Left Main Pulmonary Artery Research Articles

Nonneoplastic diseases of aorta and pulmonary trunk--Part IV.

This five-part review focuses on selected nonneoplastic diseases of the aorta and pulmonary trunk. Because many more diseases affect the aorta compared with the pulmonary trunk and right and left main pulmonary arteries, most of this review will be devoted to disorders of the aorta. Part IV of the series discusses cystic medial degeneration, trauma, and congenital diseases of the aorta.

Nonneoplastic diseases of aorta and pulmonary trunk--Part III.

The five-part review focuses on selected nonneoplastic diseases of the aorta and pulmonary trunk. Because many more disease affect the aorta compared with the pulmonary trunk and right and left main pulmonary arteries, most of this review will be devoted to disorders of the aorta. Part III of this five-part series discusses the etiology of aortic aneurysms and aortitis.

Nonneoplastic diseases of aorta and pulmonary trunk--Part II.

AbstractThis five‐part review focuses on selected nonneoplastic diseases of the aorta and pulmonary trunk. Because many more diseases affect the aorta compared with the pulmonary trunk and right and left main pulmonary arteries, most of this review will be devoted to disorders of the aorta. Part II of this five‐part series discusses complications of aortic dissection and aortic aneurysm.

Nonneoplastic diseases of aorta and pulmonary trunk--Part I.

This five-part review focuses on selected nonneoplastic diseases of the aorta and pulmonary trunk. Because many more diseases affect the aorta compared with the pulmonary trunk and right and left main pulmonary arteries, most of this review will be devoted to disorders of the aorta. Part I of this five-part review discusses general concepts of aorta anatomy and aortic dissection.

Vasodilator effects of adrenomedullin on small pulmonary arteries and veins in anaesthetized cats.

1. This study was conducted to determine adrenomedullin (AM) action sites in the pulmonary vascular bed and the relation between its vasodilator effects and vascular tone. Moreover, an examination was made into whether calcitonin gene-related peptide (CGRP) receptors mediate pulmonary vasodilatations induced by AM. To this end, we directly measured internal diameter (i.d.) changes in small pulmonary arteries and veins (100-1100 microns i.d.) by use of an X-ray television system on the in vivo cat lung. 2. Under control (resting vascular tone) conditions, AM injections into the left main pulmonary artery caused dose-related i.d. increases in both small arteries and veins. The mean i.d. increase of the 100-1100 microns arteries (4 +/- 1, 11 +/- 2, and 17 +/- 2% with 0.01, 0.1, and 1 nmol kg-1 AM, respectively) was significantly larger than that for the veins (1 +/- 1, 5 +/- 2, and 7 +/- 2% with 0.01, 0.1 and 1 nmol kg-1 AM, respectively) whatever the injected dose of AM. 3. When unilobar hypoxia (5% O2) had decreased the i.d. of the 100-1100 microns arteries and veins by 16 +/- 3 and 6 +/- 3%, respectively, AM (0.1 nmol kg-1) was able to induce significantly larger i.d. increases in the arteries (28 +/- 3%) and veins (11 +/- 3%) than those under control conditions. 4. The AM-induced i.d. response pattern in the serially connected pulmonary arteries was quite different from that induced by CGRP; AM caused a greater increase in smaller vessels (100-500 microns) than in larger vessels (500-1100 microns). In the case of CGRP, a greater increase was observed in the larger vessels. 5. CGRP8-37 (100 nmol kg-1, i.v., followed by a continuous infusion of 0.2 nmol kg-1 min-1) had no significant effect on the i.d. increase induced by AM (0.1 nmol kg-1) in any serial segments of the arteries and veins. 6. The results indicate that, in the cat, AM induces greater vasodilatation in small pulmonary arteries and lesser vasodilatation in small veins, the maximum dilatation being in the more peripheral arterial segment (100-500 microns). The vasodilator effect of AM was enhanced when vascular tone was elevated. The data suggest that the AM-induced pulmonary vasodilatation is not mediated by CGRP receptors but by its own specific receptor.

