scholarly journals Left Pulmonary Artery Coarctation Associated with Pneumonia and Pulmonary Hypertension in a Cat

2021 ◽  
Vol 8 (12) ◽  
pp. 325
Author(s):  
Carlotta Valente ◽  
Massimiliano Tursi ◽  
Helen Poser ◽  
Carlo Guglielmini
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Artery ◽  
Physical Examination ◽  
Cardiac Hypertrophy ◽  
Respiratory Distress ◽  
Cardiac Remodeling ◽  
Left Pulmonary Artery ◽  
Pathological Findings ◽  
Thoracic Radiography ◽  
Presumptive Diagnosis

A five-month-old European shorthair female kitten was referred because of recurrent episodes of respiratory distress. Results of physical examination, thoracic radiography, and echocardiography led to a presumptive diagnosis of severe precapillary pulmonary hypertension (PH) and interstitial pneumonia associated with right-sided cardiac remodeling. The cat rapidly died because of respiratory insufficiency. Pulmonary and cardiovascular pathological findings evidenced left pulmonary artery coarctation, severe right-sided cardiac hypertrophy, and bilateral pneumonia. This is the first report of pulmonary artery coarctation associated with pneumonia and PH in a cat.

scholarly journals Spontaneous pulmonary artery thrombus in a neonate

2021 ◽  
Vol 73 (1) ◽  
Author(s):  
Y. S. Shrimanth ◽  
Krishna Prasad ◽  
Adari Appala Karhtik ◽  
Parag Barwad ◽  
C. R. Pruthvi ◽  
...  
Keyword(s):  
Pulmonary Artery ◽  
Respiratory Distress ◽  
Disease Risk ◽  
Maternal Diabetes ◽  
Left Pulmonary Artery ◽  
Pulmonary Angiography ◽  
Haemodynamic Instability ◽  
Artery Thrombosis ◽  
Heart Disease Risk Factors ◽  
Heart Disease Risk

Abstract Background Pulmonary artery thrombosis is rare in neonates and mimics as persistent pulmonary hypertension or congenital heart disease. Risk factors include septicemia, dehydration, polycythemia, maternal diabetes, asphyxia, and inherited thrombophilias. They present with cyanosis and respiratory distress. Careful echocardiogram assessment helps in identifying the thrombus in the pulmonary artery and its branches. Computed tomography pulmonary angiography confirms the diagnosis. Case presentation We present a case of term neonate who presented with respiratory distress and cyanosis and a detailed echocardiogram revealed thrombus in the origin of left pulmonary artery. The neonate was managed initially with unfractionated heparin and later with low molecular weight heparin with which there was significant resolution of the thrombus Conclusion Spontaneous pulmonary artery thrombosis though rare should be suspected in any cyanotic neonate with respiratory distress. Management in these cases depends on the haemodynamic instability and lung ischemia.

scholarly journals Cinaciguat, a soluble guanylate cyclase activator, causes potent and sustained pulmonary vasodilation in the ovine fetus

2009 ◽  
Vol 297 (2) ◽  
pp. L318-L325 ◽  
Author(s):  
Marc Chester ◽  
Pierre Tourneux ◽  
Greg Seedorf ◽  
Theresa R. Grover ◽  
Jason Gien ◽  
...  
Keyword(s):  
Blood Flow ◽  
Pulmonary Hypertension ◽  
Pulmonary Artery ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Guanylate Cyclase ◽  
Soluble Guanylate Cyclase ◽  
Left Pulmonary Artery ◽  
Flow Transducer ◽  
Pulmonary Vasodilation

