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      Hypertension and related diseases in the era of COVID-19: a report from the Japanese Society of Hypertension Task Force on COVID-19

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          Abstract

          Coronavirus disease-2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has affected more than seven million people worldwide, contributing to 0.4 million deaths as of June 2020. The fact that the virus uses angiotensin-converting enzyme (ACE)-2 as the cell entry receptor and that hypertension as well as cardiovascular disorders frequently coexist with COVID-19 have generated considerable discussion on the management of patients with hypertension. In addition, the COVID-19 pandemic necessitates the development of and adaptation to a “New Normal” lifestyle, which will have a profound impact not only on communicable diseases but also on noncommunicable diseases, including hypertension. Summarizing what is known and what requires further investigation in this field may help to address the challenges we face. In the present review, we critically evaluate the existing evidence for the epidemiological association between COVID-19 and hypertension. We also summarize the current knowledge regarding the pathophysiology of SARS-CoV-2 infection with an emphasis on ACE2, the cardiovascular system, and the kidney. Finally, we review evidence on the use of antihypertensive medication, namely, ACE inhibitors and angiotensin receptor blockers, in patients with COVID-19.

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          Most cited references 60

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          Clinical features of patients infected with 2019 novel coronavirus in Wuhan, China

          Summary Background A recent cluster of pneumonia cases in Wuhan, China, was caused by a novel betacoronavirus, the 2019 novel coronavirus (2019-nCoV). We report the epidemiological, clinical, laboratory, and radiological characteristics and treatment and clinical outcomes of these patients. Methods All patients with suspected 2019-nCoV were admitted to a designated hospital in Wuhan. We prospectively collected and analysed data on patients with laboratory-confirmed 2019-nCoV infection by real-time RT-PCR and next-generation sequencing. Data were obtained with standardised data collection forms shared by WHO and the International Severe Acute Respiratory and Emerging Infection Consortium from electronic medical records. Researchers also directly communicated with patients or their families to ascertain epidemiological and symptom data. Outcomes were also compared between patients who had been admitted to the intensive care unit (ICU) and those who had not. Findings By Jan 2, 2020, 41 admitted hospital patients had been identified as having laboratory-confirmed 2019-nCoV infection. Most of the infected patients were men (30 [73%] of 41); less than half had underlying diseases (13 [32%]), including diabetes (eight [20%]), hypertension (six [15%]), and cardiovascular disease (six [15%]). Median age was 49·0 years (IQR 41·0–58·0). 27 (66%) of 41 patients had been exposed to Huanan seafood market. One family cluster was found. Common symptoms at onset of illness were fever (40 [98%] of 41 patients), cough (31 [76%]), and myalgia or fatigue (18 [44%]); less common symptoms were sputum production (11 [28%] of 39), headache (three [8%] of 38), haemoptysis (two [5%] of 39), and diarrhoea (one [3%] of 38). Dyspnoea developed in 22 (55%) of 40 patients (median time from illness onset to dyspnoea 8·0 days [IQR 5·0–13·0]). 26 (63%) of 41 patients had lymphopenia. All 41 patients had pneumonia with abnormal findings on chest CT. Complications included acute respiratory distress syndrome (12 [29%]), RNAaemia (six [15%]), acute cardiac injury (five [12%]) and secondary infection (four [10%]). 13 (32%) patients were admitted to an ICU and six (15%) died. Compared with non-ICU patients, ICU patients had higher plasma levels of IL2, IL7, IL10, GSCF, IP10, MCP1, MIP1A, and TNFα. Interpretation The 2019-nCoV infection caused clusters of severe respiratory illness similar to severe acute respiratory syndrome coronavirus and was associated with ICU admission and high mortality. Major gaps in our knowledge of the origin, epidemiology, duration of human transmission, and clinical spectrum of disease need fulfilment by future studies. Funding Ministry of Science and Technology, Chinese Academy of Medical Sciences, National Natural Science Foundation of China, and Beijing Municipal Science and Technology Commission.
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            Mal (MyD88-adapter-like) is required for Toll-like receptor-4 signal transduction.

