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Up to 50% of people worldwide are affected by periodontal disease (PD); cardiovascular diseases are a serious concern for the major portion of the world's population. Observational data have shown a connection between PD and CVD. The current systemic review investigates the incidence of the CVD in individuals with PD through various designs of the previous research.
Cardiovascular diseases (CVDs) are the leading cause of mortality worldwide. Coronary heart disease (CHD) is the main cause of mortality in heart patients following stroke, rheumatic heart disease and myocardial infarctions. Approximately 80% of individuals succumb to CVDs, due to poor living conditions in low and middle income families and malnutrition. Infectious diseases, human immunodeficiency, tuberculosis, malaria, high blood pressure or hypertension, obesity and overweight, and nutritional disorders including smoking, excessive alcohol consumption, high salt and sugar intake, as well as other factors are responsible for CVDs and CHDs in young as well as elderly individuals. The focus of the present review are recent epidemiological aspects of CVD and CHD as well as the usefulness of a Mediterranean diet for heart patients and the prevention of heart diseases.
Environmental contamination has exposed humans to various metal agents, including mercury. It has been determined that mercury is not only harmful to the health of vulnerable populations such as pregnant women and children, but is also toxic to ordinary adults in various ways. For many years, mercury was used in a wide variety of human activities. Nowadays, the exposure to this metal from both natural and artificial sources is significantly increasing. Recent studies suggest that chronic exposure, even to low concentration levels of mercury, can cause cardiovascular, reproductive, and developmental toxicity, neurotoxicity, nephrotoxicity, immunotoxicity, and carcinogenicity. Possible biological effects of mercury, including the relationship between mercury toxicity and diseases of the cardiovascular system, such as hypertension, coronary heart disease, and myocardial infarction, are being studied. As heart rhythm and function are under autonomic nervous system control, it has been hypothesized that the neurotoxic effects of mercury might also impact cardiac autonomic function. Mercury exposure could have a long-lasting effect on cardiac parasympathetic activity and some evidence has shown that mercury exposure might affect heart rate variability, particularly early exposures in children. The mechanism by which mercury produces toxic effects on the cardiovascular system is not fully elucidated, but this mechanism is believed to involve an increase in oxidative stress. The exposure to mercury increases the production of free radicals, potentially because of the role of mercury in the Fenton reaction and a reduction in the activity of antioxidant enzymes, such as glutathione peroxidase. In this review we report an overview on the toxicity of mercury and focus our attention on the toxic effects on the cardiovascular system.
Acute rheumatic fever (ARF) is an autoimmune disease affecting the heart-valve endocardium in its final stage. Although rare in developing countries, ARF persists in third-world countries, particularly Senegal, where rheumatic heart diseases (RHDs) are the most common pediatric cardiovascular pathology. This study aimed to investigate mutations in MT-CYB in ARF and RHD in Senegalese patients. MT-CYB was amplified from blood samples from ARF patients at the Clinical of Thoracic and Cardiovascular Surgery of Fann National University Hospital Centre, Dakar, Senegal (control group, healthy individuals) and sequenced. More than half of the MT-CYB mutations (58.23%) were heteroplasmic. Transitions (61.67%) were more frequent than transversions (38.33%), and non-synonymous substitutions represented 38.33% of mutations. Unoperated RHD patients harbored frequent MT-CYB polymorphisms (7.14 ± 14.70 mutations per sample) and accounted for 72.73% of mutations. Paradoxically, subjects undergoing valvular replacement harbored infrequent polymorphisms (1.39 ± 2.97 mutations per patient) and lacked 36 mutations present in unoperated subjects. A genetic differentiation was observed between these two populations, and the mutations in operated subjects were neutral, while those in unoperated subjects were under positive selection. These results indicate a narrow link (perhaps even causal) between MT-CYB mutations and ARF and its complications (i.e., RHDs) and that these mutations are largely deleterious.
Background: Although sleep respiratory disorders are known as a relevant source of cardiovascular risk, there is a substantial lack of trials aimed to evaluate the eventual occurrence of associations between sleep apnea (SA) and valvular heart diseases (VHD). Methods: We recruited 411 patients referring to our sleep disorder unit, among which 371 had SA. Ninety-three subjects with SA also suffered from VHD. Physical examination, echocardiography, nocturnal cardio-respiratory monitoring, and laboratory tests were performed in each patient. Patient subgroups were comparatively evaluated through cross-sectional analysis. Results: A statistically significant increase in the prevalence of VHD was detected in relation to high apnea hypopnea index (AHI) values (p = 0.011). Obstructive sleep apnea occurrence was higher in SA patients without VHD (p < 0.0001). Conversely, central and mixed sleep apneas were more frequent among SA patients with VHD (p = 0.0003 and p = 0.002, respectively). We observed a direct correlation between AHI and BMI values (p < 0.0001), as well as between AHI and serum uric acid levels (p < 0.0001), high sensitivity C-reactive protein (p < 0.0001), and indexed left ventricular end-diastolic volume (p < 0.015), respectively. BMI and VHD resulted to be the main predictors of AHI values (p < 0.0001). Conclusions: Our study suggests that a significant association can occur between SA and VHD. It is clinically relevant that when compared to SA patients without VHD, higher frequencies of central and mixed apneas were found in subjects with SA and VHD. Moreover, after elevated BMI, VHD represented the second predictor of AHI values.