Impaired nitric oxide-cGMP signaling contributes to severe pulmonary hypertension after birth, which may in part be due to decreased soluble guanylate cyclase (sGC) activity. Cinaciguat (BAY 58-2667) is a novel sGC activator that causes vasodilation, even in the presence of oxidized heme or heme-free sGC, but its hemodynamic effects have not been studied in the perinatal lung. We performed surgery on eight fetal (126 ± 2 days gestation) lambs (full term = 147 days) and placed catheters in the main pulmonary artery, aorta, and left atrium to measure pressures. An ultrasonic flow transducer was placed on the left pulmonary artery to measure blood flow, and a catheter was placed in the left pulmonary artery for drug infusion. Cinaciguat (0.1–100 μg over 10 min) caused dose-related increases in pulmonary blood flow greater than fourfold above baseline and reduced pulmonary vascular resistance by 80%. Treatment with 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ), an sGC-oxidizing inhibitor, enhanced cinaciguat-induced pulmonary vasodilation by >120%. The pulmonary vasodilator effect of cinaciguat was prolonged, decreasing pulmonary vascular resistance for >1.5 h after brief infusion. In vitro stimulation of ovine fetal pulmonary artery smooth muscle cells with cinaciguat after ODQ treatment resulted in a 14-fold increase in cGMP compared with non-ODQ-treated cells. We conclude that cinaciguat causes potent and sustained fetal pulmonary vasodilation that is augmented in the presence of oxidized sGC and speculate that cinaciguat may have therapeutic potential for severe neonatal pulmonary hypertension.

scholarly journals Left Lung and Pulmonary Artery Hypoplasia: A Rare Case of Hemoptysis

2020 ◽  
Author(s):  
Guiomar Pinheiro ◽  
Ana Margarida Alves ◽  
Isabel Neves ◽  
Teresa Sequeira
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Artery ◽  
Pulmonary Hypoplasia ◽  
Left Lung ◽  
Left Pulmonary Artery ◽  
Pulmonary Infections ◽  
Rare Congenital Disorder ◽  
History Of ◽  
Pulmonary Artery Hypoplasia

Pulmonary hypoplasia or agenesis is a rare congenital disorder that results in lung underdevelopment. This disease is usually found in children but rarely encountered in adults. We describe the case of an 84-year-old woman diagnosed with a unilateral pulmonary hypoplasia presenting simultaneously with left pulmonary artery hypoplasia. Due to this condition, the patient had a lifelong history of pulmonary infections that resulted in several bronchiectases in the affected lung. Moreover, the pulmonary artery hypoplasia led to the development of pulmonary hypertension and collateral circulation causing hemoptysis, giving rise to the patient attending the emergency department. Although we were able to medically manage the hemoptysis, it can be fatal and require surgical intervention. Hence, an early diagnosis is essential so that appropriate follow-up and prompt prevention and treatment of complications, such as pulmonary infections, hemoptysis and pulmonary hypertension, are achieved.

scholarly journals Noninvasive pulmonary artery wave intensity analysis in pulmonary hypertension

2015 ◽  
Vol 308 (12) ◽  
pp. H1603-H1611 ◽  
Author(s):  
Michael A. Quail ◽  
Daniel S. Knight ◽  
Jennifer A. Steeden ◽  
Liesbeth Taelman ◽  
Shahin Moledina ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Artery ◽  
Left Pulmonary Artery ◽  
Wave Intensity ◽  
Healthy Controls ◽  
Intensity Analysis ◽  
Wave Intensity Analysis ◽  
Pulmonary Vessel ◽  
Golden Angle ◽  
Angiographic Data

