This study evaluates the pathogenesis of COVID-19 and the therapeutic efficacy of sitagliptin in diabetic and obese mice. Using a novel double-transgenic mouse model (db/db and K18-hACE2), the findings demonstrates that SARS-CoV-2 infection (Delta variant) causes severe multi-organ damage, glucose metabolism abnormalities, insulin resistance, and pancreatic islet cell damage in diabetic mice. Infected diabetic mice displayed higher mortality, inflammation (elevated TNF-α, IL-6, IL-1β), and fibrinolytic activity (PAI-1), alongside dysregulated diabetes-related hormones (GLP-1, leptin, ghrelin, resistin) compared to non-diabetic controls. Sitagliptin treatment reduced organ injury, hyperglycemia, inflammation, and fibrinolytic activity while improving insulin resistance and glucose metabolism. This was evidenced by decreased fasting blood glucose levels, improved insulin sensitivity, and elevated insulin and GLP-1 levels. These findings suggest sitagliptin is a promising therapeutic strategy to mitigate the severity of COVID-19 in experimental diabetes by modulating inflammation and improving metabolic syndrome. Further mechanistic investigations revealed that the level of hACE2 expression, along with the activation of NF-κB and IRS-1, play critical roles in the development of SARS-CoV-2-induced diabetes, the exacerbation of pre-existing diabetes, and the therapeutic efficacy of sitagliptin.

Cardiovascular diseases, including stroke driven by atherosclerosis, remain a leading global health concern. Current diagnostic imaging modalities such as magnetic resonance imaging fail to characterize oxidative stress within atherosclerotic plaques. Here, we introduce difuranfluoreno-dithiophen-based polymers designed for afterglow imaging, offering ultrabright luminescence, ultralow-power excitation (0.087 milliwatts per square centimeter), and ultrashort acquisition times (0.01 seconds). Through a molecular engineering strategy, we have optimized polymers for enhanced reactive oxygen species (ROS) generation capability, ROS capturing capability, and fluorescence quantum yield, resulting in an increase in afterglow intensity (~130-fold) compared to commonly used 2-methoxy-5-(2'-ethylhexyloxy)-1,4-phenylenevinylene polymer (MEHPPV). Additionally, we have developed ratiometric afterglow nanoparticles doped with oxidative stress-responsive molecules, enabling imaging of oxidative stress markers in atherosclerotic plaque. This approach provides a tool for cardiovascular imaging and diagnostics, which is conducive to the auxiliary diagnosis and risk stratification of atherosclerosis.

N-acetylcysteine (NAC) can take part in the treatment of chronic respiratory diseases because of the potent mucolytic, antioxidant, and anti-inflammatory effects of NAC. However, less is known about its use in the treatment of acute lung injury. Nowadays, an increasing number of studies indicates that early administration of NAC may reduce markers of oxidative stress and alleviate inflammation in animal models of acute lung injury (ALI) and in patients suffering from distinct forms of acute respiratory distress syndrome (ARDS) or pulmonary infections including community-acquired pneumonia or Coronavirus Disease (COVID)-19. Besides low costs, easy accessibility, low toxicity, and rare side effects, NAC can also be combined with other drugs. This article provides a review of knowledge on the mechanisms of inflammation and oxidative stress in various forms of ALI/ARDS and critically discusses experience with the use of NAC in these disorders. For preparing the review, articles published in the English language from the PubMed database were used.

COVID-19 is associated with increased risk of post-acute cardiovascular outcomes. Population-based evidence for long periods of observation is still limited.

This population-based cohort study was conducted using data (2020-2021) from the British Columbia COVID-19 Cohort. The exposure of interest was severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, identified through reverse transcription-polymerase chain reaction (RT-PCR) assay. Individuals who tested positive (exposed) on RT-PCR were matched to negative controls (unexposed) on sex, age, and RT-PCR collection date in a 1:4 ratio. Outcomes of interest were incident major adverse cardiovascular events and acute myocardial infarction, identified more than 30 days after RT-PCR collection date. The association between SARS-CoV-2 infection and cardiovascular risk was assessed through multivariable survival models. Population attributable fractions were computed from Cox models.

We included 649,320 individuals: 129,864 exposed and 519,456 unexposed. The median duration of follow-up was 260 days; 1,786 events (0.34%) took place among the unexposed, and 702 (0.54%) in the exposed. The risk of major adverse cardiovascular events was higher in the exposed (adjusted hazard ratio [aHR] 1.34; 95% confidence interval [CI], 1.22-1.46), with greater risk observed in those who were hospitalized (aHR 3.81; 95% CI, 3.12-4.65) or required intensive care unit admission (aHR 6.25; 95% CI, 4.59-8.52) compared with the unexposed group. The fraction of cardiovascular events attributable to SARS-CoV-2 was 7.04% (95% CI, 4.67-9.41%). Comparable results were observed for acute myocardial infarction.

SARS-CoV-2 infection was associated with higher cardiovascular risk, with graded increase across the acute COVID-19 severity, contributing to 7% of incident major adverse cardiovascular events. These findings suggest that long-term monitoring of cardiovascular risk is required in COVID-19 survivors.

Viral infection by SARS-CoV2 is a pandemic affecting over 600 million people worldwide. One of five hospitalized patients may present myocardial injury, strongly associated with disease severity and mortality.

Retrospective cross-sectional study of hospitalized COVID-19 patients diagnosed between May 01, 2020, and June 30, 2021, from the database of the Registro Latinoamericano de Enfermedad Cardiovascular y COVID-19 (CARDIO COVID 19-20) with a troponin value recorded during hospitalization. A descriptive analysis of sociodemographic and clinical characteristics was performed. Bivariate analysis was conducted according to the presence or absence of myocardial injury. Survival analysis was made using Kaplan-Meier curves, by the presence of myocardial injury. A multivariate Poisson regression model was performed to determine factors associated with mortality. Statistical analyses were performed using the RStudio V.1.4.1717 package.

A total of 2,134 patients were included, 64.2% were male, and 911 patients had myocardial injury. The median age of the total population was 61 years. Individuals with myocardial injury had a higher prevalence of hypertension, diabetes, and dyslipidemia. Survival probability was lower in this subgroup. Patients with myocardial injury had a 1.95 times higher risk of death. Age, male sex, chronic kidney disease, arrhythmias, decompensated heart failure, requirement of inotropic/vasopressor, and invasive mechanical ventilation were related to higher mortality risk in patients with myocardial injury.

Patients with COVID-19 and myocardial injury exhibit a broad spectrum of cardiac abnormalities. Myocardial injury is associated with a higher disease severity and risk of in-hospital mortality. This multicenter study uniquely represents data from 13 Latin American countries, offering regional insights into the impact of myocardial injury during the COVID-19 pandemic.

