Stroke in atrial fibrillation and improving the identification of ‘high‐risk’ patients: the crossroads of immunity and thrombosis

Shantsila, Eduard; Lip, Gregory Y.H.

doi:10.1111/jth.13121

Cited by 13 publications

(9 citation statements)

References 21 publications

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“…However, the release of inflammatory cytokines from neutrophils can induce apoptosis of lymphocytes, which suggests that the N/L may not only reflect the number of neutrophils and lymphocytes, but also reflect the over-activation of neutrophils, which increases the disparity in number between these two types of white blood cells. This emphasizes the utility of the N/L [24]. We found that the model containing the N/L was more predictive than the other models.…”

Section: Agingsupporting

confidence: 55%

A high neutrophil-to-lymphocyte ratio predicts hemorrhagic transformation of large atherosclerotic infarction in patients with acute ischemic stroke

Zhang

Zeng

Wang³

et al. 2020

Aging

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Increasing evidence suggests that inflammation is associated with the development of acute ischemic stroke (AIS). The neutrophil-to-lymphocyte ratio (N/L) is an important marker of inflammation and is highly correlated with mortality in stroke patients in recent studies. The N/L of patients who experience hemorrhagic transformation (HT) after AIS is know, but any relationship between N/L and large artery atherosclerosis (LAA) remains unclear, this is our present topic. We enrolled 185 patients with LAA-type HT in the development cohort from a prospective, consecutive, hospital-based stroke registry to this end. We matched these patients to 213 LAA patients who did not develop HT as controls. The incidence of HT after LAA was significantly greater (P<0.01) in patients with higher N/L. We developed a predictive nomogram (incorporating age, systolic blood pressure, the National Institutes of Health Stroke Scale, and the N/L) for LAA patients. The predictive power was good (area under the curve, AUC: 0.832, 95%CI: 0.791-0.872). Our findings were further validated in a validation cohort of 202 patients with AIS attributable to LAA (AUC:0.836, 95%CI:0.781-0.891). In summary, a high N/L is associated with an increased risk for HT after LAA.

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Section: Agingsupporting

confidence: 55%

A high neutrophil-to-lymphocyte ratio predicts hemorrhagic transformation of large atherosclerotic infarction in patients with acute ischemic stroke

Zhang

Zeng

Wang³

et al. 2020

Aging

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“…In this sense, the NLR is superior to only the neutrophil count or lymphocyte count for distinguishing the occurrence of HT, and this may also explain why the AUC for the NLR appeared to be greater than those for neutrophil and lymphocyte counts at each corresponding time point (Additional file 1: Table S4). On the other hand, inflammatory cytokines released by neutrophils may trigger lymphocyte apoptosis [34]. This suggests that the NLR may not simply reflect the neutrophil and lymphocyte counts but also overactivation of neutrophils, thus leading to a wider gap between the two leukocyte types, and this also supports the superiority of the NLR.…”

Section: Discussionmentioning

confidence: 99%

Dynamic change of neutrophil to lymphocyte ratio and hemorrhagic transformation after thrombolysis in stroke

Guo

Xiao

et al. 2016

J Neuroinflammation

114

107

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BackgroundThe neutrophil to lymphocyte ratio (NLR) has been shown to predict short- and long-term outcomes in ischemic stroke patients. We sought to explore the temporal profile of the plasma NLR in stroke patients treated with intravenous thrombolysis (IVT) and its relationship with intracranial bleeding complications after thrombolysis.MethodsA total of 189 ischemic stroke patients were prospectively enrolled. Blood samples for leukocyte, neutrophil, and lymphocyte counts were obtained at admission and at 3–6, 12–18, and 36–48 h after IVT. Head CT was performed on admission and repeated after 36–48 h, and a CT scan was done immediately in case of clinical worsening. Hemorrhagic events were categorized as symptomatic intracranial hemorrhage (sICH) and parenchymal hematomas (PH) according to previously published criteria.ResultsAn increasing trend in the NLR was observed after stroke, and the NLR was higher in patients who developed PH or sICH at 3–6, 12–18, and 36–48 h after IVT (P < 0.01) than in those without PH or sICH. The optimal cutoff value for the serum NLR as an indicator for auxiliary diagnosis of PH and sICH was 10.59 at 12–18 h. Furthermore, the NLR obtained at 12–18-h post-treatment was independently associated with PH (adjusted odds ratio [OR] 1.14) and sICH (adjusted OR 1.14). In addition, patients with a NLR ≥10.59 had an 8.50-fold greater risk for PH (95 % confidence interval [CI] 2.69–26.89) and a 7.93-fold greater risk for sICH (95 % CI 2.25–27.99) than patients with a NLR <10.59.ConclusionsNLR is a dynamic variable, and its variation is associated with HT after thrombolysis in stroke patients.Electronic supplementary materialThe online version of this article (doi:10.1186/s12974-016-0680-x) contains supplementary material, which is available to authorized users.