Pulmonary wave reflections are a potential hemodynamic biomarker for pulmonary hypertension (PH) and can be analyzed using wave intensity analysis (WIA). In this study we used pulmonary vessel area and flow obtained using cardiac magnetic resonance (CMR) to implement WIA noninvasively. We hypothesized that this method could detect differences in reflections in PH patients compared with healthy controls and could also differentiate certain PH subtypes. Twenty patients with PH (35% CTEPH and 75% female) and 10 healthy controls (60% female) were recruited. Right and left pulmonary artery (LPA and RPA) flow and area curves were acquired using self-gated golden-angle, spiral, phase-contrast CMR with a 10.5-ms temporal resolution. These data were used to perform WIA on patients and controls. The presence of a proximal clot in CTEPH patients was determined from contemporaneous computed tomography/angiographic data. A backwards-traveling compression wave (BCW) was present in both LPA and RPA of all PH patients but was absent in all controls ( P = 6e−8). The area under the BCW was associated with a sensitivity of 100% [95% confidence interval (CI) 63–100%] and specificity of 91% (95% CI 75–98%) for the presence of a clot in the proximal PAs of patients with CTEPH. In conclusion, WIA metrics were significantly different between patients and controls; in particular, the presence of an early BCW was specifically associated with PH. The magnitude of the area under the BCW showed discriminatory capacity for the presence of proximal PA clot in patients with CTEPH. We believe that these results demonstrate that WIA could be used in the noninvasive assessment of PH.

Cellular adaptation during chronic neonatal hypoxic pulmonary hypertension

1991 ◽  
Vol 261 (4) ◽  
pp. L97-L104 ◽  
Author(s):  
Kurt R. Stenmark ◽  
Almas A. Aldashev ◽  
Ernest C. Orton ◽  
A. G. Durmowicz ◽  
D. B. Badesch ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Smooth Muscle ◽  
Pulmonary Artery ◽  
Arterial Wall ◽  
Chronic Hypoxia ◽  
Left Pulmonary Artery ◽  
Right Atrial ◽  
Vascular Changes ◽  
Hypoxic Pulmonary Hypertension

Newbor animals develop more severe hypoxic pulmonary hypertension than do adults, their vascular changes are greater, and both the hypertension and vascular changes occur more rapidly. We hypothesize that this differential developmentally controlled response may arise from either a difference in the type or quantity of endogenously secreted mediators in response to a given injury or a difference in the replicative and/or matrix-producing response of the vascular cells to physical or chemical stimuli. We investigated the effect of chronic hypoxia (14 days) on the proliferative and matrix-producing phenotype of the neonatal (14-day-old) pulmonary artery smooth muscle cell (SMC) and examined the heterogeneity and potential mechanisms responsible for this response. In situ hybridization studies demonstrated a remarkable change in the distribution of cells hybridizing with a tropoelastin cRNA probe after 14 days of hypoxia. Studies also demonstrated a population of SMC that did not hybridize with the elastin or collagen probes, indicating that the pulmonary artery contains SMC of multiple phenotypes and that the response to hypoxic and hemodynamic stress is not uniform for the various types. Bromodeoxyuridine labeling experiments indicated a large increase in DNA synthesis in hypertensive vessels, which, again, was not uniform either across or along the arterial wall. In vitro experiments with neonatal SMC suggested that hypoxia alone could not be responsible for the proliferative or matrix changes. These observations were supported by in vivo experiments in which coarctation of the left pulmonary artery, which markedly decreased pressure and flow to the left lung in hypoxic animals (14 days), resulted in significant decreases in collagen and elastin message levels in the left pulmonary artery distal to the coarctation compared with location-matched vessels from the right lung. Finally, we noted marked decreases in B-receptor density and adenyl cyclase activity in right atrial and pulmonary artery tissue from the chronically hypoxic animals. Decreases in the ability of the cell to produce adenosine 3',5'-cyclic monophosphate could significantly affect both the proliferative and matrix-producing potential of the SMC. We conclude that in vivo adaptation of the pulmonary artery SMC to chronic hypoxia includes changes in protein synthesis, cell proliferation, receptor expression, and enzyme activity. Further, there is a marked heterogeneity of these responses both across and along the arterial wall. hypoxia; phenotype; signal transductions; smooth muscle cells

Anomalous origin of left pulmonary artery from the ascending aorta: echocardiography assessment

2019 ◽  
Vol 30 (1) ◽  
pp. 145-147
Author(s):  
Samir Atmani ◽  
Imane Bendris
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Artery ◽  
Cardiac Failure ◽  
Left Pulmonary Artery ◽  
Ascending Aorta ◽  
High Flow ◽  
Anomalous Origin ◽  
Cardiac Anomaly ◽  
Rare Anomaly

