Whitaker syndrome: A case report of autoimmune polyendocrine syndrome type 1 with dilated cardiomyopathy.

Key Clinical Message: This case report highlights dilated cardiomyopathy as a cardiovascular complication in autoimmune polyendocrine syndrome type 1 (APS-1), emphasizing the need for early recognition and a multidisciplinary approach. Comprehensive care and regular follow-up are crucial in managing these atypical presentations to optimize patient outcomes. Abstract: APS-1, also known as Whitaker syndrome, is characterized by a triad of mucocutaneous candidiasis, adrenal insufficiency, and hypoparathyroidism. This rare autosomal recessive disorder results from mutations in the autoimmune regulator (AIRE) gene. Cardiovascular and pulmonary manifestations in APS-1 are infrequently reported in the literature. We present a case of a 28-year-old male who presented with shortness of breath and pedal edema. Physical examination revealed alopecia, absence of eyebrows, hyperpigmentation on joints, oral candidiasis, and nail dystrophy. Echocardiography demonstrated dilated cardiomyopathy (DCM) and pericardial effusion. Chest x-ray showed left-sided pleural effusion. Laboratory investigations revealed hypocalcemia, hyperphosphatemia, low parathyroid hormone (PTH), low cortisol, and high adrenocorticotropic hormone (ACTH) levels. The combination of chronic mucocutaneous candidiasis (CMC), hypoparathyroidism, and adrenal insufficiency confirmed the diagnosis of APS-1. To the best of our knowledge, this is the first Pakistani and second worldwide reported case of APS-1 presenting with such a combination of manifestations. Early recognition and multidisciplinary management are crucial for improving outcomes in these patients.

Treatment of malignant primary cardiac tumors requires attention to cardiovascular complications: a single-center, retrospective study.

BACKGROUND: Malignant primary cardiac tumors require multimodal approaches including surgery, chemotherapy and radiotherapy, but these treatments can be associated with cardiovascular complications. However, few reports have described the cardiovascular complications related to primary cardiac tumor treatment because of their rarity. METHODS: Clinical records of patients with primary cardiac tumors treated at Kyushu University Hospital from January 2010 to August 2021 were retrospectively examined. RESULTS: Of the 47 primary cardiac tumor patients, 13 (28%) were diagnosed with malignancy, including 5 angiosarcomas, 3 intimal sarcomas, 3 diffuse large B-cell lymphomas, 1 Ewing's sarcoma and 1 fibrosarcoma. Cardiovascular events were observed in 10 patients (77%), including cardiac dysfunction in 6 patients, arrhythmias in 5 patients, right heart failure in 2 patients, and excessively prolonged prothrombin time due to the combination of warfarin and chemotherapy in 1 patient. Two patients who showed notable cardiac complications are described. Case A involved a 69-year-old woman who underwent surgery for a left atrial intimal sarcoma, followed by postoperative chemotherapy with doxorubicin plus ifosfamide and radiotherapy. After three cycles of chemotherapy and sequential radiotherapy, her left ventricular ejection fraction decreased to 34%, and ongoing heart failure therapy was required. Case B involved a 66-year-old man who received chemotherapy for primary cardiac lymphoma, resulting in tumor shrinkage. However, due to tumor involvement of the intraventricular septum, atrioventricular block developed, requiring cardiac pacemaker implantation. CONCLUSION: High incidences of cardiac failure and arrhythmias were observed during multimodal treatments for malignant primary cardiac tumors. Proper management of complications may lead to a favorable prognosis in patients with malignant primary cardiac tumors.

Exploring the clinical effectiveness of glucagon-like peptide-1 receptor agonists in managing cardiovascular complications: an updated comprehensive review and future directives.

