Cardiovascular Manifestations Research Articles

Exploring the impact of recent COVID-19 infection on perfusion and functional parameters derived from gated myocardial perfusion imaging in patients undergoing evaluation for coronary artery disease.

This study seeks to evaluate how recent COVID-19 infection affects myocardial perfusion and functional parameters derived from gated myocardial perfusion imaging in patients undergoing evaluation for coronary artery disease. The goal is to enhance our understanding of COVID-19's influence on the cardiovascular system. Conducted at Farshchian Heart Hospital from 2022 to 2023, this case-control study enrolled patients suspected of coronary artery disease, stratified into two groups: those with confirmed COVID-19 infection within the past 6months (study group) and those without prior COVID-19 infection (control group). Employing a 2-day protocol, stress testing and gated SPECT MPI were performed. Statistical analysis included descriptive statistics, Chi-square test, Student's t test, and Mann-Whitney U test. Among the 86 patients included, 43 were in each group. Significantly higher summed stress core and summed difference score values were observed in the study group compared to the control group (p < 0.05). In addition, the study group exhibited significantly altered global left ventricular ejection fraction, end-diastolic volume, and end-systolic volume (p < 0.05). Non-perfusion findings, including transient ischemic dilation and transient right ventricular visualization, were more prevalent in the study group. Recent COVID-19 infection is associated with impaired myocardial perfusion and altered functional parameters as detected by MPI. These findings underscore the intricate interplay between COVID-19 and cardiovascular health, emphasizing the importance of comprehensive evaluation and management strategies to address cardiac complications in affected individuals. Further research is warranted to elucidate the underlying mechanisms and optimize patient care in the context of COVID-19-associated cardiovascular manifestations.

#174 Valvulopathies and left ventricular hypertrophy in ADPKD: prevalence and association with genotype and phenotype

Abstract Background and Aims Autosomal dominant polycystic kidney disease (ADPKD) is the most common inherited nephropathy due to mutations in PKD1 or PKD2 genes. In addition to kidney involvement, ADPKD is also characterized by extrarenal manifestations including the presence of cysts in other organs, intracranial aneurysms, arterial hypertension, valvulopathies and left ventricular hypertrophy (LVH). Cardiac abnormalities are an important cause of morbidity and mortality in ADPKD patients. Limited data on the association between these cardiovascular manifestations with phenotypic (both renal and systemic) and genotypic features of ADPKD are currently available. In this study we report the prevalence of the main cardiac abnormalities (valvulopathies, with a focus on aortic, mitral, tricuspid valve regurgitation, mitral prolapse, and LVH) observed in a large cohort of ADPKD patients, and investigated their association with renal diameter, renal function, other systemic manifestations such as pancreatic cysts, intracranial cysts, intracranial aneurysm and genotype. Method This retrospective study was conducted at the A. Gemelli Hospital, Rome in a single-center cohort of 129 ADPKD patients, who had previously undergone echocardiogram, abdominal ultrasound, brain MRI, and blood tests, between January 2018 and July 2023. Genetic testing was performed in 58 of the 129 patients. For the statistical analysis the average bilateral renal diameter of each patient was used. An interventricular septum cut-off thickness of 11 mm was used to define left ventricular hypertrophy. Non-parametric (Mann–Whitney and Spearman) and chi-square tests were applied as appropriate. Results In our cohort of 129 patients, the prevalence of valvulopathies was the following: 68% of mitral regurgitation, 22% of mitral prolapse, 20% of aortic regurgitation and 56% of tricuspid regurgitation. Left ventricular hypertrophy was identified in 28% of the entire cohort. We found that in ADPKD patients with aortic regurgitation, renal diameters are larger (p = 0.027) and the eGFR is lower (p &amp;lt; 0.01) than in patients without this echocardiographic abnormality (Fig. 1a,b). In the subset of genotyped ADPKD patients (58), mutations in PKD 1 were associated with mitral prolapse (p = 0.02). Interventricular septal thickness, regardless of the presence of hypertrophy was positively correlated (Fig. 1c) with renal diameter (p = 0.001 r = +0.289) and negatively (Fig. 2a) with eGFR (p &amp;lt; 0.001 r = −0.422). Both correlations, also adjusted for arterial hypertension, remained statistically significant (p = 0.008, coefficient r = +0.235 and p &amp;lt; 0.001, coefficient r = −0.304, respectively). In addition, patients with LVH featured a larger renal diameter (p = 0.03), and a lower eGFR (p &amp;lt; 0.001) (Fig. 2b-c). Moreover LVH was associated with the presence of PKD1 mutations (p = 0.03). Neither valvulopathies nor LVH were associated with other systemic manifestations of the disease. Conclusion We show for the first time an association of LVH with ADPKD genotype (specifically mutations in PKD1) and the association of a specific valvulopathy (aortic regurgitation) with the renal phenotype of ADPKD patients. To date only one study found an association of another valvulopathy, mitral regurgitation, with mutations in PKD1 [1]. Heart valves disease and LVH are risk factors for the subsequent development of further cardiovascular complications therefore understanding the pathogenetic mechanisms responsible for the higher incidence of these abnormalities in ADPKD would be useful to identify high-risk subgroups of patients and tailor personalised interventions.