Relationship between pulmonary artery diameter at computed tomography and pulmonary artery pressures at right-sided heart catheterization. Massachusetts General Hospital Lung Transplantation Program.

The purpose of the study was to determine the relationship between pulmonary artery (PA) size at computed tomography (CT) and PA pressures, to develop a noninvasive CT method of PA pressure measurement, and to determine a PA diameter that can enable differentiation of normal subjects from those with pulmonary hypertension. PA vessel diameters in 55 candidates for lung and heart-lung transplantation were measured at CT and correlated with PA pressures with both linear and stepwise multiple regression. The multiple regression equations were then tested prospectively in 35 pretransplantation patients. Combined main and left main PA cross-sectional area corrected for body surface area showed the best correlation with mean PA pressure (r = .87). The multiple regression equations helped predict mean PA pressure within 5 mm Hg in 50% of patients with chronic lung disease and in only 8% of patients with pulmonary vascular disease. There was a very good correlation between main and left main PA size and mean PA pressure. At present, however, CT has not demonstrated sufficient accuracy to be used clinically.

Endovascular stenting for treatment of an adult patient with pulmonary artery stenosis with 1-year follow-up

This report describes the occurrence of symptomatic proximal left main pulmonary artery stenosis in a 58-yr-old man that was successfully treated with endovascular stenting with 1-yr follow-up. The technique and pitfalls of this procedure are described. Endovascular stenting provided a well-tolerated, nonsurgical approach to alleviating isolated pulmonary artery stenosis in this patient.

Thrombektomie mit Hilfe eines Hochgeschwindigkeits-Rotationskatheters - Erste Erfahrungen

Evaluation of the Amplatz rotational catheter for the recanalisation of acute thrombotic occlusions in various vascular regions. The Amplatz air-driven rotational catheter was used in 5 patients with acute vessel occlusion in various vascular regions: superficial and profundal femoral artery respectively and popliteal artery with tibiofibular trunk (case 1 and 2), a Collier-Shunt (case 3), the left main pulmonary artery (case 4) and the portal vein after TIPS procedure (case 5). A complete or partial recanalisation was achieved in all cases. Time accounted for recanalisation was between 40 and 90 seconds. No adjunctive intervention was necessary. No complications occurred. The Amplatz thrombectomy device allows a fast, safe and effective mechanical thrombectomy of peripheral arteries and haemodialysis shunts. Partial recanalisation of large caliber vessels is also possible.

PH-stat cooling improves cerebral metabolic recovery after circulatory arrest in a piglet model of aortopulmonary collaterals

Cardiopulmonary bypass with deep hypothermic circulatory arrest increases the risk of neurologic injury in patients with aortopulmonary collaterals. Experimental studies have demonstrated that such collaterals decrease the rate of cerebral cooling before arrest and cerebral metabolic recovery after circulatory arrest. Use of pH-stat blood gas management has been shown to increase cerebral blood flow during cooling. The current study was designed to test whether cooling with pH-stat blood gas management can decrease the cerebral metabolic impact of aortopulmonary collaterals. Twenty 4- to 6-week-old piglets underwent placement of a shunt between the left subclavian artery and main pulmonary artery. In control animals ( n = 10) the shunts were immediately ligated, whereas in the shunt animals ( n = 10) the shunts were left patent. All animals were supported with cardiopulmonary bypass, cooled to 18º C by means of either alpha-stat (five control and five shunt animals) or pH-stat (five control and five shunt animals) blood gas management, subjected to circulatory arrest for 90 minutes, and rewarmed to 37º C. The cerebral metabolic rate of oxygen consumption (a marker for neurologic function) was significantly lower after circulatory arrest in the shunt animals cooled with alpha-stat blood gas management than in the control animals subjected to alpha-stat management (1.2 ± 0.2 vs 2.3 ± 0.2 ml oxygen per 100 gm/min, p < 0.05). By contrast, there was no difference between the pH-stat shunt animals and either control group (2.1 ± 0.2 vs 2.3 ± 0.2 [alpha-stat] and 2.0 ± 0.3 [pH-stat] ml oxygen per 100 gm/min, p = not significant). pH-Stat cooling protected the brain from shunt-related injury. When circulatory arrest is used in the presence of aortopulmonary collaterals, the use of pH-stat blood gas management during cooling results in better cerebral protection than alpha-stat blood gas management. (J T HORAC C ARDIOVASC S URG 1996;111:147-57)

Clinical evaluation of pulmonary 3D time-of-flight MRA with breath holding using contrast media.