The possible cardiovascular advantages of glucagon-like peptide-1 receptor agonists (GLP-1RAs), a class of drugs predominantly used to treat type 2 diabetes (T2D), have garnered increasing attention in recent years. Clinical trials have looked into the possibility that GLP-1RAs have extra cardioprotective benefits in addition to their ability to manage T2D, demonstrating significant major adverse cardiovascular events (MACE) reduction and a favorable safety profile. GLP-1 RAs improve cardiovascular outcomes, especially in those with existing cardiovascular disease. MACE has been steadily declining with this class of drugs, which results in a noticeable rise in cardiovascular outcome trials (CVOTs). GLP-1 RAs have a variety of impacts on the cardiovascular system beyond their function in glycemic control. They offer direct cardioprotection, vasodilation, promotion of salt excretion, reduction of weight, improved lipid profile, and anti-inflammatory qualities through a variety of mechanisms. Thus, this review focuses on GLP-1RAs, its mechanism of action, its clinical effectiveness in CVOTs, the mechanism behind its cardiovascular benefits, its potential role in heart failure, cardiovascular outcomes, its underutilization, and future directives. In conclusion, GLP-1 RAs shows potential in controlling T2D while also lowering cardiovascular risk, but warrants further study into long-term results and real-world data to optimize treatment regimens, ultimately increasing patient outcomes and lowering the burden of cardiovascular disease in T2D populations.

Exposure to aircraft noise exacerbates cardiovascular and oxidative damage in three mouse models of diabetes.

BACKGROUND: Epidemiology links noise to increased risk of metabolic diseases like diabetes and obesity. Translational studies in humans and experimental animals showed that noise causes reactive oxygen species (ROS)-mediated cardiovascular damage. The interaction between noise and diabetes, specifically potential additive adverse effects, remains to be determined. METHODS AND RESULTS: C57BL/6 mice were treated with streptozotocin (i.p. injections, 50 mg/kg/d for 5d) to induce type-1 diabetes, with S961 (subcutaneous osmotic minipumps, 0.57 mg/kg/d for 7d) or fed a high-fat diet (HFD, 20 weeks) to induce type-2 diabetes. Control and diabetic mice were exposed to aircraft noise to an average sound pressure level of 72 dB(A) for 4d. While body weight was unaffected, noise reduced insulin production in all diabetes models. The oral glucose tolerance test showed only an additive aggravation by noise in the HFD model. Noise increased blood pressure and aggravated diabetes-induced aortic, mesenteric, and cerebral arterioles endothelial dysfunction. ROS formation in cerebral arterioles, the aorta, the heart, and isolated mitochondria was consistently increased by noise in all models of diabetes. Mitochondrial respiration was impaired by diabetes and noise, however without additive effects. Noise increased ROS and caused inflammation in adipose tissue in the HFD model. RNA sequencing data and alteration of gene pathway clusters also supported additive damage by noise in the setting of diabetes. CONCLUSION: In all three models of diabetes, aircraft noise exacerbates oxidative stress, inflammation, and endothelial dysfunction in mice with pre-existing diabetes. Thus, noise may potentiate the already increased cardiovascular risk in diabetic patients.

Traffic noise significantly contributes to an increased risk of cardiometabolic diseases (including diabetes and obesity) in the general population via stress hormones, inflammation and oxidative stress, all of which contribute to impaired vascular function and high blood pressure. However, the extent to which noise affects pre-existing diabetes is not sufficiently explained, which prompted us to investigate the molecular mechanisms responsible for noise-mediated exacerbation of cardiometabolic complications in three different animal models with diabetes mellitus: Noise exposure in diabetic mice caused further impairment of insulin signalling, increased blood pressure, and damage of small and large blood vessels as well as oxidative stress in the aorta, brain, and heart.Our functional observations were supported by gene analyses indicating combined effects of noise and diabetes on gene groups related to inflammation and metabolism, suggesting a need for further studies in humans to investigate how noise impacts cardiovascular risk in vulnerable groups such as patients with diabetes.

Lipid-Lowering Treatment Gaps in Patients after Acute Myocardial Infarction: Using Global Database TriNetX.