The heart is the first organ formed during mammalian development. A properly sized and functional heart is vital throughout the entire lifespan. Loss of cardiomyocytes because of injury or diseases leads to heart failure, which is a major cause of human morbidity and mortality. Unfortunately, regenerative potential of the adult heart is limited. The Hippo pathway is a recently identified signaling cascade that plays an evolutionarily conserved role in organ size control by inhibiting cell proliferation, promoting apoptosis, regulating fates of stem/progenitor cells, and in some circumstances, limiting cell size. Interestingly, research indicates a key role of this pathway in regulation of cardiomyocyte proliferation and heart size. Inactivation of the Hippo pathway or activation of its downstream effector, the Yes-associated protein transcription coactivator, improves cardiac regeneration. Several known upstream signals of the Hippo pathway such as mechanical stress, G-protein-coupled receptor signaling, and oxidative stress are known to play critical roles in cardiac physiology. In addition, Yes-associated protein has been shown to regulate cardiomyocyte fate through multiple transcriptional mechanisms. In this review, we summarize and discuss current findings on the roles and mechanisms of the Hippo pathway in heart development, injury, and regeneration.
One of the major causes of death all over the world is heart disease or cardiac dysfunction. These diseases could be identified easily with the variations in the sound produced due to the heart activity. These sophisticated auscultations need important clinical experience and concentrated listening skills. Therefore, there is an unmet need for a portable system for the early detection of cardiac illnesses. This paper proposes a prototype model of a smart digital-stethoscope system to monitor patient's heart sounds and diagnose any abnormality in a real-time manner. This system consists of two subsystems that communicate wirelessly using Bluetooth low energy technology: A portable digital stethoscope subsystem, and a computer-based decision-making subsystem. The portable subsystem captures the heart sounds of the patient, filters and digitizes, and sends the captured heart sounds to a personal computer wirelessly to visualize the heart sounds and for further processing to make a decision if the heart sounds are normal or abnormal. Twenty-seven t-domain, f-domain, and Mel frequency cepstral coefficients (MFCC) features were used to train a public database to identify the best-performing algorithm for classifying abnormal and normal heart sound (HS). The hyper parameter optimization, along with and without a feature reduction method, was tested to improve accuracy. The cost-adjusted optimized ensemble algorithm can produce 97% and 88% accuracy of classifying abnormal and normal HS, respectively.
Chronic heart diseases have in common an unresolved inflammatory status. In atherosclerosis, myocarditis, myocardial infarction, or atrial fibrillation, mounting evidence suggests that unresolved inflammation contributes to the chronicity, aggravation, and morbidity of the disease. Following cardiac injury or infection, acute inflammation is a normal and required process to repair damaged tissues or eliminate pathogens and promote restoration of normal functions and structures. However, if acute inflammation is not followed by resolution, a chronic and deleterious inflammatory status may occur, characterized by the persistence of inflammatory biomarkers, promoting aggravation of myocardial pathogenesis, abnormal structural remodeling, development of cardiac fibrosis, and loss of function. Although traditional antiinflammatory strategies, including the use of COX-inhibitors, to inhibit the production of inflammation promotors failed to promote homeostasis, mounting evidence suggests that activation of specific endogenous autacoids may promote resolution and perpetuate cardioprotective effects. The recent discovery of the active mechanism of resolution suggests that proresolving signals and cellular processes may help to terminate inflammation and combat the development of its chronic profile in cardiac diseases. This review discussed (I) the preclinical and clinical evidence of inflammation-resolution in cardiac disorders including atrial fibrillation; (II) how and why many traditional antiinflammatory treatments failed to prevent or cure cardiac inflammation and fibrosis; and (III) whether new therapeutic strategies may interact with the resolution machinery to have cardioprotective effects. RvD D-series resolving, RvE E-series resolving, LXA4 lipoxin A4, MaR1 maresin-1.
