The earliest evidence from China suggested that COVID-19 patients are even more vulnerable to succumbing from complications in the presence of a multimorbid status, including metabolic syndrome. Due to ongoing metabolic abnormalities, non-alcoholic fatty liver disease (NAFLD) appears to be a potential risk factor for contracting SARS-CoV-2 infection and developing related complications. This is because of the interplay of chronically active inflammatory pathways in NAFLD- and COVID-19-associated acute cytokine storm. The risk of severe disease could also be attributed to compromised liver function as a result of NAFLD. We systematically reviewed current literature to ascertain the relationship between NAFLD and severe COVID-19, independent of obesity, which is considered the major factor risk factor for both NAFLD and COVID-19. We found that NAFLD is a predictor of severe COVID-19, even after adjusting for the presence of obesity (OR 2.358; 95% CI: 1.902–2.923, p < 0.001).

Acute pulmonary embolism (PE) can present with non-specific signs and symptoms and thus the diagnosis and management might not be as straightforward. This review outlines the new PE management guidelines in the Indian context. The exact prevalence in the Indian population is not well defined; despite recent studies suggesting an increasing trend in the Asian population. A delay in treatment can be fatal, especially in massive PE. The nuances associated with stratification and management have led to heterogeneity in acute PE management. The purpose of the review is. 1: To highlight the principles of stratification, diagnosis and management of acute PE with a special attention towards the Indian population. 2: To aid patient selection for newer catheter based therapies. To conclude, formulation of pulmonary embolism guidelines in the Indian setting is required underlying the role of further research in this area.

Background: Cardiorenal syndrome (CRS) refers to the bidirectional interactions between the acutely or chronically dysfunctioning heart and kidney that lead to poor outcomes. Due to the evolving literature on renal impairment and heart failure with preserved ejection fraction (HFpEF), this review aimed to highlight the pathophysiological pathways, diagnosis using imaging and biomarkers, and management of CRS in patients with HFpEF. Summary: The mechanism of CRS in HFpEF can be hypothesized due to the interplay of elevated central venous pressure, renin-angiotensin-aldosterone system (RAAS) activation, oxidative stress, endothelial dysfunction, coronary microvascular dysfunction, and chronotropic incompetence. The correlation between HFpEF and worsening renal function seen in both long-term trials and observational data points to the evidence for these mechanisms. Upcoming biomarkers such as cystatin C, NGAL, NAG, KIM-1, ST-2, and galectin-3, along with conventional ones, are promising for early diagnosis, risk stratification, or response to therapy. Despite the lack of specific treatment for CRS in HFpEF, the management can be discussed with similar medications used in goal-directed medical therapy for heart failure with reduced ejection fraction (HFrEF). Additionally, there is increasing evidence for the role of vasodilators, inotropes, assist devices, and renal denervation, although long-term studies are necessary. Key Message: The management of CRS in HFpEF is an evolving field that currently shows promise for using diagnostic and prognostic biomarkers, conventional heart failure medications, and novel therapies such as renal denervation, interatrial shunt, and renal assist devices. Further studies are needed to understand the pathophysiological pathways, validate the use of novel biomarkers, especially for early diagnosis and prognostication, and institute new management strategies for CRS in patients with HFpEF.

The severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2), the causative agent of the novel coronavirus disease 2019 (COVID 19), was reported to the World Health Organization in late 2019. This disease quickly evolved into a public health concern and was declared a pandemic on March 11, 2020. COVID-19’s high transmission rate and potential to cause a spectrum of systemic diseases makes it imperative for researchers and clinicians worldwide to collaborate and develop a strategy to manage and contain this disease. Studies have shown a wide range of hematological abnormalities and virus-related coagulopathies in affected patients, resulting in an increased propensity to develop serious thrombotic complications or disseminated intravascular coagulation (DIC) in severe cases. The fatal implications of coagulopathy in the form of pulmonary embolism (PE), myocardial infarction (MI), and cerebral infarction compelled us to study in-depth the pathophysiology and treatment options related to COVID-19. This analysis reviews published reports on patients with confirmed SARS-COV-2 infection and associated coagulopathy, defined as abnormalities in the coagulation parameters prothrombin time (PT), activated partial thromboplastin time (aPTT), antithrombin time, fibrinogen, fibrin degradation products, and D-dimer. In this review, we present the hematological manifestations of COVID-19, focusing on virus-associated coagulopathy and relevant pathophysiology, clinical outcomes, and treatment.

Coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV- 2) was declared a pandemic by WHO in March 2020. The causative organism has since undergone a series of mutations. COVID-19 primarily being a respiratory illness causes pre-existing pulmonary diseases to show worse clinical outcomes. About one-third of the world’s population is thought to be infected with latent Mycobacterium tuberculosis (MTB). Both previous and newly developed tuberculosis (TB) infection are risk factors for COVID-19 and are associated with poor outcomes. T lymphocytes play a pivotal role in defense against MTB and with evidence suggesting depletion of T lymphocytes in COVID-19, it can be postulated that COVID-19 can increase the risk of reactivation of latent TB. Given that a large population around the globe is infected with latent tuberculosis, it is interesting to study and note cases where the virus leads to the reactivation of latent tuberculosis infection. Herein, we present a 76-year-old Brazilian male recently treated for COVID-19 pneumonia, presenting with new-onset cough and weakness diagnosed with latent MTB reactivation.

There is a paucity of data and minimal literature on outcomes of percutaneous coronary intervention (PCI) among liver cirrhosis patients. Therefore, we conducted a systematic review and meta-analysis to evaluate the clinical outcomes among liver cirrhosis patients post-PCI. We conducted a comprehensive literature search in the PubMed, Embase, Cochrane, and Scopus databases for relevant studies. Effect sizes were pooled using the DerSimonian and Laird random-effects model as an odds ratio (OR) with 95% confidence intervals (CI). A total of 3 studies met the inclusion criteria, providing data from 10,705,976 patients. A total of 28,100 patients were in the PCI + Cirrhosis group and 10,677,876 patients were in the PCI-only group. The mean age of patients with PCI + Cirrhosis and PCI alone was 63.45 and 64.35 years. The most common comorbidity was hypertension among the PCI + Cirrhosis group compared with PCI alone (68.15% vs. 73.6%). Cirrhosis patients post-PCI were had higher rates of in-hospital mortality (OR, 4.78 (95%CI: 3.39–6.75), p < 0.001), GI bleeding (OR, 1.91 (95%CI:1.83–1.99), p < 0.001, I² = 0%), stroke (OR, 2.48 (95%CI:1.68–3.66), p < 0.001), AKI (OR, 3.66 (95%CI: 2.33–6.02), p < 0.001), and vascular complications (OR, 1.50 (95%CI: 1.13–1.98), p < 0.001) compared with the PCI group without cirrhosis. Patients with cirrhosis are at a high risk for mortality and adverse outcomes post-PCI procedure compared to the PCI-only group of patients.