Can left atrial mechanics predict anticoagulation in cryptogenic stroke?

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
A Azul Freitas ◽  
J Milner ◽  
J Ferreira ◽  
C Ferreira ◽  
S Martinho ◽  
...  

Abstract Introduction Ischemic stroke is a leading cause of death and disability in the Western world, frequently due to cardioembolism and atherothromboembolism. Cryptogenic strokes occur without a well-defined aetiology after a standard vascular and cardiac evaluation, and secondary prevention may include antiplatelet therapy while awaiting results of long-term cardiac monitoring. In this study, we aimed to identify echocardiographic predictors of paroxysmal atrial fibrillation (AF) latter identified in follow-up of patients with cryptogenic stroke. Methods We retrospectively assessed all patients with cryptogenic stroke admitted in our hospital in the last 2 years. Only patients in normal sinus rhythm with a minimum of 24 hours of cardiac monitoring at admission and 24 hours Holter monitor within 6 months after discharge were included. Echocardiographic measures included left ventricle ejection fraction, left atrium (LA) volume, left and right atrium longitudinal strain, left and right ventricle longitudinal strain, E/A ratio, E/e' ratio, isovolumetric relaxation time (IVRT) and E wave deacceleration time. Echocardiographic data was assessed to determine its accuracy to identify AF. Results The study included 32 patients with a mean age of 72±10 years and a male preponderance (87.5%). AF was identified in 12 (37.5%) patients. This group of patients had a larger indexed LA volume (44.3 vs 29.1 mL/m2, p=0.043), a lower IVRT (87 vs 116 ms, p=0.028), and a lower LA longitudinal strain in contractile (6.7 vs 13.6%, p<0.001) and in reservoir phase (17.1 vs 23.6%, p=0.042). All other variables were not significantly different among groups, including LA longitudinal strain in conduit phase. LA longitudinal strain in contractile phase showed the best predictive power with an area under the ROC curve of 0.925 (95% CI 0.82–1 p=0.001). The cut-off value that best predicted AF was 8.17% with a sensitivity of 1 and specificity of 0.9. Conclusion LA longitudinal strain in contractile phase is a powerful method to identify AF in cryptogenic stroke. When reduced, anticoagulation may be considered in order to prevent recurrence. Further studies are warranted to reproduce these results in larger cohorts. Funding Acknowledgement Type of funding source: None

2021 ◽  
pp. 85-85
Author(s):  
Milovan Stojanovic ◽  
Bojan Ilic ◽  
Marina Deljanin-Ilic ◽  
Stevan Ilic

Introduction: Electrical injury can cause various cardiac dysrhythmias such as asystole, ventricular fibrillation, sinus tachycardia, and heart blocks. However, it rarely causes atrial fibrillation. Case report: Patient S.M, born in Nis in 1973, was admitted to the emergency department after receiving an electric shock (<600 V). He subsequently lost consciousness, fell down, and sustained back and head injuries. During the examination heart rate was irregular but with no heart murmurs. There was an entry wound on the front of the left thigh and an exit wound on the front of the neck. An electrocardiogram showed newly appearing atrial fibrillation. The laboratory tests showed no pathological deviation and focus cardiac ultrasound showed that contractile force was preserved with no wall-motion abnormalities and normal left atrium dimensions. The patient was administered low-molecular-weight heparin subcutaneously and propafenone (600 mg) orally. At follow up after 24 hours, an electrocardiogram showed normal sinus rhythm. Conclusion: We report a rare case of an electrical injury-induced atrial fibrillation, which was converted to sinus rhythm by pocket therapy. Although most cases of an electrical injury-induced AF represent benign conditions which are self-limited, cardiac monitoring as a routine measure should be considered.