A Comprehensive Review of Lyme Disease: A Focus on Cardiovascular Manifestations

A Comprehensive Review of Lyme Disease: A Focus on Cardiovascular Manifestations

Parachute mitral valve and mid-aortic syndrome – unusual associations of Alagille syndrome

Background: Alagille syndrome (ALGS) is a multisystem disorder involving at least three systems among the liver, heart, skeleton, face, and eyes. Common cardiac associations include pulmonary artery stenosis/atresia, atrial septal defect (ASD), ventricular septal defect (VSD) and tetralogy of fallot (ToF). Coarctation of aorta (CoA), renal and intracranial arteries are commonly involved vessels in Alagille syndrome. We present two cases with rare cardiovascular manifestations of Alagille syndrome. Case description: Case 1: A 25-year-old female with a history of Alagille syndrome presented to the cardiologist office for progressive exertional dyspnoea, orthopnoea, and palpitations. She was tachycardiac on examination and had an apical diastolic rumble. A transthoracic echocardiogram (TTE) showed a left ventricular ejection fraction (LVEF) of 60% and parachute mitral valve (PMV) with severe mitral stenosis. A transoesophageal echocardiogram (TOE) showed insertion of chordae into the anterolateral papillary muscle, severe mitral stenosis with a valve area of 0.7 cm. She was referred to a congenital heart disease specialist and underwent robotic mitral valve replacement with improvement in her symptoms. Case 2: A 27-year-old female with known Alagille syndrome and resistant hypertension presented to the cardiologist office due to progressive exertional dyspnoea for a year. She was hypertensive and had a new 2/6 systolic ejection murmur along the left upper sternal border. TTE revealed an LVEF of 60% and pulmonary artery pressure of 19 mmHg. A CoA was suspected distal to the left subclavian artery due to a peak gradient of 38 mmHg. Cardiac magnetic resonance (CMR) imaging ruled out CoA, and diffuse narrowing of the descending thoracic aorta measuring 13–14 mm in diameter was noted. The patient was referred to a congenital heart disease specialist for further management. Conclusion: PMV presenting as mitral stenosis and mid-aortic syndrome are not commonly described anomalies in association with Alagille syndrome. TTE, TOE and CMR played a key role in diagnosis and management of these patients.

Cardiovascular manifestations in pediatric multisystem inflammatory syndrome associated with COVID-19 in a tertiary care pediatric center in Mexico City

The objective is to expose the cardiovascular alterations in patients diagnosed with pediatric inflammatory multisystem syndrome (PIMS) associated with COVID-19 during the SARS-CoV-2 pandemic, in order to understand the disease, its evolution, and optimal management upon diagnosis. Retrospective, observational, cross-sectional analytical study of patients diagnosed with PIMS according to the criteria of the World Health Organization at the National Institute of Pediatrics, from March 2020 to December 2021. During the study period, 77 patients with PIMS were diagnosed. The results showed correlation between the shock state and alteration of laboratory markers (platelets 144217.29 ± 139321.6 μL [p < 0.001], procalcitonin 27.37 ± 38.37 ng/ml [p = 0.05] and ferritin 1937.87 ± 2562.63 [p < 0.001]). The ventricular function in patients with shock was significantly lower compared to those without shock (49.6 ± 9.1% vs. 58.1 ± 8.4 %; t-Student p < 0.001), as well as injury to the left coronary artery (p = 0.02). There is a correlation between NT-proBNP and ventricular dysfunction (Kruskal-Wallis p = 0.007). Statistical significance was found in the association between death, elevation of inflammatory markers and ventricular dysfunction (p < 0.001). The cardiovascular alterations observed, in order of frequency, were pericardial effusion (25.7%), myocarditis (15%), mild ventricular dysfunction (13.5%) and small coronary aneurysm with predominance of the left coronary artery and the anterior descending one.

