Collateral bronchopulmonary circulation after spontaneous recanalisation of pulmonary thromboemboli in the dog.

STUDY OBJECTIVE: The aim was to study the fate of enlarged bronchial arteries after resolution of experimental pulmonary embolism. DESIGN: Embolisation of the pulmonary arteries of both lungs was performed with intravenous gelfoam. Pulmonary pressure and pulmonary arteriolar resistance were measured 1 h, 40 d and 80 d after embolisation. Pulmonary angiography and aortography were performed at the same time to evaluate the pulmonary emboli and the collateral bronchopulmonary circulation. Aortography and gross pathological and histological examination of the lungs was performed after 80 d. EXPERIMENTAL MATERIAL: 15 adult mongrel dogs of either sex were studied, weight 22-25 kg. Nine dogs were embolised and there were six controls. MEASUREMENTS AND MAIN RESULTS: All animals survived until 80 d. There was a rise (p less than 0.001) in mean pulmonary artery pressure and arteriolar resistance 1 h after embolisation. Pulmonary artery pressures and resistances were still raised 40 d after embolisation but had returned to normal after 80 d. Pulmonary arteriography at 1 h confirmed massive thromboembolism. After 40 d antegrade pulmonary blood flow was almost completely restored, and the thromboemboli had largely disappeared. Pulmonary angiograms were completely normal after 80 d. Aortography after 40 d showed a well developed collateral bronchopulmonary circulation, most pronounced in the lower lobes, which persisted unchanged until 80 d. Aortography and gross pathological and histological examination at necropsy confirmed the presence of hypertrophic well developed bronchial arteries to both lower lobes and to a lesser extent to the middle and upper lobes, with only a few organised and recanalised thrombi in segmental arteries of both lower lobes. CONCLUSIONS: Our data show a temporal dissociation between the resolution of pulmonary thromboemboli in the present model and the eventual regression of developed bronchopulmonary collateral vessels. The mechanism of this dissociation could not be elucidated.

Bronchial arteries in experimental pulmonary infarction: angiographic and morphometric study.

OBJECTIVES: The aim was to investigate (1) whether collateral bronchopulmonary circulation developing due to chronic pulmonary embolism could prevent the evolution of pulmonary infarction after induction of pulmonary venous outflow impairment; and (2) how collateral bronchopulmonary circulation developed after acute embolisation of the lung with impaired pulmonary venous outflow. METHODS: Fifty two mongrel dogs were studied. Thirty six dogs were experimental animals and 16 were in a control group. Unilateral impairment of pulmonary venous outflow was induced by constriction of the left pulmonary veins in two groups of experimental dogs: (1) three months after and (2) one hour before bilateral embolisation of the pulmonary artery. All animals were killed 12 days after constriction. The size of the bronchial arteries was evaluated from angiograms. The diameter and the wall thickness of the arteries were measured during histology. RESULTS: In all experimental dogs, haemorrhagic infarctions developed distally to emboli in the left lung regardless of whether the bronchial arteries were dilated before induction of pulmonary venous constriction or whether collateral circulation started to develop after pulmonary venous constriction. Constriction of the pulmonary veins was an essential factor for pulmonary infarction to develop as no infarction developed in the embolised regions of the right lungs with intact pulmonary venous outflow. Pulmonary venous constriction alone did not cause dilatation or hypertrophy of the bronchial arteries. After pulmonary artery embolisation, the same enlargement and hypertrophy of the bronchial arteries occurred both in the left lung with previously impaired venous outflow and in the right lung with intact pulmonary veins. CONCLUSIONS: Expanded bronchopulmonary circulation did not prevent the development of infarction in the embolised region of the lung with impaired pulmonary venous outflow. Development of collateral bronchopulmonary circulation was not influenced by previously impaired pulmonary venous outflow.

Iliofemoral venous thrombectomy followed by percutaneous closure of the temporary arteriovenous fistula.

Iliofemoral venous thrombosis treated by anticoagulants alone almost invariably results in postthrombotic sequelae with deep venous reflux alone or combined with an outflow obstruction. This study evaluates the result of iliofemoral venous thrombectomy with temporary proximal arteriovenous fistula (AVF) performed on 48 consecutive patients. In 10 patients the thrombus extended in the inferior vena cava, and the thrombectomy was combined with inferior vena cava interruption. The AVF closed spontaneously in 8 of 48 patients (patency rate, 84%). An attempt to close the AVF by placing a detachable balloon percutaneously under radiographic control was made 6 to 12 weeks later (success rate, 87%; complications, rare). A preclosure arteriovenography of the femoro-iliaco-caval segment revealed 34 of 38 segments open (patency rate, 89%). Four patients had severe stenosis of the iliac segment, and a transvenous percutaneous dilatation was successfully performed in three of the four patients, keeping the fistula. At AVF closure 4 weeks later the arteriovenography showed sustained dilatation in only two patients. Thirty-seven patients were followed for 3 to 48 months (median, 24 months) and 30 of 37 patients (81%) who had no symptoms were not using compression stockings. Doppler investigation revealed patent and competent femoral and popliteal veins and normal photoplethysmography in 56% of the patients. Four iliac veins were occluded (patency rate, 88%). No recurrence of fistula had occurred. Venous iliofemoral thrombectomy seems to better preserve valve function. The percutaneous balloon closure of the AVF has decreased the complication rate, facilitated venographic evaluation of the result, and made possible the performance of percutaneous interventions under the protection of the AVF.

