Pulmonary Venous Occlusion Research Articles

Unilateral pulmonary venous occlusion caused by a localized pericardial clot.

Unilateral pulmonary venous occlusion caused by a localized pericardial clot.

Atrial flow dynamics as a determinant of tissue temperature during balloon cryoablation.

Balloon cryoablation is an accepted method of achieving pulmonary vein isolation for the treatment of atrial fibrillation. The relationship between blood flow in the atrium and cryo energy delivery to the tissue remains poorly understood. Controlled cryoablations were performed in vitro using a pulmonary vein phantom constructed from bovine muscle, providing a 20 mm vein ostium. A temperature sensor was mounted within the 'vein wall' at a 1 mm tissue depth. Apparatus was constructed to assess the effect of incomplete pulmonary venous occlusion causing a leak, simulated atrial stasis, atrial circulation, and mitral regurgitation. Controlled ablations using the 2nd generation 28 mm cryoballoon catheter were repeated three times and mean values compared. Leak volume significantly affected both balloon temperatures and tissue temperatures. Simulated mitral regurgitation (MR) significantly impaired the effectiveness of cryo energy delivery resulting in significantly warmer balloon and tissue temperatures. With high leak volumes and moderate to severe MR there was a marked disparity between the cryoballoon temperature and the tissue temperature of approximately 60 degrees. Balloon warming times varied inversely with both leak volume and simulated MR flow volume. Incomplete venous occlusion and MR result in warmer balloon and tissue temperatures, and shorter balloon warming times, and are likely to significantly impair the effectiveness of cryoablation. Balloon temperature is poor indicator of tissue temperature under higher flow conditions.

Pulmonary and Thoracic Vascular Involvement in Behcet's Disease on CT

Behcet’s disease (BD) is characterized by recurrent oral and genital ulcerations, ocular and additional clinical manifestations. The exact cause of the disease is unknown. Thoracic manifestations of BD show a wide spectrum including vascular, mediastinal, pleural and parenchymal involvement. CT is the imaging modality that provides the assessment of the thoracic presentations of BD. The typical presentations of BD are aneurysms of the pulmonary arteries and venous occlusion. Aneurysms of the aorta, occlusion of vena cava superior, venous aneurysms, mediastinal lymphadenopathy, mediastinal fibrosis, pneumonia, pulmonary hemorrhage, infarction, pleural and pericardial effusions, and pleural nodules are other thoracic manifestations of BD. Assessment of these thoracic involvements can be used in the diagnosis of BD.

Pulmonary vein stenosis after atrial fibrillation ablation.

Pulmonary vein stenosis (PVS) is an uncommon but devastating complication of atrial fibrillation (AF) ablation. Patients are often misdiagnosed due to non-specific symptoms and the challenges of visualising the pulmonary veins on standard chest imaging. Delays in treatment result in worsening symptoms and pulmonary venous occlusion. The optimal method of intervening for PVS has not been well established. Restenosis after successful intervention is common, warrants active surveillance, and is the focus of research into prevention and management strategies. In this article we review the existing literature on PVS, and discuss our own experience in managing patients with severe PVS.

Massive Intractable Hemoptysis Due to Idiopathic Granulomatous Pulmonary Veno-occlusive Disease

Pulmonary veno-occlusive disease is a rare condition with limited treatment options. The pathological hallmark of the disease is occlusion of pulmonary venules and small veins in the lobular septa. The etiology of the disease remains obscure. We report and discuss an extremely unusual case presenting as massive and intractable hemoptysis, in which pulmonary venous occlusion was attributed to granulomatous venulitis in the absence of other pulmonary or systemic inflammatory abnormalities.

Off -label use of Amplatzer devices in congenital heart disorders during childhood

Background Certain medical devices used to treat congenital cardiac lesions in the cardiac catheterization laboratory are used on an off -label and non-routine basis. This article discusses the non-routine use of Amplatzer medical devices.Methods In a retrospective study, from-11-2006 to-12-2011, Amplatzer devices used in our paediatric cardiology ward were reviewed.Results Children (n = 436) were catheterized to close their defects (438 defects) using Amplatzer devices. The mean age and body weight of the patients were 5.87 ± 4.2 years and 20.8 ± 13.6 kg. On-label devices were used for 421 patients (96.1%) and off -label devices for 17 patients (3.9%). The off -label use indications and used devices were the Amplatzer septal occluder (aortopulmonary window closure), the muscular ventricular septal occluder (perimembranous ventricular septal defect occlusion, patent ductus arteriosus occlusion, and right pulmonary artery to left atrium fi stulous connection closure), the vascular plug (coronary fi stula occlusion, left ventricle pseudoaneurysm occlusion, atypical patent ductus arteriosus occlusion, and anomalous pulmonary venous drainage occlusion), and the ductal occluder (ventricular septal defect occlusion). These devices were successfully implanted in exclusively extraordinary, diffi cult, or extreme cases.Conclusions The use of a medical device outside of its approved purpose is commonly referred to as “off -label use”. This study showed that the issue of off -label, non-routine use of devices exists in paediatric cardiology. Furthermore, the percutaneous closure of defects with non-routine Amplatzer devices is safe and eff ective, with a high success rate and a high follow-up term outcome.

