Comparison and Analysis on the Existing Single-Herbal Strategies against Viral Myocarditis.

Purpose: Herbal medicine is one of crucial symbols of Chinese national medicine. Investigation on molecular responses of different herbal strategies against viral myocarditis is immeasurably conducive to targeting drug development in the current international absence of miracle treatment. Methods: Literature retrieval platforms were applied in the collection of existing empirical evidences for viral myocarditis-related single-herbal strategies. SwissTargetPrediction, Metascape, and Discovery Studio coordinating with multidatabases investigated underlying target genes, interactive proteins, and docking molecules in turn. Results: Six single-herbal medicines consisting of Huangqi (Hedysarum Multijugum Maxim), Yuganzi (Phyllanthi Fructus), Kushen (Sophorae Flavescentis Radix), Jianghuang (Curcumaelongae Rhizoma), Chaihu (Radix Bupleuri), and Jixueteng (Spatholobus Suberectus Dunn) meet the requirement. There were 11 overlapped and 73 unique natural components detected in these herbs. SLC6A2, SLC6A4, NOS2, PPARA, PPARG, ACHE, CYP2C19, CYP51A1, and CHRM2 were equally targeted by six herbs and identified as viral myocarditis-associated symbols. MCODE algorithm exposed the hub role of SRC and EGFR in strategies without Jianghuang. Subsequently, we learned intermolecular interactions of herbal components and their targeting heart-tissue-specific CHRM2, FABP3, TNNC1, TNNI3, TNNT2, and SCN5A and cardiac-myocytes-specific IL6, MMP1, and PLAT coupled with viral myocarditis. Ten interactive characteristics such as π-alkyl and van der Waals were modeled in which ARG111, LYS253, ILE114, and VAL11 on cardiac troponin (TNNC1-TNNI3-TNNT2) and ARG208, ASN106, and ALA258 on MMP1 fulfilled potential communicating anchor with ellagic acid, 5α, 9α-dihydroxymatrine, and leachianone g via hydrogen bond and hydrophobic interaction, respectively. Conclusions: The comprehensive outcomes uncover differences and linkages between six herbs against viral myocarditis through component and target analysis, fostering development of drugs.

Imaging of Cardiac Infections: A Comprehensive Review and Investigation Flowchart for Diagnostic Workup.

Infections of the cardiovascular system may present with nonspecific symptoms, and it is common for patients to undergo multiple investigations to arrive at the diagnosis. Echocardiography is central to the diagnosis of endocarditis and pericarditis. However, cardiac computed tomography (CT) and magnetic resonance imaging also play an additive role in these diagnoses; in fact, magnetic resonance imaging is central to the diagnosis of myocarditis. Functional imaging (fluorine-18 fluorodeoxyglucose-positron emission tomography/CT and radiolabeled white blood cell single-photon emission computed tomography/CT) is useful in the diagnosis in prosthesis-related and disseminated infection. This pictorial review will detail the most commonly encountered cardiovascular bacterial and viral infections, including coronavirus disease-2019, in clinical practice and provide an evidence basis for the selection of each imaging modality in the investigation of native tissues and common prostheses.

Extrapulmonary complications of COVID-19: A multisystem disease?

The outbreak of coronavirus disease 2019 (COVID-19), caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has been recently declared a pandemic by the World Health Organization. In addition to its acute respiratory manifestations, SARS-CoV-2 may also adversely affect other organ systems. To date, however, there is a very limited understanding of the extent and management of COVID-19-related conditions outside of the pulmonary system. This narrative review provides an overview of the current literature about the extrapulmonary manifestations of COVID-19 that may affect the urinary, cardiovascular, gastrointestinal, hematological, hematopoietic, neurological, or reproductive systems. This review also describes the current understanding of the extrapulmonary complications caused by COVID-19 to improve the management and prognosis of patients with COVID-19.

The COSEVAST Study Outcome: Evidence of COVID-19 Disease Severity Proportionate To Surge in Arterial Stiffness (preprint)

