Key result
Atrial cardiopathy linked to ~610% higher risk of early neurological deterioration after endovascular stroke treatment.
Why the study?
Thromboembolism is a possible consequence of underlying atrial cardiopathy that can occur before atrial fibrillation onset, motivating examination of atrial cardiopathy biomarkers and acute ischemic stroke outcomes after endovascular treatment.
Does the presence of atrial cardiopathy increase the risk of poor outcomes in patients with acute ischemic stroke undergoing endovascular treatment?
Cohort (n=87)
Does the presence of atrial cardiopathy increase the risk of poor outcomes in patients with acute ischemic stroke undergoing endovascular treatment?
Absolute Event Rate: 41.4% vs 32.8%
Biomarkers of atrial cardiopathy, such as elevated PTFV1 and NT-proBNP, are strongly associated with early neurological deterioration in patients with acute ischemic stroke following endovascular treatment.
May warrant closer post-EVT monitoring for deterioration; leaves open whether atrial cardiopathy should guide trials or care.
Thromboembolism is a possible consequence of underlying atrial cardiopathy, which can occur even before the onset of atrial fibrillation. Our objective was to examine the association between biomarkers of atrial cardiopathy and outcomes of acute ischemic stroke (AIS) following endovascular treatment (EVT). We conducted a retrospective study that collected data from patients with AIS who underwent EVT and compared the outcomes between those with and without atrial cardiopathy. Neurological function was assessed using the modified Rankin Scale (mRS), with an mRS score >2 indicating poor function at day 90. Additionally, we evaluated secondary consequences, including symptomatic intracerebral hemorrhage (sICH), early neurological deterioration (END), and malignant cerebral edema (MCE). Our study included 87 patients (77.6 % male; mean age 60.93 ± 12.47 years). Among these patients, 29 (33.3 %) had atrial cardiopathy, while the remaining 58 (66.7 %) did not. In the atrial cardiopathy group, 12 patients (41.4 %) had poor functional outcomes (mRS>2), compared to 19 (32.8 %) in the non-atrial cardiopathy group. We observed sICH in 22 (25.3 %) patients, END in 14 (16.1 %) patients, MCE in 11 (12.6 %) patients, and two (2.3 %) patients who died in the hospital. We found that patients with PTFV1>5000 μV/ms (OR: 8.39, 95 % CI: 1.43-105.95, P = 0.02) and NT-proBNP>250 pg/mL (OR: 5.09, 95 % CI: 1.20-27.63, P = 0.03) had significantly higher risk of END. After adjusting for covariates in the Firth logistic regression, we further found that atrial cardiopathy was significantly associated with END, as revealed by both univariate (OR: 6.31, 95 % CI: 1.42-59.87, P = 0.01) and multivariable firth regression models (Modle 1, OR: 7.10, 95 % CI: 1.57-67.38, P < 0.01; Modle 2, OR: 7.82, 95 % CI: 1.69, 76.36, P < 0.01; Modle 3, OR: 8.59, 95 % CI: 1.72-91.70, P < 0.01). Moreover, we observed that atrial cardiopathy was associated with an increased risk of END in AIS patients with large artery atherosclerosis (LAA) receiving EVT. Therefore, clinicians should consider atrial cardiopathy as a possible underlying cause of AIS in their patients. Further investigation is warranted to elucidate the relationship between atrial cardiopathy and AIS's occurrence, progression, and prognosis.
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Zhao et al. (2024) conducted a cohort in Acute ischemic stroke (AIS) following endovascular treatment (EVT) (n=87). Atrial cardiopathy vs. No atrial cardiopathy was evaluated on Poor neurological function (mRS score >2) at day 90. Atrial cardiopathy was significantly associated with an increased risk of early neurological deterioration in acute ischemic stroke patients following endovascular treatment (OR 7.10; 95% CI 1.57-67.38; P<0.01).
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