Pulmonary venous occlusion and death in pulmonary arterial hypertension: survival analyses using radiographic surrogates

BackgroundRecent studies find that a considerable number of patients with pulmonary arterial hypertension (PAH) develop fibrous obstruction of the pulmonary veins. Such obstruction more commonly accompanies connective tissue disorder (CTD)-associated PAH than idiopathic PAH. However, few researchers have gauged the risk of death involving obstruction of the pulmonary veins.MethodsThirty-seven patients with PAH were enrolled (18 patients, idiopathic PAH; 19 patients, CTD-associated PAH). The patients were 49 ± 18 years and had a World Health Organization functional class of 3.2 ± 0.6. Thickening of the interlobular septa, centrilobular ground-glass attenuation, and mediastinal adenopathy were surrogates for obstruction of the pulmonary veins, and were detected by a 16-row multidetector computed tomography scanner.ResultsThe follow-up period was 714 ± 552 days. Fifteen deaths occurred. Thickening of the interlobular septa, centrilobular ground-glass attenuation, and mediastinal adenopathy were found in 37.8%, 24.3%, and 16.2% of patients, respectively. Cox proportional hazard analysis revealed an increased risk of death with each radiographic surrogate (mediastinal adenopathy: p < 0.0001, hazard ratio = 13.9; thickening of interlobular septa: p < 0.001, hazard ratio = 12.0; ground-glass attenuation: p = 0.02, hazard ratio = 3.7). The statistical significance of these relationships was independent of the cause of PAH and plasma concentration of brain natriuretic peptide.ConclusionsThe results of this study imply that obstruction of the pulmonary veins is associated with an increased risk of death in patients with PAH.

Myocardial tuberculosis presenting with congestive heart failure and pulmonary venous occlusion

Myocardial tuberculosis is a rare but well recognized disease entity. It can either remain clinically silent or present in various different forms. The presentation of myocardial tuberculosis depends upon the structures involved by the disease process. We report a case of cardiac tuberculosis with pulmonary venous obstruction presenting with congestive cardiac failure.

A 50-Year-Old Woman With a History of Atrial Fibrillation Presents With Acute Dyspnea and Pleuritic Chest Pain

A 50-Year-Old Woman With a History of Atrial Fibrillation Presents With Acute Dyspnea and Pleuritic Chest Pain

Successful stenting of the ductus venosus in 2 neonates with asplenia syndrome complicated by infracardiac type total anomalous pulmonary venous connection

In the neonatal period, the surgical mortality of palliation is extremely high for asplenia syndrome complicated by single ventricle combined with total anomalous pulmonary venous connection (TAPVC). Recently, stent implantation for the pulmonary venous drainage route soon after birth has been used instead of surgery to prevent pulmonary venous occlusion and to maintain stable hemodynamics in the neonatal period or in early infancy. Here, we successfully implanted stents in the ductus venosus (DV) in 2 neonates with asplenia syndrome complicated by infracardiac type TAPVC. The first patient was a 3-day-old male neonate with severe cyanosis. Immediately after TAPVC was diagnosed, we implanted a stent in the DV. The second patient was a 0-day-old female neonate. She was diagnosed as TAPVC by fetal echocardiogram. After the scheduled delivery, a stent was successfully implanted. We believe that stent implantation in the DV in the neonatal period is effective and less invasive than surgery in patients with infracardiac type TAPVC.

Complete Pulmonary Venous Occlusion After Radiofrequency Ablation for Atrial Fibrillation

Pulmonary vein stenosis is a known, yet under-recognized complication of radiofrequency ablation for atrial fibrillation. We present the case of a patient developing complete left-sided pulmonary venous occlusion following radiofrequency ablation. Recommendations are made to allow earlier diagnosis of this complication.

Metastatic leiomyosarcoma presenting with pulmonary venous occlusion and infarction

A 67-year-old, non-smoking man, presented 1 yearafterresectionofacutaneousleiomyosarcomawithacute, pleuritic chest pain. Computed tomography(CT) and magnetic resonance imaging (MRI) demon-strated a left superior pulmonary venous fillingdefect, which was subsequently demonstratedhistologically to be an intravascular metastasisfrom the primary tumour. The evolving role of CTisemphasized,andthiscaseappearstobeuniqueinterms of diagnosis and images.