Epicardial adipose tissue (EAT), a unique fat depot surrounding the heart, plays a multifaceted role in glucose and lipid metabolism, thermogenesis, and the secretion of bioactive molecules that influence cardiac structure and function. Its proximity to the myocardium allows it to contribute directly to CVDs, including coronary artery disease, arrhythmias, and heart failure. In particular, excessive EAT has emerged as a significant factor in heart failure with preserved ejection fraction (HFpEF), the most common form of heart failure, especially in individuals with obesity and diabetes. Traditional metrics like body mass index (BMI) fail to capture the complexities of visceral fat, as patients with similar BMIs can exhibit varying CVD risks. EAT accumulation induces mechanical stress and fosters a pro-inflammatory and fibrotic environment, driving cardiac remodeling and dysfunction. Pharmacological modulation of EAT has shown promise in delivering cardiometabolic benefits. Recent advancements in diabetes therapies, such as SGLT2 inhibitors and GLP-1 receptor agonists, and antilipidemic drugs have demonstrated their potential in reducing pro-inflammatory cytokine production and improving glucose regulation, which directly influences EAT. These discoveries suggest that EAT could be a significant therapeutic target, though further investigation is necessary to elucidate its role in HFpEF and other CVDs. Recent advances have identified the prokineticin/PKR1 signaling pathway as pivotal in EAT development and remodeling. This pathway regulates epicardial progenitor cells (EPDCs), promoting angiogenesis while reducing EAT accumulation and metabolic stress on the heart, particularly under high-calorie conditions. Prokineticin, acting through its receptor PKR1, limits visceral adipose tissue growth, enhances insulin sensitivity, and offers cardioprotection by reducing oxidative stress and activating cellular survival pathways. In this review, we provide a comprehensive analysis of EAT's role in CVDs, explore novel therapeutic strategies targeting EAT, and highlight the potential of prokineticin signaling as a promising treatment for HFpEF, obesity, and diabetes.

Since its emergence in 2019, COVID-19 has continued to pose significant threats to both the physical and mental health of the global population, as well as to healthcare systems worldwide (Raman et al., Eur Heart J 43:1157-1172, 2022). Emerging evidence indicates that COVID-19 may lead to post-acute COVID-19 syndrome (PACS) with cardiovascular implications, potentially driven by factors such as ACE2 interaction with viruses, systemic inflammation, and endothelial dysfunction. However, there remains a limited amount of research on the cardiovascular manifestations of PACS, which may delay the development of optimal treatment strategies for affected patients. Therefore, it is crucial to investigate the prevalence of cardiovascular sequelae in COVID-19 patients and to determine whether COVID-19 infection acts as an independent risk factor for these outcomes.

This meta-analysis adhered to PRISMA guidelines and was registered in PROSPERO (CRD42024524290). A systematic search of PubMed, Embase, and the Cochrane Library was conducted up to March 17, 2024. The primary outcomes included hypertension, palpitations, and chest pain, with pooled effect estimate reported as proportions and odds ratios (ORs) with 95% confidence intervals (CIs). Sensitivity and subgroup analysis were performed to assess the robustness of the results and to identify sources of heterogeneity.

A total of 37 studies, encompassing 2,965,467 patients, were included in the analysis. Pooled results from case-control studies revealed that, compared to the control group, the ORs of chest pain in the COVID-19 group was 4.0 (95% CI: 1.6, 10.0). The ORs for palpitation and hypertension were 3.4 (95% CI: 1.1, 10.2) and 1.7 (95% CI: 1.6, 1.8), respectively. The proportions of PACS patients experiencing chest pain, palpitation, and hypertension as sequelae were 22% (95% CI: 14%, 33%), 18% (95% CI: 13%, 24%), and 19% (95% CI: 12%, 31%), respectively.

Our findings indicate that 15% of COVID-19 patients experience cardiovascular sequelae. Furthermore, COVID-19 infection significantly increases the likelihood of developing these sequelae compared to uninfected individuals. Future research should prioritize investigating the underlying pathological mechanisms and developing targeted preventive and management strategies.

CRD42024524290.

We test the robustness of the self-controlled risk interval (SCRI) design in a setting where time between doses may introduce time-varying confounding, using both negative control outcomes (NCOs) and quantitative bias analysis (QBA). All vaccinated cases identified from 5 European databases between September 1, 2020, and end of data availability were included. Exposures were doses 1-3 of the Pfizer, Moderna, AstraZeneca, and Janssen COVID-19 vaccines; outcomes were myocarditis and, as the NCO, otitis externa. The SCRI used a 60-day control window and dose-specific 28-day risk windows, stratified by vaccine brand and adjusted for calendar time. The QBA included two scenarios: (1) baseline probability of the confounder was higher in the control window and (2) vice versa. The NCO was not associated with any of the COVID-19 vaccine types or doses except Moderna dose 1 (IRR = 1.09; 95% CI 1.01-1.09). The QBA suggested that even the strongest literature-reported confounder (COVID-19; RR for myocarditis = 18.3) could only explain away part of the observed effect, from IRR = 3 to IRR = 1.40. The SCRI seems robust to unmeasured confounding in the COVID-19 setting, although a strong unmeasured confounder could bias the observed effect upward. Replication of our findings for other safety signals would strengthen this conclusion. This article is part of a Special Collection on Pharmacoepidemiology.

The molecular mechanisms regulating coronavirus pathogenesis are complex, including virus-host interactions associated with replication and innate immune control. However, some genetic and epigenetic conditions associated with comorbidities increase the risk of hospitalization and can prove fatal in infected patients. This systematic review will provide insight into host genetic and epigenetic factors that interfere with COVID-19 expression in light of available evidence.

This study conducted a systematic review to examine the genetic and epigenetic susceptibility to COVID-19 using a comprehensive approach. Through systematic searches and applying relevant keywords across prominent online databases, including Scopus, PubMed, Web of Science, and Science Direct, we compiled all pertinent papers and reports published in English between December 2019 and June 2023.

The findings reveal that the host's HLA genotype plays a substantial role in determining how viral protein antigens are showcased and the subsequent immune system reaction to these antigens. Within females, genes responsible for immune system regulation are found on the X chromosome, resulting in reduced viral load and inflammation levels when contrasted with males. Possessing blood group A may contribute to an increased susceptibility to contracting COVID-19 as well as a heightened risk of mortality associated with the disease. The capacity of SARS-CoV-2 involves inhibiting the antiviral interferon (IFN) reactions, resulting in uncontrolled viral multiplication.

There is a notable absence of research into the gender-related predisposition to infection, necessitating a thorough examination. According to the available literature, a significant portion of individuals affected by the ailment or displaying severe ramifications already had suppressed immune systems, categorizing them as a group with elevated risk.

