Characterization of myocardial injury in a cohort of patients with SARS-CoV-2 infection

Caro‐Codón, Juan; Rey, J.; Buño, Antonio; Iniesta, Ángel M.; Rosillo, Sandra; Castrejón‐Castrejón, Sergio; Merino, C; Marco, I; Martínez, Luis A.; Garcia-Veas, Jose M; Martín‐Polo, Lorena; Rodríguez‐Sotelo, Laura; Martínez‐Cossiani, Marcel; Gonzalez‐Valle, Luis; Herrero, Alicia; López-de-Sá, Esteban; Merino, José Luís

doi:10.1016/j.medcli.2021.02.001

Cited by 13 publications

(8 citation statements)

References 28 publications

(38 reference statements)

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“…In addition, studies have also shown a correlation of elevated serum troponin levels and a higher risk of myocardial injury and substantially higher mortality in COVID-19 patients (Knight et al, 2020;Shi et al, 2020;Wei et al, 2020;Caro-Codón et al, 2021). Notably, in a large study with 1,053 patients with COVID-19 in whom troponin-I, B-type natriuretic peptide, C-reactive protein, ferritin, and D-dimer were measured, only troponin was identified as the only independent predictor of 30-days mortality (Manocha et al, 2021).…”

Section: Long Term Consequences Of Covid-19 On the Heartmentioning

confidence: 99%

COVID-19 and the Vasculature: Current Aspects and Long-Term Consequences

Martínez-Salazar

Holwerda

Stüdle

et al. 2022

Front. Cell Dev. Biol.

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Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) was first identified in December 2019 as a novel respiratory pathogen and is the causative agent of Corona Virus disease 2019 (COVID-19). Early on during this pandemic, it became apparent that SARS-CoV-2 was not only restricted to infecting the respiratory tract, but the virus was also found in other tissues, including the vasculature. Individuals with underlying pre-existing co-morbidities like diabetes and hypertension have been more prone to develop severe illness and fatal outcomes during COVID-19. In addition, critical clinical observations made in COVID-19 patients include hypercoagulation, cardiomyopathy, heart arrythmia, and endothelial dysfunction, which are indicative for an involvement of the vasculature in COVID-19 pathology. Hence, this review summarizes the impact of SARS-CoV-2 infection on the vasculature and details how the virus promotes (chronic) vascular inflammation. We provide a general overview of SARS-CoV-2, its entry determinant Angiotensin-Converting Enzyme II (ACE2) and the detection of the SARS-CoV-2 in extrapulmonary tissue. Further, we describe the relation between COVID-19 and cardiovascular diseases (CVD) and their impact on the heart and vasculature. Clinical findings on endothelial changes during COVID-19 are reviewed in detail and recent evidence from in vitro studies on the susceptibility of endothelial cells to SARS-CoV-2 infection is discussed. We conclude with current notions on the contribution of cardiovascular events to long term consequences of COVID-19, also known as “Long-COVID-syndrome”. Altogether, our review provides a detailed overview of the current perspectives of COVID-19 and its influence on the vasculature.

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Section: Long Term Consequences Of Covid-19 On the Heartmentioning

confidence: 99%

COVID-19 and the Vasculature: Current Aspects and Long-Term Consequences

Martínez-Salazar

Holwerda

Stüdle

et al. 2022

Front. Cell Dev. Biol.

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“…Myocardial injury is an important pathogenic feature of COVID-19, where cardiovascular histopathology findings are reported in up to 48% of patients; moreover, cardiovascular magnetic resonance abnormalities are detected in 26% to 60% of recovered hospitalized patients [ 687 , 688 , 689 , 690 ]. The frequent presence of elevated high-sensitive troponin I (hs-TnI) in COVID-19 patients is significantly associated with higher rates of cardiac complications [ 691 ]. Even though immune-mediated inflammation and hypercoagulability [ 692 ], the dysregulation in the CD147-cyclophilin pathway [ 693 ], as well as other potential direct and indirect mechanisms have been proposed [ 694 ], the exact causal mechanisms for myocardial injury in COVID-19 still await further elucidation [ 695 ].…”

Section: Melatonin Regulates Sars-cov-2-mediated Crosstalk Between Th...mentioning

confidence: 99%

Melatonin: Regulation of Viral Phase Separation and Epitranscriptomics in Post-Acute Sequelae of COVID-19

