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Query: UMLS:C0042373 (vascular disease)
 17,070 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Fourteen patients with pulmonary vascular disease, either primary pulmonary hypertension or the result of cardiac defects, underwent balloon atrial septostomy (BAS) over the period of July 1981 to June 1988 because of symptoms of syncope, fatigue, right heart failure, and cardiac arrest. Ages ranged from 4 mo to 50 yr. Two moribund patients died within 24 h of the septostomy due to severe hypoxemia and unrelieved low cardiac output; three others died 2 wk to 35 mo later; the remaining 9 patients have improved symptomatically and are alive 11 to 96 mo after septostomy. One received a heart and lung transplant 19 mo later. We conclude that, in patients with symptomatic cor pulmonale secondary to pulmonary vascular disease, atrial septostomy can improve symptoms and may serve as a palliative bridge to heart and/or lung transplantation.
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PMID:Effects of atrial septostomy in patients with terminal cor pulmonale due to pulmonary vascular disease. 172 34

The natural history of patients with complete atrioventricular canal defect is one of unrelenting development of pulmonary vascular obstructive disease. Corrective surgery, which can be performed with low mortality during infancy, reduces the time that the pulmonary vascular bed is exposed to excessively high pressure and blood flow. In some patients, however, advanced vascular disease may already be established at operation. Surgical intervention in these patients may not prevent the progression of obliterative pulmonary vascular disease and may in time even result in right ventricular failure, since after the corrective operation there is no ventricular septal defect to shunt away the right ventricular pressure overload. This article outlines a numeric method for predicting pulmonary vascular resistance after surgical correction; the method is based on age and hemodynamic data available from preoperative cardiac catheterization. Retrospective analysis of preoperative and postoperative data from 20 patients produced a regression equation in which a linear combination of inverse pulmonary/systemic blood flow ratio and age at operation predicted pulmonary vascular resistance after operation, with a multiple correlation coefficient of 0.85. This newly discovered relationship may provide valuable insight into the probable outcome of surgical intervention in cases in which pulmonary vascular obstructive disease is suspected as significant.
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PMID:Preoperative prediction of postoperative pulmonary arteriolar resistance after surgical repair of complete atrioventricular canal defect. 194 97

Cor pulmonale is right ventricular enlargement secondary to pulmonary hypertension. Although most often caused by parenchymal lung disease, derangements of the ventilatory drive, the respiratory pumping mechanism, or the pulmonary vascular bed may also result in right ventricular hypertrophy and dilatation. Arterial hypoxemia (and resultant polycythemia), hypercapnia, and respiratory acidosis all contribute to the increased afterload on the right ventricle. Diagnosis is often difficult, since pulmonary vascular disease, pulmonary hypertension, and cor pulmonale have few specific manifestations, especially early in their evolution. Treatment is primarily directed at the underlying pulmonary or ventilatory disorder, rather than at the right ventricular failure per se. Supplemental oxygen is essential to avoid hypoxia; corticosteroids, anticoagulants, vasodilators, and other specific therapies are used as indicated to treat the underlying pulmonary disorders. When medical therapies fail, lung or heart-lung transplantation has become a possibility for selected patients.
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PMID:Chronic cor pulmonale. Etiology and management. 239 36

The reduction of pulmonary hypertension that occurs within 24 hours of valve replacement for mitral stenosis is well documented, but patients who die after surgery have not been adequately studied. Clinical and autopsy data for 16 patients who died following mitral valve replacement were reviewed. The emphasis was on preoperative and postoperative pulmonary arterial pressure and pulmonary vascular disease, including arterial, venous, and capillary changes. Morphologic features were graded and summed to obtain an additive histologic assessment (AHA). Patients were divided into three groups: 1) those who had uneventful operations and early postoperative periods but died prior to discharge; 2) those who had postoperative difficulty, with identifiable acute anatomic causes of death; and 3) those who had postoperative difficulty, with no apparent acute anatomic cause of death. In group 1 (n = 4) the preoperative pulmonary arterial pressure was 43 +/- 17 mm Hg, and AHA ranged from 0 to 4; in group 2 (n = 5) the preoperative pulmonary arterial pressure was 60 +/- 15 mm Hg, but AHA ranged only from 2 to 5. In group 3 (n = 7) the preoperative pulmonary arterial pressure was 59 +/- 12 mm Hg; AHA ranged from 6 to 9, significantly higher than that of the other groups (P less than 0.005). Three patients from group 3 had elevated pulmonary arterial pressure (60, 52, and 50 mm Hg three, six, and 15 days after surgery, respectively). Two additional patients had right heart failure with normally contracting left ventricles terminally. It is concluded that some patients with mitral stenosis who die after surgery with persistently elevated pulmonary arterial pressure have sufficiently severe pulmonary vascular disease to account for their persistent pulmonary hypertension and death.
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PMID:Pulmonary vascular disease and hypertension after valve surgery for mitral stenosis. 397 87