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“…Furthermore, compared with other subtypes of ischemic stroke, patients with cardioembolic ischemic stroke have significantly higher plasma levels of tumour necrosis factor-alpha (TNF-α), IL-1β and IL-6 [ 19 ]. Interestingly, all these inflammatory markers have also been implicated in the genesis of atrial fibrillation [ 20 ] and have been shown to be related to autonomic imbalance [ 21 ]. In fact, elevated levels of IL-6 and C-reactive protein have been associated with decreased heart rate variability, a marker of autonomic dysfunction [ 21 – 23 ].…”

Section: Pathophysiology Of Neurogenic Atrial Fibrillation Detected Amentioning

confidence: 99%

“…In fact, elevated levels of IL-6 and C-reactive protein have been associated with decreased heart rate variability, a marker of autonomic dysfunction [ 21 – 23 ]. A prolonged inflammatory response can result in atrial remodeling and atrial fibrillation perpetuation through re-entry circuits, further contributing to the prothrombotic state of atrial fibrillation [ 1 , 20 ].…”

Section: Pathophysiology Of Neurogenic Atrial Fibrillation Detected Amentioning

confidence: 99%

“…echocardiographic evidence of left atrial enlargement, left atrial function, impaired systolic function, left ventricular hypertrophy, mitral valve disease and epicardial fat) [ 6 , 44 – 47 , 52 , 62 – 65 , 68 , 69 , 73 ▪ ]; history of congestive heart failure [ 67 ] and coronary artery disease [ 57 , 68 ]; duration of stroke symptoms [ 57 ]; stroke severity [ 62 , 63 , 67 ]; prior cortical [ 50 , 65 ], anterior circulation [ 54 ], and posterior circulation [ 50 ] infarctions; white matter lesions [ 52 ], haemorrhagic transformation [ 45 , 65 ], susceptibility sign [ 65 ] and multiple infarcts [ 45 ] on brain MRI; and free fatty acid and triglyceride levels [ 65 ]. In patients with acute atrial fibrillation, there is depletion of lymphocytes, possibly due to excessive apoptosis mediated by inflammatory responses and decreased survival modulated by catecholamines [ 20 ]. As such, an increased neutrophil to lymphocyte ratio seems to predict incident and postprocedural atrial fibrillation; however, it has never been investigated as a marker of AFDAS to the best of our knowledge [ 74 ].…”

Section: Markers Of Atrial Fibrillation Detected After Stroke and Tramentioning

confidence: 99%

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The complexity of atrial fibrillation newly diagnosed after ischemic stroke and transient ischemic attack: advances and uncertainties

Cerasuolo¹,

Cipriano²,

Sposato

2017

Current Opinion in Neurology

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Purpose of reviewAtrial fibrillation is being increasingly diagnosed after ischemic stroke and transient ischemic attack (TIA). Patient characteristics, frequency and duration of paroxysms, and the risk of recurrent ischemic stroke associated with atrial fibrillation detected after stroke and TIA (AFDAS) may differ from atrial fibrillation already known before stroke occurrence. We aim to summarize major recent advances in the field, in the context of prior evidence, and to identify areas of uncertainty to be addressed in future research.Recent findingsHalf of all atrial fibrillations in ischemic stroke and TIA patients are AFDAS, and most of them are asymptomatic. Over 50% of AFDAS paroxysms last less than 30 s. The rapid initiation of cardiac monitoring and its duration are crucial for its timely and effective detection. AFDAS comprises a heterogeneous mix of atrial fibrillation, possibly including cardiogenic and neurogenic types, and a mix of both. Over 25 single markers and at least 10 scores have been proposed as predictors of AFDAS. However, there are considerable inconsistencies across studies. The role of AFDAS burden and its associated risk of stroke recurrence have not yet been investigated.SummaryAFDAS may differ from atrial fibrillation known before stroke in several clinical dimensions, which are important for optimal patient care strategies. Many questions remain unanswered. Neurogenic and cardiogenic AFDAS need to be characterized, as it may be possible to avoid some neurogenic cases by initiating timely preventive treatments. AFDAS burden may differ in ischemic stroke and TIA patients, with distinctive diagnostic and treatment implications. The prognosis of AFDAS and its risk of recurrent stroke are still unknown; therefore, it is uncertain whether AFDAS patients should be treated with oral anticoagulants.

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Stroke in atrial fibrillation and improving the identification of ‘high‐risk’ patients: the crossroads of immunity and thrombosis

Cited by 13 publications

References 21 publications

A high neutrophil-to-lymphocyte ratio predicts hemorrhagic transformation of large atherosclerotic infarction in patients with acute ischemic stroke

A high neutrophil-to-lymphocyte ratio predicts hemorrhagic transformation of large atherosclerotic infarction in patients with acute ischemic stroke

Dynamic change of neutrophil to lymphocyte ratio and hemorrhagic transformation after thrombolysis in stroke

The complexity of atrial fibrillation newly diagnosed after ischemic stroke and transient ischemic attack: advances and uncertainties

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