Search

Background: Atrial cardiopathy is a proposed mechanism of embolic stroke of undetermined source (ESUS). Left atrial (LA) strain may identify early atrial cardiopathy prior to structural changes. We aim to study the associations between LA strain, ESUS, and atrial fibrillation (AF) detection in ESUS. Methods: The study population included patients with ESUS and noncardioembolic (NCE) stroke presenting to the Rhode Island Hospital Stroke Center between January 2016 and June 2017 who underwent transthoracic echocardiography. Speckle tracking echocardiography (STE) was used to measure the three phases of LA strain (reservoir, conduit, and contractile). Binary logistic regression analysis was performed to determine the associations between LA strain and stroke subtype (ESUS vs. NCE) as well as follow‐up detection of AF in ESUS patients. Results: We identified 656 patients, 307 with ESUS and 349 with NCE. In binary logistic regression, the lowest tertiles of LA reservoir (adjusted OR 1.944, 95% CI 1.266–2.986, p =.002), contractile (aOR 1.568, 95% CI 1.035–2.374, p =.034), and conduit strain (aOR 2.288, 95% CI 1.448–3.613, p =.001) were more likely to be significantly associated with ESUS compared to NCE stroke. Among all ESUS patients, the lowest tertiles of LA reservoir strain (OR 2.534, 95% CI 1.029–6.236, p =.043), contractile strain (OR 2.828, 95% CI 1.158–6.903, p =.022), and conduit strain (OR 2.614, 95% CI 1.003–6.815, p =.049) were significantly associated with subsequent detection of AF. Conclusion: Reduced LA strain is associated with ESUS occurrence and AF detection in ESUS patients. Therefore, quantification of LA strain in ESUS patients may improve risk stratification and guide secondary prevention strategies. [ABSTRACT FROM AUTHOR]

Objective: Anticoagulation therapy is commonly interrupted in patients with atrial fibrillation (AF) for elective procedures. However, the risk factors of acute ischemic stroke (AIS) during the periprocedural period remain uncertain. We performed a nationwide analysis to evaluate AIS risk factors in patients with AF undergoing elective surgical procedures. Methods: Using the Nationwide Readmission Database, we included electively admitted adult patients with AF and procedural Diagnosis‐Related Group codes from 2016 to 2019. Diagnoses were identified based on International Classification of Disease, 9th revision‐Clinical Modification (ICD‐10 CM) codes. We constructed a logistic regression model to identify risk factors and developed a new scoring system incorporating CHA2DS2VASc to estimate periprocedural AIS risk. Results: Of the 1,045,293 patients with AF admitted for an elective procedure, the mean age was 71.5 years, 39.2% were women, and 0.70% had a perioperative AIS during the index admission or within 30 days of discharge. Active cancer (adjusted OR [aOR] = 1.58, 95% confidence interval [CI] = 1.42–1.76), renal failure (aOR = 1.14, 95% CI = 1.04–1.24), neurological surgery (aOR = 4.51, 95% CI = 3.84–5.30), cardiovascular surgery (aOR = 2.74, 95% CI = 2.52–2.97), and higher CHA2DS2VASc scores (aOR 1.25 per point, 95% CI 1.22–1.29) were significant risk factors for periprocedural AIS. The new scoring system (area under the receiver operating characteristic curve [AUC] = 0.68, 95% CI = 0.67 to 0.79) incorporating surgical type and cancer outperformed CHA2DS2VASc (AUC = 0.60, 95% CI = 0.60 to 0.61). Interpretation: In patients with AF, periprocedural AIS risk increases with the CHA2DS2VASc score, active cancer, and cardiovascular or neurological surgeries. Studies are needed to devise better strategies to mitigate perioperative AIS risk in these patients. ANN NEUROL 2023;94:321–329 [ABSTRACT FROM AUTHOR]