As the coronavirus disease 2019 (COVID-19) pandemic persists, the exploration of adjunct therapies to mitigate disease severity remains a priority. Statins, known for their pleiotropic effects, have been under investigation for their potential role in managing COVID-19 complications. The study was conducted in a single referral hospital and adhered to Consolidated Standards of Reporting Trials guidelines. Eligible participants were randomized in a 1:1 ratio into either the rosuvastatin group or the control group. Outcome measures included vital signs, laboratory data, clinical outcomes, and patient symptoms. Statistical analysis was performed using SPSS software (version 26.0, IBM Corp., Armonk, New York). A total of 100 patients were enrolled. No significant differences were observed between the rosuvastatin and control groups in terms of baseline characteristics and laboratory parameters, except for the fact that rosuvastatin-treated patients showed lower levels of C-reactive protein in comparison with the controls on both the 1st and 5th days (38.1 ± 16.3 vs 50.5 ± 25.3) compared to the control group. Clinical outcomes, including hospital length of stay, intensive care unit admission, need for intubation, and 1-month mortality, did not differ significantly between the two groups. Symptom scales, as assessed by the Borg Rating of Perceived Exertion and Leicester Cough Questionnaire, showed significant improvement in the rosuvastatin group compared to controls. Our study provides insights into the short-term efficacy of moderate-intensity rosuvastatin in COVID-19 patients. Further research is warranted to elucidate the long-term effects and optimal dosing of statins in COVID-19 management.

Coronavirus disease 2019 (COVID-19) was declared a global pandemic in 2019. It remains uncertain to what extent COVID-19 effects the heart in heathy individuals. To evaluate the effect of the COVID-19 on cardiac structure and function in middle-aged and older individuals.

A single-centre prospective observational study enroled a total of 124 participants (84 with history of COVID-19 [COVID-19 group] and 40 without a history of COVID-19 [non-COVID group]). All participants underwent echocardiography with speckle tracking to assess cardiac structure and function at rest and during peak exercise.

There were no differences in left and right ventricular diastolic function (p ≥ 0.05) between the COVID-19 and non-COVID-19 groups. Participants in COVID-19 group demonstrated higher left ventricular mass (130 ± 39.8 vs. 113 ± 27.2 g, p = 0.008) and relative wall thickness (0.38 ± 0.07 vs. 0.36 ± 0.13, p = 0.049). Left ventricular global longitudinal strain was reduced in the COVID-19 group at rest and at peak-exercise (rest: 18.3 ± 2.01 vs. 19.3 ± 1.53%, p = 0.004; peak exercise: 19.1 ± 2.20 vs. 21.0 ± 1.58%, p ≤ 0.001). However, no difference was seen in resting left ventricular ejection fraction (58 ± 2.89 vs. 59 ± 2.51%, p = 0.565) between groups. Right ventricular fractional area change was reduced in the COVID-19 group (p = 0.012).

Cardiac structural and functional remodelling was observed in middle-aged and older otherwise healthy individuals with a history of COVID-19.

Epidemiological studies link COVID-19 to increased cardiac arrest (CA) risk, but causality remains unclear due to potential confounding factors in observational studies . We conducted a Mendelian randomization (MR) analysis using genome-wide association study (GWAS) data, employing COVID-19-associated single nucleotide polymorphisms (SNPs) with significance values smaller than 5 × 10⁻⁸. We calculated inverse-variance weighted (IVW) MR estimates and performed sensitivity analyses using MR methods robust to horizontal pleiotropy. Additionally, a reverse MR analysis was conducted using CA-associated SNPs with significance values smaller than 1 × 10⁻⁵. Results indicated that infected COVID-19 (OR = 1.12, 95% CI = 0.47-2.67, p = 0.79), hospitalized COVID-19 (OR = 1.02, 95% CI = 0.70-1.49, p = 0.920), and severe respiratory COVID-19 (OR = 0.99, 95% CI = 0.81-1.21, p = 0.945) did not causally influence CA risk. Reverse MR analysis also did not support a causal effect of CA on COVID-19. Thus, associations in observational studies may stem from shared biological factors or environmental confounding.

Background and Objectives: Fever in patients who have suffered an out-of-hospital cardiac arrest (OHCA) has been linked to poor clinical outcomes, as a fever can exacerbate neurological damage, increase metabolic demands, and trigger inflammatory responses. This study evaluates the impact of the COVID-19 outbreak and associated fevers on OHCA outcomes and examines how they can worsen patient prognosis. Materials and Methods: Our retrospective observational analysis used data from the National Emergency Department Information System (NEDIS), comprising adult OHCA patients at 402 EDs in Korea between 27 January and 31 December 2020 (COVID-19 pandemic period) and the corresponding period in 2019 (pre-COVID-19). The primary outcome was in-hospital mortality, with the COVID-19 outbreak as the main exposure variable and fever as an important interaction variable. We employed multilevel multivariate logistic regression with an interaction term (year of visit × fever) to examine the effects of COVID-19 and fever on mortality. Risk-adjusted mortality rates were calculated, and a difference-in-difference analysis evaluated the impact of COVID-19 on excess mortality by fever status. Results: During COVID-19, in-hospital mortality was higher among OHCA patients compared to the pre-pandemic period (adjusted OR 1.22, 95% CI 1.11-1.34), particularly among febrile patients (adjusted OR 1.40, 95% CI 1.24-1.59). Interaction analysis revealed that COVID-19 disproportionately increased mortality in febrile OHCA patients compared with non-febrile patients (difference-in-difference: 0.8%, 95% CI 0.2-1.5). Conclusions: Our study found that the COVID-19 pandemic significantly increased mortality among OHCA patients, with febrile patients experiencing disproportionately worse outcomes due to systemic delays and pandemic-related disruptions.

Sepsis, characterized as life-threatening organ dysfunction resulting from dysregulated host responses to infection, remains a significant challenge in clinical practice. Despite advancements in understanding host-bacterial interactions, molecular responses, and therapeutic approaches, the mortality rate associated with sepsis has consistently ranged between 10 and 16%. This elevated mortality highlights critical gaps in our comprehension of sepsis etiology. Traditionally linked to bacterial and fungal pathogens, recent outbreaks of acute viral infections, including Middle East respiratory syndrome coronavirus (MERS-CoV), influenza virus, and severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), among other regional epidemics, have underscored the role of viral pathogenesis in sepsis, particularly when critically ill patients exhibit classic symptoms indicative of sepsis. However, many cases of viral-induced sepsis are frequently underdiagnosed because standard evaluations typically exclude viral panels. Moreover, these viruses not only activate conventional pattern recognition receptors (PRRs) and retinoic acid-inducible gene-I (RIG-I)-like receptors (RLRs) but also initiate primary antiviral pathways such as cyclic guanosine monophosphate adenosine monophosphate (GMP-AMP) synthase (cGAS)-stimulator of interferon genes (STING) signaling and interferon response mechanisms. Such activations lead to cellular stress, metabolic disturbances, and extensive cell damage that exacerbate tissue injury while leading to a spectrum of clinical manifestations. This complexity poses substantial challenges for the clinical management of affected cases. In this review, we elucidate the definition and diagnosis criteria for viral sepsis while synthesizing current knowledge regarding its etiology, epidemiology, and pathophysiology, molecular mechanisms involved therein as well as their impact on immune-mediated organ damage. Additionally, we discuss clinical considerations related to both existing therapies and advanced treatment interventions, aiming to enhance the comprehensive understanding surrounding viral sepsis.

Although COVID-19 has been linked to worse outcomes in patients with neurological disorders, its impact on those with essential tremor (ET) remains unclear. To investigate clinical outcomes of ET patients with and without COVID-19 three and a half years post-pandemic.

