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Since its recognition in December 2019, covid-19 has rapidly spread globally causing a pandemic. Pre-existing comorbidities such as hypertension, diabetes, and cardiovascular disease are associated with a greater severity and higher fatality rate of covid-19. Furthermore, COVID-19 contributes to cardiovascular complications, including acute myocardial injury as a result of acute coronary syndrome, myocarditis, stress-cardiomyopathy, arrhythmias, cardiogenic shock, and cardiac arrest. The cardiovascular interactions of COVID-19 have similarities to that of severe acute respiratory syndrome, Middle East respiratory syndrome and influenza. Specific cardiovascular considerations are also necessary in supportive treatment with anticoagulation, the continued use of renin-angiotensin-aldosterone system inhibitors, arrhythmia monitoring, immunosuppression or modulation, and mechanical circulatory support.

ObjectiveWe sought to explore the prevalence and immediate clinical implications of acute myocardial injury in a cohort of patients with COVID-19 in a region of China where medical resources are less stressed than in Wuhan (the epicentre of the pandemic).MethodsWe prospectively assessed the medical records, laboratory results, chest CT images and use of medication in a cohort of patients presenting to two designated covid-19 treatment centres in Sichuan, China. Outcomes of interest included death, admission to an intensive care unit (ICU), need for mechanical ventilation, treatment with vasoactive agents and classification of disease severity. Acute myocardial injury was defined by a value of high-sensitivity troponin T (hs-TnT) greater than the normal upper limit.ResultsA total of 101 cases were enrolled from January to 10 March 2020 (average age 49 years, IQR 34–62 years). Acute myocardial injury was present in 15.8% of patients, nearly half of whom had a hs-TnT value fivefold greater than the normal upper limit. Patients with acute myocardial injury were older, with a higher prevalence of pre-existing cardiovascular disease and more likely to require ICU admission (62.5% vs 24.7%, p=0.003), mechanical ventilation (43.5% vs 4.7%, p<0.001) and treatment with vasoactive agents (31.2% vs 0%, p<0.001). Log hs-TnT was associated with disease severity (OR 6.63, 95% CI 2.24 to 19.65), and all of the three deaths occurred in patients with acute myocardial injury.ConclusionAcute myocardial injury is common in patients with COVID-19 and is associated with adverse prognosis.

ObjectiveThe present study tested the hypothesis that arterial stiffness will be elevated across overall and specific inflammatory disorders compared with an inflammation-free comparison group.MethodsAdults (n=171 125) aged 40–70 years from the UK Biobank who were cardiovascular disease (CVD) free and who had their arterial stiffness assessed at the time of study recruitment between 2006 and 2010 were included. The main exposure was represented by a global measure of chronic inflammatory disorders. Two inflammatory biomarker measures (eg, leucocytes count, granulocytes count) were included as markers of inflammation severity. The arterial stiffness index assessed by a non-invasive technique represented the study primary outcome measure.ResultsA total of 5976 (3%) participants diagnosed with inflammatory disorders and 165 149 participants without an inflammatory disorder had data on arterial stiffness. Adjusted linear regression analyses revealed a 14% increment in mean arterial stiffness for chronic inflammatory disorders (beta coefficient (β) 1.14, 95% CI 1.05 to 1.24, P=0.002) compared with no chronic inflammatory disorder. Arterial stiffness tended to increase (P value=0.031) with tertiles of leucocytes and granulocytes count. For instance, mean arterial stiffness values increased from 1.11 (95% CI 0.96 to 1.29) in the first tertile to 1.17 (95% CI 1.02 to 1.34) in the second tertile, and 1.21 (95% CI 1.05 to 1.39) in the third tertile of leucocytes count. There was evidence for similar associations with some of the most common individual inflammatory disorders, including psoriasis and rheumatoid arthritis.ConclusionArterial stiffness was associated with multiple chronic inflammatory disorders. An increasing trend in mean arterial stiffness was also documented with increasing tertiles of different inflammatory biomarkers. Future studies are needed to investigate the discriminant value of arterial stiffness to predict major CVD events within various inflammatory disorders.

