Patient-level and system-level barriers associated with treatment delays for ST elevation myocardial infarction in China.

OBJECTIVE: This study aims to understand the current ST elevated myocardial infarction (STEMI) treatment process in Guangdong Province and explore patient-level and system-level barriers associated with delay in STEMI treatment, so as to provide recommendations for improvement. METHODS: This is a qualitative study. Data were collected using semistructured, face-to-face individual interviews from April 2018 to January 2019. Participants included patients with STEMI, cardiologists and nurses from hospitals, emergency department doctors, primary healthcare providers, local health governors, and coordinators at the emergency medical system (EMS). An inductive thematic analysis was adopted to generate overarching themes and subthemes for potential causes of STEMI treatment delay. The WHO framework for people-centred integrated health services was used to frame recommendations for improving the health system. RESULTS: Thirty-two participants were interviewed. Patient-level barriers included poor knowledge in recognising STEMI symptoms and not calling EMS when symptoms occurred. Limited capacity of health professionals in hospitals below the tertiary level and lack of coordination between hospitals of different levels were identified as the main system-level barriers. Five recommendations were provided: (1) enhance public health education; (2) strengthen primary healthcare workforce; (3) increase EMS capacity; (4) establish an integrated care model; and (5) harness government's responsibilities. CONCLUSIONS: Barriers associated with delay in STEMI treatment were identified at both patient and system levels. The results of this study provide a useful evidence base for future intervention development to improve the quality of STEMI treatment and patient outcomes in China and other countries in a similar situation.

Inhibitory effect of melatonin on Mst1 ameliorates myocarditis through attenuating ER stress and mitochondrial dysfunction.

Viral myocarditis has been found to be one of the leading causes of sudden death in young adults. However, no effective drugs have been developed to intervene the progression of myocarditis. Accordingly, the present study is carried out to explore the protective role played by melatonin in the setting of viral myocarditis with a focus on Mst1-Hippo pathway, mitochondrial dysfunction and ER stress. Cardiac function was determined via echocardiographic examination. Mitochondrial function and ER stress were detected via ELISA, western blots, and immunofluorescence. Our data demonstrated that virus injection induced cardiac dysfunction as evidenced by reduced contractile function in myocardium. Besides, LDH release assay and western blotting analysis demonstrated that cardiomyocyte death was activated by virus injection. Interestingly, melatonin treatment improved cardiac function and repressed virus-mediated cardiomyocyte apoptosis. At the molecular levels, mitochondrial dysfunction was induced by virus infection, as indicated by mitochondrial membrane potential reduction, mPTP opening rate elevation and caspase-9-related apoptosis activation. Besides, ER stress parameters were also elevated in virus-treated cardiomyocytes. Interestingly, melatonin treatment maintained mitochondrial dysfunction and repressed ER stress. To the end, we found that Mst1 was upregulated by virus infection; this effect was attenuated through supplementation with melatonin. However, Mst1 overexpression reduced the beneficial impact exerted by melatonin on cardiomyocyte viability, mitochondrial function and ER homeostasis. Our study illustrated that melatonin treatment attenuated viral myocarditis via sustaining cardiomyocyte viability, repressing mitochondrial dysfunction and inhibiting ER stress in a manner dependent on Mst1 inhibition.