1074 ET patients were evaluated in this retrospective study in the Montefiore Health System from January 2016 to July 2023. Comparisons between ET patients with and without a positive SARS-CoV-2 polymerase chain reaction test were made. Outcomes included post-index date major adverse cardiovascular events (MACEs), new-onset sleep disturbances, fatigue, dyspnea, first-time fall, new-onset anxiety, new-onset depression, headache, new-onset imbalance, new-onset mild cognitive impairment, and all-cause mortality, adjusted hazard ratios (aHR) adjusting for covariates were calculated.

ET patients with COVID-19 had higher prevalence of pre-existing type-2 diabetes, depression, and anxiety compared to ET patients without COVID-19. COVID-19 was significantly associated with higher risk of MACEs, (aHR = 2.39 [1.49, 3.82]), new-onset sleep disturbance, (aHR = 2.12 [1.44, 3.13]), fatigue, (aHR = 1.83 [1.27, 2.65]), dyspnea, (aHR = 1.98 [1.40, 2.80]), first-time fall, (aHR = 4.76 [2.24, 10.14]), new-onset anxiety, (aHR = 3.66 [2.02, 6.64]), and new-onset depression, (aHR = 2.38 [1.20, 4.70]). COVID-19 was not associated with all-cause mortality.

In patients with ET, COVID-19 significantly increases the risk of several long-term adverse health outcomes, but not mortality.

Background: Understanding the interactions between age and comorbidities is crucial for assessing COVID-19 mortality, particularly in patients with cardiac and pulmonary conditions. This study investigates the relationship between comorbidities and mortality outcomes in a cohort of hospitalized COVID-19 patients, emphasizing the interplay of age, cardiac, and pulmonary conditions. Methods: We analyzed a cohort of 3005 patients hospitalized with COVID-19 between 2020 and 2022. Key variables included age, comorbidities (diabetes, cardiac, pulmonary, and neoplasms), and clinical outcomes. Chi-square tests and logistic regression models were used to assess the association between comorbidities and mortality. Stratified analyses by age, diabetes, and pulmonary conditions were conducted to explore interaction effects. Additionally, interaction terms were included in multivariable logistic regression models to evaluate the combined impact of age, comorbidities, and mortality. Results: Cardiac conditions such as hypertension, ischemic cardiopathy, and myocardial infarction showed significant protective effects against mortality in younger patients and in those without pulmonary conditions (p < 0.001). However, these protective effects were diminished in older patients and those with pulmonary comorbidities. Age was found to be a significant modifier of the relationship between cardiac conditions and mortality, with a stronger protective effect observed in patients under the median age (p < 0.001). Pulmonary comorbidities significantly increased the risk of mortality, particularly when co-occurring with cardiac conditions (p < 0.001). Diabetes did not significantly modify the relationship between cardiac conditions and mortality. Conclusions: The findings highlight the complex interactions between age, cardiac conditions, and pulmonary conditions in predicting COVID-19 mortality. Younger patients with cardiac comorbidities show a protective effect against mortality, while pulmonary conditions increase mortality risk, especially in older patients. These insights suggest that individualized risk assessments incorporating age and comorbidities are essential for managing COVID-19 outcomes.

The pandemic COVID-19 (coronavirus disease 2019) is caused by the severe acute respiratory syndrome corona virus 2 (SARS-CoV-2), which devastated the global economy and healthcare system. The infection caused an unforeseen rise in COVID-19 patients and increased the mortality rate globally. This study gives an overall idea about host-pathogen interaction, immune responses to COVID-19, recovery status of infection, targeted organs and complications associated, and comparison of post-infection immunity in convalescent subjects and non-infected individuals. The emergence of the variants and episodes of COVID-19 infections made the situation worsen. The timely introduction of vaccines and precautionary measures helped control the infection's severity. Later, the population that recovered from COVID-19 grew significantly. However, understanding the impact of healthcare issues resulting after infection is paramount for improving an individual's health status. It is now recognised that COVID-19 infection affects multiple organs and exhibits a broad range of clinical manifestations. So, post COVID-19 infection creates a high risk in individuals with already prevailing health complications. The identification of post-COVID-19-related health issues and their appropriate management is of greater importance to improving patient's quality of life. The persistence, sequelae and other medical complications that normally last from weeks to months after the recovery of the initial infection are involved with COVID-19. A multi-disciplinary approach is necessary for the development of preventive measures, techniques for rehabilitation and strategies for clinical management when it comes to long-term care.

Risk of cardiovascular events is increased after COVID-19. However, information on cardiovascular risk trends after COVID-19 infection is lacking and estimates by sex are inconsistent. Our aim was to examine cardiovascular outcomes and mortality in a large cohort (164,346 participants) of SARS-CoV-2 positive individuals compared to non-positive individuals, stratified by sex. Data were obtained from the Spanish Health System's electronic medical records. Selected individuals were ≥ 45 years old with/without a positive SARS-CoV-2 test in the period March-May 2020. Follow-up was obtained until January 31, 2021, for cardiovascular events (angina/myocardial infarction, arrhythmias, bypass/revascularization, heart failure, peripheral artery disease, stroke/transient ischemic attack, and thrombosis), and until March 31, 2021, for mortality. Individuals were matched by propensity score. Incidence of cardiovascular events and mortality was compared with accelerated failure time models. The effect of matching and of COVID-19 severity was assessed with sensitivity analyses. In the first 3 months of follow-up, SARS-CoV-2 positive individuals had a higher risk of mortality and of all cardiovascular events. From 4-12 months, there was increased risk of mortality in SARS-CoV-2 positive individuals overall, of heart failure in SARS-CoV-2 positive females (HR= 1.26 [1.11-1.42]), and of arrhythmias and thrombosis in SARS-CoV-2 positive males (HR= 1.29 [1.14-1.47] and HR= 1.35 [1.03-1.77], respectively). When COVID-19 patients admitted to the ICU were excluded, incidence of thrombosis was similar in males regardless of positive/non-positive SARS-CoV-2 status. In the full year of follow-up, increased incidence of heart failure and of arrhythmias and thrombosis was observed in SARS-CoV-2 positive females and males, respectively.

This editorial article is intended to perform a discussion on the manuscript entitled "Simultaneous portal vein thrombosis and splenic vein thrombosis in a COVID-19 patient: A case report and review of literature" written by Abramowitz et al. The article focuses on the diagnostic processes in a 77-year-old-male patient with a simultaneous portal vein and splenic artery thrombosis accompanying coronavirus disease 2019 (COVID-19). The authors postulated that splanchnic thrombosis should be on the list of differential diagnoses in a patient presenting with abdominal pain in presence of a COVID-19 infection. The tendency for venous and arterial thrombosis in COVID-19 patients is encountered, largely attributed to hypercoagulopathy. In general, venous thromboembolism mostly manifest as deep vein thrombosis (DVT), pulmonary embolism (PE) or catheter-related thromboembolic events. Acute PE, DVT, cerebrovascular events and myocardial infarction are seen as the most common thromboembolic complications in COVID-19 patients. COVID-19-associated hemostatic abnormalities include mild thrombocytopenia and increased D-dimer level. Similar to other coagulopathies, the treatment of the underlying condition is the mainstay. Addition of antiplatelet agents can be considered in critically ill patients at low bleeding risk, not on therapeutic anticoagulation, and receiving gastric acid suppression Early administration of antithrombotic drugs will have a beneficial effect in both the prevention and treatment of thrombotic events, especially in non-ambulatory patients. Low molecular weight heparin (LMWH) should be started if there is no contraindication, including in non-critical patients who are at risk of hospitalization LMWH (enoxaparin) is preferred to standard heparin.