AbstractAnomalous origin of one pulmonary artery from the ascending aorta is a rare cardiac anomaly in which the pulmonary artery abnormally arises from the ascending aorta. Physiologically, most patients develop signs of cardiac failure due to high flow to both lungs. The purpose of this study is to demonstrate, with this rare anomaly, the accurate place of the echocardiography to establish diagnosis especially in the systemic or supra-systemic pulmonary hypertension.

scholarly journals Left Pulmonary Artery Ligation and Chronic Pulmonary Artery Banding Model for Inducing Right Ventricular—Pulmonary Hypertension in Sheep

ASAIO Journal ◽  
2020 ◽  
Vol 67 (1) ◽  
pp. e44-e48
Author(s):  
Rei Ukita ◽  
Yuliya Tipograf ◽  
Andrew Tumen ◽  
Rachel Donocoff ◽  
John W. Stokes ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Artery ◽  
Right Ventricular ◽  
Left Pulmonary Artery ◽  
Pulmonary Artery Banding ◽  
Artery Ligation

scholarly journals P1728 Pulmonary hypertension in a pregnant Women - a rare anatomical aetiology

2020 ◽  
Vol 21 (Supplement_1) ◽  
Author(s):  
J Grade Santos ◽  
F Ferreira ◽  
M Loureiro ◽  
A Almeida ◽  
A Pereira ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Artery ◽  
Pulmonary Artery Pressure ◽  
Medical Therapy ◽  
Cardiac Mri ◽  
Left Pulmonary Artery ◽  
Severe Pulmonary Hypertension ◽  
Right Pulmonary Artery ◽  
History Of

Abstract A 32 year old female patient, with a medical history of an ill-characterized Pulmonary Arterial Hypertension associated with congenital heart disease, lost in the follow up with no medical therapy, attended an emergency department for a gynecological hemorrhage at 16 weeks of pregnancy. Due to high maternity mortality risk, informed consent was obtained, and termination of pregnancy was performed. She was then referred to our pulmonary hypertension center. At our center she had complains of fatigue with moderate intensity exertion, classified in a class II of the World Health Organization (WHO) classification, but was otherwise asymptomatic, with no history of dyspnea, angina or syncope. There was allusion to a self-limited episode of hemoptysis in the past. On physical examination she had an increased pulmonary component of the second heart sound, continuous heart murmur in left sternal border and no cyanosis (O2 peripheral saturation in the upper and lower limbs of 99% at room air). The performed echocardiograms (both transthoracic and transesophageal) showed an estimated systolic pulmonary artery pressure of 120 mmHg with severe right ventricular hypertrophy and systolic dysfunction. There was dilatation of the trunk and right pulmonary artery. The left pulmonary artery was not seen. Biochemical evaluation and viral serologies were unremarkable. The pulmonary function tests and the arterial blood gases were normal. Cardiac MRI demonstrated the presence of a right aortic arch and a right patent arterial duct. An anomalous origin of the left pulmonary artery from the ascending thoracic aorta could be noted. Associated congenital cardiac defects were excluded. A right heart catheterization confirmed the presence of severe pulmonary hypertension with mean pulmonary artery pressure of 86 mmHg and Pulmonary vascular resistance of 11 Wood Units. A large persistent arterial duct to the right pulmonary artery was confirmed with persistent left to right shunt. The left pulmonary artery was visualized when injection was performed in the aortic root. Coronary arteries were normally implanted. The patient was started on Sildenafil and Bosentan (later replaced by Macitentan due to hepatic toxicity). After 3 years of follow up, there was an improvement in symptoms and in the 6 minutes walking test, remaining in a low risk category and on a WHO class I. This case reports a very rare congenital abnormality identified in an adult patient. Despite the complex anatomy and severe pulmonary hypertension, the patient is reasonably well under medical therapy and close follow up. Abstract P1728 Figure. Cardiac MRI Cine Sequences

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