            The recognition of microbial pathogens by the innate immune system involves Toll-like receptors (TLRs), which recognize pathogen-associated molecular patterns. Different TLRs recognize different pathogen-associated molecular patterns, with TLR-4 mediating the response to lipopolysaccharide from Gram-negative bacteria. All TLRs have a Toll/IL-1 receptor (TIR) domain, which is responsible for signal transduction. MyD88 is one such protein that contains a TIR domain. It acts as an adapter, being involved in TLR-2, TLR-4 and TLR-9 signalling; however, our understanding of how TLR-4 signals is incomplete. Here we describe a protein, Mal (MyD88-adapter-like), which joins MyD88 as a cytoplasmic TIR-domain-containing protein in the human genome. Mal activates NF-kappaB, Jun amino-terminal kinase and extracellular signal-regulated kinase-1 and -2. Mal can form homodimers and can also form heterodimers with MyD88. Activation of NF-kappaB by Mal requires IRAK-2, but not IRAK, whereas MyD88 requires both IRAKs. Mal associates with IRAK-2 by means of its TIR domain. A dominant negative form of Mal inhibits NF-kappaB, which is activated by TLR-4 or lipopolysaccharide, but it does not inhibit NF-kappaB activation by IL-1RI or IL-18R. Mal associates with TLR-4. Mal is therefore an adapter in TLR-4 signal transduction.
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              ST-Segment Elevation in Patients with Covid-19 — A Case Series

              To the Editor: Myocardial injury with ST-segment elevation has been observed in patients with coronavirus disease 2019 (Covid-19). Here, we describe our experience in the initial month of the Covid-19 outbreak in New York City. Patients with confirmed Covid-19 who had ST-segment elevation on electrocardiography were included in the study from six New York hospitals. Patients with Covid-19 who had nonobstructive disease on coronary angiography or had normal wall motion on echocardiography in the absence of angiography were presumed to have noncoronary myocardial injury. We identified 18 patients with Covid-19 who had ST-segment elevation indicating potential acute myocardial infarction (Fig. S1 in the Supplementary Appendix, available with the full text of this letter at NEJM.org). The median age of the patients was 63 years, 83% were men, and 33% had chest pain around the time of ST-segment elevation (Table 1). A total of 10 patients (56%) had ST-segment elevation at the time of presentation, and the other 8 patients had development of ST-segment elevation during hospitalization (median, 6 days) (Fig. S2A). Of 14 patients (78%) with focal ST-segment elevation, 5 (36%) had a normal left ventricular ejection fraction, of whom 1 (20%) had a regional wall-motion abnormality; 8 patients (57%) had a reduced left ventricular ejection fraction, of whom 5 (62%) had regional wall-motion abnormalities. (One patient did not have an echocardiogram.) Of the 4 patients (22% of the overall population) with diffuse ST-segment elevation, 3 (75%) had a normal left ventricular ejection fraction and normal wall motion; 1 patient had a left ventricular ejection fraction of 10% with global hypokinesis. A total of 9 patients (50%) underwent coronary angiography; 6 of these patients (67%) had obstructive disease, and 5 (56%) underwent percutaneous coronary intervention (1 after the administration of fibrinolytic agents) (Fig. S3). The relationship among electrocardiographic, echocardiographic, and angiographic findings are summarized in Figure S4. The 8 patients (44%) who received a clinical diagnosis of myocardial infarction had higher median peak troponin and d-dimer levels than the 10 patients (56%) with noncoronary myocardial injury (Fig. S2B and S2C). A total of 13 patients (72%) died in the hospital (4 patients with myocardial infarction and 9 with noncoronary myocardial injury). In this series of patients with Covid-19 who had ST-segment elevation, there was variability in presentation, a high prevalence of nonobstructive disease, and a poor prognosis. Half the patients underwent coronary angiography, of whom two thirds had obstructive disease. Of note, all 18 patients had elevated d-dimer levels. In contrast, in a previous study involving patients who presented with ST-segment elevation myocardial infarction, 64% had normal d-dimer levels. 1 Myocardial injury in patients with Covid-19 could be due to plaque rupture, cytokine storm, hypoxic injury, coronary spasm, microthrombi, or direct endothelial or vascular injury. 2 Myocardial interstitial edema has been shown on magnetic resonance imaging in such patients. 3
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                Author and article information