Introduction. Post-coronavirus disease-2019 (COVID-19) patients may develop cardiac symptoms. We hypothesized that cardiovascular magnetic resonance (CMR) can assess the background of post-COVID-19 cardiac symptoms using multi-parametric evaluation. We aimed to conduct an investigation of symptomatic patients with post-COVID-19 syndrome using CMR (INSPIRE-CMR). Methods. INSIPRE-CMR is a retrospective multicenter study including 174 patients from five centers referred for CMR due to cardiac symptoms. CMR was performed using 3.0 T/1.5 T system (24%/76%, respectively). Myocardial inflammation was determined by the updated Lake Louise criteria. Results. Further, 174 patients with median age of 40 years (IQR: 26-54), 72 (41%) were women, and 17 (9.7%) had a history of autoimmune disease, muscular dystrophy, or cancer. In total, 149 (86%) patients were late gadolinium enhanced (LGE)-positive with a non-ischemic pattern, and of those evaluated with the updated Lake Louise criteria, 141/145 (97%) had ≥1 pathologic T1 index. Based on the T2-criterion, 62/173 (36%) patients had ≥1 pathologic T2 index. Collectively, 48/145 (33%) patients had both positive T1- and T2-criterion. A positive T2-criterion or a combination of a positive T1- and T2-criterion were significantly more common amongst patients with severe COVID-19 [45 (31%) vs. 17 (65%), p = 0.001 and 32 (27%) vs. 16 (64%), p < 0.001, respectively]. During the one-year evaluation, available for 65/174 patients, shortness of breath, chest pain, and arrhythmia were identified in 7 (4%), 15 (8.6%), and 43 (24.7%), respectively. CMR evaluation, available in a minority of them, showed mildly reduced LVEF, while nat T1 mapping and EVC remained at levels higher than the normal values of the local MRI units. Conclusions. The majority of post-COVID-19 patients with cardiac symptoms presented non-ischemic LGE and abnormalities in T1 and T2-based indices. Multi-parametric CMR reveals important information on post-COVID-19 patients, supporting its role in short/long-term evaluation.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) not only posed major health and economic burdens to international societies but also threatens patients with comorbidities and underlying autoimmune disorders, including Crohn's disease (CD) patients. As the vaccinated population is gradually relieved from the stress of the latest omicron variant of SARS-CoV-2 due to competent immune responses, the anxiety of CD patients, especially those on immunosuppressive treatment, has not subsided. Whether the use of immunosuppressants for remission of CD outweighs the potential risk of severe coronavirus disease 2019 (COVID-19) has long been discussed. Thus, for the best benefit of CD patients, our primary goal in this study was to navigate the clinical management of CD during the COVID pandemic. Herein, we summarized COVID-19 outcomes of CD patients treated with immunosuppressive agents from multiple cohort studies and also investigated possible mechanisms of how SARS-CoV-2 impacts the host immunity with special consideration of CD patients. We first looked into the SARS-CoV-2-related immunopathology, including lymphocytopenia, T-cell exhaustion, cytokine storms, and their possible molecular interactions, and then focused on mechanistic actions of gastrointestinal systems, including interruption of tryptophan absorption, development of dysbiosis, and consequent local and systemic inflammation. Given challenges in managing CD, we summarized up-to-date clinical and molecular evidence to help physicians adjust therapeutic strategies to achieve the best clinical outcomes for CD patients.

This review discusses the pivotal role of microcirculation in maintaining tissue oxygenation and waste removal and highlights its significance in various pathological conditions. It delves into the cellular mechanisms underlying hemodynamic coherence, elucidating the roles of the endothelium, glycocalyx, and erythrocytes in sustaining microcirculatory integrity. Furthermore, the review gives comprehensive information about microcirculatory changes observed in cardiac surgery, sepsis, shock, and COVID-19 disease. Through comprehensive exploration, the review underscores the intricate relationship between microcirculation, disease states, and clinical outcomes, emphasizing the importance of understanding and monitoring microvascular dynamics in critical care settings.

SARS-CoV-2 infection can result in long-term chronic cardiovascular (CV) damage after the acute phase of the illness. COVID-19 frequently causes active myocarditis, SARS-CoV-2 can directly infect and kill cardiac cells, causing severe pathology and dysfunction across the organs and cells. Till now, the pathogenesis of COVID-19-associated cardiac injuries has not been understood, but there are several factors that contribute to the progression of cardiac injuries, such as genetic, dietary, and environmental. Among them ranges of host genetic factor including metabolizing, inflammation, and coagulation related genes have a role to contribute the cardiac injuries induced by COVID-19. Hereditary DNA sequence variations contribute to the risk of illness in almost all of these diseases. Hence, we comprehended the occurrence of genetic variations of metabolizing, inflammation and coagulation-related genes in the general population, their expression in various diseases, and their impact on cardiac injuries induced by COVID-19.

We utilized multiple databases, including PubMed (Medline), EMBASE, and Google Scholar, for literature searches.

The genes involved in metabolism (APOE, MTHFR), coagulation (PAI-1, ACE2), and immune factors (CRP, ESR, and troponin I) may have a role in the progression of COVID-19-associated cardiac injuries. The risk factors for CVD are significantly varied between and within different regions. In healthy individuals, the ACE I allele is responsible for the predisposition to CAD, but the ACE D haplotype is responsible for susceptibility and severity, which ultimately leads to heart failure. Patients who carry the T allele of rs12329760 in the TMPRSS2 gene are at risk for developing the severe form of COVID-19. IL-6 (rs1800796/rs1800795) polymorphism is associated with an increased mortality rate and susceptibility to severe COVID-19 disease. While the putative role of IL-6 associated with chronic, inflammatory diseases like cardiac and cerebrovascular disease is well known.

The occurrence of genetic variations in the ACE-2, AGT, DPP-IV, TMPRSS2, FUIRN, IL-4, IL-6, IFN-γ, and CYP2D6 genes is varied among different populations. Examining the correlation between these variations and their protein levels and cardiac injuries induced by COVID-19 may provide valuable insights into the pathogenesis of cardiac injuries induced by COVID-19.

COVID-19 is associated with acute risk of major adverse cardiac events (MACE), including myocardial infarction, stroke, and mortality (all-cause). However, the duration and underlying determinants of heightened risk of cardiovascular disease and MACE post-COVID-19 are not known.