1993 ◽  
Vol 27 (7-8) ◽  
pp. 877-880 ◽  
Author(s):  
Kamal Kishore ◽  
Abhinav Raina ◽  
Vijay Misra ◽  
Ernesto Jonas

OBJECTIVE: To report a case of acute toxicity in a patient with chronic verapamil toxicity, possibly precipitated by intravenous administration of the highly protein-bound drugs ceftriaxone and clindamycin. DATA SOURCES: Case reports, review articles, and relevant laboratory and clinical studies identified by MEDLINE (1984-forward), and relevant cross references from those articles. DATA EXTRACTION: Data were abstracted from pertinent sources by one author and reviewed by the remaining authors. CASE SUMMARY: A 59-year-old man who had been receiving sustained-release verapamil 240 mg ql2h for more than two years for hypertension, and phenytoin 300 mg/d for many years for prophylaxis against seizures, was noted to be in junctional rhythm when he presented to the emergency room with bilateral pneumonia. Administration of intravenous ceftriaxone 1 g and clindamycin 900 mg precipitated symptoms of acute verapamil toxicity in this patient. The toxicity led to complete heart block requiring cardiopulmonary resuscitation and insertion of a temporary pacemaker. He spontaneously reverted to normal sinus rhythm after 16 hours. Subsequent cardiac evaluation, including echocardiogram, 48-hour dynamic electrocardiographic recording (Holter), and exercise stress test were normal. The patient has remained in sinus rhythm for more than one year after this episode. CONCLUSIONS: We believe that junctional rhythm on admission was a result of chronic verapamil toxicity. This may have been because of increased bioavailability of the drug or increased sensitivity of the receptors. Administration of ceftriaxone, clindamycin, or both agents might have precipitated acute verapamil toxicity by displacing verapamil from its protein-binding sites. Extreme caution is necessary when a highly protein-bound drug is given to a patient already receiving verapamil.


2020 ◽  
Vol 21 (Supplement_1) ◽  
Author(s):  
L E Sade ◽  
S Keskin ◽  
A Colak ◽  
O Ciftci ◽  
U Can ◽  
...  

Abstract Purpose Detection of atrial fibrillation (AF) after stroke impacts patient management. However, detection of AF is difficult due to its paroxsysmal nature. We sought to test the hypothesis that echocardiographic quantification left atrial (LA) mechanics in patients with stoke can be an imaging biomarker to predict AF. Methods We enrolled prospectively and consecutively 131 patients in normal sinus rhythm with a new diagnosis of ischemic stroke. All patients underwent 48-hour Holter monitorization, transthoracic echocardiography with saline injection in addition to routine work-up of stroke evaluation. Two-dimensional and Doppler studies, together with most up-to-date LA quantification tools were performed including 3-dimensional LA phasic volumes (maxiumum and minimum LA Volume index - LAVImax, LAVImin) and LA strain quantification (average strain from apical 4- and 2-chamber during reservoir (Ss) and contraction (Sa) phases). Patients were followed-up and underwent second 48-hour Holter monitorization 6-12 months later if no etiologic cause was found. Any AF episode lasting &gt;30 seconds was considered significant parosysmal AF. Results In 49 patients, causes other than AF were identified (Noncryptogenic). In 43 patients no discernable cause was found (NoAF Cryptogenic). Paroxysmal AF episodes lasting longer than 30 sec were documented in 27 patients at first 48-hour Holter and in 12 patients during follow-up (9.2 ± 3.1 months) either by second 48-hour Holter monitorization or clinically (AF cryptogenic). LAVImax and LAVImin were significantly increased, Ss and Sa were significantly reduced in patients with AF as compared to No AF and Noncryptogenic groups (Table). LA volumes and strain measures predicted AF development independently of CHA2DS2-VASc score. Better discrimination between No AF and AF groups was obtained after second Holter monitorization that enabled detection of more cases with paroxysmal AF (Figure). Conclusions Our findings underscore the value of echocardiographic assessment of LA function as a marker of AF development and for selection of patients who could benefit from empiric anticoagulation. Noncryptogenic AF cryptogenic No AF cryptogenic 3D LAVI max (ml/m&sup2;) 30.1 ± 9,4 38.1 ± 12.7 28.9 ± 9.2 3D LAVI min (ml/m&sup2;) 13.9 ± 7.5 20.7 ± 10.7 13.4 ± 5.3 3D LA EF (%) 55.5 ± 9.4 50.0 ± 10.5 53.8 ± 10.0 Ss (%) 17.4 ± 8.5 12.7 ± 5.3 17.5 ± 8.5 Sa (%) 12.7 ± 6.3 9.0 ± 5.0 12.8 ± 6.3 CHA2DS2-VASc 4.0 ± 1.6 5.0 ± 1.6 3.9 ± 1.5 Abstract P1797 Figure.