Our goal was to evaluate the clinical utility of pulmonary 3D TOF MRA using a contrast medium and breath holding. To determine an optimal imaging time in a pilot study, 30 sequential axial images were obtained for each of 18 patients by using a turbo fast low angle shot sequence immediately after a bolus injection of 5 ml Gd-DTPA. MRA consisted of five sequential MR scans performed using a 3D fast imaging with steady-state precession sequence on 13 patients. The imaging start time after a bolus injection of 10 ml Gd-DTPA was determined from the results of the pilot study. We hoped that the acquisition of the center of k-space of the first MRA was matched to the period of maximum effect of the first pass bolus for the pulmonary arteries. In a pilot study on average, pulmonary artery signal intensities were relatively high from 10.4 to 20.7 s after the contrast medium injection. The MR angiograms obtained at the optimal time were superior to those that followed. All pulmonary trunks and the right and left main pulmonary arteries were accurately recognized. MRA had a sensitivity of 80.0%, a specificity of 95.0%, and an accuracy of 94.5% for the detection of segmental artery stenosis or occlusion. Abnormal vessels were visualized in both patients with pulmonary sequestration. Pulmonary 3D TOF MRA using breath holding and a contrast medium is useful in demonstrating proximal pulmonary vasculature and pulmonary sequestration.

Intermediate-Term Outcome After Intracardiac Repair of Associated Cardiac Defects in Patients With Atrioventricular and Ventriculoarterial Discordance

Limited information is available concerning long-term results, especially systemic right ventricular (RV) or tricuspid valvular function, after intracardiac repair of anomalies associated with discordant atrioventricular (AV) and ventriculoarterial (VA) connections ("congenitally corrected transposition of the great arteries"). We retrospectively reviewed the intermediate-term follow-up of 28 patients, totaling 158 patient-years (median, 60 months), after intracardiac repair involving closure of a ventricular septal defect (VSD) with or without additional surgery. Seven patients had VSD closure alone, 5 had VSD repair with pulmonary stenosis relief, and 16 had VSD closure with conduit insertion between left ventricle and main pulmonary artery. Hospital mortality was 4% (1 of 28 patients; 70% confidence limits, 0.07% to 12%) and the 1-, 5-, and 10-year actuarial survival probabilities were 89%, 83%, and 83%, respectively. Twenty-one of 24 long-term survivors were in New York Heart Association functional class I and 3 were in class II. Sixteen of 24 patients showed increasing tricuspid regurgitation (TR) of more than moderate degree, which occurred within 3 years after surgery in 7 patients. Twelve of 22 patients showed deterioration of RV pump function, mainly (9 of 12 patients) within 3 years postoperatively. The pulmonary to systemic flow ratio at the preoperative cardiac catheter study was significantly (P < .05) higher in patients who developed RV dysfunction (2.3 +/- 1.0, mean +/- SD) than in those with well-maintained RV function (1.4 +/- 0.6). Intermediate-term results of intracardiac repair for AV and VA discordance were satisfactory in terms of survival and clinical functional status; however, there is concern about systemic RV dysfunction with development of TR relatively early after the operation. Alternative surgical approaches such as anatomic correction or Fontan repair for cases unsuitable for biventricular repair may improve the long-term results, including ventricular and valvular function.