Data from the UK Biobank was used to identify COVID-19 cases (n=10 005) who were positive for polymerase chain reaction (PCR+)-based tests for SARS-CoV-2 infection (n=8062) or received hospital-based International Classification of Diseases version-10 (ICD-10) codes for COVID-19 (n=1943) between February 1, 2020 and December 31, 2020. Population controls (n=217 730) and propensity score-matched controls (n=38 860) were also drawn from the UK Biobank during the same period. Proportional hazard models were used to evaluate COVID-19 for association with long-term (>1000 days) risk of MACE and as a coronary artery disease risk equivalent. Additional analyses examined whether COVID-19 interacted with genetic determinants to affect the risk of MACE and its components.

The risk of MACE was elevated in COVID-19 cases at all levels of severity (HR, 2.09 [95% CI, 1.94-2.25]; P<0.0005) and to a greater extent in cases hospitalized for COVID-19 (HR, 3.85 [95% CI, 3.51-4.24]; P<0.0005). Hospitalization for COVID-19 represented a coronary artery disease risk equivalent since incident MACE risk among cases without history of cardiovascular disease was even higher than that observed in patients with cardiovascular disease without COVID-19 (HR, 1.21 [95% CI, 1.08-1.37]; P<0.005). A significant genetic interaction was observed between the ABO locus and hospitalization for COVID-19 (Pinteraction=0.01), with risk of thrombotic events being increased in subjects with non-O blood types (HR, 1.65 [95% CI, 1.29-2.09]; P=4.8×10-5) to a greater extent than subjects with blood type O (HR, 0.96 [95% CI, 0.66-1.39]; P=0.82).

Hospitalization for COVID-19 represents a coronary artery disease risk equivalent, with post-acute myocardial infarction and stroke risk particularly heightened in non-O blood types. These results may have important clinical implications and represent, to our knowledge, one of the first examples of a gene-pathogen exposure interaction for thrombotic events.

COVID-19 is a new disease caused by the recently discovered SARS-CoV-2 virus. The COVID-19 disease manifests in several ways and it may affect various systems, including the gastrointestinal, musculoskeletal, neurological, cardiovascular, and pulmonary systems. Individuals who have ad-additional health conditions, such as cardiovascular disorders, are particularly more likely to experience illness and death. This study aimed to assess the clinical effect of COVID-19 on myocardial injury, as measured by troponin elevation, and to determine if this effect has an impact on the outcome.

This retrospective study was conducted at King Saud Medical City. The electronic medical records used to identify all admitted patients between March 23 and June 15, 2020, with a laboratory-confirmed positive COVID-19 diagnosis who had troponin I measured.

During the study period, 768 COVID-19-positive patients were hospitalized. Of those, 187 patients were excluded because the troponin level was not measured. The remaining 581 (75.7%) had troponin I measured. Overall, 89 of 581 (15.3%) patients died. Of those, 67.8% were in the markedly elevated cTnI group, 8.5% were in the mildly elevated cTnI group, whereas no deaths were reported in the group with normal cTnI levels.

Myocardial injury was observed in COVID-19-admitted patients at a significant level that warrants attention to this consequence. In older individuals with pre-existing cardiovascular comorbidities, the diagnosis of myocardial injury was linked to a higher likelihood of being admitted to the intensive care unit, experiencing a worse prognosis, and ultimately, death.

The COVID-19 pandemic has presented unprecedented challenges for healthcare systems globally, impacting critical care resources and patient outcomes. Understanding its multifaceted effects is crucial for future crisis response.

Analyze the repercussions of the COVID-19 pandemic on mechanical ventilation cases and mortality among non-SARS-CoV-2 patients.

A nationwide database encompassing all patients receiving mechanical ventilation in Spain was used to compare the number of cases and clinical outcomes during COVID-19 (March 2020 - December 2021) to pre-pandemic cases (May 2018 - February 2020). Univariate and multivariate analyses were employed.

COVID-19 significantly reduced access to ventilation for non-COVID-19 patients. A 16 % decrease (12,099 fewer patients) was observed during the pandemic compared to pre-pandemic times. This reduction affected all analyzed conditions except self-inflicted injuries, coinciding with a rise in overall mortality risk (34.5% vs 35.6 %, OR 1.09, 95 %CI 1.06-1.12). The increased mortality was consistent across diverse admission types, including cancer (37.1% vs. 41.5 %, OR 1.18, 95 %CI 1.09-1.29), hemorrhagic strokes (55.4% vs. 56.6 %, OR 1.07, 95 %CI 1.02-1.20), acute myocardial infarction (35.6% vs. 38 %, OR 1.11, 95 %CI 1.01-1.21), non-SARS-CoV-2 pneumonia (44.5% vs. 45.8 %, OR 1.12, 95 %CI 1.02-1.24), septic shock (54.7% vs. 56.3 %, OR 1.10, 95 %CI 1.06-1.15), and prolonged ventilation (≥96 h) (37% vs. 38.2 %, OR 1.10, 95 %CI 1.06-1.10).

The findings underscore the profound impact of the COVID-19 pandemic on critical care utilization and patient outcomes among non-SARS-CoV-2 patients. As healthcare systems strive to mitigate future crises, these insights emphasize adaptable strategies for equitable access to life-saving treatments.

Hepatocellular carcinoma (HCC) is a highly heterogeneous malignancy with poor prognosis and a common cause of cancer-related death worldwide, and despite ongoing therapeutic breakthroughs, patient survival benefits are limited. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the cause of coronavirus disease 2019 (COVID-19) and poses a major threat to humanity worldwide. As the epidemic continues to develop, more and more people are infected with SARS-CoV-2, including patients with HCC. However, the relationship between COVID-19 and HCC has not yet been fully elucidated. Our study aimed to identify the shared genetic characteristics and molecular mechanisms between COVID-19 and HCC. The data involved in this study come from Gene Expression Omnibus (GEO), The Cancer Genome Atlas (TCGA), Genotype-Tissue Expression(GTEx), and Cancer Cell Line Encyclopedia(CCLE) databases. We used differentially expressed genes to perform enrichment analysis to reveal the biological landscape of COVID-19 combined with HCC. In addition, weighted gene co-expression network analysis (WGCNA) was used to study the co-expression network related to COVID-19 and HCC. We then combined the validation datasets to screen out immunoglobulin superfamily member 1 (IGSF1) as the most important core gene. Finally, we extensively studied the functional expression of IGSF1 in tumor samples, normal tissues, and cancer cell lines. The molecular mechanisms related to COVID-19 and HCC are rarely studied. Our study identifies IGSF1 as a potential therapeutic target and immune-related biomarker for patients with COVID-19 and HCC.

Cardiovascular involvements are one of the most important and threatening problems of SARS-CoV-2 infection and can cause a wide range of clinical manifestations in children. Therefore, a review of previous studies is necessary to prevent the occurrence of cardiovascular complications and reduce the risk of mortality in this age group of patients. To investigate the cardiovascular complications in children with COVID-19, international authoritative databases including PubMed, Scopus, Embase, Web of Science, Google Scholar, and Persian databases were searched using the main concepts, all articles were published between January 2020 and November 2022. According to the results of the present study, no deaths due to cardiovascular involvement were reported in the studied healthy children with COVID-19. In addition, in electrocardiogram (ECG) findings, supraventricular arrhythmias (SVA) and ventricular arrhythmias (VA) and in echo findings, left ventricular dysfunction (LVD) have had the most consequences.