Background and Objectives: Patients with previous acute myocardial infarction are at significantly higher risk of recurrent events. Early and intensive lipid-lowering therapy targeting low-density lipoprotein cholesterol is a key strategy for reducing cardiovascular risk in post-acute myocardial infarction patients worldwide. This study aimed to assess patients' real-life lipid-lowering treatment gaps after acute myocardial infarction using a global network, TriNetX, of anonymous, real-time patient data. The uniqueness of the study was the use of the novel, evolving, and constantly improving TriNetX platform and the evaluation of its feasibility for clinical research. Materials and Methods: A retrospective study was conducted on global repository patients in 2020, diagnosed with acute myocardial infarction, with a three-year follow-up. Results: After acute myocardial infarction, the prescribing rate of lipid-lowering medication (statins, ezetimibe and PCSK9I) was insufficient to reach target LDL-C values. The mean LDL-C level decreased from 2.7 mmol/L (103 mg/dL) as measured on the day of AMI to 1.97 mmol/L (76 mg/dL) between 31D and 3M. During the second and third years, the mean LDL-C value was stable (around 2.0 mmol/L (78 mg/dL)). LDL-C goals were not sufficiently reached, as only 7-12% of patients were reported to have LDL-C values < 55 mg/dL (1.4 mmol/L) and 13-20% of patients were reported to have LDL-C values < 70 mg/dL (1.8 mmol/L) during the follow-up periods. This means that a substantial number of patients remain at a very high risk for CV complications and mortality. Most cardiovascular complications happen within three months after acute myocardial infarction. Conclusions: Gaps remain between the recommendations for managing LDL-C in guidelines and what occurs in real life. The TriNetX platform is an innovative platform with significant potential and should be further developed for clinical research, as it enables the use of valuable interinstitutional data.

Investigating the research trajectory and future trends of immune disorders in diabetes cardiovascular complications: A bibliometric analysis over the past decade based on big data.

INTRODUCTION: Cardiovascular complications of diabetes are a top cause of death in diabetics and often involve immune system problems. Despite numerous studies, there's a shortage of extensive data to advance this field. This study aims to systematically analyze the role of immune dysregulation in these complications using bibliometric methods, to outline the research path and predict future directions. METHODS: Published from January 1, 2014 to December 31, 2023, 2826 records from the Web of Science Core Collection were analyzed. Collaboration networks, keyword co-occurrences, references, and research hotspots were visualized and analyzed using Microsoft Office Excel 2019, VOSviewer, CiteSpace, and R software. RESULTS: The number of research papers and citations on this topic has been increasing from 2014 to 2023, with significant contributions from the United States and China. Studies have focused on the effects of oxidative stress, inflammation, metabolism, gut microbiota, and COVID-19 on diabetic heart problems, highlighting the role of immune dysregulation in these diseases. CONCLUSION: This research provides an overview of immune dysregulation in the cardiovascular complications of diabetes, explores potential treatments including immunomodulation, insulin resistance, and the benefits of vitamin D on cardiovascular disease, and helps advance the field.

Clonal hematopoiesis of indeterminate potential and cardiovascular disease: Pathogenesis, clinical presentation, and future directions.

Clonal hematopoiesis of indeterminate potential (CHIP) is a well-studied phenomenon in hematologic malignancies. With advancements in gene sampling and analysis and the use of large cohort studies, CHIP has recently been linked to cardiovascular disease (CVD). The relationship between CHIP and CVD appears to be bidirectional, with traditional risk factors for cardiovascular disease increasing the mutation burden in CHIP, and CHIP itself effecting the incidence or prognosis of a variety of CVD. The purpose of this review is to understand the epidemiology, risk factors, and pathogenesis of CHIP in the context of various CVD conditions.

Epigenetic mechanisms in cardiovascular complications of diabetes: towards future therapies.