2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
G Rajagopal ◽  
S.R Landman

Abstract Background Cardiac monitoring technologies often utilize monitoring centers or services in which technicians adjudicate arrhythmia episodes. Arrhythmias with a high prevalence of false detections (such as pauses) can slow down the review process while also delaying review of time-sensitive true episodes. Objective To develop algorithms that can stratify device-detected pause episodes into low- and high-priority queues to facilitate monitoring center review. Methods The high priority queue algorithm identifies episodes which are likely to be true pause episodes. The algorithm consists of four conditions, which identify features that were found to be predictive of true pauses, including the number of beats in the episode, the noise status of the last pre-pause beat, and the relative flatness of the ECG signal. Using a similar set of features, a set of criteria was determined that would identify pause-triggered episodes that were highly unlikely to be true pauses. 11,567 pause episodes were used for development with 19,520 separate episodes used for validation. All episodes were adjudicated by a cardiac monitoring center. The validation dataset consisted of 18,280 (93.6%) false pauses and 1240 (6.4%) true pauses. Results The high-priority queue algorithm identified true pause episodes with a sensitivity of 82.3% and specificity of 96.8% in the validation dataset (see table). The low-priority queue algorithm flagged 78.4% of all pause episodes as low-priority in the validation dataset, with only 4 true pause episodes (&lt;0.1%) flagged as low priority. Conclusion The high-priority queue algorithm for device detected pause episodes could potentially identify ∼82% of all true pause notifiable episodes, expediting their review process. The low-priority queue successfully identifies a large percentage (∼80%) of false pause-triggered episodes, which would help to improve monitoring center efficiency as false pause-triggered episodes are a large driver of artifact / normal sinus rhythm episodes. Funding Acknowledgement Type of funding source: Private company. Main funding source(s): Medtronic


Heart Rhythm ◽  
2021 ◽  
Vol 18 (8) ◽  
pp. S62
Author(s):  
Matthew R. Reynolds ◽  
Candace L. Gunnarsson ◽  
Michael P. Ryan ◽  
Sarah Rosemas ◽  
Paul D. Ziegler ◽  
...  

2015 ◽  
Vol 308 (2) ◽  
pp. H126-H134 ◽  
Author(s):  
Erin Harleton ◽  
Alessandra Besana ◽  
Parag Chandra ◽  
Peter Danilo ◽  
Tove S. Rosen ◽  
...  

Atrial fibrillation (AF) is a common arrhythmia with significant morbidities and only partially adequate therapeutic options. AF is associated with atrial remodeling processes, including changes in the expression and function of ion channels and signaling pathways. TWIK protein-related acid-sensitive K+ channel (TASK)-1, a two-pore domain K+ channel, has been shown to contribute to action potential repolarization as well as to the maintenance of resting membrane potential in isolated myocytes, and TASK-1 inhibition has been associated with the induction of perioperative AF. However, the role of TASK-1 in chronic AF is unknown. The present study investigated the function, expression, and phosphorylation of TASK-1 in chronic AF in atrial tissue from chronically paced canines and in human subjects. TASK-1 current was present in atrial myocytes isolated from human and canine hearts in normal sinus rhythm but was absent in myocytes from humans with AF and in canines after the induction of AF by chronic tachypacing. The addition of phosphatase to the patch pipette rescued TASK-1 current from myocytes isolated from AF hearts, indicating that the change in current is phosphorylation dependent. Western blot analysis showed that total TASK-1 protein levels either did not change or increased slightly in AF, despite the absence of current. In studies of perioperative AF, we have shown that phosphorylation of TASK-1 at Thr383 inhibits the channel. However, phosphorylation at this site was unchanged in atrial tissue from humans with AF or in canines with chronic pacing-induced AF. We conclude that phosphorylation-dependent inhibition of TASK-1 is associated with AF, but the phosphorylation site responsible for this inhibition remains to be identified.


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