                Contributors
                shigeru.shibata@med.teikyo-u.ac.jp
                Journal
                Hypertens Res
                Hypertens. Res
                Hypertension Research
                Springer Singapore (Singapore )
                0916-9636
                1348-4214
                31 July 2020
                : 1-19
                Affiliations
                [1 ]ISNI 0000 0000 9239 9995, GRID grid.264706.1, Division of Nephrology, Department of Internal Medicine, , Teikyo University School of Medicine, ; Tokyo, Japan
                [2 ]ISNI 0000 0001 0672 2176, GRID grid.411497.e, Department of Preventive Medicine and Public Health, Faculty of Medicine, , Fukuoka University, ; Fukuoka, Japan
                [3 ]ISNI 0000 0000 9239 9995, GRID grid.264706.1, Department of Hygiene and Public Health, , Teikyo University School of Medicine, ; Tokyo, Japan
                [4 ]ISNI 0000000123090000, GRID grid.410804.9, Division of Cardiovascular Medicine, Department of Medicine, , Jichi Medical University School of Medicine, ; Tochigi, Japan
                [5 ]ISNI 0000 0001 0720 6587, GRID grid.410818.4, Department of Endocrinology and Hypertension, , Tokyo Women’s Medical University, ; Tokyo, Japan
                [6 ]ISNI 0000 0001 0702 8004, GRID grid.255137.7, Department of Nephrology and Hypertension, , Dokkyo Medical University, ; Tochigi, Japan
                [7 ]ISNI 0000 0004 0531 3030, GRID grid.411731.1, Department of Graduate School of Medicine (Cardiology), , International University of Health and Welfare, ; Fukuoka, Japan
                [8 ]ISNI 0000 0001 1011 3808, GRID grid.255464.4, Department of Pharmacology, , Ehime University Graduate School of Medicine, ; Ehime, Japan
                [9 ]ISNI 0000 0000 8662 309X, GRID grid.258331.e, Department of Pharmacology, Faculty of Medicine, , Kagawa University, ; Kagawa, Japan
                [10 ]ISNI 0000 0001 1167 1801, GRID grid.258333.c, Department of Cardiovascular Medicine and Hypertension, Graduate School of Medical and Dental Sciences, , Kagoshima University, ; Kagoshima, Japan
                [11 ]ISNI 0000 0001 1033 6139, GRID grid.268441.d, Department of Medical Science and Cardiorenal Medicine, , Yokohama City University Graduate School of Medicine, ; Yokohama, Japan
                [12 ]ISNI 0000 0004 1936 9959, GRID grid.26091.3c, Department of Endocrinology, Metabolism and Nephrology, , Keio University School of Medicine, ; Tokyo, Japan
                [13 ]ISNI 0000 0001 0660 6749, GRID grid.274841.c, Department of Cardiovascular Medicine, Faculty of Life Sciences, Graduate School of Medical Science, , Kumamoto University, ; Kumamoto, Japan
                [14 ]ISNI 0000 0004 0373 3971, GRID grid.136593.b, Department of Geriatric and General Medicine, , Osaka University Graduate School of Medicine, ; Osaka, Japan
                Article
                515
                10.1038/s41440-020-0515-0
                7393334
                © The Japanese Society of Hypertension 2020

                This article is made available via the PMC Open Access Subset for unrestricted research re-use and secondary analysis in any form or by any means with acknowledgement of the original source. These permissions are granted for the duration of the World Health Organization (WHO) declaration of COVID-19 as a global pandemic.

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