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170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The authors studied the bronchoscopic appearance of bronchial mucosa's vessel contour in pulmonary venous hypertension in 20 patients with mitral stenosis and in 20 with cardiomyopathy and/or aortic vitium. The submucous venous congestion was scored on the base of its extent and severity according to Ohmichi. They have observed a linear relation between the PPA (wedge) and PPA values in patients with mitral stenosis and the total scores indicatory of submucous venous congestion. The mean total scores of patients with mitral stenosis as well as cardiomyopathic patients showing volume-loading of the pulmonary circuit and/or aortic vitium differed to the benefit of the former. Mucosa's vessel contour of grade 3 was found in 12 patients with mitral stenosis and only in 4 cases of cardiomyopathy and/or aortic vitium, so that is more characteristic of mitral stenosis. In spite of this, condition of patients with cardiomyopathy and/or aortic vitium are considered more severe on the base of NYHA values. Taking both patient populations into consideration relation between NYHA-phase and the degree of total scores could not have been proved. Venous congestion on lower part of the left main bronchus was observed in every patient. Appearance of congestive bronchial mucosa has not occurred in pure precapillary pulmonary hypertension.
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PMID:[Bronchoscopic appearance of the bronchial mucosa in pulmonary venous hypertension]. 194 61

The conventional chest radiographs were studied of 18 patients with primary pulmonary hypertension, waiting for, or treated with lung transplantation in the Papworth Hospital. The goal of the study was to find out whether there is a pattern characteristic of primary pulmonary hypertension. The following points were considered: a) pulmonary transparency; b) the hila; c) the left hemidiaphragm; d) the pulmonary artery; e) the right ventricle; f) the right atrium; g) the left ventricle. A score was assigned for any degree of abnormality of the points mentioned above. As a result, a radiological pattern was found that can: 1) confirm the presence of pulmonary hypertension; 2) exclude that this hypertension has a detectable cause; 3) measure the severity of the disease, particularly with regard to hypertension degree. The conclusion is that there is a radiological pattern strongly suggestive of primary pulmonary hypertension and that conventional radiology can help in detecting and monitoring this rare disease, which today can only be treated by means of transplantation.
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PMID:[Is there a typical radiologic picture of primary pulmonary hypertension? Study of 18 cases]. 194 63

Systemic venous hypertension after the Fontan procedure is a major cause of mortality and morbidity, accounting for 11 of 16 deaths in our series of 228 Fontan procedures. A partial Fontan with a residual atrial septal defect (ASD) would allow controlled right-to-left shunting to reduce venous pressure and improve cardiac output while maintaining a reduced but acceptable arterial oxygen saturation. This allows complete or graded closure of the ASD after the discontinuation of cardiopulmonary bypass in the operating room or at any time in the postoperative period by exposing the snare under local anesthesia. From 1987 to 1990, 36 patients undergoing the modified Fontan procedure had placement of an adjustable interatrial communication. Indications for placement of an adjustable ASD included increased pulmonary artery pressures, increased pulmonary vascular resistance, reactive airway disease, previously increased or unknown pulmonary vascular resistance, small pulmonary arteries, and borderline ventricular function. Fourteen patients had the adjustable ASD closed at the time of operation, 8 patients underwent narrowing, and 12 underwent closure of the ASD in the postoperative period. Eight patients were discharged with the ASD partially open, and 2 patients underwent delayed closure. The partial Fontan with an adjustable ASD may increase the safety of the Fontan procedure for high-risk groups such as those with increased pulmonary vascular resistance, pulmonary hypertension, and impaired left ventricular function and for infants, who tolerate venous hypertension poorly. The ability to adjust the ASD in stages depending on the hemodynamic response increases flexibility and safety.
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PMID:Partial Fontan: advantages of an adjustable interatrial communication. 195 28