From 1976 through 1981, 8 corrective operations for truncus arteriosos communis type I have been performed. The patient's ages ranged from 2 months to 4 1/2 years; 2 of the children had previously undergone banding of the pulmonary artery. Intracardiac correction consisted in closure of the ventricular septal defect (VSD) and disconnection of the pulmonary trunk from the aorta with reconstruction of the right ventricular outflow tract using a valved Dacron conduit. One 3 1/2-year-old child died postoperatively because of right heart failure. In this child the pulmonary vascular resistance had risen to 13 U x m2 despite banding of the pulmonary artery in infancy. All other children have survived the operation without major complications and are in good condition. Postoperative follow-up (re-catheterization in 6 out of 7 survivors) showed a faultless function of the conduits in all instances. Persistence of pulmonary hypertension was ascertained in one patient. According to these findings, which are in agreement with the experience of others, it is concluded that primary correction of truncus arteriosus should be undertaken in early infancy prior to development of pulmonary vascular disease.
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PMID:Surgical correction of truncus arteriosus type I. 618 May 11

Eleven patients with Tetralogy of Fallot and congenital or acquired absence of one pulmonary artery (PA) have been operated upon at the Department of Cardiac Surgery of Ospedali Riuniti-Bergamo-Italy. Eight children had agenesis of the left PA, one of the right PA and two had complete occlusion of the right PA after a palliative operation. Four patients had only a palliative procedure (one Blalock-Taussig, two Waterston, three PTFE shunts) with one operative death. Two patients underwent a two-staged procedure, that is an initial shunt (one Blalock and one PTFE shunt) followed by subsequent total correction. Five patients underwent primary total correction. No operative death occurred among the patients who had total correction. Right ventricular outflow reconstruction has been accomplished with an infundibular patch in one patient, an external valved conduit in two patients, and a transanular patch plus orthotopic bioprosthesis in 4 patients. One patient with a valved conduit died one year postoperatively in right heart failure caused by pulmonary hypertension. The pulmonary vascular disease was probably due to pulmonary microembolization following the severe hemolysis that lasted for twenty days in the early postoperative period. The nine surgical survivors are in good general condition with maximum follow-up of 7 years. The surgical approach either in case of palliation or in case of corrective surgery is finally discussed. In our experience TOF with unilateral absence of a PA is a congenital anomaly that can be corrected with results comparable to those of uncomplicated TOF.
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PMID:[Surgical treatment of the tetralogy of Fallot with a single pulmonary artery]. 620 74

The hemodynamic and clinical responses to calcium channel blockade with verapamil and nifedipine were compared with those of hydralazine in 12 patients with pulmonary hypertension secondary to obliterative pulmonary vascular disease. All three drugs produced a marked and similar decrease in pulmonary vascular resistance; however, this was accompanied by a significant increase in cardiac index with hydralazine (+0.71 liter/min per m2, p less than 0.01), no change in cardiac index with nifedipine and a significant decrease in cardiac index with verapamil (-0.25 liter/min per m2, p less than 0.05). Mean pulmonary artery pressure decreased markedly with both calcium channel blocking drugs (-16.0 mm Hg with verapamil and -14.5 mm Hg with nifedipine, both p less than 0.01), but this was associated with a concomitant increase in mean right atrial pressure (+6.2 mm Hg with verapamil and +4.4 mm Hg with nifedipine, both p less than 0.01); neither variable changed after hydralazine. Hence, right ventricular performance (as reflected by right ventricular stroke work index) deteriorated during treatment with both calcium channel blocking drugs, despite the decrease in resistance to right ventricular ejection; in contrast, right ventricular stroke work index increased after hydralazine. The unfavorable hemodynamic effects of calcium channel blockade were accompanied by severe adverse clinical events, including profound hypotension and cardiogenic shock during acute drug administration and the exacerbation of right heart failure during long-term treatment. These deleterious responses to verapamil and nifedipine are likely the result of a direct depressant effect exerted by these drugs on right ventricular function independent of their pulmonary vasodilatory actions.
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PMID:Adverse hemodynamic and clinical effects of calcium channel blockade in pulmonary hypertension secondary to obliterative pulmonary vascular disease. 649 Oct 82

