Rout, Amit

Background Older adults with non–ST‐segment–elevation acute coronary syndrome are less likely to undergo an invasive strategy compared with younger patients. Randomized controlled trials traditionally exclude older adults because of their high burden of geriatric conditions. Methods and Results We searched for randomized controlled trials comparing invasive versus medical management or a selective invasive (conservative) strategy for older patients (age≥75 years) with non–ST‐segment–elevation acute coronary syndrome. Fixed effects meta‐analysis was conducted to estimate the odds ratio (OR) with 95% CI for the composite of death or myocardial infarction (MI) and individual secondary end points of all‐cause death, cardiovascular death, MI, revascularization, stroke, and major bleeding. Nine studies with 2429 patients (invasive: 1228 versus control: 1201) with a mean follow‐up of 21 months were included. An invasive strategy was associated with a significantly decreased risk of a composite of death and MI (OR, 0.67 [95% CI, 0.54–0.83], P <0.001), MI (OR, 0.56 [95% CI, 0.45–0.70], P <0.001) and subsequent revascularization (OR, 0.27 [95% CI, 0.16–0.48], P <0.001). There was no difference in all‐cause death (OR, 0.84 [95% CI, 0.65–1.10], P =0.21), cardiovascular death (OR, 0.85 [95% CI, 0.63–1.15], P =0.30), stroke (OR, 0.74 [95% CI, 0.38–1.47], P =0.39), or major bleeding (OR, 1.24 [95% CI, 0.42–3.66], P =0.70). Conclusions In older patients ≥75 years old with non–ST‐segment–elevation acute coronary syndrome, an invasive strategy reduced the risk of a composite of death and MI, MI, and subsequent revascularization compared with a conservative strategy alone. Older adults with higher burden of geriatric conditions should be included in future trials to improve generalizability to this growing population.

BRASH syndrome is characterized by bradycardia, renal failure, AV nodal blockade, shock, and hyperkalemia. The proposed mechanism involves a vicious cycle between AV nodal blockers, hyperkalemia, and renal failure and was first described in 2016. We present a case of a 52-year-old woman who presented with progressively worsening shortness of breath and hypertensive urgency who subsequently developed profound bradycardia and shock that was refractory to resuscitative measures, she was diagnosed with BRASH syndrome. In this article, we explore the predisposing factors and challenges faced during the management of patients with BRASH syndrome.

Introduction: Thrombo-inflammatory syndrome (TIS) characterized by a pathophysiological state of hypercoagulability, heightened platelet function, and inflammation has been observed in patients with acute myocardial infarction, and HIV. Hypothesis: The incidence of TIS is observed at a high rate in COVID-19 patients and worsens with symptom severity Methods: Blood samples from COVID-19 positive hospitalized patients (n=24) was collected for coagulation and platelet function analysis using point-of-care thromboelastography, TEG6s (Haemonetics, Corp) and routine labs were collected to measure markers of inflammation, coagulation, and organ damage (Table). Disease severity was grouped according to oxygen supplementation requirements and comparisons were made using unpaired t-test and chi-squared tests. Thrombo-inflammation was defined as the presence of both hypercoagulability by TEG [Clot initiation (R) < 4.6, fibrin clot strength (FCS) >32mm, and platelet fibrin clot strength (PFCS) >69] and D-dimer >ULN. Results: Ninety- five percent of COVID positive patients had at least one co-morbidity with the incidence of hypertension (71%), diabetes (50%), and obesity (42%) being the most frequent. A total of 63% (16/24) of patients had TIS, the incidence was significantly increased with escalating disease severity (p=0.03). A significant stepwise (p<0.05) increase in FCS, D-Dimer, WBC count, lactate dehydrogenase, and procalcitonin was observed with worsening respiratory function (table). MA-ADP a measure of platelet function was in the high normal range for 81 % of patients. Conclusions: Thrombo-inflammatory is observed with most COVID patients, importantly heightened platelet function is a component of the syndrome and raises the question if antiplatelet therapy is needed in select COVID patients. Selective assessments with TEG6s may facilitate antithrombotic personalization.

Background: Thromboelastography (TEG®) is used across a wide range of clinical settings to identify patients at risk for thrombosis and coagulopathic bleeding and may be a useful diagnostic tool to guide antithrombotic treatment in patients with COVID-19. Hypothesis: TEG® identifies symptom progression in COVID -19 patients, particularly in the high-risk minority population known to have worse clinical outcomes. Methods: Whole blood from African American and Hispanic hospitalized COVID positive (n=22) and negative outpatients (n=24) was analyzed using point-of-care TEG®6s (Haemonetics, Corp). TEG® parameters including clot initiation (R), fibrin clot strength (FCS), platelet-fibrin clot strength (PFCS) and clot lysis (LY30) were compared across disease severity groups (table). Routine labs including D-Dimer, C-reactive protein (CRP), ferritin, and procalcitonin were also collected. Results: Ninety- five percent of COVID positive patients had at least one co-morbidity with the incidence of hypertension (73%), diabetes (55%), and obesity (45%) being the most frequent. R time was more rapid, and FCS and PFCS was significantly higher in COVID positive as compared to negative groups (p<0.03). A stepwise increase in FCS and PFCS was observed with worsening respiratory function (table). Similarly, D-Dimer, CRP, ferritin, and procalcitonin levels were highest in patients receiving ventilator support. No differences were observed in clot lysis between the groups despite elevated D-Dimer levels. Conclusion: We have demonstrated that TEG®6s can identify a prothrombotic phenotype characterized by rapid clot initiation and increased fibrin and platelet-fibrin clot strength in a minority population with COVID-19. Future studies are warranted implementing the TEG6s® in clinical trials to personalize antithrombotic therapy in COVID-19 and improve outcomes.