Acellular matrix: A biomaterials approach for coronary artery bypass and heart valve replacement

We have developed a multistep detergent-enzymatic extraction process (involving hypotonic and hypertonic solutions, the detergents octyl-phenoxy-polyethoxyethanol and sodium dodecyl sulfate, as well as DNAse and RNAse) which, while inhibiting autolysis, removes all cells from tissues and, with them, cellular antigens together with lipids and more soluble glycosaminoglycans. What remains is acellular matrix with the structural proteins well conserved and normally arranged. Canine arteries extracted to acellular matrix were implanted as coronary artery bypass allografts in a canine model, without the use of cardiopulmonary bypass, and compared with autogenous saphenous veins. Of nine pilot acellular matrix implants, four were patent, as compared with four of seven saphenous vein grafts. All occlusions in both graft types occurred acutely soon after implantation, with almost all patent grafts followed up for 6 months. The acellular matrix allografts showed no inflammation and only minimal cellular repopulation. This model needs further development, but appears promising for preclinical evaluation. Canine aortic and pulmonic valves extracted to acellular matrix using a modification of our extraction process, eliminating the detergent sodium dodecyl sulfate, were implanted heterotopically as allografts in the left main pulmonary artery in dogs, a location chosen to avoid the need for cardiopulmonary bypass. At 1 month, two-dimensional echocardiography of six implants showed leaflet motion and 3- to 5-mm Hg transvalvular gradients. Explant histology of four valves at 1 month showed no inflammation, cellular repopulation at the base of the valve, and partial endothelialization.(ABSTRACT TRUNCATED AT 250 WORDS)

Echinococcal Cyst of the Pericardium

Figure 1. A 56-year-old man from Saudi Arabia presented with dyspnea. A chest film (Panel A) revealed a large mass in the left hemithorax, with contralateral mediastinal shift and depression of the gas-filled stomach (arrow). Computed tomography after the injection of intravenous contrast medium (Panel B and Panel C) showed a large multilocular cyst in the left hemithorax with contralateral displacement of mediastinal structures, including the trachea (T), the ascending aorta (AA) and the descending aorta (DA), the superior vena cava (SVC), and the right pulmonary artery (RPA). The left main bronchus (arrow) and left pulmonary artery (LPA) were compressed. . . .

Aortic implantation is possible in all cases of anomalous origin of the left coronary artery from the pulmonary artery

Anomalous origin of the left coronary artery from the pulmonary artery (PA) optimally is treated by creation of a multiple coronary system. This study explores the use of aortic implantation employing alternative methods to achieve coronary transfer in all patients, regardless of the site of origin of the anomalous coronary artery, avoiding the problems of bypass grafts and tunnel procedures. During the period 1986 to 1994, 11 patients aged 6 months to 8 years (mean age, 2.6 years) underwent repair. Coronary artery origin from the PA included left sinus in 3, posterior in 2, right sinus in 2, intramural aorta with its orifice at the bifurcation of the main and right PA in 1, high left main PA in 1, high at the bifurcation of main and right PA in 1, and anterior in 1. Findings included angina in 4, prior infarctions in 3, ischemia in 7, left ventricular dysfunction in 6, mitral regurgitation in 5, atrial septal defect in 2, and echocardiograms suggestive of endocardial fibrosis in 4. One patient had prior ligation with ventricular dysfunction and collateralization and recanalization. A single patient was asymptomatic. Repair was accomplished by direct transfer using the PA sinus of Valsalva as a button in only 6; tubular reconstruction was used in 4 when the distance was too great to avoid tension; 2 short tubes were constructed with PA wall in 2 of the 3 left sinus origins, whereas 2 long tubes of PA wall were used (1 high on the left side of the main PA and 1 with left anterior descending origin from the anterior sinus of Valsalva in a patient with malrotation [end neo-artery to side aortic reconstruction]); finally, in situ transfer and intraaortic reconstruction (unroofing and anastomosis) was performed in 1 intramural coronary artery. Division of the PA, mobilization of the distal PA, division of the ductus, and direct reanastomosis of the PA was performed in 3 tubular reconstructions, as well as all 6 direct coronary transfers. There were no operative or late deaths. Follow-up of 2 to 100 months (mean, 46 months) revealed no new angina or infarctions, improved function and decreased mitral regurgitation. Echocardiographic and angiographic studies demonstrated patency and prograde flow in the new coronary systems. Aortic implantation is the treatment of choice for anomalous origin of the left coronary artery. Methods such as direct transfer, tubular reconstruction, and in situ transfer make such implantation possible in all patients regardless of the site of coronary origin, distance from the aorta, or coronary artery configuration.