Although pulmonary hypertension is frequently mentioned as a complication of the sicklemic state, careful review of the medical literature revealed only a single subject in whom cardiac catheterization data substantiated this diagnosis. In two additional patients, both clinical and autopsy findings of pulmonary vascular disease and cor pulmonale were described, although no hemodynamic studies had been performed. We have therefore detailed the clinical history, cardiac catheterization results, and autopsy findings in three previously undescribed patients. These three patients, along with the three case reports culled from the medical literature, from the substance of this review. Pulmonary hypertension should be suspected in patients with sickle hemoglobinopathy in whom either fixed dyspnea or unexplained syncope develops. Early in the course of the disease, right heart catheterization remains the only way to establish the diagnosis with certainty. Noninvasive studies such as chest x-ray, electrocardiography, and echocardiography tend to be nondiagnostic until late in the course of right ventricular failure. Although specific therapy has yet to be defined, the ominous prognosis of this complication of sickle hemoglobinopathy supports the application of experimental modalities such as continuous oxygen therapy, partial exchange transfusion, or even limited phlebotomy.
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PMID:Pulmonary hypertension and cor pulmonale in the sickle hemoglobinopathies. 714 75

We performed correction of intracardiac lesions in 10 patients with coarctation. All cardiovascular lesions were corrected except coarctation. Six patients had a large left-to-right shunt though a ventricular septal defect (VSD), two patients had left ventricular outflow obstruction, two patients had mitral insufficiency, and one patient had mitral stenosis. Arterial perfusion was through the ascending aorta. Urine output was 6.0 +/- 1.5 cc/kg/hr during cardiopulmonary bypass. There was no morbidity related to cardiopulmonary bypass or inadequate perfusion of the lower body, and left ventricular failure did not occur. One patient with Taussig-Bing abnormality and pulmonary vascular disease died postoperatively of right ventricular failure. Intracardiac repair with aortic perfusion in the presence of coarctation is a safe alternative to coarctation repair or combined procedures.
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PMID:Cardiopulmonary bypass in the presence of uncorrected coarctation. 720 67

To test a hypothesis that reduction in pulmonary perfusion pressure and flow affect underlying vascular disease, pulmonary pathology was studied in monocrotaline-treated rats undergoing single lung transplantation. Inbred rats were treated with 40 mg/kg (group T1, n = 6) and 80 mg/kg of monocrotaline (group T2, n = 9), received a left lung isograft 2 and 4 weeks after medication, and were killed 4 and 6 weeks after single lung transplantation, respectively. For each group, rats receiving the same amount of monocrotaline (M1, M2) or vehicle (N1, N2) served as controls. Monocrotaline-treated rats developed pulmonary vascular disease and right heart failure, resulting in severe exercise intolerance in M1 or death in M2 unless single lung transplantation had been carried out. At death, pulmonary blood flow was directed toward the left lung isograft, and the retained right lung received a significantly reduced fraction of cardiac output. Right to left ventricular weight ratio was significantly reduced in both groups as compared to the respective control rats, suggesting reduced perfusion pressure. Although thickness of media in small pulmonary arteries (media/radius) was normal (34% +/- 4%) in the lung isografts, it was significantly increased in the contralateral lung (group T1, 45% +/- 5%; group T2, 48% +/- 3%), which was not significantly different from that of monocrotaline-treated control rats, respectively (group M1, 47% +/- 7%; group M2, 49% +/- 6%). Although single lung transplantation reduced perfusion pressure and flow toward the monocrotaline-treated native lung, it failed to affect vascular morphology significantly.
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PMID:Monocrotaline-induced pulmonary vascular disease after contralateral lung transplantation in the rat. 847 5


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