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SARS-CoV-2 can elicit intense release of cytokines and chemokines, possibly leading not only to vascular inflammation and atherosclerotic plaque instability but also to myocardial inflammation. Therefore, possible mechanisms for elevated troponin levels in these patients include demand ischaemia, stress cardiomyopathy, microvascular thrombosis, and secondary effects of systemic inflammation. Direct viral infection of the myocardium is another possible causal pathway of myocardial damage. The unique affinity of SARS-CoV-2 for the host angiotensin-converting enzyme 2 receptor raises the possibility of direct viral infection of vascular endothelium and myocardium, such that in some patients, COVID-19-associated myocardial injury could represent viral myocarditis.8 Any of these mechanisms may exacerbate underlying cardiovascular conditions.9
For the purposes of this study, myocarditis was defined as the presence of an inflammatory infiltrate associated with myocyte injury not due to some other cause, which was present in multiple foci. The opinions put forth here do not necessarily represent the opinions of all members of the Society for Cardiovascular Pathology or the Association for European Cardiovascular Pathology.
Quantification of inflammatory cells. There were more CD68+ macrophages (A) and CD3+ lymphocytes (B) in the myocarditis group compared with the no myocarditis group. There were no differences in inflammatory cell density between the left and right ventricles for either group. Horizontal bars indicate the median values. Overall P = 0.01 (A) and P = 0.005 (B).
While there was a non-significant trend toward higher troponin levels in the patients with myocarditis in this study, myocarditis does not fully explain the elevated troponin levels seen in patients with COVID-19. Other forms of myocardial injury such as right ventricular strain are clearly contributing to elevated troponin levels in these patients. All of the patients with multifocal myocarditis in this series had new electrocardiography changes including atrial fibrillation in two cases, and new ST-segment depression in the setting of chronic atrial fibrillation in the third case. Given that the majority of patients with COVID-19 have increased macrophages in the heart, it may also be challenging to discern which of these patients have actual lymphocytic myocarditis by imaging studies.
While the presence of virus in cardiac macrophages on electron microscopy has been reported, we were unable to verify this finding.13 However, so far, the electron microscopy in this patient series has only been completed in three cases without actual myocarditis.
Preliminary observations in the literature, together with the observations in this series, suggest that myocardial injury with or without depressed cardiac function in these patients may result from aetiologies other than viral myocarditis. Acute myocardial tissue injury might be related to elevated cytokines, hypoxaemia, right ventricular strain, and thrombotic complications. Both myocardial microvascular thrombi and right ventricular strain injury were present in some of the patients in this series. Thus, the term myocarditis should be used cautiously in describing patients with elevated troponin levels in the setting of COVID-19, particularly in the absence of more specific diagnostic testing such as endomyocardial biopsy and/or cardiac magnetic resonance imaging, which may be difficult to obtain in these patients.
Details of the cardiac pathology from autopsies of patients dying with COVID-19 are currently very limited. Despite the high mortality rate worldwide, only a few studies, comprising a small number of patients, have so far reported information concerning the cardiac pathology in these patients.10,12,14,15 Some of these studies employed limited diagnostic approaches such as biopsies. Thus, it is not surprising that in the few studies published to date, no substantial myocardial changes have been identified. Our study represents the first series with extensive histological cardiac examination, with a median of 20 full-thickness blocks of myocardium per case.
This study has several limitations. Molecular analysis for virus in the myocardium was not performed. While this is the largest and most detailed study of the cardiac pathology in the setting of COVID-19 to date, this study is still relatively small, and underpowered for identifying and excluding differences between the groups. Also this series focused on a subset of patients who died from COVID-19, and the observations may not be readily extended to all patients with COVID-19. The definition for diagnosing COVID-19 in patients infected with SARS-CoV-2 may not have been uniform across the institutions of this multicentre study. Only limited bedside echocardiography was performed on a small number of the patients. Electrocardiographic findings were based on documented clinical observations, and were not obtained in a standardized fashion. Likewise, there was not a uniform process for obtaining the autopsies in this series, and the results may not be readily extended to all patients dying with COVID-19. This study was retrospective in nature, and not all cases were sampled for histology in the same manner. For this study, we used the stringent criterion of multiple foci of inflammation associated with myocardial injury for a diagnosis of myocarditis. Thus, there is high confidence that the three cases meeting this criterion have myocarditis. There were six additional cases with lymphocytic infiltrates but no or only focal myocyte injury. In some previous studies not related to COVID-19, particularly involving endomyocardial biopsies, such pathology was regarded as myocarditis.22,23 However, the significance of these lymphocytic infiltrates with no to only focal myocardial injury in the COVID-19 autopsy population is currently unclear and may not be indicative of myocarditis.
The rear of these switch does not reveal any EU certification as such, so if you were thinking of buying one, despite them only having just been launched in Mainland China, you would ultimately be better off waiting for the H1 switches to become available. Aside from this, the H1 has a higher power rating, at 100-250VAC, 50/60Hz, Max. 8A, compared to the E1, which is listed as 220VAC at 50Hz, with a maximum of 5A.
A question: when a Z-wave controller (not these switches) is down, the Z-wave switches can continue to operate manually (pushing physically on the switch) so the lights can be switched on or off all the same. What happens if one unplug the Aqara hub from the LAN at home? Do the Aqara switches are completely inoperable, or can they still be hand-operated?
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I love to see metal parts, joints, bolts, cooling fans behind trellis work, yellow / black strips that warn you of danger in a certain zone. Stuff like that. And above all, i hate touchscreens & love tactile feedback. 781b155fdc