Aims  To chart the effect of the COVID-19 pandemic on the activity of interventional electrophysiology services in affected regions. Methods and results  We reviewed the electrophysiology laboratory records in three affected cities: Wenzhou in China, Milan in Italy, and London in the UK. We inspected catheter lab records and interviewed electrophysiologists in each centre to gather information on the impact of the pandemic on working patterns and on the health of staff members and patients. There was a striking decline in interventional electrophysiology activity in each of the centres. The decline occurred within a week of the recognition of widespread community transmission of the virus in each region and shows a striking correlation with the national figures for new diagnoses of COVID-19 in each case. During the period of restriction, workflow dropped to <5% of normal, consisting of emergency cases only. In two of three centres, electrophysiologists were redeployed to perform emergency work outside electrophysiology. Among the centres studied, only Wenzhou has seen a recovery from the restrictions in activity. Following an intense nationwide programme of public health interventions, local transmission of COVID-19 ceased to be detectable after 18 February allowing the electrophysiology service to resume with a strict testing regime for all patients. Conclusion  Interventional electrophysiology is vulnerable to closure in times of great social difficulty including the COVID-19 pandemic. Intense public health intervention can permit suppression of local disease transmission allowing resumption of some normal activity with stringent precautions.

Our previous studies have reported that agonist of α7 nicotinic acetylcholine receptors prevented electrophysiological dysfunction of rats with ischaemic cardiomyopathy (ICM) by eliciting the cholinergic anti‐inflammatory pathway (CAP). Adenosine monophosphate‐activated protein kinase (AMPK) signalling is widely recognized exerting cardioprotective effect in various cardiomyopathy. Here, we aimed to investigate whether the protective effects of the CAP are associated with AMPK signalling in ICM. In vivo, coronary artery of rats was ligated for 4 weeks to induce the ICM and then treated with PNU‐282987 (CAP agonist) and BML‐275 dihydrochloride (AMPK antagonist) for 4 weeks. In vitro, primary macrophages harvested from rats were induced inflammation by Lipopolysaccharide (LPS) treatment and then treated with PNU‐282987 and BML‐275 dihydrochloride. In vivo, exciting CAP by PUN‐282987 elicited an activation of AMPK signalling, alleviated ventricular remodeling, modified the cardiac electrophysiological function, reduced the cardiac expression of collagens and inflammatory cytokines and maintained the integrity of ultrastructure in the ischemic heart. However, the benefits of CAP excitation were blunted by AMPK signaling antagonization. In vitro, excitation of the CAP was observed inhibiting the nuclear transfer of NF‐κB p65 of macrophages and promoting the transformation of Ly‐6C high macrophages into Ly‐6C low macrophages. However, inhibiting AMPK signalling by BML‐275 dihydrochloride reversed the CAP effect on LPS‐treated macrophages. Finally, our findings suggest that eliciting the CAP modulates the inflammatory response in ICM through regulating AMPK signalling.

Aims: To chart the effect of the COVID-19 pandemic on the activity of interventional electrophysiology services in affected regions. Methods: We reviewed the electrophysiology laboratory records in 3 affected cities: Wenzhou in China, Milan in Italy and London, United Kingdom. We interviewed electrophysiologists in each centre to gather information on the impact of the pandemic on working patterns and on the health of staff members. Results: There was a striking decline in interventional electrophysiology activity in each of the centres. The decline occurred within a week of the recognition of widespread community transmission of the virus in each region and shows a striking correlation with the national figures for new diagnoses of COVID-19 in each case. During the period of restriction, work-flow dropped to <5% of normal, consisting of emergency cases only. In 2 of 3 centres, electrophysiologists were redeployed to perform emergency work outside electrophysiology. Among the centres studied, only Wenzhou has seen a recovery from the restrictions in activity. Following an intense nationwide program of public health interventions, local transmission of COVID-19 ceased to be detectable after February 18th allowing the electrophysiology service to resume with a strict testing regime for all patients. Conclusion: Interventional electrophysiology is vulnerable to closure in times of great social difficulty including the COVID-19 pandemic. Intense public health intervention can permit suppression of local disease transmission allowing resumption of some normal activity.

With the chronic ischemia persisting after acute myocardial infarction, the accompanying low-degree inflammation and subsequent fibrosis result in progression of cardiac remodeling and heart failure. Recently, Sodium Houttuyfonate (SH), a pure compound extracted from Houttuynia cordata, has been confirmed exerting anti-inflammatory and anti-fibrotic effects under diseased situations. Here, we aimed to investigate whether SH could reverse the cardiac remodeling post-myocardial infarction by alleviating cardiac inflammation and fibrosis. Left anterior descending coronary artery of adult male Sprague-Dawley rats was ligated to elicit myocardial infarction. Low and high dose of SH was administered by oral gavage for four consecutive weeks post-myocardial infarction. Long-term SH treatment decreased heart rate, heart weight/ body weight (HW/BW), and left ventricle weight/body weight (LVW/BW), reduced cardiac expression of brain natriuretic peptide (BNP), improved left ventricular heart function, and ameliorated the histopathological changes caused by myocardial infarction. Western blotting revealed the expression of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), transforming growth factor-β (TGF-β), collagen I, and collagen III of the infarcted ventricle were reduced by SH treatment. Meanwhile, we found that SH treatment post-myocardial infarction activated AMP-activated protein kinase (AMPK) and suppressed nuclear factor-κB p65 (NF-κB p65). Furthermore, on H9C2 cells induced hypoxic injury with cobalt chloride (CoCl2), the reduction of inflammatory cytokines (IL-6, TNF-α, and TGF-β), activation of AMPK, and suppression of NF-κB p65 were also observed by SH treatment. However, transfection of H9C2 with AMPKα siRNA blunted the suppression of NF-κB p65 and inflammatory cytokines (IL-6, TNF-α, and TGF-β) by SH post-hypoxia. Taken together, these findings suggested that long-term administration of SH post-myocardial infarction reduced cardiac inflammatory and fibrotic responses, and reversed cardiac remodeling process. The underlying mechanism may be activating AMPK and suppressing NF-κB pathway.

BackgroundIn patients with triple valve replacement developing third-degree atrioventricular block (AVB), the most appropriate approach for permanent pacemaker implantation remains questionable.Case presentationIn this case presentation, we first described the approach of implantation of the cardiac resynchronization therapy pacemaker (CRT-P) via one bipolar pacing lead in middle cardiac vein (MCV) and one quadripolar pacing lead in anterior interventricular vein (AIV) in a patient developing complete AVB, who had been previously diagnosed with rheumatic valvular heart disease with triple valve replaced. After the CRT-P implantation, the two pacing leads in coronary sinus (CS) provided a dual-site ventricular pacing from the anterior septum and posterior septum, which resulted in a narrow QRS complex and an increased ventricular synchrony. During the long-term follow-up, no deterioration of heart function was documented and pacing parameters remained good.ConclusionIn this patient developing complete AVB with triple valve replaced, our approach of CRT-P implantation provides an effective and reliable ventricular pacing, and is an alternative option when transvenous right ventricular pacing, transseptal left ventricular pacing and transpericardial epicardium pacing are not possible. Further prospective randomized trials are required to confirm the efficiency of our approach of dual-site ventricular pacing by CRT-P in this kind patients.