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COVID-19 has been associated with a hypercoagulable state causing cardiovascular and neurovascular complications. To further characterize cerebrovascular disease (CVD) in COVID-19, we review the current literature of published cases and additionally report the clinical presentation, laboratory and diagnostic testing results of 12 cases with COVID-19 infection and concurrent CVD from two academic medical centers in Houston, TX, USA, between March 1 and May 10, 2020. To date, there are 12 case studies reporting 47 cases of CVD in COVID-19. However, only 4 small case series have described the clinical and laboratory findings in patients with COVID-19 and concurrent stroke. Viral neurotropism, endothelial dysfunction, coagulopathy and inflammation are plausible proposed mechanisms of CVD in COVID-19 patients. In our case series of 12 patients, 10 patients had an ischemic stroke, of which 1 suffered hemorrhagic transformation and two had intracerebral hemorrhage. Etiology was determined to be embolic without a clear cause identified in 6 ischemic stroke patients, while the remaining had an identifiable source of stroke. The majority of the patients had elevated inflammatory markers such as D-dimer and interleukin-6. In patients with embolic stroke of unclear etiology, COVID-19 may have played a direct or indirect role in the processes that eventually led to the strokes while in the remaining cases, it is unclear if infection contributed partially or was an incidental finding.

The field of acute stroke treatment has made tremendous progress in reducing the overall burden of disability. Understanding the pathophysiology of acute ischemic injury, neuroimaging to quantify the extent of penumbra and infarction, and acute stroke reperfusion therapies have together contributed to these advancements. In this review we highlight advancements in reperfusion therapies for acute ischemic stroke.

Introduction: COVID-19 has been associated with venous and arterial thrombotic complications. The objective of our study was to determine whether markers of coagulation and hemostatic activation (MOCHA) on admission could identify COVID-19 patients at risk for thrombotic events. Methods: COVID-19 patients admitted to a tertiary academic healthcare system from April 3, 2020 to July 31, 2020 underwent admission testing of MOCHA profile parameters (plasma d-dimer, prothrombin fragment 1.2, thrombin-antithrombin complex, and fibrin monomer). For this analysis we excluded patients on outpatient anticoagulation therapy preceding admission. Prespecified endpoints monitored during hospitalization included deep vein thrombosis, pulmonary embolism, myocardial infarction, ischemic stroke and access line thrombosis. Results: During the study period, 276 patients were included in the analysis cohort (mean age 59 ± 6.3 years, 47% female, 83% non-white race). Arterial and venous thrombotic events occurred in 43 (16%) patients (see Table). Each coagulation marker was independently associated with the composite endpoint (p Conclusion: Admission MOCHA with ≥ 2 abnormalities identified COVID-19 patients at risk for a thrombotic event, ICU admission and intubation while < 2 abnormalities identified a subgroup of patients who were at low risk for thrombotic events. Our results suggest that an admission MOCHA profile can be useful to risk stratify COVID-19 patients. Further studies are needed to determine whether an admission MOCHA profile can guide anticoagulation therapy and improve overall clinical outcomes.

BackgroundCoronavirus disease 2019 (COVID-19) has been associated with a coagulopathy giving rise to venous and arterial thrombotic events. The objective of our study was to determine whether markers of coagulation and hemostatic activation (MOCHA) on admission could identify COVID-19 patients at risk for thrombotic events and other complications.MethodsCOVID-19 patients admitted to a tertiary academic healthcare system from April 3, 2020 to July 31, 2020 underwent standardized admission testing of MOCHA profile parameters (plasma d-dimer, prothrombin fragment 1.2, thrombin-antithrombin complex, and fibrin monomer) with abnormal MOCHA defined as ≥ 2 markers above the reference. Prespecified thrombotic endpoints included deep vein thrombosis, pulmonary embolism, myocardial infarction, ischemic stroke, and access line thrombosis; other complications included ICU admission, intubation and mortality. We excluded patients on anticoagulation therapy prior to admission and those who were pregnant.ResultsOf 276 patients (mean age 59 ± 6.4 years, 47% female, 62% African American race) who met study criteria, 45 (16%) had a thrombotic event. Each coagulation marker on admission was independently associated with a vascular endpoint (pConclusionsAdmission MOCHA with ≥ 2 abnormalities identified COVID-19 patients at increased risk of ICU admission and intubation during hospitalization more effectively than isolated admission D-dimer measurement. Admission MOCHA with