Dioscin has been widely used in clinics for coronary artery disease (CAD) treatment for years in China. However, the underlying mechanism for Dioscin-mediated cardioprotective effect has not been elucidated. Here, we showed that Dioscin significantly rescues the cardiac function in mouse model of myocardial infarction (MI), accompanied by the reduction of cardiac fibrosis and apoptosis, resulting from elevated angiogenesis. Mechanistically, Dioscin promotes the proliferation and migration of hypoxic endothelial cells via the up-regulation of lncRNA MANTIS, which serves as a scaffolding lncRNA within a chromatin remodeling complex. Meanwhile, it enables pol II binding to the transcription start sites, which leads to induced expression of angiogenesis-related genes, including SOX18, SMAD6, and COUP-TFII. Conversely, IncRNA MANTIS silencing prevents Dioscin-induced migration and angiogenesis in hypoxic endothelial cells. Taken together, these data provide new insights that clarifies the cardioprotective effects of Dioscin against myocardial infarcted injury and confirms the effect on angiogenic activity of endothelial cells. This will build a solid theoretical basis for clinical therapeutic strategies.
Echocardiography and catheterization angiography suffer certain limitations in the evaluation of congenital heart diseases in adults, though these are overcome by MRI, in which a wide field-of view, unlimited multiplanar imaging capability and three-dimensional contrast-enhanced MR angiography techniques are used. In adults, recently introduced fast imaging techniques provide cardiac MR images of sufficient quality and with less artifacts. Ventricular volume, ejection fraction, and vascular flow measurements, including pressure gradients and pulmonary-to-systemic flow ratio, can be calculated or obtained using fast cine MRI, phase-contrast MR flow-velocity mapping, and semiautomatic analysis software. MRI is superior to echocardiography in diagnosing partial anomalous pulmonary venous connection, unroofed coronary sinus, anomalies of the pulmonary arteries, aorta and systemic veins, complex heart diseases, and postsurgical sequelae. Biventricular function is reliably evaluated with cine MRI after repair of tetralogy of Fallot, and Senning's and Mustard's operations. MRI has an important and growing role in the morphologic and functional assessment of congenital heart diseases in adolescents and adults.
Background and Objectives: Cancer patients are at increased short- and long-term risk of cardiac toxicity and mortality. It is well-known that cardiac morbidity and mortality follows a seasonal pattern. Here we address the question of whether heart disease-related fatalities among cancer patients also follow a seasonal pattern. Materials and Methods: We performed a retrospective analysis of seasonality of deaths due to heart diseases (n = 503,243) in patients with newly diagnosed cancer reported during the period from 1975 to 2016 in the US's largest cancer registry-the Surveillance, Epidemiology, and End Results (SEER) database. Seasonality was assessed through a classical cosinor model assuming a single annual peak. Results: We identified a significant seasonal peak in the first half of November. A peak with identical features was for all subgroups of patients defined based on demographic characteristics. This was also the case when analysis was performed on subgroups defined by the type of malignancy. Only patients with acute leukemias, pancreatic cancer and nervous system malignancies did not have a seasonal pattern in heart disease-related fatalities. Conclusion: the rate of heart disease-related fatalities after cancer diagnosis follows a seasonal pattern similar to that observed for the general population, albeit with an earlier peak in November. This suggests that close monitoring of the cardiovascular system in cancer survivors must be particularly active from late autumn and during the entire winter period.
Introduction: Patients with inflammatory rheumatic diseases have an increased risk of developing cardiovascular manifestations. The high risk of cardiovascular pathology in these patients is not only due to traditional cardiovascular risk factors (age, gender, family history, smoking, sedentary lifestyle, cholesterol), but also to chronic inflammation and autoimmunity. Aim: In this review, we present the mechanisms of cardiovascular comorbidities associated with inflammatory rheumatic diseases, as they have recently been reported by different authors, grouped in electrical abnormalities, valvular, myocardial and pericardial modifications and vascular involvement. Methods: We conducted a systematic search of published literature on the following online databases: EBSCO, ScienceDirect, Scopus and PubMed. Searches were limited to full-text English-language journal articles published between 2010 and 2017 using the following key words: heart, systemic inflammation, autoimmunity, rheumatic diseases and disease activity. After the primary analysis we included 50 scientific articles in this review. Results: The results showed that cardiac manifestations of systemic inflammation can occur frequently with different prevalence in rheumatoid arthritis (RA), systemic lupus erythematosus(SLE), systemic sclerosis(SSc) and ankylosing spondylitis(AS). Rheumatologic diseases can affect the myocardium, cardiac valves, pericardium, conduction system and arterial vasculature. Conclusions: Early detection, adequate management and therapy of specific cardiac involvement are essential in rheumatic disease. Electrocardiographic and echocardiographic evaluation should be performed as routine investigations in patients with inflammatory rheumatic diseases.
