Features and risk factors of post-COVID-19 syndrome: findings from a longitudinal study in Bangladesh.

Background: A comprehensive study of the post-COVID syndrome (PCS) remains scarce in low-and middle-income countries. We assessed the prevalence, incidence rate, evolution over time, and risk factors of PCS among hospitalized (HS) and non-hospitalized (NHS) COVID-19 survivors. Methods: We undertook a prospective longitudinal study of COVID-19 survivors at months 1, 3, and 5 post-discharge or post-isolation period. The study was conducted at two COVID-19-designated hospitals in Dhaka, Bangladesh, between December 2020 and October 2021. Findings: 362 participants were enrolled in the study; the median time from the onset of COVID-19 to enrolment was 57 days (IQR 41, 82). At enrolment, after adjusting for potential confounders, the HS more often had one or more symptoms, peripheral neuropathy (PN), depression and anxiety disorder, poor quality of life, dyspnea, tachycardia, restrictive lung disease on spirometry, anemia, proteinuria, and need for insulin therapy than the non-hospitalized group (95% CI > 1 for all). Although most of these findings decreased significantly over time in HS, PN increased in both groups. The incidence of diabetes was 9.8/1000 person-month, and the new requirement of insulin therapy was higher (aOR, 6.71; 95% CI, 2.87, 15.67) among HS than the NHS. Older age, being female, comorbidity, cigarette smoking, hospitalization, and contact with COVID-19 cases were independently associated with PCS. Interpretation: We observed a high burden of PCS in hospitalized and non-hospitalized survivors despite most findings' decreasing trend over time. Our results underscore the importance of continuing long-term follow-up and subsequent management. Funding: The United States Agency for International Development (USAID).

Correlation between Myocardial Strain by 2-D Speckle-Tracking Echocardiography and Angiographic findings by Coronary Angiogram in Stable Angina.

Background and aims: Identification of coronary artery disease by non-invasive means is a subject of interest for all. Myocardial strain has shown some promising results. This study intends to see if change in strain value correlates with the angiographic findings in patients with stable angina. It is also assessing whether myocardial strain can predict the presence of coronary artery disease (CAD) in stable angina patients. Method: This cross-sectional study was carried out on 84 stable angina patients with no previous cardiac history and normal LV function undergoing coronary angiogram for guideline-based indication. After careful history, clinical examination and investigations, including conventional echocardiography, selected participants underwent 2-D speckle tracking echocardiography for measurement of myocardial strain by automated functional imaging. All participants underwent coronary angiogram and stenosis >70% was considered significant. Gensini score was calculated. The myocardial strain value and Gensini score were correlated. Results: Global longitudinal strain (GLS) was significantly lower in patients with significant CAD than those with non-significant CAD (-16.1±2.6% vs -19.4±2.2%; p < 0.001). The optimal cut-off value of GLS, which discriminated between patients with and without significant coronary artery disease, was -18.05% (sensitivity=81.8% and specificity=85%). Also, GLS declined incrementally with the increasing severity of CAD defined by increasing number of stenotic vessels. There was an inverse correlation between GLS and severity of CAD (expressed in Gensini score) in this study (r = 0.669, p< 0.001), meaning that GLS decreased with increasing severity of CAD. GLS remained an independent predictor for the presence of significant CAD after multivariate adjustment for other significant baseline characteristics and echocardiographic parameters. Conclusions: The myocardial strain by 2DSE correlates with the angiographic severity by coronary angiogram in patients with stable angina. It is an independent predictor of significant coronary artery disease, which it can detect with good sensitivity and specificity.

Influence of maternal diabetes on serum leptinemic and insulinemic status of the offspring: a case study of selected patients in a tertiary care hospital in Bangladesh.

INTRODUCTION: Leptin is now known to be an important hormone affecting intrauterine fetal growth. Since growth of fetus is also affected by the glycemic status of the mother. Serum leptin of infant is influenced by the maternal diabetic state. Investigation of cord blood leptin in babies of DM (Diabetes Mellitus) and GDM (Gestational Diabetes Mellitus) mothers (controlled blood glucose levels) may provide some indication about involvement of genetic factor in the development of leptin abnormalities in fetus. AIM: The study was taken to investigate whether cord blood insulin, c-peptide and leptin levels correlate with birth weight in offspring of DM mother. METHODS: Blood was drawn from umbilical cord of 30 babies from GDM mothers (GDM-babies), 45 babies from Type 2 DM Mothers (DM-babies), and 30 babies from ND (Nondiabetic) mothers (ND-babies) of term pregnancy. Weight, blood glucose, placenta, serum leptin and c-peptide of the babies were measured. RESULTS: Birth weight of GDM and DM babies were significantly higher compared to ND-babies. Glucose level in GDM babies was significantly higher than ND and DM babies. Leptin levels in GDM babies were significantly higher than that of ND and DM babies. Serum c-peptide in GDM babies was significantly higher than DM and ND babies. However, there was no significant difference in leptin-glucose ratio among the three groups. Irrespective of degree of hyperglycemia leptin is a major determinant of fetal growth. CONCLUSIONS: DM mother produces different insulinemic and leptinemic responses in the fetus indicating a possible genetic involvement.

An investigation into genetic contribution to the relationship between insulin resistance and birth weight.

BACKGROUND: Insulin resistance has been proposed to be the most likely phenotypic trait that could represent a genetic link between low birth weight and type 2 diabetes, especially in Southeast Asia. Insulin resistance can persist for many years, even decades, before the manifestation of overt diabetes. There have been many studies suggesting a strong genetic basis in the etiology of type 2 diabetes mellitus. There is also ample evidence providing a link with low birth weight and type 2 diabetes in later life. Hence, parental insulin sensitivity could well serve as a representation of the offspring's future insulin resistance state. Association between maternal insulin sensitivity and the incidence of type 2 diabetes mellitus in low birth weight babies is confounded by many factors and hence, has limited value in the determination of any genetic origin of the disease. Therefore, the present study was done to investigate the relationship between paternal insulin sensitivity and the growth parameters of the foetus to determine a genetic link between poor early growth and the increased risk of type 2 diabetes mellitus in later life. MATERIALS AND METHODS: The study was performed on 30 healthy fathers and their babies born from nondiabetic mothers. Each father underwent a low-dose short insulin tolerance test (ITT) as a measure of insulin sensitivity. Placental weight was recorded and a blood sample was collected from the placental side of the umbilical cord at birth for measurement of insulin. Measurement of birth weight, length, and head circumference were recorded and ponderal index was calculated from the formula: weight (kg)/ length (cm)(3). Individual parameters of insulin resistance syndrome were measured in the fathers. RESULTS: The degree of insulin sensitivity, K(m) (constant for insulin tolerance test) did not correlate with the fetal growth parameters (Ponderal Index r = 0.031, P = 0.870; weight of baby r = 0.010, P = 0.959; length of baby r = 0.087, P = 0.464; head circumference r = 0.280, P = 0.142) or with the fathers' anthropometric measures: body mass index (BMI), blood pressure, fasting glucose, insulin, and lipid profiles. CONCLUSION: The data suggest that the mechanism linking insulin resistance with low birth weight is not a genetically determined defect.