OBJECTIVEAlthough intensive glycemic control achieved with insulin therapy increases the incidence of both moderate and severe hypoglycemia, clinical reports of cognitive impairment due to severe hypoglycemia have been highly variable. It was hypothesized that recurrent moderate hypoglycemia preconditions the brain and protects against damage caused by severe hypoglycemia.RESEARCH DESIGN AND METHODSNine-week-old male Sprague-Dawley rats were subjected to either 3 consecutive days of recurrent moderate (25–40 mg/dl) hypoglycemia (RH) or saline injections. On the fourth day, rats were subjected to a hyperinsulinemic (0.2 units · kg−1 · min−1) severe hypoglycemic (∼11 mg/dl) clamp for 60 or 90 min. Neuronal damage was subsequently assessed by hematoxylin-eosin and Fluoro-Jade B staining. The functional significance of severe hypoglycemia–induced brain damage was evaluated by motor and cognitive testing.RESULTSSevere hypoglycemia induced brain damage and striking deficits in spatial learning and memory. Rats subjected to recurrent moderate hypoglycemia had 62–74% less brain cell death and were protected from most of these cognitive disturbances.CONCLUSIONSAntecedent recurrent moderate hypoglycemia preconditioned the brain and markedly limited both the extent of severe hypoglycemia–induced neuronal damage and associated cognitive impairment. In conclusion, changes brought about by recurrent moderate hypoglycemia can be viewed, paradoxically, as providing a beneficial adaptive response in that there is mitigation against severe hypoglycemia–induced brain damage and cognitive dysfunction.
Background Coronavirus Disease 2019 (COVID-19) results in increased inflammatory markers previously associated with atrial arrhythmias. However, little is known about their incidence or specificity in COVID-19, or their association with outcomes. We determined the incidence, predictors and outcomes of atrial fibrillation or flutter (AF/AFL) in patients hospitalized with COVID-19, or hospitalized with Influenza. Methods This is a retrospective analysis of 3,970 patients admitted with PCR-positive COVID-19 between 2/4/2020-4/22/2020 with manual review performed of 1,110. The comparator arm included 1,420 patients with influenza hospitalized between 1/1/2017-1/1/2020. Results Among 3970 inpatients with COVID-19, the incidence of AF/AFL was 10% (N=375) and in patients without a history of atrial arrhythmias, 4% (N=146). Patients with new-onset AF/AFL were older with increased inflammatory markers including Interleukin-6 (93 vs 68 pg/ml, P<0.01), and more myocardial injury (Troponin-I: 0.2 vs 0.06ng/ml, P<0.01). AF/AFL were associated with increased mortality (46% vs 26%, P<0.01). Manual review captured a somewhat higher incidence of AF/AFL (13%, N=140). Compared to inpatients with COVID-19, patients with Influenza (N=1420) had similar rates of AF/AFL (12%, n=163) but lower mortality. The presence of AF/AFL correlated with similarly increased mortality in both COVID-19 (RR 1.77) and Influenza (RR 1.78). Conclusions AF/AFL occurs in a subset of patients hospitalized with either COVID-19 or Influenza, and is associated with inflammation and disease severity in both infections. The incidence and associated increase in mortality in both cohorts suggests that AF/AFL in not specific to COVID-19, but is rather a generalized response to the systemic inflammation of severe viral illnesses.
Introduction: Recent studies have described several cardiovascular manifestations of COVID-19 including myocardial ischemia, myocarditis, thromboembolism, and malignant arrhythmias. However, to our knowledge, syncope in COVID-19 patients has not been systematically evaluated. We sought to characterize syncope and/or presyncope in COVID-19. Methods: This is a retrospective analysis of consecutive patients hospitalized with laboratory-confirmed COVID-19 with either syncope or presyncope. This "study" group (n = 37) was compared with an age and gender-matched cohort of patients without syncope ("control") (n = 40). Syncope was attributed to various categories. We compared telemetry data, treatments received, and clinical outcomes between the two groups. Results: Among 1000 COVID-19 patients admitted to the Mount Sinai Hospital, the incidence of syncope/presyncope was 3.7%. The median age of the entire cohort was 69 years (range 26-89+ years) and 55% were men. Major comorbidities included hypertension, diabetes, and coronary artery disease. Syncopal episodes were categorized as (a) unspecified in 59.4% patients, (b) neurocardiogenic in 15.6% patients, (c) hypotensive in 12.5% patients, and (d) cardiopulmonary in 3.1% patients with fall versus syncope and seizure versus syncope in 2 of 32 (6.3%) and 1 of 33 (3.1%) patients, respectively. Compared with the "control" group, there were no significant differences in both admission and peak blood levels of d-dimer, troponin-I, and CRP in the "study" group. Additionally, there were no differences in arrhythmias or death between both groups. Conclusions: Syncope/presyncope in patients hospitalized with COVID-19 is uncommon and is infrequently associated with a cardiac etiology or associated with adverse outcomes compared to those who do not present with these symptoms.
IMPORTANCEEarly rhythm control of atrial fibrillation (AF) with either antiarrhythmic drugs (AADs) or catheter ablation has been reported to improve cardiovascular outcomes compared with usual care; however, the optimal therapeutic modality to achieve early rhythm control is unclear.OBJECTIVE To assess the safety and efficacy of AF ablation as first-line therapy when compared with AADs in patients with paroxysmal AF.
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