Intracranial hemorrhage remains one of the most feared acute neurological emergencies. However, apart from the acute management, secondary risk factor management and prevention of ischemic events remains ambiguous. We present a thorough review of the current data available regarding management of antithrombotics after intracranial hemorrhage. The most robust evidence comes from the investigators of the RESTART trial which reassured the safety of resuming antiplatelet therapy after ICH, namely in patients with prior indication and treatment with antithrombotics. We conclude that based on available data, the risk of recurrent ICH is probably too small to exceed the found benefits of antiplatelet therapy in the secondary prevention of ischemic vascular disease.

Background There is limited data on the markers of coagulation and hemostatic activation (MOCHA) profile in Coronavirus disease 2019 (COVID-19) and its ability to identify COVID-19 patients at risk for thrombotic events and other complications. Methods Hospitalized patients with confirmed SARS-COV-2 from four Atlanta hospitals were included in this observational cohort study and underwent admission testing of MOCHA parameters (plasma d-dimer, prothrombin fragment 1.2, thrombin-antithrombin complex, fibrin monomer). Clinical outcomes included deep vein thrombosis, pulmonary embolism, myocardial infarction, ischemic stroke, access line thrombosis, ICU admission, intubation and mortality. Main results Of 276 patients (mean age 59 ± 6.4 years, 47% female, 62% African American), 45 (16%) had a thrombotic endpoint. Each MOCHA parameter was independently associated with a thrombotic event (p Conclusions An admission MOCHA profile is useful to risk-stratify COVID-19 patients for thrombotic complications and more effective than isolated d-dimer for predicting risk of ICU admission and intubation.

Background: There has been debate in the role of exogenous testosterone as a risk factor for stroke. Hormone replacement therapy (HRT) is considered a risk factor for stroke. The risk of ischemic stroke may increase when using testosterone-containing HRT. Methods: Using data from the observational component of the Women’s Health Initiative (WHI) [WHI Observational Study (OS)], we analyzed the 93,676 women aged 50-79 years, who participated in the OS over a period of 12±1 years. We compared the outcome of stroke in participants with reported use of a combination of testosterone and estrogen, estrogen alone, progesterone alone, and a combination of estrogen and progesterone, as recorded at the baseline visit. A logistic regression analysis was run to determine the odds of developing stroke. Results: Of the 93, 676 participants, 1772 used a combination of testosterone and estrogen (Estratest) HRT, 11,282 used progesterone alone, 10,808 used a combination of estrogen and progesterone, and 31,673 used estrogen alone. A smaller proportion of participants who developed an outcome of stroke had used Estratest as compared to estrogen alone or a combination of estrogen and progesterone (1.9% vs. 96.3% p=0.62). In the logistic regression, participants who had used Estratest were 1.2 times as likely to develop stroke as users of other hormone replacement therapy (OR 1.2 95%CI (0.96-1.6)), while women who had used progesterone only were 0.87 times less likely to develop stroke than users of other hormone replacement therapy (OR 0.874 95%CI (0.77-0.99)). After adjusting for confounders, the risk of developing stroke increased in users of Estratest (OR 1.25 95%CI (0.96-1.6) p=0.04), and decreased in users of progesterone only (OR 0.873 95%CI (0.77-0.99) p=0.038). Conclusion: Use of testosterone-containing HRT slightly increased the risk of stroke in women when compared to progesterone alone HRT, although this was not found to be significant. Stroke risk with Estratest may be considered to be similar to estrogen only and combination of estrogen plus progesterone HRT. Future studies are required to investigate these correlations.