scholarly journals The Presence of a Large Chiari Network in a Patient with Atrial Fibrillation and Stroke

2016 ◽  
Vol 2016 ◽  
pp. 1-3
Author(s):  
Nneka Schwimmer-Okike ◽  
Johannes Niebuhr ◽  
Grit Gesine Ruth Schramek ◽  
Stefan Frantz ◽  
Heike Kielstein

The Chiari network is an embryological remnant found in the right atrium, mostly without any significant pathophysiological consequences. However, several cardiac associations are reported in the literature including supraventricular tachyarrhythmias. We present a case of a 96-year-old body donor with a stroke episode and intermittent atrial fibrillations. The dissection of the heart revealed the presence of an immense Chiari network with a large central thrombus. The role of a Chiari network in the pathogenesis of stroke and pulmonary embolism is discussed.

2019 ◽  
Vol 47 (8) ◽  
pp. 470-476 ◽  
Author(s):  
Uğur Aksu ◽  
Kamuran Kalkan ◽  
Oktay Gulcu ◽  
Emrah Aksakal ◽  
Mustafa Öztürk ◽  
...  

2020 ◽  
Vol 46 (08) ◽  
pp. 895-907
Author(s):  
Nina D. Anfinogenova ◽  
Oksana Y. Vasiltseva ◽  
Alexander V. Vrublevsky ◽  
Irina N. Vorozhtsova ◽  
Sergey V. Popov ◽  
...  

AbstractPrompt diagnosis of pulmonary embolism (PE) remains challenging, which often results in a delayed or inappropriate treatment of this life-threatening condition. Mobile thrombus in the right cardiac chambers is a neglected cause of PE. It poses an immediate risk to life and is associated with an unfavorable outcome and high mortality. Thrombus residing in the right atrial appendage (RAA) is an underestimated cause of PE, especially in patients with atrial fibrillation. This article reviews achievements and challenges of detection and management of the right atrial thrombus with emphasis on RAA thrombus. The capabilities of transthoracic and transesophageal echocardiography and advantages of three-dimensional and two-dimensional echocardiography are reviewed. Strengths of cardiac magnetic resonance imaging (CMR), computed tomography, and cardiac ventriculography are summarized. We suggest that a targeted search for RAA thrombus is necessary in high-risk patients with PE and atrial fibrillation using transesophageal echocardiography and/or CMR when available independently on the duration of the disease. High-risk patients may also benefit from transthoracic echocardiography with right parasternal approach. The examination of high-risk patients should involve compression ultrasonography of lower extremity veins along with the above-mentioned technologies. Algorithms for RAA thrombus risk assessment and protocols aimed at identification of patients with RAA thrombosis, who will potentially benefit from treatment, are warranted. The development of treatment protocols specific for the diverse populations of patients with right cardiac thrombosis is important.


2019 ◽  
Vol 9 (1) ◽  
pp. 36
Author(s):  
Laurence Jesel ◽  
Malak Abbas ◽  
Sin-Hee Park ◽  
Kensuke Matsushita ◽  
Michel Kindo ◽  
...  

Background: Whilst the link between aging and thrombogenicity in atrial fibrillation (AF) is well established, the cellular underlying mechanisms are unknown. In AF, the role of senescence in tissue remodeling and prothrombotic state remains unclear. Aims: We investigated the link between AF and senescence by comparing the expression of senescence markers (p53 and p16), with prothrombotic and inflammatory proteins in right atrial appendages from patients in AF and sinus rhythm (SR). Methods: The right atrial appendages of 147 patients undergoing open-heart surgery were harvested. Twenty-one non-valvular AF patients, including paroxysmal (PAF) or permanent AF (PmAF), were matched with 21 SR patients according to CHA2DS2-VASc score and treatment. Protein expression was assessed by tissue lysates Western blot analysis. Results: The expression of p53, p16, and tissue factor (TF) was significantly increased in AF compared to SR (0.91 ± 0.31 vs. 0.58 ± 0.31, p = 0.001; 0.76 ± 0.32 vs. 0.35 ± 0.18, p = 0.0001; 0.88 ± 0.32 vs. 0.68 ± 0.29, p = 0.045, respectively). Expression of endothelial NO synthase (eNOS) was lower in AF (0.25 ± 0.15 vs. 0.35 ± 0.12, p = 0.023). There was a stepwise increase of p53, p16, TF, matrix metalloproteinase-9, and an eNOS progressive decrease between SR, PAF, and PmAF. AF was the only predictive factor of p53 and p16 elevation in multivariate analysis. Conclusions: The study brought new evidence indicating that AF progression is strongly related to human atrial senescence burden and points at a link between senescence, thrombogenicity, endothelial dysfunction and atrial remodeling.