Acute coronary syndrome (ACS) is frequently reported in patients with coronavirus disease 2019 (COVID-19). Cytokine storm induced by interleukin-6 (IL-6) has been suggested to potentially cause myocardial injury in COVID-19. We investigated the association between baseline level of IL-6 and development of ACS in COVID-19 patients.

Demographic and clinical data of hospitalized COVID-19 patients from 2020 to 2022 were reviewed. Extracted data including patient characteristics, laboratory biomarkers, and systemic inflammation indexes in patients with or without ACS were reviewed and analyzed. Logistic regression models were applied to analyze predictors of ACS development and receiver-operating characteristic (ROC) curves were used to assess discriminatory power of IL-6 and other risk factors for predicting ACS development.

Among 1,753 COVID-19 patients, 37 cases experienced ACS and 159 patients without main COVID-19 complications were randomly selected as controls. ACS patients were older (p = 0.001) and suffered from more comorbidities including diabetes (43% vs. 18%, p = 0.001), hypertension (40.5% vs. 24.5%, p = 0.050), ischemic heart disease (49% vs. 9%, p = 0.001), and hyperlipidemia (19% vs. 5%, p = 0.010). Also, decreased level of consciousness (31.6% vs. 2.5%, p = 0.001), ICU admission (65% vs. 2%, p = 0.001), and mortality events (70% vs. 0.6%, p = 0.001) were more prevalent in the ACS group. Baseline levels of IL-6 (p = 0.001), D-dimer (p = 0.026), troponin (p = 0.001), blood urea nitrogen (p = 0.002), and creatinine (p = 0.008) were higher in ACS patients but erythrocyte sedimentation rate (p = 0.013), hemoglobin (p = 0.033), and red blood cells (p = 0.028) were lower compared with controls. Also, age (OR: 1.06, p = 0.019), IL-6 (OR: 1.44, p = 0.047), and cardiovascular disease (CVD) (OR: 3.66, p = 0.043) were associated with ACS development. The area under the curve (AUC) of IL-6 and combined predictors respectively was 0.661 (p = 0.002) and 0.829 (p = 0.001).

High IL-6 concentration at baseline is a strong predictor for ACS development in COVID-19 patients. Also, elderly and concurrent CVD are significantly associated with ACS development.

The rapid global spread of a new coronavirus disease known as COVID-19 has led to a significant increase in mortality rates, resulting in an unprecedented worldwide pandemic.

The impact of COVID-19, particularly its long-term effects, has also had a profound effect on the health and well-being of individuals.Metabolic syndrome increases the risk of heart and brain diseases, presenting a significant danger to human well-being.

The prognosis of long COVID and the progression of metabolic syndrome interact with each other, but there is currently a lack of systematic reports.In this paper, the pathogenesis, related treatment and prognosis of long COVID and metabolic syndrome are systematically reviewed.

Since December 2019, coronavirus disease 2019 (COVID-19) has been spreading worldwide with devastating immediate or long-term effects on people's health. Although the lungs are the primary organ affected by COVID-19, individuals infected with SARS-CoV-2 also develop systemic lesions involving multiple organs throughout the body, such as the cardiovascular system. Emerging evidence reveals that COVID-19 could generate myocardial fibrosis, termed "COVID-19-associated myocardial fibrosis." It can result from the activation of fibroblasts via the renin-angiotensin-aldosterone system (RAAS), transforming growth factor-β1 (TGF-β1), microRNAs, and other pathways, and can also occur in other cellular interactions with SARS-CoV-2, such as immunocytes, endothelial cells. Nonetheless, to gain a more profound insight into the natural progression of COVID-19-related myocardial fibrosis, additional investigations are necessary. This review delves into the underlying mechanisms contributing to COVID-19-associated myocardial fibrosis while also examining the antifibrotic potential of current COVID-19 treatments, thereby offering guidance for future clinical trials of these medications. Ultimately, we propose future research directions for COVID-19-associated myocardial fibrosis in the post-COVID-19 era, such as artificial intelligence (AI) telemedicine. We also recommend that relevant tests be added to the follow-up of COVID-19 patients to detect myocardial fibrosis promptly.

Adverse life occurrences (e.g., severe accidents, violence/abuse, organic disorders such as COVID-19) can elicit traumatic responses that heighten fear, anxiety, and depression. However, scientific research has shown that certain variables, such as self-esteem, based on theories like terror management theory (TMT) and the anxiety-buffering hypothesis (ABH), can mitigate the negative effects of trauma. This study aimed to test the ABH by assessing the buffering role of self-esteem in the relationships among the impact of traumatic experiences, fear, anxiety, and depression.

An observational research design was used. This study involved 321 participants who experienced COVID-19 as a traumatic experience. A sequential multiple-mediation model with observed variables (path analysis) was used to test the impact of the traumatic experience on fear, anxiety, and depression, examining the protective role of self-esteem.

A path analysis revealed that fear and anxiety mediated the relationship between the impact of the traumatic experience of COVID-19 and depression. Additionally, in line with the ABH, self-esteem was found to mediate the relationship between the predictors and their adverse psychological consequences. This suggests that self-esteem played a buffering role, mitigating the negative impact of traumatic experiences on mental health outcomes.

These findings underscore the central mediating role of self-esteem, as well as fear and anxiety, in the pathway from trauma-related factors to depression. These insights advocate for evidence-based interventions aimed at alleviating the psychological suffering associated with traumatic experiences, fostering adaptation, and supporting psychological health.

TTE is the main modality used to assess RV function, but conventional TTE parameters have limited diagnostic value because they may fail to detect early abnormalities in RV systolic function. Due to its ability to detect subclinical impairment of cardiac function, 2D STE has been widely used to investigate RV function. In this study, we aimed to investigate whether there are sequelae of RV function in recovered COVID-19 patients with pulmonary involvement.

This is a prospective observational cohort study of 57 healthy volunteers and 54 patients. Participants had no history of chronic illness and no evidence of respiratory or cardiac symptoms. The patients had been hospitalised with COVID-19 with pulmonary involvement but did not require intensive care unit follow-up or non-invasive mechanical ventilation support. TTE was performed. Demographic and clinical characteristics and laboratory test results were collected.

LVEF, TAPSE, St and FAC were significantly lower in the patient group. LV-LS 3-chamber, LV-GLS, RV-FWS, RV-GLS were significantly lower in the patient group.

RV-LS and LV-GLS were shown to decrease in the patient group. Although no obvious pathological values were observed in RV parameters on conventional echocardiography, TAPSE, St and FAC values were lower in the patient group.

