Background Coronavirus disease 2019 (COVID-19) has been implicated in a wide spectrum of cardiac manifestations following the acute phase of the disease. Objectives To assess the range of cardiac sequelae after COVID-19 recovery. Data sources PubMed, Embase, Scopus (inception through 17 February 2021), and Google scholar (2019 through 17 February 2021). Study eligibility criteria Prospective and retrospective studies, case reports and case series. Participants Adult patients assessed for cardiac manifestations after COVID-19 recovery. Exposure Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection diagnosed by polymerase chain reaction (PCR). Methods Systematic review. Results Thirty-five studies (fifteen prospective cohort, seven case reports, five cross-sectional, four case series, three retrospective cohort and one ambidirectional cohort) evaluating cardiac sequelae in 52609 patients were included. Twenty-nine studies utilized objective cardiac assessments, mostly cardiac magnetic resonance imaging (CMR) in sixteen studies, echocardiography in fifteen, electrocardiography (ECG) in sixteen and cardiac biomarkers in eighteen. Most studies had a fair risk of bias. The median time from diagnosis/recovery to cardiac assessment was 48 days (1-180). Common short-term cardiac abnormalities (<3 months) included increased T1 (proportion: 30%), T2 (16%), pericardial effusion (15%) and late gadolinium enhancement (LGE, 11%) on CMR, with symptoms such as chest pain (25%) and dyspnea (36%). In the medium term (3-6 months), common changes included reduced left ventricular global longitudinal strain (30%) and LGE (10%) on CMR, diastolic dysfunction (40%) on echocardiography and elevated NT-proBNP (18%). In addition, COVID-19 survivors had higher risk (RR = 3; 95% CI: 2.7-3.2) of developing heart failure, arrythmias and myocardial infarction. Conclusions COVID-19 appears to be associated with persistent/de novo cardiac injury after recovery, particularly subclinical myocardial injury in the earlier phase and diastolic dysfunction later. Larger well-designed and controlled studies with baseline assessments are needed to better measure the extent of cardiac injury and its clinical impact.

Purpose The urothelium of cats diagnosed with feline interstitial cystitis (FIC) was analyzed to determine if abnormalities in protein expression patterns could be detected, and whether the pattern of expression was similar to that observed in human Interstitial Cystitis/Bladder Pain Syndrome (IC) patients. The proteins that were analyzed are involved in cell adhesion, barrier function, comprise the glycosaminoglycan (GAG) layer, or are markers of differentiation. Methods Formalin-fixed biopsies from 8 cats with FIC and 7 healthy controls were labeled using immunohistochemistry and scored using a modified version of a system previously used for human samples. Cluster analysis was performed to investigate relationships between the markers and samples. Results The results showed that 89% of the FIC bladders displayed abnormal protein expression and chondroitin sulfate (CS) patterns, whereas only 27% of the normal tissues exhibited slight abnormalities. Abnormalities were found in most of the FIC samples, biglycan (87.5%), CS (100%), decorin (100%), E-cadherin (100%), keratin-20 (K20, 100%), uroplakin (50%), ZO-1 (87.5%). In the FIC bladders, about 75% of the CS, biglycan, and decorin samples displayed absence of luminal staining or no staining. Results from the cluster analysis revealed that the FIC and normal samples fell into two clearly separate groups, demonstrating that the urothelium of cats with FIC is altered from normal. Conclusions FIC produces similar changes in luminal GAG and several proteins as is seen in human patients, suggesting some commonality in mechanism and supporting the use of FIC as a model for human IC.

Growing reports since the beginning of the pandemic and till date describe increased rates of cardiac complications (CC) in the active phase of coronavirus disease 2019 (COVID-19). CC commonly observed include myocarditis/myocardial injury, arrhythmias and heart failure, with an incidence reaching about a quarter of hospitalized patients in some reports. The increased incidence of CC raise questions about the possible heightened susceptibility of patients with cardiac disease to develop severe COVID-19, and whether the virus itself is involved in the pathogenesis of CC. The wide array of CC seems to stem from multiple mechanisms, including the ability of the virus to directly enter cardiomyocytes, and to indirectly damage the heart through systemic hyperinflammatory and hypercoagulable states, endothelial injury of the coronary arteries and hypoxemia. The induced CC seem to dramatically impact the prognosis of COVID-19, with some studies suggesting over 50% mortality rates with myocardial damage, up from ~ 5% overall mortality of COVID-19 alone. Thus, it is particularly important to investigate the relation between COVID-19 and heart disease, given the major effect on morbidity and mortality, aiming at early detection and improving patient care and outcomes. In this article, we review the growing body of published data on the topic to provide the reader with a comprehensive and robust description of the available evidence and its implication for clinical practice.

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Serum levels of CA 125, CA 15-3 and CEA are not affected by molar pregnancy. The mean level of CA 19-9 in maternal serum is significantly lower in cases of molar pregnancy when compared with cases of normal pregnancy. The amnion cell origin of CA 19-9 could explain the statistically significant difference between cases of therapeutic abortion and cases of HM (complete HM lacks amniotic membrane).

This study attempts to determine the analgesic properties of nalbuphine, pentazocine and butorphanol during labor and their potential effects on maternal and fetal blood gases and pH. Butorphanol analgesia was superior to either nalbuphine or pentazocine in relieving labor pain. The studied analgesics caused significant maternal respiratory acidosis and fetal metabolic acidosis. These acidotic changes were most marked with pentazocine, moderate with nalbuphine and minimal with butorphanol.

The liver-heart axis is a growing field of interest owing to rising evidence of complex bidirectional interplay between the two organs. Recent data suggest non-alcoholic fatty liver disease (NAFLD) has a significant, independent association with a wide spectrum of structural and functional cardiac diseases, and seems to worsen cardiovascular disease (CVD) prognosis. Conversely, the effect of cardiac disease on NAFLD is not well studied and data are mostly limited to cardiogenic liver disease. We believe it is important to further investigate the heart-liver relationship because of the tremendous global health and economic burden the two diseases pose, and the impact of such investigations on clinical decision making and management guidelines for both diseases. In this review, we summarize the current knowledge on NAFLD diagnosis, its systemic manifestations, and associations with CVD. More specifically, we review the pathophysiological mechanisms that govern the interplay between NAFLD and CVD and evaluate the relationship between different CVD treatments and NAFLD progression.

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