Cardiovascular manifestations in a complex case of thyroid storm secondary to graves: challenges and therapeutic considerations

Cardiovascular manifestations in a complex case of thyroid storm secondary to graves: challenges and therapeutic considerations

Endothelial dysfunction and complement activation are independently associated with disease duration in patients with systemic vasculitis

ObjectivesSystemic vasculitis is a heterogenous group of autoimmune diseases characterized by enhanced cardiovascular mortality. Endothelial dysfunction is associated with accelerated vascular damage, representing a core pathophysiologic mechanism contributing to excess CV risk. Recent studies have also shown that complement activation holds significant role in the pathogenesis of Anti-Neutrophilic Cytoplasmic Autoantibody (ANCA) -associated vasculitis (AAV). Given the potential crosstalk between the endothelium and complement, we aimed to assess, for the first time simultaneously, easily accessible biomarkers of endothelial dysfunction and complement activation in SV. MethodsWe measured circulating endothelial microvesicles (EMVs) and soluble complement components representative of alternative, classical and terminal activation (C5b-9, C1q, Bb fragments, respectively) in a meticulously selected group of patients with systemic vasculitis, but without cardiovascular disease. Individuals free from systemic diseases, who were matched with patients for cardiovascular risk factors(hypertension, diabetes, smoking, dyslipidemia), comprised the control group. ResultsWe studied 60 individuals (30 in each group). Patients with systemic vasculitis had elevated EMVs, higher levels of C5b-9 [536.4(463.4) vs 1200.94457.3), p = 0.003] and C1q [136.2(146.5 vs 204.2(232.9), p = 0.0129], compared to controls [232.0 (243.5) vs 139.3(52.1), p < 0.001]. In multivariate analysis both EMVs and C5b-9 were independently associated with disease duration (p = 0.005 and p = 0.004 respectively), yet not with disease activity. ConclusionPatients with systemic vasculitis exhibit impaired endothelial function and complement activation, both assessed by easily accessible biomarkers, even in the absence of cardiovascular disease manifestations. EMVs and soluble complement components such as C5b-9 and C1q could be used as early biomarkers of endothelial dysfunction and complement activation, respectively, in clinical practice during the course of SV, yet their predictive value in terms of future cardiovascular disease warrants further verification in appropriately designed studies.

Proteomic mapping identifies serum marker signatures associated with MIS-C specific hyperinflammation and cardiovascular manifestation

Multisystem inflammatory syndrome in children (MIS-C) shares several clinical and immunological features with Kawasaki Disease (KD) and pediatric hyperinflammation, but the immuno-phenotypic overlap among these clinical mimics is still incompletely understood. Here we analyzed serum samples from treatment-naïve patients with MIS-C (n = 31) and KD (n = 11), pediatric hyperinflammation (n = 13) and healthy controls (HC, n = 10) by proximity extension assay (PEA) to profile 184 blood biomarkers. Collectively, immunophenotypic overlap between MIS-C and hyperinflammation exceeds overlap with KD. Overexpression of IL-17 A in MIS-C and KD could best separate these conditions from hyperinflammatory conditions, while those were hallmarked by overabundance of adenosin deaminase and IL-18. Depletion in serum TNF-related subfamily member 9 (TNFRSF9) and apoptosis inducing ligand (TRAIL) linked with cardiovascular manifestations and myocarditis in MIS-C. Altogether, our analysis highlights important differences in molecular marker signatures also across different MIS-C and KD cohorts and suggests several previously unidentified molecular associations in context of cardiovascular inflammation.