ObjectiveRisk stratification is crucial to optimise treatment strategies in patients with COVID-19. We aimed to evaluate the impact on mortality of an early assessment of cardiac biomarkers in patients with COVID-19.MethodsHumanitas Clinical and Research Hospital (Rozzano-Milan, Lombardy, Italy) is a tertiary centre that has been converted to the management of COVID-19. Patients with confirmed COVID-19 were entered in a dedicated database for cohort observational analyses. Outcomes were stratified according to elevated levels (ie, above the upper level of normal) of high-sensitivity cardiac troponin I (hs-TnI), B-type natriuretic peptide (BNP) or both measured within 24 hours after hospital admission. The primary outcome was all-cause mortality.ResultsA total of 397 consecutive patients with COVID-19 were included up to 1 April 2020. At the time of hospital admission, 208 patients (52.4%) had normal values for cardiac biomarkers, 90 (22.7%) had elevated both hs-TnI and BNP, 59 (14.9%) had elevated only BNP and 40 (10.1%) had elevated only hs-TnI. The rate of mortality was higher in patients with elevated hs-TnI (22.5%, OR 4.35, 95% CI 1.72 to 11.04), BNP (33.9%, OR 7.37, 95% CI 3.53 to 16.75) or both (55.6%, OR 18.75, 95% CI 9.32 to 37.71) as compared with those without elevated cardiac biomarkers (6.25%). A multivariate analysis identified concomitant elevation of both hs-TnI and BNP as a strong independent predictor of all-cause mortality (OR 3.24, 95% CI 1.06 to 9.93).ConclusionsAn early detection of elevated hs-TnI and BNP predicts mortality in patients with COVID-19. Cardiac biomarkers should be systematically assessed in patients with COVID-19 at the time of hospital admission in order to optimise risk stratification.

ObjectiveSepsis-induced myocardial dysfunction (SIMD) can involve both the left and right ventricles. However, the characteristics and outcomes across various manifestations of SIMD remain unknown.MethodsThis was a retrospective cohort study using a prospective registry of septic shock from January 2011 and April 2017. Patients with clinically presumed cardiac dysfunction underwent echocardiography within 72 hours after admission and were enrolled (n=778). SIMD was classified as left ventricle (LV) systolic/diastolic and right ventricle (RV) dysfunction, which were defined based on the American Society of Echocardiography criteria. The primary outcome was 28-day mortality.ResultsOf the 778 septic shock patients who underwent echocardiography, 270 (34.7%) showed SIMD. The median age was 67.0 years old, and the male was predominant (57.3%). Among them, 67.3% had LV systolic dysfunction, 40.7% had RV dysfunction and 39.3% had LV diastolic dysfunction. Although serum lactate level and sequential organ failure assessment score were not significantly different between groups, SIMD group showed higher troponin I (0.1 vs 0.1 ng/mL; p=0.02) and poor clinical outcomes, including higher 28-day mortality (35.9 vs 26.8%; p<0.01), longer intensive care unit length of stay (5 vs 2 days; p<0.01) and prolonged mechanical ventilation (9 vs 4 days; p<0.01). Multivariate analysis showed that isolated RV dysfunction was an independent risk factor of 28-day mortality (OR 2.26, 95% CI 1.04 to 4.91).ConclusionsOne-third of patients with septic shock showed various myocardial dysfunctions. LV systolic dysfunction was common; however, only RV dysfunction was associated with short-term mortality.

ObjectivesThe present study aimed to assess the relationship between inflammatory disorders with cardiometabolic diseases and mortality within a community-based population.MethodsThe UK Biobank data were used to conduct two investigations: a cross-sectional study to estimate cardiometabolic risk and a prospective cohort study to estimate mortality risk. Binary regression analyses were used to model the association between coronary heart disease, stroke, type 2 diabetes, venous thromboembolism and peripheral artery disease diagnoses with seven inflammatory disorders (eg, rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), psoriasis, ankylosing spondylitis (AS), systemic vasculitis, Crohn’s disease and ulcerative colitis (UC)). Cox proportional hazards was used to estimate all-cause and cardiovascular-related mortality.ResultsAbout 4% (n=19, 082) of the study population (n=5 02 641) were diagnosed with a chronic inflammatory disorder. The most common inflammatory disorder was psoriasis (n=6286), and the least common was SLE (n=654). SLE showed the strongest association with multiple (relative risk (RR) 6.36, 95% CI 4.37 to 9.25) risk of cardiometabolic diseases, followed by the RA (RR 1.70, 95% CI 1.59 to 1.83), UC (RR 1.69, 95% CI 1.51 to 1.89), AS (RR 1.28, 95% CI 1.09 to 1.52), vasculitis (RR 1.64, 95% CI 1.42–1.90) and psoriasis (RR 1.25, 95% 1.16 to 1.35) disorders. The magnitude of the association was higher among participants prescribed non-steroidal anti-inflammatory drugs or corticosteroids drugs, with multiple cardiometabolic risk being greater within SLE (RR 12.35, 95% CI 7.18 to 21.24), followed by UC (RR 3.81, 95% CI 2.69 to 5.38), Crohn’s disease (RR 3.07, 95% CI 1.85 to 5.11), RA (RR 3.06, 95% CI 2.44 to 3.85), psoriasis (RR 2.36, 95% CI 1.88 to 2.95), AS (RR 2.25, 95% CI 1.48 to 3.41) and vasculitis (RR 1.89, 95% CI 1.28 to 2.79). Similar pattern was observed with respect to the cumulative cardiometabolic risk.ConclusionInflammatory disorders are associated with heightened risk of cardiometabolic events, which may vary by anti-inflammatory therapy and duration. All-cause mortality was also higher among specific inflammatory disorders compared with the absence of inflammatory disorders.