2020 ◽  
Vol 21 (Supplement_1) ◽  
Author(s):  
S M Binno ◽  
L Moderato ◽  
G Pastorini ◽  
B Matrone ◽  
D Aschieri ◽  
...  

Abstract We report a case of a 83-year-old female, who had an admission for dyspnea. Laboratory showed D-dimer 1000 ng/ml, haemoglobin 12.4 mg/dL, CPR 0.08mg/dl whereas on Arterial Blood Gas test she had hypoxia with respiratory alkalosis. In view of suspected pulmonary embolism, she underwent Thoracic Computed Tomography scan that excluded it. During the stay the patient seemed more symptomatic while in standing position(with SpO2s 89% while supine plunging to 50% while standing): ABGs were performed both standing (reservoir 15 l/min pH 7.50, pO2 37.2 mmHg, pCO2 37.1 mmHg, HCO3 28.9 mmol/l) and recumbent position (reservoir 15 l/min pH 7.47, pO2 65.5 mmHg, pCO2 35.1 mmHg, HCO3 25.6 mmol), showing a difference of 28 mmHg. Subsequently the patient underwent v/p pulmonary scintigraphy: no signs of pulmonary embolism though it revealed a multiple focus of capitation Tc-99m macro aggregated albumin in brain, thyroid and kidneys (IMG top), compatible for veno-arterial shunt. Trans-esophageal echocardiography (TOE) revealed a massive stretched patent foramen ovale (PFO) with continuous right-to-left shunting through the atria. The bubble test (IMG bottom) confirmed the presence of patency along with sudden passage of microbubbles through the foramen. Qp/Qs = 0.8, due to volume overload in the left atrium from the right atrium. The imaging along with clinical scenario confirmed the suspected diagnosis of platypnea-orthodeoxia, finding the patent foramen ovale as the anatomical cause. Platypnea-orthodeoxia syndrome is a clinical condition characterized by dyspnea. Typically blood oxygen saturation declines with standing position while it resolves with recumbent. The classification entails 3 groups: intracardiac shunting (most common presentation), pulmonary shunting, ventilation-perfusion mismatch. Presence of multiple focus of albumin macroaggregates outside the lungs in v/p scintigraphy examination is suggestive for veno-arteriuous shunt: without shunt, normally all the albumin aggregates are hampered in the lungs’ field. Images in bottom are taken in sequence from a single acquisition during the TOE, in one single cardiac beat. Here is depicted the evidence of the PFO, the influx of bubbles in the right atrium and the instantaneous and massive shunt of the bubbles across the interatrial septum, in the left atrium. Usually the diagnosis is performed within 55 years old: it is interesting how late the diagnosis occurred in this patient with such resounding clinical manifestation. Top Scintigraphy with ventilation and perfusion lung scan sequences. Next, scintigraphy with capitation of Tc-99m macro aggregated albumin in brain, thyroid and kidneys. Bottom, Transesophageal echocardiogram: images taken within the same heart beat proving right-to-left passage of bubble across the septum. Abstract P1317 Figure. Scintigraphy and Transesophageal echo


2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
N I Bork ◽  
N G Pavlidou ◽  
B Reiter ◽  
H Reichenspurner ◽  
T Christ ◽  
...  