Loh¹,

Reíter

2022

IJMS

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The relentless, protracted evolution of the SARS-CoV-2 virus imposes tremendous pressure on herd immunity and demands versatile adaptations by the human host genome to counter transcriptomic and epitranscriptomic alterations associated with a wide range of short- and long-term manifestations during acute infection and post-acute recovery, respectively. To promote viral replication during active infection and viral persistence, the SARS-CoV-2 envelope protein regulates host cell microenvironment including pH and ion concentrations to maintain a high oxidative environment that supports template switching, causing extensive mitochondrial damage and activation of pro-inflammatory cytokine signaling cascades. Oxidative stress and mitochondrial distress induce dynamic changes to both the host and viral RNA m6A methylome, and can trigger the derepression of long interspersed nuclear element 1 (LINE1), resulting in global hypomethylation, epigenetic changes, and genomic instability. The timely application of melatonin during early infection enhances host innate antiviral immune responses by preventing the formation of “viral factories” by nucleocapsid liquid-liquid phase separation that effectively blockades viral genome transcription and packaging, the disassembly of stress granules, and the sequestration of DEAD-box RNA helicases, including DDX3X, vital to immune signaling. Melatonin prevents membrane depolarization and protects cristae morphology to suppress glycolysis via antioxidant-dependent and -independent mechanisms. By restraining the derepression of LINE1 via multifaceted strategies, and maintaining the balance in m6A RNA modifications, melatonin could be the quintessential ancient molecule that significantly influences the outcome of the constant struggle between virus and host to gain transcriptomic and epitranscriptomic dominance over the host genome during acute infection and PASC.

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“…It has been shown that myocardial damage occurs in about 20% of patients with severe COVID-19 ( 26 ). In such circumstances, even mild increases of cTnI (well below the 99th percentile) are associated with a higher prevalence of cardiac and non-cardiac complications, and a higher mortality ( 8 , 27 ). In 2,700 patients with severe COVID-19, signs of myocardial injury were common and usually associated with mild elevations in troponin concentration ( 28 ).…”

Section: Discussionmentioning

confidence: 99%

“…Recent evidence suggests that increased troponin levels in patients with severe (1) COVID-19 are associated with an increased likelihood of cardiovascular disease, critical illness (2, 3), and death (4,5). Patients with COVID-19 not only show troponin levels above the 99th percentile more frequently, but also show measurably increased levels of troponins (below the 99th percentile but above the limit of detection) more frequently (6)(7)(8)(9).…”

Section: Introductionmentioning

confidence: 99%

Mild COVID-19 induces early, quantifiable, persistent troponin I elevations in elder men

Bürgi¹,

Rösslein²,

Nolte³

et al. 2022

Front. Cardiovasc. Med.

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ImportanceElderly patients, especially men, are at risk of increased morbidity from coronavirus disease 2019 (COVID-19). Long-term data on troponin I levels in longitudinal observational studies of outpatients with mild to moderate COVID-19 are scarce.ObjectiveThis controlled cohort study aimed to evaluate the course of troponin I concentrations over a long period in convalescent COVID-19 outpatients with mild to moderate symptoms.Setting and participantsIn this cohort study, individuals with PCR-confirmed, mild to moderate SARS-CoV-2 infection as well as control individuals with confirmed negative PCR and negative SARS-CoV-2 serology were included. Study visits were performed from April 2020 through July 2021 (initialized during the first wave of the corona pandemic in Switzerland). A study visit in patients comprised blood draws every week in the first month and additionally after 8 weeks. This course was repeated in patients observed long-term.ResultsThis study enrolled 278 individuals from the Canton of St. Gallen, Switzerland, aged 12–92 years (59.5% women), who had mild to moderate COVID-19 symptoms (outpatients only) and a diagnosis confirmed by positive RT-PCR. Fifty-four of the participants with confirmed SARS-CoV-2 infection were followed for 14 months with repeat cycles of the testing protocol. In addition, 115 symptomatic patients that were PCR and serology negative were enrolled in the same time period as a control group. In COVID-19 patients, low-level troponin I concentrations (cTnI) were significantly increased from baseline until week 9 after positive RT-PCR diagnosis in men older than 54 years [ΔcTnI = 5.0 ng/L (median); 95% CI 4.1–6.0; p = 0.02]. The troponin I concentration remained elevated throughout 14 months in men older than 54 years within the cohort with a prolonged observation period. This statistically significant change in troponin I concentration was not dependent on co-morbidities in this group. ALT, Creatinine, BNP, and D-Dimer values after convalescence did not differ in comparison to the control cohort.ConclusionIn this analysis of individuals with confirmed SARS-CoV-2 infection, hs troponin I levels of men aged 54 or older significantly increased after infection. They remained elevated for at least 14 months after diagnosis. This suggests the possibility of an ongoing, long-term, low-grade myocardial injury. Further studies with focus on elderly patients and a prolonged observational period are necessary to elucidate whether the phenomenon observed is associated with detectable structural changes to the heart muscle or is without further clinical consequences.

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Characterization of myocardial injury in a cohort of patients with SARS-CoV-2 infection

Cited by 13 publications

References 28 publications

COVID-19 and the Vasculature: Current Aspects and Long-Term Consequences

COVID-19 and the Vasculature: Current Aspects and Long-Term Consequences

Melatonin: Regulation of Viral Phase Separation and Epitranscriptomics in Post-Acute Sequelae of COVID-19

Mild COVID-19 induces early, quantifiable, persistent troponin I elevations in elder men

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