Auto-immune and inflammatory diseases are heterogenous in their clinical manifestations and prognosis, even among individuals presenting with the same pathology. Understanding the immunological alterations involved in their pathogenesis provides valuable insights in different clinical phenotypes and treatment responses. Immunophenotyping could lead to significant improvements in diagnosis, monitoring, initial treatment decisions and follow-up in autoimmune and inflammatory diseases. Mass cytometry provides measurement of over 40 simultaneous cellular parameters at single-cell resolution, and therefore holds immense potential to evaluate complex cellular systems and for high-dimensional single-cell analysis. The high dimensionality of mass cytometry provides better coverage of immune populations dynamics, with sufficient power to identify rare cell types compared to flow cytometry. In this comprehensive review, we explore how mass cytometry findings contributed in the past decade to a deeper understanding of the cellular actors involved in systemic auto-immune and auto-inflammatory diseases with their respective therapeutic and prognostic impact. We also delve into the bioinformatical approaches applied to mass cytometry to analyze the high volumes of data generated, as well as the impact of the use of complementary single cell RNA sequencing, and their spatial modalities. Our analysis highlights the fact that mass cytometry captures major information on cell populations providing insights on the complex pathogenesis of autoimmune diseases. Future research designs could include mass cytometry findings in association to other -omics to stratify patients in adequate therapeutic arms and provide advancements in personalized therapies in the field of auto-immune and inflammatory diseases.

Immunoglobulin G4-related disease (IgG4-RD) is a systemic fibroinflammatory disease characterised by multiorgan lymphoplasmacytic infiltration, obliterative phlebitis and storiform fibrosis. It can be associated with cardiovascular pathology. The objective of this narrative review is to summarise the published literature on cardiovascular manifestations of IgG4-RD and to provide a basis for diagnosis and management of the condition by the practising cardiologist.We propose the following categorisations of cardiovascular IgG4-RD: aortitis, medium-vessel arteritis, pulmonary vascular disease, phlebitis, valvulopathy, pericarditis, myocardial disease and antineutrophilic cytoplasmic antibody-associated vasculitis. We also review herein developments in radiological diagnosis and reported medical and surgical therapies. Cardiovascular lesions frequently require procedural and/or surgical interventions, such as aortic aneurysm repair and valve replacement. IgG4-RD of the cardiovascular system results in serious complications that can be missed if not evaluated aggressively. These are likely underdiagnosed, as clinical presentations frequently mimic cardiovascular disease due to more common aetiologies (myocardial infarction, abdominal aortic aneurysm and so on). While systemic corticosteroids are the mainstay of IgG4-RD treatment, biological and disease-modifying agents are becoming more widely used. Cardiologists should be aware of cardiovascular IgG4-RD as a differential diagnosis, and understand the roles of corticosteroids, disease-modifying agents and biologicals, as well as their integration with surgical approaches. There are several knowledge gaps, including diagnosis, risk factors, pathogenesis and appropriate management in Ig4-RD of the cardiovascular system. Areas lacking well-conducted randomized trials include safety of steroids in the setting of vascular aneurysms and the role of disease-modifying drugs and biological agents in patients with established cardiovascular complications of this multifaceted enigmatic disease.