To determine the clinical, laboratory and hemodynamic profile in patients with primary pulmonary hypertension and associated portal hypertension, 7 new cases and 71 previously reported cases were analyzed. There was no gender predilection and the average age at diagnosis was 41 years. Liver cirrhosis was the most frequent cause of hypertension (82%) and a surgical portosystemic shunt was present in 29%. Almost invariably, portal hypertension either preceded or was diagnosed concurrently with pulmonary hypertension, favoring the hypothesis that in portal hypertension, the pulmonary vasculature may be exposed to vasoactive substances normally metabolized or produced by the diseased liver, possibly inducing vasoconstriction or direct toxic damage to the pulmonary arteries. Clinically, exertional dyspnea was the most frequent presenting symptom (81%); other symptoms, such as syncope, chest pain and fatigue, were present in less than 33%. An accentuated pulmonary component of the second heart sound (82%) and a systolic murmur (69%) were the most common physical findings. At least 75% of these patients had evidence of pulmonary hypertension on electrocardiography (right ventricular hypertrophy) or roentgenography (cardiomegaly or dilated main pulmonary arteries, or both). Hemodynamic findings included severe pulmonary hypertension (mean pulmonary artery pressure 59 +/- 19 mm Hg) with normal pulmonary capillary wedge pressure and cardiac output. Treatment was basically palliative and the mean and median survival times were 15 and 6 months, respectively. In brief, on the basis of clinical presentation and laboratory features, patients with combined primary pulmonary hypertension and portal hypertension seldom represent a diagnostic challenge. Further research is needed on treatment, which remains palliative. The survival rate is poor and worse than that seen in isolated primary pulmonary hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Association between primary pulmonary hypertension and portal hypertension: analysis of its pathophysiology and clinical, laboratory and hemodynamic manifestations. 199 8

We describe a patient who developed fatal pulmonary artery hypertension secondary to diffuse venulitis. This otherwise healthy young woman first presented with generalized venulopathy, with chemosis, facial swelling, pleural effusions, and pericardial tamponade. The symptoms partially responded to steroid therapy, but over a 2-year course, a rapidly progressive and fatal venoocclusive disease developed. No other primary condition was diagnosed, and at autopsy, the patient had striking venulitis throughout, including the pulmonary bed. We believe that this is a unique case of pulmonary hypertension resulting from a generalized venulopathy.
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PMID:Fatal pulmonary venoocclusive disease secondary to a generalized venulopathy: a new syndrome presenting with facial swelling and pericardial tamponade. 199 22

Thrombolytic therapy has been used fairly extensively in the management of acute proximal deep-vein thrombophlebitis of the extremities, acute pulmonary embolism, and acute peripheral arterial thrombosis and embolism in addition to acute thrombotic coronary events. In the presence of acceptable indications and a favorable benefit to risk ratio, this form of therapy, when successful, has served as a useful adjunct in the management of these disorders. In deep-vein thrombophlebitis, lysis of the thrombus before permanent pathological changes (eg, organization, scarring) have occurred can prevent venous valvular dysfunction and postural venous hypertension and its complications, especially the postphlebitic syndrome. In the more severe forms of acute pulmonary embolism, thrombolytic therapy, when applied early after symptom onset, decreases morbidity and is likely to prevent a chronic increase in pulmonary vascular resistance and persistent pulmonary hypertension. In peripheral arterial thrombo-occlusive events, early restoration of flow through thrombolysis has been shown to limit ischemic damage and serve as a useful supplement to angioplasty or surgery. Thrombolytic therapy has been used less extensively in acute strokes. Here the danger of reperfusion causing bleeding into a softened area of brain undergoing infarction has slowed its evaluation for this disorder; its application to stroke remains experimental.
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PMID:Thrombolytic therapy for noncoronary diseases. 200 69

The effect of oral molsidomine (M) on the pulmonary artery hypertension of patients with chronic obstructive pulmonary disease (COPD) was investigated during an acute study (4 mg once) and after a 3 week-treatment (3 times 4 mg a day), on a double-blind basis in 16 patients, 8 receiving a placebo, and 8 molsidomine. Ventilatory and cardiocirculatory indices were obtained at rest and during exercise. When acutely given, molsidomine reduces the mean pulmonary arterial pressure (PAP), the pulmonary vascular resistance (PVR) and the arterial O2 partial pressure (PaO2), increasing heart rate (HR) as well as the alveo-arterial O2 partial pressure difference (P(A-a)O2). During exercise, pulmonary arterial pressure and pulmonary vascular resistance decrease while heart rate increases without modification of arterial blood gases. After a 3-week treatment, molsidomine no more improves any index but significantly reduces cardiac output during exercise and consequently the O2 delivery to the tissues. The same feature has already been observed for other nitrates. It thus seems inappropriate to prescribe nitrates or nitrate-like drugs to chronic obstructive pulmonary disease patients with a view to lower their pulmonary hypertension.
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PMID:Disappearance of molsidomine effects on pulmonary circulation of patients with chronic obstructive pulmonary disease after a three week treatment. 201 6

