Novel coronavirus disease (COVID-19) has led to a major public health crisis globally. Currently, myocardial damage is speculated to be associated with COVID-19, which can be seen as one of the main causes of death of patients with COVID-19. We therefore, aim to investigate the effects of COVID-19 disease on myocardial injury in hospitalized patients who have been tested positive for COVID-19 pneumonia in this study. A prospective study was conducted among 201 patients with COVID-19 in the Pakistan Military Hospital from April 1 to August 31, 2020, including non-critical cases and critical cases. COVID-19 patients were stratified as critical and non-critical according to the signs and symptoms severity; with those requiring intensive care and invasive mechanical ventilation as critical, and those did not requiring invasive mechanical ventilation as non-critical. A total of 201 COVID-19 patients with critical and non-critical categories presented with myocardial injury. All patients with myocardial injury had an elevation in CKMB and Troponin-I levels. Of these patients, 43.7% presented with new electrocardiography (ECG) changes, and ST depression was typically observed in 36.3% patients. In addition, 18.7% patients presented with abnormal echocardiography findings, with right ventricular dilatation and dysfunction commonly seen among critical group patients. Results analyzed by a logistic regression model showing COVID-19 direct contribution to myocardial injury in these patients. COVID-19 disease directly leads to cardiovascular damage among critical and non-critical patients. Myocardial injury is associated not only with abnormal ECG changes but also with myocardial dysfunction on echocardiography and more commonly observed among critical patients.

The world's number one cause of death is cardiovascular diseases. The pathogenesis of different disease entities in the cardiovascular disease spectrum is complicated and multifactorial. Inflammation in these complicated etiologies serves as a key position and is a significant cause of atherosclerosis, which contributes to the underlying pathology. Therefore, therapeutic targeting of inflammatory pathways in patients with cardiovascular diseases such as atherosclerosis enhances cardiovascular results. Inflammasomes are intracellular protein complexes engaged in atherosclerosis pathogenesis and activated by multiple danger signals. Emerging proof has revealed that Nod-like receptor protein 3 (NLRP3) inflammasome, which regulates caspase-1 activation and later pro-interleukin processing, triggers inflammatory reactions in the vascular wall and leads to atherosclerotic plaque formation. Inflammasome-mediated signaling interference could decrease inflammation and mitigate illness severity. In this section, we provide an overview of the present literature on the underlying mechanisms leading to the activation of NLRP3 inflammasome and the role of NLRP3 inflammasome in the progression of atherogenesis and highlight the possibility of therapeutic interventions due to mechanisms involved in the of inhibition of NLRP3 activation.

Background and Objectives: A dispute over interaction of warfarin with two quinolones—i.e., moxifloxacin and levofloxacin—leading to significant increase in international normalized ratio (INR) levels and coagulopathies is currently in debate. The study objective was to compare the INR values due to addition of quinolones and cefixime in warfarin treated patients after replacement of disease valves with metallic valves. Material and Methods: A prospective evaluation of patients who undergone valve replacement surgeries in the cardiology hospital setup in Pakistan during the period 2018–2019 was done, including all those subjects treated concurrently with levofloxacin, moxifloxacin, cefixime, and warfarin for the study. Data organized included demographic information, concurrent medications, and appropriate analytical parameters, especially INR values taken before and within seven days after prescribing three antibiotics in discharged patients who had undergone valve replacement surgeries. Patients for whom laboratory INR values were not given at the time of discharge and with deranged liver function, renal function, low albumin levels, and febrile patients were removed from study. Furthermore, patients were advised on possible food interactions and evaluated to examine if these factors have any possible influence on the interaction being studied. Results: Differences in INR were analyzed statistically by means of SPSS analysis before and after the possible interaction. Following the administration of levofloxacin and moxifloxacin to warfarin therapy, statistical analysis showed remarkable increase in INR (p < 0.001) and no significant change in INR was observed after cefixime treatment (p > 0.05). Conclusion: Results showed that, after adding levofloxacin and moxifloxacin in patients on warfarin, therapy contributed to remarkable increase in INR. However, addition of cefixime prevented frequent coagulopathies; therefore, close monitoring of INR and switching to a safe antibiotic such as cefixime is recommended.

Background: Novel coronavirus disease (COVID-19) has led to a major public health crisis globally. Currently, myocardial damage is speculated to be associated with COVID-19, which can be seen as one of the main causes of death of patients with COVID-19. Therefore, in this study, we aim to investigate the effects of COVID-19 diagnosed patients on myocardial injury. Methods: A prospective study was conducted among 201 patients with COVID-19 in the Pakistan Military Hospital from April 1 to August 31, 2020, including non-critical cases and critical cases. COVID-19 patients were stratified as critical and non-critical according to signs and symptoms with those requiring intensive care and ventilator support as critical and those don’t require ventilator support as non-critical Results: A total of 201 COVID-19 patients with critical and non-critical categories presented with myocardial injury. All patients with myocardial injury had an elevation in CKMB and Trop 1 levels. Of these patients, 43.7% presented with new electrocardiography (ECG) changes, ST depression is observed in 36.3% patients, and 16.9% presented with abnormal electrocardiogram findings, with right ventricular dilatation and dysfunction. Results analyzed by a logistic regression model showing COVID-19 direct contribution to myocardial injury in these patients. Conclusion: COVID-19 disease directly leads to cardiovascular damage among critical and non-critical patients. Myocardial injury is associated not only with abnormal ECG changes but also with myocardial dysfunction on echocardiography and more commonly observed among critical patients.

Background Despite the fact that a number of therapeutic agents have been tested for the treatment of coronavirus disease 2019 (Covid-19), no antiviral agents have yet been proven to be effective. Objectives This study aims to evaluate the favorable clinical outcomes after remdesivir treatment in hospitalized patients with moderately severe COVID-19 disease in Pakistan. Methods A prospective study in hospitalized patients with moderately severe Covid-19 disease was conducted between January 2021- October 2021. The patients were divided into remdesivir-treated and control groups. The Remdesivir-treated group received 200mg IV, followed by 100mg once daily for four days. In addition to standard care, all patients received corticosteroid therapy. The clinical status of remdesivir patients was assessed after the 5th day of treatment, including proportion negative polymerase chain reaction test for COVID-19, length of hospitalization, improvement in oxygen demand, and effects on C-reactive protein (CRP) levels. Multivariate analysis and paired sample T-test were performed to evaluate a favorable response to remdesivir treatment and results were compared with a control group. Result In total, 328 patients were enrolled in the study, with 162 of them receiving IV remdesivir on the day of admission. The C-reactive protein level in the remdesivir treated group [median 22.0 (14.0–36.7)] was significantly lower (p < 0.001) than in the remdesivir naive group [median 79.1 (57.4–139.0)]. The number of days spent in the hospital was significantly different between the remdesivir-treated and remdesivir-naive groups [6.2 0.5] (p < 0.001). In the remdesivir-treated group, 36.7% of patients were discharged with a negative PCR, compared to 21.6% in the control group (p < 0.001). In comparison to the control group, the remdesivir treated group showed a significant improvement in the ratio of arterial oxygen partial pressure to fractional inspired oxygen (p < 0.001). Conclusion The remdesivir treatment was found to be superior to improve clinical outcomes among moderately severe Covid-19 disease patients.