Patients with SARS-CoV-2 infection carry an increased risk of cardiovascular disease encompassing various implications, including acute myocardial injury or infarction, myocarditis, heart failure, and arrhythmias. A growing volume of evidence correlates SARS-CoV-2 infection with myocardial injury, exposing patients to higher mortality risk. SARS-CoV-2 attacks the coronary arterial bed with various mechanisms including thrombosis/rupture of preexisting atherosclerotic plaque, de novo coronary thrombosis, endotheliitis, microvascular dysfunction, vasculitis, vasospasm, and ectasia/aneurysm formation. The angiotensin-converting enzyme 2 receptor plays pivotal role on the cardiovascular homeostasis and the unfolding of COVID-19. The activation of immune system, mediated by proinflammatory cytokines along with the dysregulation of the coagulation system, can pose an insult on the coronary artery, which usually manifests as an acute coronary syndrome (ACS). Electrocardiogram, echocardiography, cardiac biomarkers, and coronary angiography are essential tools to set the diagnosis. Revascularization is the first-line treatment in all patients with ACS and obstructed coronary arteries, whereas in type 2 myocardial infarction treatment of hypoxia, anemia and systemic inflammation are indicated. In patients presenting with coronary vasospasm, nitrates and calcium channel blockers are preferred, while treatment of coronary ectasia/aneurysm mandates the use of antiplatelets/anticoagulants, corticosteroids, immunoglobulin, and biologic agents. It is crucial to untangle the exact mechanisms of coronary involvement in COVID-19 in order to ensure timely diagnosis and appropriate treatment. We have reviewed the current literature and provide a detailed overview of the pathophysiology and clinical spectrum associated with coronary implications of SARS-COV-2 infection. Patients with SARS-CoV-2 infection carry an increased risk of cardiovascular disease encompassing various implications, including acute myocardial injury or infarction, myocarditis, heart failure, and arrhythmias. A growing volume of evidence correlates SARS-CoV-2 infection with myocardial injury, exposing patients to higher mortality risk. SARS-CoV-2 attacks the coronary arterial bed with various mechanisms including thrombosis/rupture of preexisting atherosclerotic plaque, de novo coronary thrombosis, endotheliitis, microvascular dysfunction, vasculitis, vasospasm, and ectasia/aneurysm formation. The angiotensin-converting enzyme 2 receptor plays pivotal role on the cardiovascular homeostasis and the unfolding of COVID-19. The activation of immune system, mediated by proinflammatory cytokines along with the dysregulation of the coagulation system, can pose an insult on the coronary artery, which usually manifests as an acute coronary syndrome (ACS). Electrocardiogram, echocardiography, cardiac biomarkers, and coronary angiography are essential tools to set the diagnosis. Revascularization is the first-line treatment in all patients with ACS and obstructed coronary arteries, whereas in type 2 myocardial infarction treatment of hypoxia, anemia and systemic inflammation are indicated. In patients presenting with coronary vasospasm, nitrates and calcium channel blockers are preferred, while treatment of coronary ectasia/aneurysm mandates the use of antiplatelets/anticoagulants, corticosteroids, immunoglobulin, and biologic agents. It is crucial to untangle the exact mechanisms of coronary involvement in COVID-19 in order to ensure timely diagnosis and appropriate treatment. We have reviewed the current literature and provide a detailed overview of the pathophysiology and clinical spectrum associated with coronary implications of SARS-COV-2 infection.

Chagas Disease (CD) can cause Chagas cardiomyopathy. The new coronavirus disease (COVID-19) also affects the cardiovascular system and may worsen Chagas cardiomyopathy. However, the cardiac evolution of patients with CD infected by COVID-19 is not known. Thus, the objective of this study is to assess, within one year, whether there was cardiac progression after COVID-19 in CD.

Longitudinal study with CD patients. The outcome was cardiac progression, defined as the appearance of new major changes in the current ECG compared to the previous ECG considered from the comparison of electrocardiograms (ECGs) performed with an interval of one year. Positive Anti-SARS-CoV2 Serology was the independent variable of interest. For each analysis, a final multiple model was constructed, adjusted for sociodemographic, clinical, and pandemic-related characteristics.

Of the 404 individuals included, 22.8 % had positive serology for COVID-19 and 10.9 % had cardiac progression. In the final model, positive serology for COVID-19 was the only factor associated with cardiac progression in the group as a whole (OR = 2.65; 95 % CI = 1.27-5.53) and for new-onset cardiomyopathy in the group with normal previous ECG (OR = 3.50; 95 % CI = 1.21-10.13).

Our study shows an association between COVID-19 and progression of Chagas cardiomyopathy, evaluated by repeated ECGs, suggesting that COVID-19 accelerated the natural history of CD.

Angiotensin converting enzyme (ACE) is not only a critical component in the renin-angiotensin system (RAS), but also suggested as an important mediator for immune response and activity, such as immune cell mobilization, metabolism, biogenesis of immunoregulatory molecules, etc. The chronic duration of cardiovascular diseases (CVD) has been increasingly considered to be triggered by uncontrolled pathologic immune reactions from myeloid cells and lymphocytes. Considering the potential anti-inflammatory effect of the traditional antihypertensive ACE inhibitor (ACEi), we attempt to elucidate whether ACE and its catalytically relevant substances as well as signaling pathways play a role in the immunity-related pathogenesis of common CVD, such as arterial hypertension, atherosclerosis and arrythmias. ACEi was also reported to benefit the prognoses of COVID-19-positive patients with CVD, and COVID-19 disease with preexisting CVD or subsequent cardiovascular damage is featured by a significant influx of immune cells and proinflammatory molecules, suggesting that ACE may also participate in COVID-19 induced cardiovascular injury, because COVID-19 disease basically triggers an overactive pathologic immune response. Hopefully, the ACE inhibition and manipulation of those associated bioactive signals could supplement the current medicinal management of various CVD and bring greater benefit to patients' cardiovascular health.

The study assessed Global longitudinal strain imaging (GLS) to detect subtle myocardial dysfunction among patients clinically recovered from COVID-19.

All patients (n = 101 76 % males, mean age 55.45 ± 11.14 years), and controls (n = 30), underwent clinical assessment and echocardiography, including GLS assessment.

The prevalence of diabetes mellitus, hypertension and dyslipidemia was comparable amongst patients and controls. The average GLS was significantly lesser in post COVID patients (-16.21 ± 1.96 vs -18.49 ± 1.64 respectively, p = 0.004) and significantly higher proportion of post COVID patients had GLS > -18 % (43 % vs 22.58 % respectively, p = 0.001) as compared to controls. The RV free wall longitudinal strain (RVFLS) was also lower in the patient group (22.35 ± 4.69 vs 24.19 ± 4.11, p = 0.004) and 21.7 % post COVID-19 patients had pathological RV FWLS (> -20 %) vs controls (6.6 %). Average GLS was significantly lesser in severe post COVID patients (viz -14.25 ± 1.92 vs -16.63 ± 1.61 vs -17.63 ± 1.91, p < 0.0001, respectively among severe, moderate and mild COVID-19 patients. On performing regression analysis, severity of COVID-19 (OR 7.762) was a significant predictor of impaired GLS.

Despite normal global LVEF, post COVID-19 recovered patients had significantly lower LV GLS and RV FWLS with severe COVID-19 infection, regardless of having a clinical recovery. This study reiterates the importance of speckle tracking echocardiography as an important imaging modality for detection of subclinical myocardial dysfunction in the post COVID-19 recovered patients.