The pathophysiological mechanisms of cardiovascular disease and microvascular complications in diabetes have been extensively studied, but effective methods of prevention and treatment are still lacking. In recent years, DNA methylation, histone modifications, and non-coding RNAs have arisen as possible mechanisms involved in the development, maintenance, and progression of micro- and macro-vascular complications of diabetes. Epigenetic changes have the characteristic of being heritable or deletable. For this reason, they are now being studied as a therapeutic target for the treatment of diabetes and the prevention or for slowing down its complications, aiming to alleviate the personal and social burden of the disease.This review addresses current knowledge of the pathophysiological links between diabetes and cardiovascular complications, focusing on the role of epigenetic modifications, including DNA methylation and histone modifications. In addition, although the treatment of complications of diabetes with "epidrugs" is still far from being a reality and faces several challenges, we present the most promising molecules and approaches in this field.

Methylglyoxal mediates the association between 2-hour plasma glucose and HbA1c with inflammation: The Maastricht Study.

CONTEXT: Glucose excursions in persons with diabetes may drive chronic inflammation. Methylglyoxal (MGO) is formed from glucose, is elevated in persons with diabetes, and is a potent glycating agent linked with inflammation. OBJECTIVE: We investigated whether glucose excursions are associated with low-grade inflammation and whether MGO mediates this association. DESIGN: We used data from The Maastricht Study, an extensive phenotyping study into the etiology of type 2 diabetes and its complications. PARTICIPANTS: Data of 3017 participants, who underwent an oral glucose tolerance test and where data on MGO levels and inflammation were available, were used. MAIN OUTCOME MEASURES: Linear regression analyses, adjusted for potential confounders, evaluated associations between fasting plasma glucose (FPG), 2-hours plasma glucose (2h-PG) and HbA1c and low-grade inflammation (stdß, [95% confidence interval]), calculated from plasma concentrations of C-reactive protein, serum amyloid A, interleukin-6, interleukin-8, tumor necrosis factor and soluble intercellular adhesion molecule-1. Mediation analyses investigated whether MGO mediated these associations. RESULTS: 2h-PG (0.172 [0.110; 0.234]) and HbA1c (0.148 [0.101; 0.196]), but not FPG (0.049 [-0.002; 0.100]), were associated with low-grade inflammation. 2h-PG and HbA1c were also associated with 2h-MGO (0.471 [0.407; 0.534], and 0.244 [0.195; 0.294], respectively). Furthermore, 2h-MGO was independently and positively associated with low-grade inflammation (0.078 [0.037, 0.120]). 2h-MGO mediated 23% of the association between 2h-PG and inflammation, and 16% of the association between HbA1c and inflammation. CONCLUSIONS: MGO mediates the association between post-load glucose excursions and HbA1c with inflammation, providing evidence for a role of postprandial MGO formation to hyperglycemia-induced low-grade inflammation.

An Unusual Presentation of an Amniotic Fluid Embolism: Fetal Bradycardia As the First Sign.

Amniotic fluid embolism (AFE) is a potentially fatal maternal condition demanding awareness from obstetricians and anesthesiologists regarding its different manifestations. The typical presentation involves maternal respiratory distress, cardiovascular collapse, neurological changes, and coagulopathy followed by fetal distress. This unusual case study emphasizes that fetal compromise may precede maternal decompensation as the initial sign of AFE. Fetal distress is a known symptom of AFE and is typically seen due to cardiorespiratory issues that lead to reduced uteroplacental perfusion, resulting in fetal hypoxia. In the case presented, fetal bradycardia occurred before any visible maternal symptoms, suggesting that fetal distress could be induced by factors independent of the mother's cardiopulmonary status. A 34-year-old healthy G4P2012 at 41 weeks and 2 days gestation who was initially laboring on the floor was emergently taken to the operating room for a cesarean delivery due to fetal bradycardia. Around the time the fetus was delivered, the patient displayed seizure activity, followed by a complete loss of consciousness and cardiac arrest. The patient was intubated and underwent cardiopulmonary resuscitation and defibrillation, subsequently converting to a wide complex tachycardia. In the operating room, there was evidence of heavy vaginal bleeding, uterine atony, and a fulminant form of disseminated intravascular coagulopathy (DIC), which required aggressive management over the next four hours. After achieving hemodynamic stability, the patient was transferred to the surgical intensive care unit (SICU), extubated on day 3, and discharged home on day 8.