Anomalous origin of the left main pulmonary artery from the ascending aorta associated with Digeorge syndrome

We place on record 2 infants with the DiGeorge syndrome and anomalous origin of the left pulmonary artery from the ascending aorta. We postulate that: (1) embryogenesis of anomalous origin of the left pulmonary artery from the ascending aorta might be due to the persistent fifth aortic arch connecting both arterial systems; (2) an anomalous pulmonary artery arising from the ascending aorta is part of the aortic arch abnormality accompanied by normal conotruncal septation; and (3) in the DiGeorge syndrome, cardiac anomalies that originate from the conotruncus or aortic arch, or both, may have the same embryologic mechanisms.

Acetazolamide slows VA/Q matching after changes in regional blood flow

Inhibition of carbonic anhydrase (CA) by acetazolamide increases ventilation-perfusion (VA/Q) heterogeneity (E. R. Swenson, H. T. Robertson, and M. P. Hlastala. J. Clin. Invest. 92: 702-709, 1993), possibly because of slowing of CO2/H(+)-dependent mechanisms of VA/Q matching with temporal fluctuations of regional ventilation and perfusion. To study this concept, we imposed abrupt changes in regional perfusion by lobar or left main pulmonary artery occlusions (PAOs) in anesthetized mechanically ventilated dogs before and after CA inhibition (20 mg/kg iv acetazolamide). The rate of ventilation redistribution and change in VA/Q distributions with changes in perfusion were measured by planar gamma imaging of the lungs during continuous inhalation of 81mKr gas ventilation scanning and the multiple inert-gas elimination technique. PAO for 5 min caused regional Kr activity to fall by 30 +/- 5% (SD) with a half time (t1/2) of 75 +/- 10 s. With release of the occlusion, counts returned to baseline with t1/2 of 79 +/- 12 s. Acetazolamide increased these respective t1/2 values (161 +/- 16 and 180 +/- 17 s). Consistent with these kinetics, VA/Q mismatch was greater with lobar PAO at 2 min but not at 10 min with CA inhibition compared with that caused by lobar PAO alone. Cyclical lobar PAO and release (10 cycles of 1-min occlusion and 1-min release) caused more VA/Q heterogeneity during CA inhibition. The arterial-to-alveolar inert-gas area difference rose minimally from 0.18 to 0.23 (P < 0.05) with cyclical PAO and from 0.24 to 0.48 (P < 0.01) after CA inhibition.(ABSTRACT TRUNCATED AT 250 WORDS)

Respiratory mechanics and gas exchange in postobstructive pulmonary vasculopathy

Chronic unilateral pulmonary artery ligation induces formation of new bronchial collateral vessels in the affected lung. These vessels form precapillary anastomoses with the pulmonary circulation and the lung is perfused with arterial blood. Inspired gas is diverted to the contralateral lung to maintain the ventilation/perfusion ratio (VA/Q) and gas exchange. This study was designed to determine the mechanism responsible for this shift of ventilation, which has not previously been investigated. We studied six dogs, before and 6 months after ligation of the left main pulmonary artery. We measured pulmonary resistance (RL) and elastance (EL), minute ventilation (VE), O2 consumption (VO2) and CO2 production (VCO2) of the right and left lungs. We also examined the effect of CO2, atropine and isoproterenol on RL and EL. In the lung with ligated pulmonary artery: 1) VE was significantly reduced; 2) RL and EL were increased and were unresponsive to CO2, atropine and isoproterenol; and 3) VO2 decreased more than VCO2 and, consequently, respiratory quotient (RQ) was greater than 1. We conclude that, with chronic pulmonary artery obstruction, ventilation shifts to the contralateral lung because of an increase in RL and EL not related to airway smooth muscle tone.

Myoendothelial junctional complexes in postobstructive pulmonary vasculopathy: a quantitative electron microscopic study.