Abstract Background Atrial fibrillation (AF) is accompanied by a profound remodeling of membrane receptors and alterations in cyclic nucleotides-dependent regulation of Ca2+-handling. Thus, while basal ryanodine receptors activity is upregulated, L-type calcium current (ICa,L) density is diminish in AF, due to local microdomain-specific cAMP dynamics. The same seems true for cGMP regulation in AF. In AF cGMP-mediated increase in ICa,L is blunted but NO-mediated attenuation of β-adrenoceptors stimulation-mediated increase is preserved. However, although the role of cGMP in controling atrial function and pathophysiology is controversial, no study has been ever performed in human myocytes to measure cGMP directly. Methods We isolated myocytes from the right and/or left atrium of 27 patients in sinus rhythm (SR), and with AF. Cells were then transfected with adenovirus to express the cytosolic FRET-based cGMP sensor red-cGES-DE5 and cultured for 48 hours. Förster resonance energy transfer (FRET) was used to measure cGMP in 61 living human atrial myocytes. We stimulated cells with the C-type natriuretic peptide CNP (100 nM and 1 μM), and the non-selective phosphodiesterases (PDEs) inhibitor IBMX (100 μM). Additionally, PDE specific inhibitors for PDE2 (Bay 60–7550, 100 nM) and PDE3 (Cilostamide, 10 μM) as well as inhibitor of the soluble guanylyl cyclase (ODQ, 50 μM) were used. We also measured PDE2 and PDE3 mRNA levels in atrial tissue samples from both groups of patients using RT-qPCR. Results We could show that stimulation with CNP increased cGMP levels in human atrial myocytes. However, in myocytes from patients with AF global cGMP responses to CNP and to IBMX was reduced compared to SR. Additionally, there was a difference in response to CNP and IBMX in patients with AF between the right and the left atria. Whereas in the right atria IBMX could further increase cGMP levels in the cell, in the left atria leaded to a reduction in cGMP levels. RT-qPCR showed a tendency of PDE3 to be reduced in AF. On the other hand, PDE2A gene expression was upregulated in the left atria. Conclusions We have shown that PDEs contributes cGMP signaling in the human atria and that they are involved in atrial pathophysiology. Now our data clearly show differences in cGMP regulation in cardiomyocytes isolated from left and right atrium from patients in atrial fibrillation and sinus rhythm. We observe a major role of PDEs, regulating cGMP pathway promoted by the reduced responses in AF, especially PDE2 in the left atria.


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


1987 ◽  
Vol 253 (4) ◽  
pp. H863-H868 ◽  
Author(s):  
D. E. Euler ◽  
P. J. Scanlon

This study was designed to evaluate the importance of local release of autonomic neuromediators when electrical stimuli are applied to the right atrium to measure the atrial fibrillation threshold (AFT). Experiments were performed in 16 open-chest dogs anesthetized with alpha-chloralose. The dogs were denervated by bilateral transection of the stellates and cervical vagi. The AFT was determined in 11 dogs by delivering either a train of stimuli (14 pulses, 4 ms, 100 Hz) or a single stimulus (10 ms) to the right atrium during its vulnerable period. In eight dogs, beta-adrenergic blockade with timolol (0.1 mg/kg) had no effect on the AFT determined with either method. Atropine (0.2 mg/kg), given after timolol, significantly increased the train-of-pulses AFT from 4.7 +/- 0.4 to 32.3 +/- 4.6 mA (P less than 0.001). The single-pulse AFT increased from 16.5 +/- 1.5 to 17.8 +/- 1.5 mA (P less than 0.05). Atropine had a similar effect on the AFT when it was given in the absence of timolol (n = 3). In five additional dogs, a monophasic action potential was recorded while a 10-mA train was delivered to the atrium during its absolute refractory period. There was marked shortening of the monophasic action potential duration (55 +/- 6 ms) in the first beat after the train. The shortening was totally abolished by atropine (0.2 mg/kg). The results suggest that a train of stimuli liberates local stores of acetylcholine, which cause a shortening of atrial repolarization time and a profound decrease in the current necessary to evoke fibrillation.


1981 ◽  
Vol 241 (3) ◽  
pp. R163-R166
Author(s):  
R. F. Munzner ◽  
D. G. Ward ◽  
D. S. Gann

To examine the role of right atrial receptors in mediating reflex vascular responses we measured, in cats anesthetized with chloralose/urethan, changes in mean arterial pressure (MAP) in response to volume pulsation of the right atrium (+/- 1 ml, 1 Hz). Changes in MAP were measured 1) with pressure in the carotid arteries normal and vagus nerves intact: right atrial pulsation led to a very small and transient fall in MAP; 2) with pressure in the carotid arteries at 75 mmHg and the vagus nerves intact: right atrial pulsation led to a larger and sustained fall in MAP; 3) with pressure in the carotid arteries at 75 mmHg and the vagus nerves cooled or sectioned bilaterally: right atrial pulsation of the right atrium led only to a very small and transient fall in MAP. These data suggest strongly that signals from right atrial receptors traveling in the vagus nerves mediate a reflex change in MAP that is normally masked by signals from carotid receptors.


Sign in / Sign up

Export Citation Format

Share Document