(1) Background: The interaction between single nucleotide variants (SNVs) associated with congenital heart diseases (CHDs) and their gene methylation status has not been well researched. The aim of the present study was to determine if there is a relationship between the methy lation status (MS) of genes and the allelic variants associated with CHDs. (2) Methods: Seven SNVs of the genes AXIN1, TBX1, TBX20, and MTHFR were selected from the literature. DNA extraction, genotyping, and a methylation analysis were performed on healthy subjects and subjects with CHDs. (3) Results: Twenty-two subjects with CHDs were selected as the case group (15 with ventricular septal defects (VSDs) and 7 with atrial septal defects (ASDs)), and 44 healthy subjects comprised the control group. The MTHFR and AXIN1 genes were hypermethylated in the control group when compared to the case group. When analyzed separately, those with atrial septum defects exhibited greater methylation, except for the gene MTHFR where there were no differences. Only the alternate alleles of MTHFR showed a significantly different methylation status in those without cardiopathy. (4) Conclusions: The MTHFR and AXIN genes were hypermethylated in the control group; however, only the alternate alleles of MTHFR (rs1801133 and rs1801131) showed a significantly different methylation status.
Development of heart diseases is driven by dynamic changes in both the activity and connectivity of gene pathways. Understanding these dynamic events is critical for understanding pathogenic mechanisms and development of effective treatment. Currently, there is a lack of computational methods that enable analysis of multiple gene networks, each of which exhibits differential activity compared to the network of the baseline/healthy condition. We describe the iMDM algorithm to identify both unique and shared gene modules across multiple differential co-expression networks, termed M-DMs (multiple differential modules). We applied iMDM to a time-course RNA-Seq dataset generated using a murine heart failure model generated on two genotypes. We showed that iMDM achieves higher accuracy in inferring gene modules compared to using single or multiple co-expression networks. We found that condition-specific M-DMs exhibit differential activities, mediate different biological processes, and are enriched for genes with known cardiovascular phenotypes. By analyzing M-DMs that are present in multiple conditions, we revealed dynamic changes in pathway activity and connectivity across heart failure conditions. We further showed that module dynamics were correlated with the dynamics of disease phenotypes during the development of heart failure. Thus, pathway dynamics is a powerful measure for understanding pathogenesis. iMDM provides a principled way to dissect the dynamics of gene pathways and its relationship to the dynamics of disease phenotype. With the exponential growth of omics data, our method can aid in generating systems-level insights into disease progression.
Background After the Chernobyl nuclear accident in 1986, an increase in the incidence of congenital heart disease ( CHD s) in the neighboring countries was reported. In 2011, Japan experienced the Great East Japan Earthquake and the nuclear accidents at Fukushima. However, a nationwide study of their effects has not been conducted yet. Methods and Results We used data covering the period between 2007 and 2014 from the annual surveys conducted by the Japanese Association for Thoracic Surgery, which included almost all of the operations pertaining to 46 types of CHD s in Japan. CHD s were divided into 2 groups based on complexity, the time of occurrence during heart development, and age at operation. We estimated the change in the number of the operations per 100 000 live births between pre- and postdisaster using a negative binomial generalized linear mixed model. Overall, a significant 14.2% (95% CI, 9.3-19.4) increase in the number of operations for complex CHD s in neonates and infants per 100 000 live births was found, whereas those performed for patients of 1 to 17 years old showed no significant change during the study period. Conclusions The number of operations for complex CHD s in neonates and infants in Japan significantly increased after the massive disaster, and its level was maintained thereafter. The number of operations for complex CHD was not equal but closely correlated to the live birth prevalence of complex CHD s. Therefore, some meaningful increase in the live birth prevalence can be assumed; however, the precise cause of the increase is unknown.
Congenital cataract (CC) and congenital heart disease (CHD) are significant birth defects. In clinical practice, the concurrence of CC and CHD is frequently observed in patients. Additionally, some monogenic diseases, copy number variation (CNV) syndromes, and diseases associated with intrauterine infection involve both cataract and heart defects. However, little is known about the association between CC and CHD. Here, we characterised the demographic, clinical, and genetic features of patients with CC and heart defects.
The data presented here are related to the research article entitled "Differential expression of the angiotensin-(1-12) [Ang-(1-12)]/chymase axis in human atrial tissue [1]. We have showed that chymase gene transcripts, chymase activity, and immunoreactive- Ang-(1-12) expression levels were higher in left compared to right atrial tissue, irrespective of cardiac disease. This article presents the echocardiographic characteristics of 111 patients undergoing heart surgery for the correction of valvular heart disease, resistant atrial fibrillation or ischemic heart disease. Left atrial chymase mRNA expression and activity, and left atrial Ang-(1-12) levels were compared between patients with stroke vs. non-stroke, congestive heart failure vs. non-heart failure, and in cardiac surgery patients who had a history of postoperative atrial fibrillation vs. non-atrial fibrillation.
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