Postobstructive pulmonary vasculopathy (POPV), produced by chronic unilateral ligation of one pulmonary artery, is characterized by (1) marked proliferation of bronchial collateral vessels, (2) increased pulmonary vascular resistance, and (3) hyperreactivity of arteries to serotonin and of veins to histamine. Electron microscopic examination of the vessels in POPV suggested an increase in myoendothelial junctional complexes (MEJC). To quantitate this change, the number of MEJC in the vessel walls of the left lung was compared with that of the right lung in 16 dogs after ligation of the left main pulmonary artery for 8.4 +/- 1.6 (SE) months. The lungs were fixed by airway instillation of 3% glutaraldehyde. Electron micrographs were taken of pulmonary arteries, capillaries, and veins and of bronchial vessels, and their external diameter and length of endothelial basal lamina were measured. The MEJC were counted and expressed as number per length of basal lamina and typed: Type I consisted of endothelial processes, type II of smooth muscle or pericyte processes, and type III of processes from each cell type. The results demonstrated that the vasculature from the control lung had the smallest number of MEJC and the majority were type I. With ligation, there was a significant increase (p < .01) in the number of MEJC for each type of vessel examined, but no significant change in the distribution of the type. In addition, no correlation was found between the number of MEJC and vascular diameter. It can be concluded that MEJC are increased in each region of the lung's vasculature in POPV and that they may play a role in the proliferative response of the bronchial vasculature, the remodeling of the pulmonary vasculature, and the pulmonary vascular hyperreactivity of this model.

Altered mechanical properties of lung parenchyma in postobstructive pulmonary vasculopathy

Postobstructive pulmonary vasculopathy (POPV) produced by chronic unilateral ligation of one pulmonary artery, results in perfusion of the pulmonary capillaries with systemic arterial blood. As a consequence, gas exchange occurs primarily in the contralateral nonligated lung. To determine whether the mechanical properties of the lung parenchyma are changed in POPV, we compared five dogs with chronic ligation of the left main pulmonary artery with five control dogs. Separate measurements of left and right lung airway flows, tracheal pressures, and alveolar pressures were made during mechanical ventilation at frequencies between 5 and 40 breaths/min. We calculated pulmonary elastance (EL) and pulmonary (RL), airway (Raw), and tissue (Rti) resistances. At all frequencies, dogs with POPV had higher left (ligated) EL and Rti and lower right (normal) lung Rti but similar EL compared with the respective lungs from control animals. Raw was the same in both lungs. Histology showed visceral pleura thickening and encroachment of new bronchial collaterals and lymphatics on the parenchyma of the ligated lungs. The contralateral lungs were entirely normal. We conclude that in POPV 1) there is an increase, in the ligated lung, of both EL and RL, the latter likely due to histological changes of the lung parenchyma, and 2) there is a reduction of Rti in the contralateral lung.

The dose-response relationship for hypoxic pulmonary vasoconstriction

In 12 pentobarbital anesthetized dogs the lungs were independently ventilated with a double piston ventilator. The right lung was ventilated throughout with 100% oxygen. Blood was drawn from the right atrium and pumped through a bubble oxygenator to a cannula in the ligated left main pulmonary artery. The pressures in the left main pulmonary artery and the left atrium were recorded during constant flow while the oxygen tension in the left lung alveolar gas and the perfusate were varied either to match each other (Protocol 1) or differ (Protocol 2) over the range from “zero” to “100%” oxygen. From the combined data a three dimensional response surface for hypoxic pulmonary vasoconstriction was derived. The maximum increase of pulmonary vascular resistance (r%PVR max) was defined at a stimulus oxygen tension (P S O 2 ) of 10 mmHg amounting to a 3.15±(0.18)-fold increase of the vascular resistance on “100%” oxygen. The stimulus oxygen tension was shown to be PS o 2 = P V o 2 0.41 × P a o 2 0.59 and the dose-response sigmoid for hypoxic pulmonary vasoconstriction in canine lungs was derived as r%PVR max = 100(PS o 2 −2.616)/(6.683x10 −5+P S o 2 −2.616) These results appear to reconcile observations from a number of laboratories and to be of quite general application.