Electrocardiographic and Echocardiographic changes in Non-Hemodialysis Chronic Kidney Disease Patients: A Cross-Sectional Study

Abstract Chronic Kidney Disease (CKD) patients have a higher risk of cardiovascular manifestations such as coronary artery disease, heart failure, arrhythmias, and sudden cardiac death. Cardiovascular diseases are the main cause of death in patients with advanced CKD, rather than end-stage kidney disease itself. Essentially, CKD speeds up the ageing process in the cardiovascular system. Objectives: To determine the prevalence of cardiovascular abnormalities in non-hemodialysis CKD patients. Methods: A descriptive cross-sectional study, was conducted in the Department of Medicine, between October 2020 to September 2022. A total of 50 CKD patients were included. The patients were evaluated &amp; enrolled in the study, based on history, general physical examination, systemic examination, Blood Urea, Serum Creatinine, Urine Routine, Electrocardiograph (ECG) and Echocardiography. Results: In the present study Electrocardiograph &amp; echocardiography determined cardiovascular abnormalities in 68% of patients. Among these 50% of patients had Left Ventricular Hypertrophy (LVH) &amp; Left Ventricular Diastolic Dysfunction (LVDD), 8% of patients had Arrhythmias and 6% patients had conduction abnormality, 2% patients had LVH and 2% patients had LVDD. Conclusion: LVH &amp; LVDD are the most common morphological abnormalities observed in our study. We can diagnose Arrhythmias and conduction abnormality by electrocardiogram &amp; echocardiography and refer them for appropriate interventions promptly.

Casting Light on The Hidden Prevalence: A Novel Perspective on Hypoplastic Coronary Artery Disease.

Background and Objectives: Coronary artery anomalies (CAAs) represent a group of rare cardiac abnormalities with an incidence of up to 1.2%. The aim of this retrospective study was to conduct a comprehensive epidemiological assessment of the prevalence of hypoplastic coronary arteries using coronary computed tomography angiography (CCTA) in patients with diagnosed CAAs and individuals presenting with cardiovascular manifestations in the north-eastern region of Romania. This study was motivated by the limited investigation of the CAAs conducted in this area. Methods: We analyzed data collected from 12,758 coronary computed tomography angiography (CCTA) records available at the "Prof. Dr. George I.M. Georgescu" Cardiovascular Diseases Institute, spanning the years 2012 to 2022. Results: Among 350 individuals with CAAs (2.7% of the total cohort), 71 patients (20.3% of the anomaly presenting group and 0.5% of the entire CCTA cohort) exhibited at least one hypoplastic coronary artery. The mean age of individuals diagnosed with hypoplastic coronary artery disease (HCAD) was 61 years, while the age distribution among them ranged from 22 to 84 years. Nearly equal cases of right and left dominance (33 and 31, respectively) were observed, with only 7 cases of co-dominance. Conclusions: HCAD may be considered underexplored in current published research, despite its potentially significant implications ranging to an increased risk of sudden cardiac arrest. The specific prevalence of HCAD among CAAs might be higher than previously reported, possibly reflecting better diagnostic accuracy of CCTA over classic coronary imaging. The absence of standard diagnostic and therapeutic protocols for HCAD underscores the necessity of a personalized approach for such cases.

Clinical Characteristics of EGPA Patients in Comparison to GPA Subgroup with Increased Blood Eosinophilia from POLVAS Registry.

