scholarly journals 324 Unilateral pulmonary artery agenesis with controlateral embolism: a double vascular trouble

2021 ◽  
Vol 23 (Supplement_G) ◽  
Author(s):  
Alessandro Pierri ◽  
Antonio De Luca ◽  
Luca Restivo ◽  
Alessandro Bologna ◽  
Angela Poletti ◽  
...  

Abstract Methods and results A 60-year-old male patient underwent coronary angiography (CA) for a non-ST segment elevation myocardial infarction (NSTEMI). CA revealed significant multivessel disease. Both internal mammary arteries (AMI) were patent, with right IMA markedly larger than the left IMA. The exam revealed also an abnormal branch arising from the proximal right coronary artery extending backwards, likely to the right lung. Pre-operative chest radiograph demonstrated asymmetry of the two hemithoraces with slight elevation of the right hemidiaphragm, small ipsilateral lung, and mediastinal shift towards the right. The patient underwent urgent CABG surgery. Myocardial revascularization was successfully performed using both AMI and one saphenous vein segment. The postoperative course was complicated by respiratory failure requiring prolonged mechanical ventilation. A chest computed tomography angiography was performed, revealing complete absence of the right pulmonary artery and a left lower lobe segmental pulmonary embolism. Furthermore, blood in the hypoplastic right lung was supplied by multiple collaterals arising from RCA and right IMA. Intravenous heparin was started with clinical improvement. Two weeks later, a lung scintigraphy was performed, ruling out perfusion defects. The patient was discharged home on oral anticoagulation with warfarin. Conclusions Unilateral pulmonary artery agenesis (UPAA) is an uncommon congenital anomaly of the great vessels. Despite the absence of the pulmonary artery, blood supply of ipsilateral lung is provided by systemic collaterals originating from bronchial, intercostal, internal mammary, and sub-diaphragmatic arteries. More rarely, these collaterals may arise from the coronary arteries with different implications, ranging from asymptomatic condition to myocardial ischaemia and infarction. In our case, the condition was previously asymptomatic. The occurrence of pulmonary embolism contributed to worsen the ventilation–perfusion mismatch, explaining the respiratory failure during the postoperative period.

2021 ◽  
Author(s):  
HuiHua Hu ◽  
XiaoCong Wang

Abstract Background: Brain stem infarction and pulmonary embolism are both serious life-threatening diseases with extremely high mortality. Central respiratory failure caused bycerebral stem infarction was considered in the initial stage of the disease. Pulmonary embolism (trunk) may have been the second cause of respiratory failure during diagnosis and treatment. The patient improved obviously after active treatment. Although the patient's condition improved significantly after active treatment, it is worth reflecting that if we had detected the right main pulmonary embolism in a timely manner during the first CTA examination, we could have determined whether the patient could benefit more from thrombolysis of the right main pulmonary artery under interventional therapy. Therefore, in clinical work, we should consider the possible complications ofthe patient while focusing on the most life-threatening primary disease.Case presentation:The patient, a 53-year-old female, she was immediately transferred from the emergency department to the ICU. Physical examination: T 37°C, HR 109/min, R 10/min, BP 105/73 mmHg, SpO 2 79%, GCS score 5, E1V2M2, coma. T CTA examination of the cervical blood vessels and cerebral blood vessels was recommended. 2) CTA examination of the cervical blood vessels and craniocerebral blood vessels performed at 10 o'clock on March 23 suggested moderate and severe stenosis at the beginning of the right vertebral artery, severe stenosis at the middle and upper segments of the basilar artery, and severe stenosis at the beginning of the bilateral posterior cerebral artery. Consideration: high possibility of brainstem infarction. After discussion with the family members, they agreed to submit the patient to percutaneous craniography and thrombectomy. 3) Cerebral artery extraction was performed from 23:50 on March 23 to 01:20 on March 24. Intraoperative diagnosis: 1. Cerebral stem infarction. 2. Upper basilar artery occlusion. Postoperative angiography showed that the basilar artery was unobstructed, and the bilateral superior cerebellar artery and posterior cerebral artery had returned to normal. Tirofiban was given 4 ml/h postoperatively. 4) The CT diagnosis room on March 24 reported the results of the vascular CTA scan from 10 'clock on March 23: A filling defect of the right main pulmonary artery and the left lower pulmonary artery lumen was observed. Pulmonary embolism was considered. Color Doppler ultrasound examination of the heart and lower limb vessels was immediately performed, and the interventional department was consulted. Cardiac ultrasonography suggested that there was no obvious thrombus in the right atrium or right ventricle of the patient. she receive anticoagulant and antiplatelet therapy.Conclusions: Central respiratory failure caused bycerebral stem infarction was considered in the initial stage of the disease. Pulmonary embolism (trunk) may have been the second cause of respiratory failure during diagnosis and treatment. The patient improved obviously after active treatment. Although the patient's condition improved significantly after active treatment, it is worth reflecting that if we had detected the right main pulmonary embolism in a timely manner during the first CTA examination, we could have determined whether the patient could benefit more from thrombolysis of the right main pulmonary artery under interventional therapy. Therefore, in clinical work, we should consider the possible complications ofthe patient while focusing on the most life-threatening primary disease.


