ABSTRACT
Background and aims: SARS-CoV2 infection may increase stroke risk. The biological mechanisms underlying ischemic stroke occurrence during COVID-19 remains unclear. Methods: A Genome-Wide Association Study (GWAS) from MEGASTROKE was used to generate Polygenic risk scores (PRSs) across four p-value thresholds (p=0.05-p=5e-8) using PRSice-2. For all ischemic stroke (AIS) we used 34217 cases and 406111 controls, large-artery atherosclerosis (LAA) 4373 cases 297290 controls, cardioembolic (CE) 7193 cases 355468 controls and small-vessel occlusion (SVO) 5386 cases 343560 controls. For undetermined stroke etiology (UND) 984 cases and 5590 controls from a Spanish stroke cohort were used. PRSs were tested in 54 patients with an ischemic stroke that occurred after COVID-19 hospitalization (<8 days)(IS-COV). IS-COV cases were genotyped with Axiom Spain Biobank Array (11 UND, 6 CE, 6 LAA, 5 SVO, 2 infrequent cause and 24 unknown etiology). 726 population controls were also genotyped. Results: We found significant associations of IS-COV with PRSAIS (threshold= 5e-5, p= 0.04;R2= 0.01, number of SNPs= 60), PRSCE (threshold= 5e-8, p= 0.02, R2= 0.01, SNPs= 4;threshold= 0.05, p= 5.9e-4, R2= 0.03, SNPs=19308), PRSLAA (threshold= 5e-5, p= 6.5e-3, R2= 0.02, SNPs= 81;threshold= 1e-4, p= 0.02, R2= 0.01, SNPs= 146;threshold= 0.05, p =1.3e-3, R2= 0.03, SNPs= 20722) and PRSUND (threshold= 1e-4, p= 0.04, R2= 0.01, SNPs=10;threshold= 0.05, p =1.5e-6, R2= 0.06, SNPs= 3416). We did not find any association between PRSSVO and IS-COV. Conclusions: CE, LAA and UND shared genetic mechanisms with ischemic stroke cases due to COVID-19. We found no association between SVO and IS-COV.
ABSTRACT
Background and Aims: We evaluated whether stroke severity, functional outcome and mortality are different in patients with ischemic stroke with or without COVID-19 infection. Methods: A prospective, observational, multicentre cohort study in Catalonia, Spain. Recruitment was consecutive from mid-March to mid-May 2020. Patients had had an acute ischemic stroke within 48 hours and a previous modified Rankin scale (mRS) score of 0 to 3. We collected demographic data, vascular risk factors, prior mRS score, NIHSS score, rate of reperfusion therapies, logistics and metrics. Primary end-point was functional outcome at 3 months. Favourable outcome was defined depending on the previous mRS score. Secondary outcome was mortality at 3 months. We performed mRS shift and multivariate analyses. Results: We evaluated 701 patients (mean age 72.3±13.3 years, 60.5% men), and 91 (13%) had COVID-19 infection. Median baseline NIHSS score was higher in COVID-19 patients compared to patients without COVID-19 [8 (3-18) vs 6 (2-14), p=0.049)]. Proportion of patients with a favourable functional outcome was 33.7% in the COVID-19 and 47% in the non-COVID-19 group. However, after a multivariate logistic regression analysis, COVID-19 infection did not increase the probability of unfavourable functional outcome. Mortality rate was 39.3% among COVID-19 patients and 16.1% in the non-COVID-19 group. In the multivariate logistic regression analysis, COVID-19 infection was a risk factor for mortality (HR 3.14 (95% CI, 2.10-4.71;p<0.001). Conclusions: Patients with ischemic stroke and COVID-19 infection have more severe strokes and higher mortality than stroke patients without COVID-19 infection. However, functional outcome is comparable in both groups.