Comparison of bronchopulmonary collaterals and collateral blood flow in patients with chronic thromboembolic and primary pulmonary hypertension.

OBJECTIVE: To compare the visualisation of bronchopulmonary collaterals and bronchopulmonary collateral blood flow in patients with chronic thromboembolic pulmonary hypertension 2nd primary pulmonary hypertension. SETTING: Referral centre for cardiology at an academic hospital. PATIENTS: Nine patients with chronic thromboembolic pulmonary hypertension and 17 with primary pulmonary hypertension. INTERVENTIONS: Bronchopulmonary collaterals were visualised by selective bronchial arteriography or thoracic aortography. Bronchopulmonary collateral blood flow was estimated by injecting indocyanine green into the ascending aorta and sampling below the mitral valve from the left ventricle. RESULTS: The degree of pulmonary hypertension was comparable in the two groups. Large bronchopulmonary collaterals were visualised in all the patients with thromboembolic pulmonary hypertension who had bronchial arteriography or aortography or both. None of the primary pulmonary hypertension group studied by aortography had bronchopulmonary collaterals (P < < 0.001). All the patients with chronic thromboembolic pulmonary hypertension had significant bronchopulmonary collateral blood flow, which was (mean (SD)) 29.8 (18.6)% of the systemic blood flow. There was no recordable collateral blood flow in 11 of 15 patients with primary pulmonary hypertension. In the remaining four patients the mean value was 1.1 (1.8)% of the systemic blood flow (P < < 0.001). CONCLUSIONS: Visualisation of bronchopulmonary collaterals by thoracic aortography or by bronchial arteriography, or the demonstration of an increased bronchopulmonary collateral flow, helps to distinguish patients with chronic thromboembolic pulmonary hypertension from those with primary pulmonary hypertension.

Life-saving balloon mitral valvuloplasty in patient with cardiogenic shock after cardiac arrest.

Balloon mitral valvuloplasty is the procedure of choice in a selected group of patients with significant mitral stenosis and suitable valve morphology. Experience in patients with cardiogenic shock is very limited. We report the case of a dying patient in cardiogenic shock, with pulmonary edema and severe hepatic damage after cardiac arrest caused by mitral restenosis. The patient was successfully treated by emergency balloon mitral valvuloplasty with a good result and complete recovery.

Mitral balloon valvuloplasty by Inoue technique without echocardiographic standby.

Mitral balloon valvuloplasty (MBV) by Inoue technique was performed in 85 patients with symptomatic rheumatic mitral stenosis (MS). Twenty-eight patients were male and 57 patients were female. The age range was nine to 59 years (mean 28). All patients were subjected to echocardiographic and Doppler examinations before and one day after the procedure. The first 57 patients were subjected to exercise tolerance tests (ETT) a few days before and a few days after the procedure. An echocardiographic score was measured regarding valve thickening, leaflet mobility, degree of calcification and the severity of involvement of subvalvular apparatus. The mitral valve area (MVA) increased from 0.9 +/- 0.2 cm2 to 1.9 +/- 0.45 cm2, (P<0.0001). The mitral gradient (MG) decreased from 20 +/- 5.8 mm/Hg to 5.05 +/-+ 3.2 mm/Hg (P<0.0001). Mean left atrial pressure (LAP) dropped from 25.85 +/- 8.4 mm/Hg to 11.05 +/- 5.4 mm/Hg (P<0.0001). Exercise tolerance test (ETT) increased from 5.59 +/- 1.3 to 11.75 +/- 1.48 min. (P<0.0001). Complications included severe mitral regurgitation (MR) in two patients (2.3%). In the first 57 patients, mild left-to-right shunt measured by green dye dilution technique had occurred in 40% of patients. In conclusion, MBV by Inoue balloon is a good alternative to surgical commissurotomy and echocardiographic standby is very helpful when it is available. However, MBV can be safely performed if echocardiography is inaccessible.