2021 ◽  
Vol 20 (1) ◽  
pp. 15-17
Author(s):  
Caroline Apsey ◽  
◽  
Muhammad Jawad ◽  
Martin Daschel ◽  
Daniel Woosey ◽  
...  

We assessed the efficacy of thrombolysis in avoiding long-term complications. Notes of patients thrombolysed for PE in the 2-year period were reviewed. The initial CTPA and echocardiogram results before thrombolysis were compared to the results of follow up imaging repeated after 6 months. Twenty-two patients were thrombolysed for PE. 14 patients had sub-massive PE and 8 patients had massive PE. The right ventricle (RV) was dilated on pre-thrombolysis echocardiogram in 16 patients. On follow up echocardiography all patients with massive PE (6 studies) had a normal RV size, with pulmonary artery pressures (PAP) of 29mmHg. Follow up echocardiography of patients with submassive PE (13 studies) showed 11 patients with a normal RV, with PAP of 28 mmHg.


Author(s):  
Safa Sabur ◽  
Rachid Taoufiq ◽  
Damesane Lamboni ◽  
Hachem Elemine ◽  
Othman Ayouche ◽  
...  

2020 ◽  
Vol 21 (Supplement_1) ◽  
Author(s):  
K Starzyk ◽  
P Dybich ◽  
K Ciuraszkiewicz ◽  
W Rokita ◽  
B Wozakowska-Kaplon

Abstract Pulmonary embolism is one of the leading causes of maternal mortality despite a low incidence of during pregnancy. We present 32-year-old woman, in the 35 week of first pregnancy, admitted to the Intensive Care Unit with dyspnea, tachycardia, cyanosis. Echocardiography confirmed the presence of embolic material in the main trunk of pulmonary artery, spreading to the right pulmonary artery. D-dimer and troponin T level were elevated, BNP remained within the normal range. The risk in PESI scale was assumed as intermediate high. LMWH therapy was initiated, the patient was constantly monitored. Venous thrombotic disease in lower extremities was excluded by ultrasonography. The treatment was carried out under obstetric supervision. The clinical state gradually improved, the patient was hemodynamically stable. Serial echocardiographic testing, revealed gradual regression of changes in the pulmonary trunk. Normalization of troponins and lowering of BNP levels were observed. The pregnancy was terminated in 39 week, by cesarean section (obstetric indications). The LMWH was continued few days after delivery, as the patient started lactation. She decided to terminate lactation in a first week after delivery so the therapy was switched into rivaroxaban for at least 3 months. Echocardiography after 3 month confirmed lack of changes in pulmonary trunk, the risk of pulmonary hypertension was low. Echocardiography can be a method of choice for confirming and monitoring pulmonary embolism during pregnancy, in a situation of high or intermediate clinical risk and good visualization of changes in pulmonary arteries Abstract P701 Figure. Embolism of pulmonary trunk and RPA


2020 ◽  
Vol 21 (Supplement_1) ◽  
Author(s):  
C M Angelescu ◽  
I Hantulie ◽  
Z Galajda ◽  
I Mocanu ◽  
A T Paduraru ◽  
...  