The Long-Term Cardiovascular Impact of COVID-19: Pathophysiology, Clinical Manifestations, and Management.

The COVID-19 pandemic, caused by the novel coronavirus SARS-CoV-2, has resulted in a substantial global health crisis, with effects extending far beyond the acute phase of infection. This review aims to provide a comprehensive overview of the long-term cardiovascular impact of COVID-19, focusing on the pathophysiology, clinical manifestations, diagnostic approaches, management strategies, and future research directions. SARS-CoV-2 induces cardiovascular complications through mechanisms such as inflammation, endothelial dysfunction, and direct myocardial injury, leading to conditions like myocarditis, heart failure, arrhythmias, and thromboembolic events. These long-term effects, collectively called "long COVID" or post-acute sequelae of SARS-CoV-2 infection (PASC), present significant challenges for healthcare systems and patient management. Diagnostic approaches include imaging techniques and laboratory tests to identify and monitor cardiovascular complications. Management strategies emphasize a holistic approach, incorporating pharmacological treatments and lifestyle modifications. Special attention is required for vulnerable populations, including those with pre-existing cardiovascular conditions. Ongoing research is essential to understand the full spectrum of long-term cardiovascular impacts and to develop effective treatments. This review highlights the critical need for continued vigilance, multidisciplinary care, and research to address the cardiovascular sequelae of COVID-19 and improve long-term health outcomes for survivors.

Cardiac biomarkers in COVID-19: what did we learn?

OBJECTIVES: COVID-19, caused by the SARS-CoV-2 virus, has generated a global pandemic with a wide range of clinical manifestations. Cardiovascular complications are frequently observed in individuals with COVID-19, particularly those with preexisting cardiovascular risk factors or diseases. Cardiac biomarkers, including troponin, natriuretic peptides, and inflammatory markers, play a vital role in risk stratification, diagnosis, monitoring, and prognosis in COVID-19 patients. These biomarkers provide valuable insights into cardiac injury, myocardial stress, inflammation, and the prediction of adverse cardiovascular outcomes. This review aims to provide better understanding of how Cardiac biomarkers correlate to clinical manifestation of COVID-19. METHODS: We retrieved studies from PubMed, Medline, and Google Scholars that included results on cardiac biomarkers in COVID-19. Total of 14 studies were reviewed. RESULTS: 8 studies showed evidence of poor progression of the disease when there is increased troponin. 6 studies out of the 14 mentioned in this review showed positive correlation between mortality and elevation in cardiac biomarkers. This shows the significance of cardiac biomarkers in predicting the mortality in patients with COVID-19. CONCLUSION: It was shown that elevated cardiac biomarkers were associated significantly to poor outcome of covid-19 infection. The outcomes that were linked to increased cardiac biomarkers included increased length of hospitalization, need of life sustaining treatment, myocarditis, invasive and non-invasive respiratory support, and even death were linked to elevated cardiac biomarkers levels.

Prognostic value of stress CMR and SPECT-MPI in patients undergoing intermediate-to-high-risk non-cardiac surgery.