To characterize the eosinophilic granulomatosis with polyangiitis (EGPA) population from the POLVAS registry depending on ANCA status and diagnosis onset, including their comparison with the granulomatosis with polyangiitis (GPA) subset with elevated blood eosinophilia (min. 400/μl) (GPA HE) to develop a differentiating strategy. A retrospective analysis of the POLVAS registry. The EGPA group comprised 111 patients. The ANCA-positive subset (n = 45 [40.54%]) did not differ from the ANCA-negative one in clinics. Nevertheless, cardiovascular manifestations were more common in ANCA-negative patients than in those with anti-myeloperoxidase (MPO) antibodies (46.97% vs. 26.92%, p = 0.045). Patients diagnosed before 2012 (n = 70 [63.06%]) were younger (median 41 vs. 49 years, p < 0.01), had higher blood eosinophilia at diagnosis (median 4,946 vs. 3,200/μl, p < 0.01), and more often ear/nose/throat (ENT) and cardiovascular involvement. GPA HE comprised 42 (13.00%) out of 323 GPA cases with reported blood eosinophil count. Both GPA subsets had a lower prevalence of respiratory, cardiovascular, and neurologic manifestations but more often renal and ocular involvement than EGPA. EGPA also had cutaneous and gastrointestinal signs more often than GPA with normal blood eosinophilia (GPA NE) but not GPA HE. The model differentiating EGPA from GPA HE, using ANCA status and clinical manifestations, had an AUC of 0.92, sensitivity of 96%, and specificity of 95%. Cardiovascular symptoms were more prevalent in the ANCA-negative subset than in the MPO-ANCA-positive one. Since EGPA and GPE HE share similarities in clinics, diagnostic misleading may result in an inappropriate therapeutic approach. Further studies are needed to optimize their differentiation and tailored therapy, including biologics.

Vascular Alterations Following COVID-19 Infection: A Comprehensive Literature Review.

SARS-CoV-2, the causative agent of the ongoing COVID-19 pandemic, has revealed a broader impact beyond the respiratory system, predominantly affecting the vascular system with various adverse manifestations. The infection induces endothelial dysfunction and immune system dysregulation, creating an inflammatory and hypercoagulable state. It affects both microvasculature and macrovasculature, leading to thromboembolic events, cardiovascular manifestations, impaired arterial stiffness, cerebrovascular complications, and nephropathy, as well as retinopathy-frequently observed in cases of severe illness. Evidence suggests that SARS-CoV-2 infection may result in persistent effects on the vascular system, identified as long-term COVID-19. This is characterized by prolonged inflammation, endotheliopathy, and an increased risk of vascular complications. Various imaging modalities, histopathological studies, and diagnostic tools such as video capillaroscopy and magnetic resonance imaging have been employed to visualize vascular alterations. This review aims to comprehensively summarize the evidence concerning short and long-term vascular alterations following COVID-19 infection, investigating their impact on patients' prognosis, and providing an overview of preventive strategies to mitigate associated vascular complications.

E012 Burden and risk factors for cardiovascular involvement in connective tissue disease

Abstract Background/Aims Connective tissue diseases (CTD) are associated with several cardiovascular manifestations. Cardiovascular diseases (CVD) are significant cause of morbidity and premature death. The pathogenesis of CVD in CTD patients is incompletely understood and likely multifactorial. Traditional risk factors for atherosclerosis are common among patients with CTD as well as metabolic syndrome. Furthermore, diabetes, dyslipidaemia, hypertension, and obesity may all be exacerbated by connective tissue disease itself or treatment with glucocorticoids. The aim of this study was to assess the burden of CVD and the risk factors for the development of cardiovascular disease in patients with CTD. Methods This was a retrospective study from a single centre. We reviewed clinical records of CTD patients as determined by treating rheumatologist. This CTD cohort included patients with systemic lupus erythematosus (SLE), myositis, systemic sclerosis, Sjogren’s syndrome, mixed and undifferentiated connective tissue diseases. Data on demographic, clinical, laboratory parameters, cardiac investigations, treatment and outcome were collected from electronic patient records. CVD and traditional risk factors were defined using standard criteria. Results A total of 298 patients with CTD were included in the analysis. Mean age of the cohort was 61±17.7 years and majority were females (n = 240, 80.5%). Of the 298 patients, 64 had CVD (21.5%). Most common CVD was ischaemic heart disease (17 patients) followed by hypertension (12), arrhythmia (9), pulmonary arterial hypertension (7), valvular diseases (5), pericardial disease (3), cardiomyopathy (3), myocarditis (2), thromboembolism (3), aortic dissection (2) and coronary spasm (1). Patient with CTD who had CVD were older (72.5±12.2 years) compared to CTD patients who did not develop CVD (non-CVD group, 57.7±17.6 years). The duration of CTD was shorter in patients with CVD (88.9±41.7 months), compared to 106±84.3 months in non-CVD group. The risk factors such as smoking, diabetes and dyslipidaemia was higher in the CVD group. Comparing CVD vs non-CVD patients respectively, systolic BP (147.1±23.0 vs 133.6±18.3mmHg), diastolic BP (83.2 ± 16.3 vs 78.2 ± 11.2mmHg) and serum uric acid (321.8±97.4 vs 292±83.9mg/dL) values were higher and statistically significant (p &amp;lt; 0.05) in CVD group. Patients with CVD had longer exposure to steroids (50%) compared to non-CVD patients (31.6%). They required high dose steroids (9.4% vs 5.6% in non-CVD patients). Current and previous DMARD use was also higher in patients who had CVD (51.6% vs 44.9%). Conclusion This study has demonstrated high burden of cardiovascular disease in CTD patients. Traditional risk factors were more prevalent in the CVD group. DMARD’s and steroid use was also higher in the CVD group. Screening for cardiovascular diseases and disease control in CTD patients is paramount for better outcomes. Further analysis will be carried out for risk factors and relevant outcomes. Disclosure K.K. Garg: None. S. Sampath: None. A. Erinjogunola: None. B. Ting: None. H. Noori: None. G.M. Koduri: None.

