Background: Takotsubo cardiomyopathy is an acute cardiomyopa-thy characterized by transient left ventricular systolic dysfunction induced by emotional or physical stress, including respiratory failure. Aim: The aim of this study was to analyze the clinical features of patients who developed takotsubo cardiomyopathy in respiratory department. Methods: We retrospectively evaluated the characteristics, causes, and outcomes of takotsubo cardiomyopathy experienced in our respiratory department Results: Of 14 patients, 35% were women over 50 years of age. The most frequent trigger was bronchoscopy. Laryngeal reflex in response to irritation of trachea results in elevation of catecholamine level, thereby inducing takotsubo cardiomyopathy. At onset, more than half of the patients did not show typical symptoms such as chest discomfort. 57.1% of cases showed type 2 respiratory failure and 42.9% showed acidosis which might related to elevation of catecholamine level as well. 50.0% of patients had comorbidities of chronic obstructive pulmonary disease (COPD) or asthma, treated regularly with β2stimulant. Since there are abundant β2-stimulant receptors in apical myocardium, repeated treatment with β2-stimulant may have contributed to the disease onset. Some cases complicated with heart failure, but all patients improved. Conclusions: In respiratory department, it is necessary to be aware of takotsubo cardiomyopathy especially when conducting procedures including tracheal manipulation, when using repetitive β2-stimulant, and when a patient shows exacerbation of respiratory failure with hypercap-nia, even without any chest complaints. AP093 SAPS II OR APACHE II IS BETTER TO PREDICT MORTALITY IN MEDICAL ICU PATIENTS

Social cognition is a complex process that requires the integration of a wide variety of behaviors, including salience, reward-seeking, motivation, knowledge of self and others, and flexibly adjusting behavior in social groups. Not surprisingly, social cognition represents a sensitive domain commonly disrupted in the pathology of a variety of psychiatric disorders including Autism Spectrum Disorder (ASD) and Schizophrenia (SCZ). Here, we discuss convergent research from animal models to human disease that implicates the prefrontal cortex (PFC) as a key regulator in social cognition, suggesting that disruptions in prefrontal microcircuitry play an essential role in the pathophysiology of psychiatric disorders with shared social deficits. We take a translational perspective of social cognition, and review three key behaviors that are essential to normal social processing in rodents and humans, including social motivation, social recognition, and dominance hierarchy. A shared prefrontal circuitry may underlie these behaviors. Social cognition deficits in animal models of neurodevelopmental disorders like ASD and SCZ have been linked to an altered balance of excitation and inhibition (E/I ratio) within the cortex generally, and PFC specifically. A clear picture of the mechanisms by which altered E/I ratio in the PFC might lead to disruptions of social cognition across a variety of behaviors is not well understood. Future studies should explore how disrupted developmental trajectory of prefrontal microcircuitry could lead to altered E/I balance and subsequent deficits in the social domain.

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