PURPOSE: The objective of this study was to investigate the role of myocardial perfusion imaging (MPI) stress tests using stress cardiac magnetic resonance (sCMR) and single-photon emission computed tomography myocardial perfusion imaging (SPECT-MPI) in non-cardiac surgery (NCS) pre-operatory management. MATERIALS AND METHODS: This monocentric retrospective study enrolled patients with coronary artery disease or a minimum of two cardiovascular risk factors undergoing intermediate-to-high-risk non-cardiac surgeries. The primary composite endpoint comprised cardiac death, cardiogenic shock, acute coronary syndromes (ACS), and cardiogenic pulmonary edema occurring within 30 days after surgery, while the secondary endpoint was ACS. RESULTS: A total of 1590 patients were enrolled; among them, 669 underwent a MPI stress test strategy (sCMR: 287, SPECT-MPI: 382). The incidence of 30-day cardiac events was lower in the stress-tested group compared to the non-stress-tested group (1.2% vs. 3.4%; p 0.006). Adopting a stress test strategy showed a significant reduction in the risk of the composite endpoint (OR: 0.33, 95% CI: 0.15-0.76, p 0.009) and ACS (OR: 0.41, 95% CI: 0.17-0.98, p 0.046) at multivariable analysis, with similar cardiac events rate between stress CMR and SPECT (1.1% vs. 1.3%, p 0.756). Stress CMR showed a greater accuracy to predict coronary artery revascularizations (sCMR c-statistic: 0.95, ischemic cut-point: 5.5%; SPECT c-statistic: 0.85, ischemic cut-point: 7.5%). CONCLUSION: Stress test strategy is related to a lower occurrence of cardiac events in high-risk patients scheduled for intermediate-to-high-risk non-cardiac surgeries. Both sCMR and SPECT-MPI comparably reduce the likelihood of cardiac complications, albeit sCMR offers greater accuracy in predicting coronary artery revascularization.

Relationship Between Glycosylated Hemoglobin Variability and the Severity of Coronary Artery Disease in Patients With Type 2 Diabetes Mellitus.

Background: Glycosylated hemoglobin (HbA1c) variability is a risk factor for cardiovascular complications in patients with Type 2 diabetes mellitus (T2DM), but its relationship with the severity of coronary artery disease (CAD) is unclear. Methods: Patients with T2DM who underwent coronary angiography due to angina were enrolled. HbA1c variability was expressed as coefficient of variation (CV), standard deviation (SD), variability independent of mean (VIM), and time in range (TIR). The severity of CAD was expressed by the number of involved vessels and Gensini score. Multivariate regression models were constructed to test the relationship between HbA1c variability, number of involved vessels, and the Gensini score, followed by linear regression analysis. Results: A total of 147 patients were included. In multivariate analysis, VIM-HbA1c (OR = 2.604; IQR: 1.15, 5.90; r = 0.026) and HbA1cTIR (OR = 0.13; IQR: 0.04, 0.41; r < 0.001) were independent risk factors for the number of involved vessels. After adjustment, HbA1cTIR (OR = 0.01; IQR: 0.002, 0.04; r < 0.001), SD-HbA1c (OR = 4.12, IQR: 1.64, 10.35; r = 0.001), CV-HbA1c (OR = 1.41, IQR: 1.04, 1.92; r = 0.007), and VIM-HbA1c (OR = 3.26; IQR: 1.43, 7.47; r = 0.003) were independent risk factors for the Gensini score. In the linear analysis, the Gensini score was negatively correlated with HbA1cTIR (ß = -0.629; r < 0.001) and positively correlated with SD-HbA1c (ß = 0.271; r = 0.001) and CV-HbA1c (ß = 0.176; r = 0.033). After subgroup analysis, HbA1cTIR was a risk factor for the number of involved vessels. The Gensini score was negatively correlated with HbA1cTIR and positively correlated with SD-HbA1c at subgroups of subjects with a mean HbA1c ≤ 7%. Conclusions: Our analysis indicates that HbA1c variability, especially HbA1cTIR, plays a role for the severity of CAD in patients with T2DM. HbA1c variability may provide additional information and require management even at the glycemic target. Translational Aspects: Studies have shown that HbA1c variability is related to cardiovascular complications. Further, we explore the correlation between HbA1c variability and the severity of CAD. HbA1c variability is a risk factor for coronary stenosis in T2DM. It may be a potential indicator reflecting glycemic control for the prevention and treatment of cardiovascular complications.

