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The Pulmonary and Bronchial Vessels, Pulmonary Vascular Abnormalities including Embolism, Pulmonary and Bronchial Angiography, and A/V Malformations.
Published in Fred W Wright, Radiology of the Chest and Related Conditions, 2022
These may be found per se, in the Osler-Weber-Rendu syndrome (haemorrhagic telangiectasia - Illus. OSLER WEBER) or in association with hepatic cirrhosis. They are more common in the lower lobes and in females. Sometimes the condition is diffuse and 'fine' but when larger vessels are involved A/V aneurysms are often present. Many A/V aneurysms are seen on chest radiographs and the feeding artery and draining vein may be shown by tomography including CT. 'Fine' lesions may be barely visible even at angiography, but the larger nodular lesions are usually well demonstrated. With multiple lesions, shunting may give rise to haemodynamic problems (e.g. patients being breathless in the upright posture and normal lying down) and polcythaemia (to compensate for unoxygenated blood). Rupture may occur into the pleura or a bronchus, the former because many are subpleural in position. Paradoxical embolism may occur with larger shunts, leading to transient ischaemic attacks, cerebral infarction or brain abscesses. Some patients may develop finger clubbing (see p. 23.1). Some lesions are undoubtedly congenital, but others arise later. Most are found by chance after the second or third decade, and outside pregnancy enlargement during adult life.
Stroke
Published in Henry J. Woodford, Essential Geriatrics, 2022
A patent foramen ovale (PFO) occurs in around 27% of the adult population.118 Essentially, it is a hole between the right and left atria (seeFigure 10.11) and is a normal component of the foetal circulation that usually closes at the time of birth. It is speculated that a PFO could allow a venous embolism to pass from the right to the left side of the heart and cause a stroke (a paradoxical embolism). This may be more likely to occur at times when right atrial pressure is elevated and the pressure gradient with the left atrium is reversed, for example during straining.119 The role of PFO in the genesis of stroke remains controversial.
Stroke and Transient Ischemic Attacks of the Brain and Eye
Published in Philip B. Gorelick, Fernando D. Testai, Graeme J. Hankey, Joanna M. Wardlaw, Hankey's Clinical Neurology, 2020
Paradoxical embolism is the embolism of a thrombus or other embolic particle from the venous circulation to the arterial circulation through a right-to-left shunt. A PFO accounts for up to 95% of paradoxical emboli, pulmonary shunts via a pulmonary arteriovenous malformation for only 5%, and atrial or ventricular septal defects for 1% or less.
Obesity in acute ischaemic stroke patients treated with intravenous thrombolysis therapy
Published in Neurological Research, 2023
Hongmin Li, Suliman Khan, Rabeea Siddique, Qian Bai, Yang Liu, Ruiyi Zhang, Yan Zhang, V. Wee Yong, Mengzhou Xue
Atrial fibrillation and flutter allow blood to stagnate, particularly in the left atrial appendage, which can allow thrombosis and subsequent embolism to the cerebral or systemic circulation. Permanent and paroxysmal atrial fibrillation increases the risk of cardioembolic ischaemic stroke [19]. The prevalence of atrial fibrillation is increasing with the aging and increasingly obese population. In utero, the cardiac foramen ovale allows the flow of placental oxygenated blood from the right to the left atrium. After birth, the increase in pressure on the left side of the heart closes the flap in most people but about 25% of individuals have a degree of residual patency (PFO) [20]. This patency creates a potential mechanism for paradoxical embolism, which could lead to ischaemic stroke. The importance of PFO in young adult stroke has been highlighted by the significant reduction in the risk of recurrent ischaemic stroke after endovascular closure of PFO [20, 21]. Bacterial endocarditis can cause septic emboli in the brain, leading to ischaemic stroke. Also, bacterial endocarditis presents difficulties for stroke treatment as it is associated with an increased risk of haemorrhagic transformation after thrombolysis owing to septic arteritis that weakens vessel walls. Surveillance for mycotic aneurysms (infected aneurysms) should be considered, as they can occur after endocarditis and can rupture, causing subarachnoid haemorrhage or ICH. Regions of segmental hypokinesis within the heart can occur following myocardial infarction, which can predispose to cardioembolic stroke [22].
Commentary: Physical activity after patent foramen ovale (PFO)-associated stroke: a personal narrative and call to action
Published in Topics in Stroke Rehabilitation, 2023
Jeff K. Vallance, I. Hale, G Hansen
Research suggests that 20% of all ischemic strokes are presumed cardioembolic.1 Paradoxical embolism through a patent foramen ovale (PFO) or other shunts in the heart [such as an atrial septal defect (ASD)] may be responsible for 5.5% of all ischemic strokes,2 and PFO may be a more common stroke mechanism than was previously thought.3 A PFO is a small flap-like opening between the right and left atria of the heart. After birth, the space most often closes but remains open in ~25% of people. In young people (<50 years of age), the presence of a PFO is a common risk factor for stroke due to the potential for paradoxical embolism.4 During paradoxical embolism, venous clots pass from the right atrium to the left atrium of the heart through the PFO and migrate to the brain instead of the lungs, where small clots are most likely filtered and reabsorbed. A recent Special Communication in JAMA Neurology recommended the use of the term PFO-associated stroke as a “ … distinct entity of ischemic stroke for all patients presenting with superficial, large deep, or retinal infarcts in the presence of a medium-risk to high-risk PFO and no other identified likely cause” (p. 884).3
Another way to the heart
Published in Acta Cardiologica, 2021
Cátia Oliveira, Carlos Braga, Glória Abreu
PLSVC occurs in 0.3–0.5% of the population and usually drains into the right atrium via the CS. In less common cases, PLSVC drains into the left atrium resulting in partial anomalous systemic venous return [1]. A RSVC is generally present. Echocardiography using agitated saline contrast plays a major role in the PLSVC diagnosis: its injection through the left antecubital vein will result in opacification of the dilated CS and subsequently the right atrium. Though usually it does not require treatment, patients with PLSVC are at higher risk of paradoxical embolism because of the possible presence of additional lesions namely atrial septal defects and direct communication of the vein to the left atrium [2]. Also, it may impair insertion of central venous catheters and pacemakers [2]. In the case of our patient, both a PLSVC and a PFO were diagnosed increasing the probability of paradoxical embolism. He is currently under vigilance and remains asymptomatic.