CELIAC DISEASE AND CARDIOVASCULAR DISEASES

Background: Celiac disease, an immune-mediated enteropathy that occurs in susceptible individuals after gluten ingestion, has clinical manifestations that go beyond the classical malabsorption syndrome and can affect other systems. Objective: To review the current literature for cardiovascular changes described in patients with celiac disease. Method: We conducted a search in the PubMed database and selected articles based on their relevance to the objective. Results: Celiac patients have a 1.2 times higher risk of cardiovascular events compared to non-celiac patients. The most common cardiovascular manifestations include atherosclerosis, cardiac arrhythmias (especially atrial fibrillation), myocarditis, coronary artery disease, dilated cardiomyopathy, impaired aortic function, and cerebrovascular diseases. There are several possible explanations for this relationship, including: prothrombotic changes, accelerated atherosclerosis compared to patients without celiac disease, associated comorbidities, such as antiphospholipid syndrome and Type 1 Diabetes mellitus, subclinical chronic inflammation and genetic factors. Celiac disease patients have a 38% higher risk of developing atrial fibrillation and a 19% higher risk of coronary artery disease. Furthermore, celiac patients have a 22% higher risk of coronary artery disease-related death, regardless of small intestine histopathology. Patients with celiac disease also show an increased prevalence of dilated cardiomyopathy (5.7%) and a 73% higher risk of developing dilated cardiomyopathy, particularly within the first year of celiac disease diagnosis. Conclusion: Celiac disease may be associated with cardiovascular changes, especially in newly diagnosed patients who have not adhered to a gluten-free diet. Therefore, cardiovascular assessment should be considered as part of the initial assessment and follow-up of individuals with celiac disease.

Addressing comprehensive complexities a striking familial hypercholesterolemia case study.

Premature aortic involvement and comprehensive management strategies in familial hypercholesterolemia familial hypercholesterolemia (FH), a rare autosomal dominant genetic disorder, poses significant challenges due to its propensity for elevated low-density lipoprotein cholesterol, premature coronary heart disease, and vascular atherosclerosis. Unraveling Cardiovascular Complexities: A Striking Familial Hypercholesterolemia. This case study delves into a remarkable instance of FH in a 16-year-old female who presented with chest pain and worsening dyspnea. Diagnostic evaluation revealed distinct electrocardiographic changes, elevated troponin levels, and profound dyslipidemia. Remarkable findings on transthoracic echocardiography, computed tomography angiography, and catheterization prompted multidisciplinary interventions and demonstrated remarkable enhancements in ventricular function, mitral regurgitation, and aortic stenosis. The case study underscores the urgency of comprehensive management strategies in confronting the myriad challenges of FH, emphasizing the value of early intervention, innovative therapies, and rigorous imaging modalities for unraveling the intricate cardiovascular manifestations of this condition.