Hypoxia elevates splanchnic sympathetic nerve activity (SNA) with differential effects during inspiration and expiration by unresolved central mechanisms. We examined the hypothesis that cardiovascular-related neurones in the caudal ventrolateral medulla (CVLM) contribute to the complex sympathetic response to hypoxia. In chloralose-anaesthetized, ventilated, vagotomized rats, acute hypoxia (10% O2, 60 s) evoked an increase in SNA (103 ± 12%) that was characterized by a decrease in activity during early inspiration followed by a prominent rise during expiration. Some recorded baro-activated CVLM neurones ( n= 13) were activated by hypoxia, and most of these neurones displayed peak activity during inspiration that was enhanced during hypoxia. In contrast, other baro-activated CVLM neurones were inhibited during hypoxia ( n= 6), and most of these neurones showed peak activity during expiration prior to the onset of hypoxia. Microinjection of the glutamate antagonist kynurenate into the CVLM eliminated the respiratory-related fluctuations in SNA during hypoxia and exaggerated the magnitude of the sympathetic response. In contrast, microinjection of a GABAA antagonist (bicuculline or gabazine) into the CVLM dramatically attenuated the sympathetic response to hypoxia. These data suggest the response to hypoxia in baro-activated CVLM neurones is related to their basal pattern of respiratory-related activity, and changes in the activity of these neurones is consistent with a contribution to the respiratory-related sympathetic responses to hypoxia. Furthermore, both glutamate and GABA in the CVLM contribute to the complex sympathetic response to acute hypoxia. [ABSTRACT FROM AUTHOR]

The sympathetic nerves that maintain blood pressure are modulated by the central respiratory generator. Neurones in the rostral ventrolateral medulla (RVLM) that drive this sympathetic nerve activity (SNA) also display central respiratory drive (CRD)-related activity, suggesting integration of respiratory and cardiovascular regulatory systems within the brainstem. Whether CRD-related activity in the RVLM is due to direct inputs from central respiratory neurones or modulation of cardiovascular-related neurones that influence the RVLM is not known. The caudal ventrolateral medulla (CVLM) contains GABAergic neurones that tonically inhibit presympathetic RVLM neurones and are essential for the production of numerous cardiovascular reflexes. The present study sought to determine whether cardiovascular-related GABAergic neurones in the CVLM display CRD-related activity. The firing patterns of individual barosensitive CVLM neurones were examined in relation to phrenic nerve activity in chloralose-anaesthetized, ventilated, neuromuscularly blocked, vagotomized rats. Histograms of phrenic-triggered CVLM neuronal activity showed that all baro-activated CVLM neurones displayed one of four patterns of CRD-related activity: (i) inspiratory peak ( n= 15), (ii) inspiratory depression ( n= 15), (iii) inspiratory peak with postinspiratory depression ( n= 10), and (iv) postinspiratory peak ( n= 9). A subset of each type of CVLM neurone was identified as GABAergic by individually filling the recorded neurone with biotinamide and observing expression of GAD67 mRNA by in situ hybridization ( n= 10). These data suggest that the activity of GABAergic neurones in the CVLM is regulated by cardiovascular and respiratory inputs, and baro-activated GABAergic CVLM neurones may contribute to CRD-related modulation of presympathetic RVLM neurones and SNA. [ABSTRACT FROM AUTHOR]

Hypoxia elevates splanchnic sympathetic nerve activity (SNA) with differential effects during inspiration and expiration by unresolved central mechanisms. Pre-sympathetic neurons in the rostral ventrolateral medulla (RVLM), which are necessary for the sympatho-excitatory response to hypoxia, are activated by hypoxia with oscillations entrained to the respiratory cycle. GABAergic baro-activated neurons in the caudal ventrolateral medulla (CVLM) provide the major tonic inhibition to RVLM neurons and have patterns of activity related to central respiratory drive. We examined the hypothesis that CVLM neurons are influenced by hypoxia and that the nature of their response may coincide with their pattern of respiratory modulation. We recorded from 18 baroactivated CVLM neurons with respiratory-related activity in choralose-anesthetised, vagotomized, paralyzed rats. Most CVLM neurons (13/18) were activated by hypoxia induced by inhalation of 10% O2, but others (5/18) were inhibited or silenced. The response to hypoxia was related to the pattern of central respiratory-related activity (P <0.05, Chi-square). Most (11/13) hypoxia-activated CVLM neurons had inspiratory-related activity. In contrast, most (4/5) hypoxia-inhibited neurons had expiratory-related activity. These data provide the first evidence that the CVLM may contribute to the complex sympathetic responses to hypoxia. [ABSTRACT FROM AUTHOR]