Abstract Introduction Right heart thrombi are rare, found in up to 20% of pulmonary emboli (PE), and associated with significantly increased mortality(1). A thrombus entrapped in a PFO is a rare form of right heart thromboembolism. Clinical Case A 73-year-old male patient who had dyspnea for 10 days, was transferred to our hospital for the surgical treatment of a cardiac tumor. We performed TTE which revealed a free floating, huge mass( measuring more than 8 cm long) in the right atrium, that protruded in the right ventricle, with high risk of embolization. Another smaller mass, attached to the interatrial septum. Severe right ventricular dysfunction and severe pulmonary hypertension were present. Contrast-enhanced computer tomography was performed, which revealed severe bilateral pulmonary artery emboli with complete occlusion of right pulmonary artery branch. Clinical and paraclinical data strongly suggested that the huge cardiac mass was a thrombus that originated from the lower extremity veins. TEE showed that the thrombus was entrapped through the PFO, with a smaller part in the left atrium and the biggest portion in the right atrium. The patient underwent an emergent on-pump surgical cardiac and right pulmonary artery embolectomy. The right atrium was opened and a huge intracardiac thrombus with a lengh of 14 cm extending from the coronary sinus, to PFO in the left atrium and also in the right ventricle was removed. The right branch of the pulmonary artery was opened and a large volume of clot- 9 cm long- was removed. The patient was removed from cardio-pulmonary by-pass (CPB) on high doses of norepinephrine and dobutamine and necessitated initiation of venous-arterial ECMO to support the severe right heart dysfunction. He was extubated after 10 days, with little improvement in the clinical status. Transthoracic echocardiography showed smaller right heart cavities), normal left ventricular function, but persistent severe RV dysfunction and severe pulmonary hypertension. In the thirteenth postoperative day, he installed cardio-respiratory arrest and he died. Discussion In this report we describe a case of a patient with a huge intracardiac thrombus, entrapped through a PFO, associated with massive pulmonary embolism, with late presentation in our hospital and severe refractory right heart dysfunction. He underwent successful embolectomy, which is a unique procedure in the treatment of an acute pulmonary embolism and entrapped thrombus in a PFO. Conclusion The treatment of choice for emboli-in-transit is controversial. In a recent review, surgical thromboembolectomy showed a trend toward improved survival and significantly reduced systemic emboli compared to anticoagulation. Thrombolysis in these patients may cause fragmentation of thrombus and systemic embolization, resulting in increased mortality. Management decisions should be made with multidisciplinary coordination and consideration of complicating factors such as PFO. Abstract P689 Figure. Extensive biatrial thrombus


1977 ◽  
Author(s):  
M.H. Todd ◽  
J.B. Forrest ◽  
J. Hirsh

Embolisation of the pulmonary vasculature with microspheres releases prostaglandin-1ike substances, PGLS (Piper and Vane, N.Y. Acad. Sei. 180: 363, 1971) but the capacity of autologous blood clots (ABC) to release pulmonary vasoactive substances is disputed. Ten normal mongrel dogs were anesthetised with pentobarbitone sodium and instrumented. Pulmonary venous blood was continuously superfused over isolated tissues for bioassay and then returned to the animal. Injection of ABC into the right atrium increased pulmonary artery pressure from 21 ± 6.5 mm Hg to 38 ± 15 mm Hg (mean ± S.D.), increased arterial pCO2 and decreased arterial pO2. No significant changes in heart rate, systemic arterial blood pressure or cardiac output occurred. In three animals contractions of the blood superfused assay tissues occurred following embolism. This effect was produced in normal assay tissues and those pretreated with antagonists of ACh, Serotonin, Histamine and Catecholamines and could therefore be attributed to PGLS. No cardiovascular or assay tissue tension changes were observed when equivalent volumes of saline or clot lysate were injected into the right atrium.Therefore, pulmonary embolism with ABC can release PGLS which may contribute to the pulmonary artery pressure rise. Vasoactive substances may normally be inactivated in the lung but in some animals appear in pulmonary venous blood.(Supported by the Ontario Heart Foundation)


1963 ◽  
Vol 204 (4) ◽  
pp. 619-625 ◽  
Author(s):  
John W. Hyland ◽  
George T. Smith ◽  
Lockhart B. McGuire ◽  
Donald C. Harrison ◽  
Florence W. Haynes ◽  
...  

Pulmonary embolism was produced in 30 closed-chest 8-kg dogs with polystyrene spheres, glass beads, or blood clots of precise graded size. The sizes matched selectively the internal diameter of pulmonary arteries from lobar branches (5–6 mm) down to atrial arteries (0.17 mm). Emboli were injected into the right atrium until the pressure in the pulmonary artery rose 5–10 mm Hg. The number of emboli of a given size required to produce this incipient pulmonary hypertension was compared with the number of vessels of that same size as determined from the literature as well as by postmortem injection with Schlesinger mass. The number of emboli bore a constant relation to the number of vessels of that same size. With each size, the majority of vessels had to be occluded before pulmonary hypertension appeared. This was true even in the absence of anesthesia. The results support the thesis that mechanical blockade rather than vasoconstriction is the mechanism by which pulmonary hypertension is produced by emboli occluding pulmonary arterial (as opposed to arteriolar) vessels.


2019 ◽  
Vol 28 ◽  
pp. 100909
Author(s):  
Jennifer M. Sunny ◽  
Bobak J. Akhavan ◽  
Ala-Eddin S. Sagar ◽  
Pushan P. Jani

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