Pulmonary hypertension resulting from venous air embolism is known to increase after ventilation with highly soluble and diffusible gases. Exacerbation of the hypertension could be due to further blockage of the circulation if the bubbles enlarge as a result of ingress of gas by diffusion. This mechanism has been frequently cited but lacks direct proof. To determine directly whether intravascular air bubbles actually enlarge when highly soluble and diffusible gases are inspired, we used microscopy to measure the size of gas emboli in vivo. When air bubbles were injected into the right atrium, the bubbles that appeared in pulmonary arterioles were larger during ventilation with helium or nitrous oxide than with air. Air bubbles injected into the pulmonary artery enlarged when the inspired gas was changed to helium or nitrous oxide. The direction, magnitude, and timing of changes in bubble size were consistent with a net diffusion of gas into the bubbles. These data support the idea that venous air emboli enlarge during ventilation with soluble and diffusible gases and thereby cause further vascular obstruction.
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PMID:Effect of ventilation with soluble and diffusible gases on the size of air emboli. 203 72

Surgery for congenital heart defects started 50 years ago with "closed" procedures, and open heart surgery is in its forth decade. Thus, long-term results are now available. Although a majority of patients lead normal lives, problems do exist. Hemodynamic anomalies can be related to residual lesions or to persistent systemic hypertension (after coarctation repair) or pulmonary hypertension (after late repair of left to right shunt lesions). Right or left ventricular dysfunction may be observed, due to longstanding overload, hypoxia or to the open heart procedure itself. Rhythm disturbances have a tendency to increase with the passage of time after surgery. After ventricular surgery (repair of ventricular septal defect and tetralogy of Fallot), conduction defects and ventricular arrhythmias are prevalent. They may lead to late sudden death. After atrial surgery, sinus node dysfunction and atrial arrhythmias are observed. Problems related to growth of the patient exist essentially in cases where foreign material (conduits, prostheses) have been implanted. Many patients, with definitive repair or palliative operation, have become adults. This is a new challenge for the adult cardiologist, and it is a duty of the pediatric cardiologist to hand over his knowledge of this pathology.
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PMID:Late results of surgery for congenital heart defects. 205 May 23

Since Shumway carried out the first successful heart-lung transplant (HLT) in Stanford in 1981, HLT has become a new therapeutic means for patients with end-stage pulmonary disease or arterial hypertension. However, it is still rarely carried out because of a lack of donors and the complexity of the surgery and postoperative course. This review described the criteria for proper donor and recipient selection, as well as the anaesthetic and postoperative management of HLT patients at Marie Lannelongue Hospital. The lack of suitable organ grafts results, at least in part, from improper donor management. Pulmonary oedema by fluid overloading and excessive haemodilution should be carefully prevented. Low doses of catecholamines and vasopressin maintain circulatory stability and convenient organ function. The indications for HLT (primary pulmonary hypertension, Eisenmenger's complex, and end-stage bronchopulmonary disease) are all characterized by severe pulmonary hypertension, hypoxaemia and cardiac failure. Careful anaesthetic induction is required to avoid circulatory collapse. Cardiopulmonary bypass (CPB) should be started early, so that mediastinal dissection may be carried out in satisfactory haemodynamic conditions. After unclamping the aorta, circulatory support with fluid and catecholamine infusion is often required. High inspired oxygen fraction and end-expiratory positive pressure may be required because of reperfusion pulmonary oedema. Blood transfusion is often needed as there are major blood losses due to dissection of the posterior mediastinum during CPB. Postoperative catecholamine administration is prolonged over several days. Negative fluid balance is often necessary to reduce pulmonary oedema. Improvement in surgical technique, early extubation, and late prescription of steroids have reduced the incidence of tracheal complications. Acute renal failure often occurs as a result of prolonged CPB, hypovolaemia, drug nephrotoxicity and sepsis. Bacterial complications (pneumonia, mediastinitis) are the main causes of early death. After the 15th postoperative day, opportunistic infections and allograft rejection are the main complications. Since 1981, major advances in HLT recipient management resulted in improved survival rates (70-80% at 1 year, and 60-70% at 2 years for the best teams). Despite the complexity of management, and the longterm threat of obliterative bronchiolitis, HLT is, at present time, the only possibility for these young patients to recover a normal quality of life.
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PMID:[Anesthesia and intensive care for heart-lung transplantation]. 205 32


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