Melatonin as a promising agent alleviating endocrine deregulation and concurrent cardiovascular dysfunction: a review and future prospect

Endocrine modulation of various growth and survival mechanisms is at the helm of cellular homeostasis and impaired endocrine balance may potentially galvanize cardiovascular health to go haywire. Melatonin, an effective antioxidant and multipotent hormone has preponderant influence on the activities of several endocrine factors including growth hormones, thyroid hormones, gastro-intestinal hormones, and those controlling reproductive and metabolic functions. Many of these hormones tightly regulate cardiovascular functions while the mammalian heart has its own endocrine machinery. Endocrine disruptions severely affect cardiovascular integrity and hormonal therapies may instigate adverse cardiac events. Therefore, this review focuses on the cardioprotective potential of melatonin concerning endocrine instability-mediated cardiovascular dysfunction. Melatonin has been reported to effectively counteract sympathetic overstimulation and also reduce the cardiotoxic attributes of catecholamines and their derivatives. Melatonin suppresses the pernicious cardiovascular manifestation of thyrotoxicosis and autoimmune thyroiditis, which is possibly attributed to its antioxidant property and regulation of iodothyronine-deiodinase activity. Interestingly, being a circadian synchronizer melatonin potentially preserves the diurnal pattern of insulin secretion and thereby improves glucose tolerance and cardiac GLUT-4 expression. Besides, melatonin modulates insulin signaling pathway by enhancing the activation of insulin receptor-associated tyrosine kinase, thus protecting the heart against diabetogenic outcomes. Further, melatonin has demonstrated its beneficial action against non-dipper hypertension by regulating the RAAS function. However, there is a plethora of unresolved research question that necessitates additional investigation into the potential therapeutic effect of melatonin in endocrine dysfunctions that emanates during various physiological and pathological states and may have potentially harmful cardiovascular implications.

The Clinical Features of Hereditary Alpha-Tryptasemia—Implications for Interdisciplinary Practice.

Hereditary alpha-tryptasemia (HAT) is a genetic predisposition of autosomal dominant inheritance that leads to a high normal (≥ 8-11.4 μg/L) or pathologically elevated (>11.4 μg/L) basal serum tryptase (BST) concentration. Its prevalence in the United Kingdom and France is reportedly 5%-6%; its prevalence in Germany is unknown. Symptomatic persons with HAT suffer from a complex constellation of symptoms. As described in this review, HAT is an important differential diagnosis in interdisciplinary practice. This review is based on publications about HAT retrieved by a selective search in PubMed, on relevant presentations at scientific meetings, and on our clinical experience. We also collected our own data on the prevalence and clinical manifestations of HAT. According to the literature, HAT is very common among patients in medical centers with BST values of 8 μg/L or above (64-74%). HAT is most commonly associated with neuropsychiatric symptoms such as exhaustion (85%), depressive episodes (59%), sleep disturbances (69%), and memory impairment (59%-68%), followed by gastrointestinal symptoms such as irritable bowel (30%-60%), nausea (51%), and reflux (49%-77%). Typical mast cell-mediated symptoms, such as flushing (47%), itch (69%), urticaria (37%), and anaphylaxis (14%-28%), are reported as well. Less commonly reported are cardiovascular manifestations, such as hypotonia, dizziness, and tachycardia (34%), and joint hypermobility (28%). HAT is more common among patients with sytemic mastocytosis (SM; 12%-21%). It is often associated with severe anaphylaxis induced by insect toxins or unknown triggers. The therapeutic options include treatment with antihistamines, mast-cell stabilizers, or IgE antibodies. A diagnosis of hereditary alpha-tryptasemia can be strongly suspected on the basis of thorough history-taking and BST measurement and then confirmed by molecular genetic testing.

Greater Disease Severity and Worse Clinical Outcomes in Patients Hospitalised with COVID-19 in Africa.

