Embolism, Ischaemia, Infarction and Shock
Jeremy R. Jass in Understanding Pathology, 2020
Most pulmonary emboli produce no clinical symptoms because they are small and the pulmonary reserve is large. Obstruction of a larger branch of a pulmonary artery tends not to produce an area of ischaemic necrosis (infarction). The lung has a dual blood supply: deoxygenated blood via the pulmonary arterial system, and oxygenated blood via the bronchial arteries. The bronchial arterial supply protects pulmonary tissues from ischaemia unless the circulation is compromised by an additional factor such as heart failure. Showers of emboli that become lodged and organised may, if present in sufficient numbers, lead to increased resistance within the pulmonary arterial tree, and so cause pulmonary hypertension. Emboli arising from the deep veins of the leg may only enter the systemic circulation if there is a septal defect in the heart. This is known as paradoxical embolism but is extremely uncommon.
Venous thrombo- embolism: pathology and clinical features
Ken Myers, Paul Hannah, Marcus Cremonese, Lourens Bester, Phil Bekhor, Attilio Cavezzi, Marianne de Maeseneer, Greg Goodman, David Jenkins, Herman Lee, Adrian Lim, David Mitchell, Nick Morrison, Andrew Nicolaides, Hugo Partsch, Tony Penington, Neil Piller, Stefania Roberts, Greg Seeley, Paul Thibault, Steve Yelland in Manual of Venous and Lymphatic Diseases, 2017
A patent foramen ovale (PFO) is present in approximately 30% of the population. Paradoxical embolism occurs if an embolus passes from the right to left atrium through to the arterial circulation, frequently to the brain causing stroke. This would not normally happen unless the right atrial pressure exceeds the left, as during a Valsalva manoeuvre or with pulmonary hypertension. The PFO increases in size with advancing age, from a mean of 3 mm in the first decade to 6 mm in the tenth decade. Paradoxical embolism is usually isolated, but it can be associated with PE if this causes the pulmonary artery pressure to rise increasing the pressure gradient between the atria.
Cerebrovascular Disease
John W. Scadding, Nicholas A. Losseff in Clinical Neurology, 2011
The term ‘paradoxical embolism’ is used when an embolus reaches the brain (or systemic arterial system) from the venous system, either through abnormal arteriovenous shunts in the lungs or via an abnormal communication between the right and the left hand sides of the heart. Congenital anomalies, e.g. atrial septal defects, especially when associated with pulmonary hypertension, are an important cause of paradoxical embolism. Patent foramen ovale also provides a potential route for paradoxical embolism. However, in many cases patent foramen ovale is an innocent finding and only appears to be relevant if associated with an atrial septal aneurysm.
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
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].
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.