A case report about anorexia nervosa and ischemic stroke: what can we learn?

INTRODUCTION: Anorexia Nervosa (AN) is a complex psychiatric illness, characterized by a high risk of developing cardiovascular complications. Given the high risk of vascular diseases in patients with AN, we can assume that patients with severe AN have a high risk of developing ischemic stroke. However, to the best of our knowledge, no reports of patients with AN presenting with ischemic stroke have been published, other than a report of the development of IS during refeeding therapy in patients with severe AN. CASE PRESENTATION: The present case report is aimed at describing the characteristics of an ischemic stroke occurring in a 19-year-old university student who had a 6-month history of AN. She was a non-smoker, had no relevant medical history and no family history of stroke. Upon hospital admission due to symptoms of stroke (aphasia and facial droop), she exhibited severe malnutrition with a BMI of 12.8 kg/m2. Computerized tomography imaging revealed occlusion of the left M2 branch and a congruous extensive area of hypoperfusion. Further investigations ruled out all common causes of stroke: she had no vascular stenosis, no heart diseases or arrhythmias, and no shunts, and gave negative results in autoimmune, toxicological and thrombophilia screenings. CONCLUSION: Clinicians should suspect development of severe complications, including ischemic stroke, in patients with severe AN. Further extensive group studies or group-based studies are needed to elucidate the etiology of ischemic stroke in patients with severe AN. This will enable us to develop more precise and effective interventions.

Comparison of Lipid Profiles Between Prediabetic and Non-prediabetic Young Adults.

Introduction Insulin resistance is considered a key component in the pathophysiology of prediabetes. Derangement in lipid parameters can occur in prediabetics that predispose to cardiovascular complications. Material and methods We performed an observational cross-sectional analytical study in a tertiary level Acharya Vinoba Bhave hospital, Sawangi, Wardha to compare the lipid profile in prediabetics with non-prediabetic young individuals between 18 and 35 age group in terms of parameters such as total cholesterol, triglyceride (TG), low-density lipoproteins (LDL) cholesterol, very low-density lipoprotein (VLDL) cholesterol, and high-density lipoprotein (HDL) cholesterol. Results We observed that prediabetics have significantly elevated total cholesterol, LDL cholesterol, VLDL cholesterol, and TG; and significantly reduced HDL cholesterol compared with the controls (p<0.001 each). Conclusion We conclude that the lipid parameters are deranged in prediabetics and this might contribute to the risk associated with dyslipidemia in this population.

Blood Viscosity Changes in Diabetes Mellitus: A 20-Year Bibliometric Review and Future Directions.

Changes in hematological parameters due to diabetes are reflected in changes in whole blood viscosity (WBV). Understanding the impact of diabetes and its cardiovascular disease (CVD) complications can provide substantiation of how laboratory tests for WBV are useful to monitor the progression and treatment. The review examines research work done in the past 20 years to provide a framework for the present agenda. This was a narrative review that followed the standard Scale for the Assessment of Narrative Review Articles (SANRA) approach. It includes both conceptual and empirical reviews. WBV was appraised in the context of bibliographic research on diabetes and other related factors such as metabolic syndrome (MetS) and oxidative stress. The association of abnormal erythrocytes as well as the relationship between WBV and MetS is established. Changes in diabetes that contribute to the development of diabetic cardiovascular complications occur through the pathway of WBV physiology. However, longitudinal analysis is very limited. There is a dearth of longitudinal study data on WBV in diabetes management. This lack of data justifies a need for further studies, especially prospective and retrospective analysis, to investigate the prevalence of diabetes mellitus about the prevalence of cardiovascular complications indices, especially estimated WBV (eWBV) between periods and within cohorts.