COVID-19 cardiovascular research from Africa is limited. This study describes cardiovascular risk factors, manifestations, and outcomes of patients hospitalised with COVID-19 in the African region, with an overarching goal to investigate whether important differences exist between African and other populations, which may inform health policies. A multinational prospective cohort study was conducted on adults hospitalised with confirmed COVID-19, consecutively admitted to 40 hospitals across 23 countries, 6 of which were African countries. Of the 5,313 participants enrolled globally, 948 were from African sites (n = 9). Data on demographics, pre-existing conditions, clinical outcomes in hospital (major adverse cardiovascular events (MACE), renal failure, neurological events, pulmonary outcomes, and death), 30-day vitality status and re-hospitalization were assessed, comparing African to non-African participants. Access to specialist care at African sites was significantly lower than the global average (71% vs. 95%), as were ICU admissions (19.4% vs. 34.0%) and COVID-19 vaccination rates (0.6% vs. 7.4%). The African cohort was slightly younger than the non-African cohort (55.0 vs. 57.5 years), with higher rates of hypertension (48.8% vs. 46.9%), HIV (5.9% vs. 0.3%), and Tuberculosis (3.6% vs. 0.3%). In African sites, a higher proportion of patients suffered cardiac arrest (7.5% vs. 5.1%) and acute kidney injury (12.7% vs. 7.2%), with acute kidney injury (AKI) appearing to be one of the strongest predictors of MACE and death in African populations compared to other populations. The overall mortality rate was significantly higher among African participants (18.2% vs. 14.2%). Overall, hospitalised African patients with COVID-19 had a higher mortality despite a lower mean age, contradicting literature that had previously reported a lower mortality attributed to COVID-19 in Africa. African sites had lower COVID-19 vaccination rates and higher AKI rates, which were positively associated with increased mortality. In conclusion, African patients were hospitalized with more severe COVID-19 cases and had poorer outcomes.

SPECIFIC BIOCHEMICAL INDICATORS AND INFLAMMATORY MARKERS IN RHEUMATOID ARTHRITIS (RA)

It is acknown that Rheumatoid inflammation is a chronic systemic autoimmune disease developing on the background of infection. Damages mainly the heart, blood vessels, musculoskeletal system and other internal organs. Multiple joints may be affected, primarily the knee, ankle and elbow undergoing destruction leads to pain, mainly symmetrical. Damaged joints swollen and skin in these foci reddens; joint morning stiffness lasts for an hour or more, this sign is accompanied by low fever and fatigue. As a result of the rheumatic process, the heart is damaged, leading to cardiovascular manifestations. Analysis of blood parameters allows the severity of the disease to be determined based on a relatively new method using Das28. The obtained results for ESR and CRP are used to calculate DAS28, which also allows monitoring of RA treatment. Most patients with rheumatoid arthritis (RA) are seropositive—they have abnormally high levels of rheumatoid factor (RF) or anti-citrullinated peptide antibodies (anti-CPP) in the blood. The article examines aspects of synthetic, chemical and alternative medicine impact on treating patients with RA as well. The article discusses comparative aspects of pharmacological and herbal medicine in the therapeutics. According to the literature, patients who have not received the expected results after treatment with pharmacological preparations successfully use herbal remedies as a means of body restoring and healing. To date, the success of traditional medicine is ahead of those of conventional using synthetic drugs.

FBN2 pathogenic variants in congenital contractural arachnodactyly with severe cardiovascular manifestations

ABSTRACT Purpose Congenital contractural arachnodactyly (CCA) is an extremely rare autosomal dominant connective tissue genetic disorder caused by pathogenic variants in FBN2. CCA is characterized by arachnodactyly, camptodactyly, contracture of major joints, scoliosis, pectus deformities, and crumpled ears, but rarely with lethal cardiovascular manifestations as in Marfan syndrome. It is imperative to conduct a comprehensive analysis and review of the pathogenesis of CCA resulting from pathogenic variants in FBN2 gene. Materials and Methods Using whole-exome sequencing and Sanger sequencing, we identified a novel pathogenic splice-altering variant (c.4472-3C>A) in intron 34 of FBN2 gene in a CCA pedigree. The transcriptional result of the splicing-altering variant was analyzed by RNA sequencing. We systematically analyzed the clinical manifestations of all reported cases of CCA caused by splicing-altering pathogenic variants and focused on all the pathogenic variants in FBN2 gene that are associated with severe cardiovascular manifestations. Results The splice-altering variant (c.4472-3C>A) in FBN2 was demonstrated to result in the exon 35 skipping and cause an in-frame deletion. Furthermore, we identified exons 31 to 35 may be a hotspot region in FBN2 gene associated with severe cardiovascular phenotype. Conclusions This study enriched the pathogenic spectrum of CCA and identified a hotspot region in FBN2 gene associated with severe cardiovascular manifestations. We recommend that patients carrying pathogenic variants in exons 31 to 35 of FBN2 pay more attention to cardiac evaluation.