Background: Arterial stiffness has been established as an independent and specific marker of various chronic cardiovascular diseases. Based on the detailed review of available research and case studies reported in reputed international journals, it can be concluded that Endothelial Damage (Endotheliitis) both in small and large arteries may be an important factor of morbidity and mortality in COVID-19 patients. Despite the pathological evidence of structural damage due to Endotheliitis in COVID-19 patients, the functional deterioration of the vasculature was not yet studied.Hyper activated inflammation of the arteries may lead to sudden rise in arterial stiffness, the functional indicator of severity of cardiovascular impairment, which develops into Multiple Organ Dysfunction Syndrome (MODS) in COVID-19. Supervising and controlling the arterial Stiffness may be a way to mitigate the morbidities and mortalities caused due to COVID-19. Objective: Our primary objective was to study functional arterial damage in COVID-19 disease and establish the non-invasive measurement of Arterial Stiffness as an independent marker of disease severity.Methods: We recorded the Arterial Stiffness of 23 Mild, 21 Moderate and 20 Severe COVID-19 patients grouped on latest NIH severity criteria. Patients with pre-existing Diabetes and Hypertension were excluded. We observed Arterial Stiffness of COVID-19 patients with standard parameters like non-invasive Carotid-Femoral Pulse Wave velocity (cfPWV), Age-Normalized increase in cfPWV (ANI_cfPWV), Age-Normalized increase in Aortic Augmentation Pressure (ANI_AugP) and Heart rate-normalized Augmentation Index (HRN_ AIx).Results: Moderate and Severe COVID-19 patients have extremely significantly elevated arterial stiffness than Mild patients. In Mild patients, cfPWV (829.1 ± 139.2 cm/s) was significantly lower than both Moderate (1067 ± 152.5 cm/s, P < 0.0001)and Severe (1416 ± 253.9 cm/s, P < 0.0001) patients. ANI_cfPWV in Moderate and Severe patients was significantly higher than Mild patients. (Mild: 101.2 ± 126.1 cm/s; Moderate: 279 ± 114.4 cm/s; Severe: 580.1 ± 216.4 cm/s; intergroup P <0.0001).Similarly, ANI_AugP also showed a significant difference in all three groups. (Mild: -1.891 ±2.817 mmHg; Moderate: 3.212 ± 3.124 mmHg; Severe: 7.246 ± 4.908 mmHg; with P <0.0001, P =0.0031, P <0.0001 respectively). HRN_ AIx also showed a significant increase in Moderate and Severe groups in comparison with the Mild Group. (Mild: 13.34 ±14.18; Moderate: 5.656±8.610; Severe: 24.80± 7.745; intergroup P <0.0001).Conclusion: This is the first study establishing the functional deterioration of vasculature in terms of abnormal increase in arterial stiffness in proportion with severity of COVID-19 disease. Our findings strongly suggest that arterial stiffness can be an independent and accurate marker for objective risk stratification and therapeutic alleviation of the acute cardiovascular complications like MODS in COVID-19.Trial Registration: The study design was registered with the Clinical Trials Registry of India (CTRI No. CTRI/2020/10/028489).Funding Statement: No external funding.Declaration of Interests: Authors declare no conflict of interest.Ethics Approval Statement: The study protocol, informed consents and other trial-related documents received the written approval of Institutional Ethics Committee (IEC No. AIIMS/Pat/IEC/2020/595).

Association of Cardiac Infection With SARS-CoV-2 in Confirmed COVID-19 Autopsy Cases.

Importance: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) can be documented in various tissues, but the frequency of cardiac involvement as well as possible consequences are unknown. Objective: To evaluate the presence of SARS-CoV-2 in the myocardial tissue from autopsy cases and to document a possible cardiac response to that infection. Design, Setting, and Participants: This cohort study used data from consecutive autopsy cases from Germany between April 8 and April 18, 2020. All patients had tested positive for SARS-CoV-2 in pharyngeal swab tests. Exposures: Patients who died of coronavirus disease 2019. Main Outcomes and Measures: Incidence of SARS-CoV-2 positivity in cardiac tissue as well as CD3+, CD45+, and CD68+ cells in the myocardium and gene expression of tumor necrosis growth factor α, interferon γ, chemokine ligand 5, as well as interleukin-6, -8, and -18. Results: Cardiac tissue from 39 consecutive autopsy cases were included. The median (interquartile range) age of patients was 85 (78-89) years, and 23 (59.0%) were women. SARS-CoV-2 could be documented in 24 of 39 patients (61.5%). Viral load above 1000 copies per µg RNA could be documented in 16 of 39 patients (41.0%). A cytokine response panel consisting of 6 proinflammatory genes was increased in those 16 patients compared with 15 patients without any SARS-CoV-2 in the heart. Comparison of 15 patients without cardiac infection with 16 patients with more than 1000 copies revealed no inflammatory cell infiltrates or differences in leukocyte numbers per high power field. Conclusions and Relevance: In this analysis of autopsy cases, viral presence within the myocardium could be documented. While a response to this infection could be reported in cases with higher virus load vs no virus infection, this was not associated with an influx of inflammatory cells. Future investigations should focus on evaluating the long-term consequences of this cardiac involvement.