Cardiac involvement in patients with myeloproliferative disorders

introduction: To evaluate cardiac involvement in myeloproliferative disorders (MPD), two-dimensional and Doppler echocardiographic studies were performed in 30 patients with MPD.patients and methods: There were 18 women and 12 men, with an age range from 35 to 76 years. Eighteen patients had polycythemia vera (PV), 8 had essential thrombocythemia (ET), and 4 had agnogenic myeloid metaplasia (AMM).results: Echocardiography revealed valvular lesions in 19 of 30 patients (63%) compared with only 1 of 22 patients (4.5%) in a control group of patients referred for echocardiography to exclude a cardiac source for idiopathic systemic thromboembolism (χ2 = 13.39, p <0.001, by χ2 test with Yates' correction). Valvular lesions were found in 77% of patients with PV, 50% with ET, and 25% with AMM (p = NS). The aortic and mitral valves were the most commonly involved valves, and the most common echocardiographic lesion was leaflet thickening, which was found in 12 patients (40%), followed by vegetations, which were observed in 5 patients (16%). In their past history, 14 of 30 (47%) MPD patients had arterial or venous thrombosis or embolism. Twelve of 19 (63%) patients with valvular lesions had thromboembolism compared with only 2 of 11 (18%) patients without evidence of valvular lesions (χ2 = 3.99, p <0.05, by χ2 test with Yates' correction). Pulmonary hypertension, unrelated to the severity of valvular disease and probably resulting from pulmonary venous occlusion, was found in four patients (13%).conclusions: We conclude that the heart is frequently involved in patients with MPD, particularly when their past history is complicated by a thromboembolic event. Some patients have clinically significant valvular disease. Pulmonary hypertension is another relatively common finding in MPD patients. Echocardiography provides information of clinical significance in MPD patients. A larger number of patients is needed to determine whether the presence of valvular lesions is of prognostic significance and may herald future thromboembolic events.

Theoretical analysis of occlusion techniques for measuring pulmonary capillary pressure.

We have developed a model including three serial compliant compartments (arterial, capillary, and venous) separated by two resistances (arterial and venous) for interpreting in vivo single pulmonary arterial or venous occlusion pressure profiles and double occlusion. We formalized and solved the corresponding system of equations. We showed that in this model 1) pulmonary capillary pressure (Pc) profile after arterial or venous occlusion has an S shape, 2) the estimation of Pc by zero time extrapolation of the slow component of the arterial occlusion profile (Pcao) always overestimates Pc, 3) symmetrically such an estimation on the venous occlusion profile (Pcvo) always underestimates Pc, 4) double occlusion pressure (Pcdo) differs from Pc. We evaluated the impact of varying parameter values in the model with parameter sets drawn either from the literature or from arbitrary arterial and venous pressures, being respectively 20 and 5 mmHg. Resulting Pcao-Pc differences ranged from 0.4 to 5.4 mmHg and resulting Pcvo-Pc differences ranged from -0.3 to -5.0 mmHg. Pcdo-Pc was positive or negative, its absolute value in general being negligible (< 1.1 mmHg).

A method for analysis of pulmonary arterial and venous occlusion data.

Recently, we presented a compartmental model of the pulmonary vascular resistance (R) and compliance (C) distribution with the configuration C1R1C2R2C3 (J. Appl. Physiol. 70: 2126-2136, 1991). This model was used to interpret the pressure vs. time data obtained after the sudden occlusion of the arterial inflow (AO), venous outflow (VO), or both inflow and outflow (DO) from an isolated dog lung lobe. In the present study, we present a new approach to the data analysis in terms of this model that is relatively simple to carry out and more robust. The data used to estimate the R's and C's are the steady-state arterial [Pa(0)] and venous [Pv(0)] pressures, the flow rate (Q), the area (A2) encompassed by Pa(t) after AO and the equilibrium pressure (Pd) after DO, and the average slope (m) of the Pa(t) and Pv(t) curves after VO. The following formulas can then be used to calculate the 2 R's and 3 C's: [Pa(0) - Pv(0)]/Q = R1 + R2 = RT, R1C1 congruent to to A2/[Pa(0) - Pd], R1 congruent to [Pa(0) - Pd]/Q, Q/m = C1 + C2 + C3 = CT, and C2 = CT - (RTC1/R2).

