlusion. Six patients had pericardial patch reconstruction, 3 terminoterminal anastomosis, 2 thrombectomy, and 1 a Blalock-Taussig shunt. There was 1 late death. At a median follow-up of 4 years (2 months to 5 years), all patients underwent cardiac catheterization: in 8 patients the reconstructed artery was patent, in 3 reoccluded. Hypoplasia of the occluded artery was reversed in 6 patients. CONCLUSIONS: Our data show that in selected patients, reconstruction of an occluded pulmonary artery can restore pulmonary vascularization and reverse hypoplasia. Strict surveillance is mandatory to prevent pulmonary artery loss.

Adolescent↗
PubMed1995

Hepatic venous blood and the development of pulmonary arteriovenous malformations in congenital heart disease.

BACKGROUND: Pulmonary arteriovenous malformations (PAVMs) are a known complication after some types of cavopulmonary anastomoses (CVPAs). Their cause is unknown, but they may be related to the absence of pulsatile flow or the presence or absence of circulating factors. These PAVMs are diffuse and are presumed to be progressive and irreversible. METHODS AND RESULTS: All patients with congenital heart disease (CHD) seen at Children's Hospital, Boston, Mass, between 1970 and 1993 were reviewed. We report on the 10 patients with CHD who were found to have developed PAVMs, as diagnosed by cardiac catheterization. Diagnoses included heterotaxy syndrome/polysplenia, with interrupted inferior vena cava and hepatic veins draining to the right atrium (n = 6); heterotaxy/asplenia (n = 1); corrected transposition with pulmonary stenosis (n = 1); and biliary atresia and associated CHD (n = 2). PAVMs were diagnosed 0.1 to 7.0 years (median, 3.5 years) after creation of a CVPA that resulted in exclusion of hepatic venous flow from one or both lungs in 8 of the 10 patients; the remaining 2 patients had normal drainage of hepatic veins to the lungs but had biliary atresia. In all, the common anatomic feature was the exclusion of normal hepatic venous return from the affected pulmonary arterial circulation. All patients with interrupted inferior vena cava, azygous continuation to the superior vena cava, and hepatic veins draining to the right atrium (polysplenia syndrome) were reviewed to determine the incidence of PAVMs in those with CVPA (ie, hepatic venous flow excluded from the pulmonary arteries) and without CVPA. Six of 28 (21%) of those with versus 1 of 56 (1.8%) of those without CVPA developed PAVMs (P = .004). The 1 patient without CVPA who had PAVMs also had biliary atresia. Among patients with CVPA, the probability of developing PAVMs was 15% and 28% at 3 and 5 years, respectively, after CVPA. The histological and angiographic appearances of PAVMs after CVPA are similar to those seen in PAVMs associated with hepatic cirrhosis. CONCLUSIONS: We postulate that PAVMs after CVPA are related to the diversion of normal hepatic venous flow from the pulmonary circulation. In this sense, these PAVMs may be analogous to those associated with liver disease, which have been found to resolve after liver transplantation. Redirection of hepatic flow to the pulmonary bed in some patients with CHD and PAVMs may lead to reversibility of the PAVMs.

Adult↗
PubMed1981

Effect of digoxin on right ventricular function in severe chronic airflow obstruction. A controlled clinical trial.

The effect of digoxin on the right and left ventricular ejection fractions in 15 patients with pulmonary heart disease caused by severe chronic airflow obstruction was studied in a double-blind, randomized, placebo-controlled trial. All patients were ambulatory and had clinical features of right but not left ventricular dysfunction. Equilibrium radionuclide angiography showed reduced right ventricular ejection fraction in all patients and reduced left ventricular ejection fraction in four. After 8 weeks of digoxin treatment, the abnormal left ventricular ejection fractions were normal; right ventricular ejection fractions increased only in those patients who had had abnormal left ventricular ejection fractions. We conclude that in patients with pulmonary heart disease, the right ventricular ejection fraction is abnormal and improves with digoxin treatment only when the left ventricular ejection fraction also is initially abnormal.

Aged↗
PubMed1977

[Misleading pulmonary emboliu].

The authors report 12 cases of pulmonary embolism with misleading signs and discuss the difficulty in diagnosis: 1) the frequency of incomplete forms; 2) lack of specificity of the clinical and paraclinical picture of pulmonary embolism which may simulate pulmonary or heart disease; 3) difficulties in interpretation of the signs of pulmonary embolism in cases of prior heart or pulmonary disease.

Aged↗
PubMed1985

Effect of long-term administration of digoxin on exercise performance in chronic airflow obstruction.

We have studied the effect of long-term digoxin on exercise performance in 15 patients with pulmonary heart disease due to severe chronic airflow obstruction (FEV1/VC ratio 29 +/- 6%: mean +/- SD). Digoxin (0.25 mg/day) was given for 8 weeks in a randomized, double-blind crossover, placebo-controlled trial. All patients were ambulatory and had clinical features of right ventricular dysfunction but no clinical evidence of left ventricular dysfunction. Assessments included progressive and steady-state exercise, pulmonary function studies and evaluation of right and left ventricular function. In all patients the right ventricular ejection fraction was reduced; in 4 patients the left ventricular ejection fraction was also reduced. In patients whose left ventricular ejection fraction was initially abnormal, 8 weeks of digoxin increased left ventricular ejection fraction to normal. In spite of the improvement in resting ventricular function, exercise performance, the cardiopulmonary response to exercise, pulmonary function and general health status did not improve. We conclude that in patients with pulmonary heart disease: 1) digoxin improves ventricular function only if left ventricular function is reduced, and 2) despite the improvement in ventricular function digoxin does not improve pulmonary function, cardiopulmonary response to exercise or general feeling of well being.

Aged↗