Response of Perfused Lung and Isolated Pulmonary Artery to Adenosine

Adenosine (AD) has been reported to induce both pulmonary arterial constriction and dilation. We investigated the effect of AD using two complementary techniques. The isolated rat lung perfused with Earle's balanced salt solution containing albumin was used to measure pulmonary arterial (Ppa), venous, and double occlusion (microvascular; Pmv) pressure, and resistance changes. AD alone had no effect on Ppa, Pmv, or resistance at any dose tested (5 x 10(-7) through 10(-3) M). However, when Ppa was elevated by pretreatment with 5 x 10(-7) M norepinephrine (NE), then 10(-4) M AD lowered Ppa by 19.5 +/- 3.2% and Pmv by 6.0 +/- 6.1% and attenuated the increase in upstream resistance caused by NE. Higher doses of AD (10(-3) M) resulted in greater relaxation. In isolated segments from rat and guinea pig pulmonary lobar arteries, isometric force production in response to AD was measured as a percentage of the active isometric force produced in response to 10(-5) M NE (% NE contraction). No response was observed in rat pulmonary arterial rings for doses of AD less than 10(-6) M. In vessels with intact endothelium, 10(-6) M AD caused a slight increase in isometric tension (2.3 +/- 1.2% NE contraction; p less than 0.05), but 10(-4) M AD caused relaxation (-17.2 +/- 2.2% NE contraction; p less than 0.05), and 10(-3) M caused further relaxation (-61.5 +/- 5.0% NE contraction; p less than 0.05). In vessels without endothelium, only relaxation was observed. Isolated guinea pig arterial rings responded to AD with vasodilation similar to the results in the rat arterial rings. Results of this study show that AD primarily causes a direct dose-dependent relaxation of pulmonary arterial smooth muscle in both the isolated perfused lung and isolated arterial ring preparation.

Determination of pulmonary microvascular reflection coefficient in sheep by venous occlusion

We devised a technique that permitted elevation of pulmonary pressures in unanesthetized sheep by occluding their pulmonary veins. Using this technique, we raised pulmonary capillary pressure from a baseline of 13.2 +/- 2.2 to 35.3 +/- 5.1 mmHg. This increased lung lymph flow (from 8.8 +/- 2.7 to 53.1 +/- 13.9 ml/h). We estimated the pulmonary microvascular oncotic reflection coefficient and found it to be 0.82 +/- 0.05 (SD). The filtration coefficient was 0.019 +/- 0.005 ml.mmHg-1.min-1. During the period of increased pressure, the animals had stable arterial pressures and cardiac outputs. None of the animals developed blood coagulation problems. These data illustrate the usefulness of pulmonary venous occlusion to elevate pulmonary microvascular pressure to obtain plasma-to-lymph protein concentration ratios independent of flow, allowing for the calculation of the oncotic reflection coefficient.

Effect of leukotrienes B4, C4, and D4 on segmental pulmonary vascular pressures

Leukotrienes (LTs) C4 and D4 are vasoconstrictors and are thought to increase both systemic and pulmonary vascular permeability. However, we and others have observed that LTC4 and LTD4 cause pulmonary vasoconstriction but do not increase the fluid filtration coefficient of excised guinea pig lungs perfused with a cell-depleted perfusate. To determine what vascular segments were exposed to an LT-induced increase in intravascular hydrostatic pressure we measured pulmonary arterial (Ppa), pulmonary arterial occlusion (Po,a), venous (Po,v) and double occlusion (Pdo) pressures in isolated guinea pig lungs perfused with a cell-depleted buffered salt solution before and after injecting 4 micrograms of LTB4, LTC4, or LTD4 into the pulmonary artery. All three LTs increased airway pressures and also increased Ppa, Po,a, and Pdo. Histamine (15 micrograms) as well as serotonin (20 or 200 micrograms) had the same effect. In excised rabbit lungs, histamine and serotonin increased only Ppa, and Po,a. LTC4 had no vasoactivity. There are marked species variations with regard to the activity and site of action of histamine, serotonin, and LTC4 on the pulmonary circulation.

Left Atrial Myxoma: Pulmonary Infarction Caused by Pulmonary Venous Occlusion

Atrial myxomas are the most common primary cardiac tumors. Typical complications include congestive heart failure, systemic emboli, or vasculitic type syndromes. Presented is a case of postpartum congestive heart failure in a 17-year-old girl. Echocardiography revealed a left atrial mass. Intraoperatively this mass was found to be extending into and occluding the left pulmonary veins. Left pulmonary infarction had occurred, and left pneumonectomy was required to completely remove the lesion. This case thus represents an unusual complication of left atrial myxoma.

Pulmonary venous dilatation in pulmonary veno-occlusive disease

A case of pulmonary veno-occlusive disease in an adult is presented. The diagnosis was suspected clinically and verified at cardiac catheterization. Balloon dilatation of the pulmonary veins was attempted at operation and later again in the catheterization laboratory. The result was a significant reduction in pulmonary venous to left atrial pressure gradient and angiographic evidence of increase in venous diameter. It appears that in the focal form of pulmonary venous occlusion, balloon dilatation may offer a therapeutic approach in an otherwise progressively lethal disease.