Inhibitory effect of microRNA-21 on pathways and mechanisms involved in cardiac fibrosis development.

Cardiac fibrosis is a pivotal cardiovascular disease (CVD) process and represents a notable health concern worldwide. While the complex mechanisms underlying CVD have been widely investigated, recent research has highlighted microRNA-21's (miR-21) role in cardiac fibrosis pathogenesis. In this narrative review, we explore the molecular interactions, focusing on the role of miR-21 in contributing to cardiac fibrosis. Various signaling pathways, such as the RAAS, TGF-ß, IL-6, IL-1, ERK, PI3K-Akt, and PTEN pathways, besides dysregulation in fibroblast activity, matrix metalloproteinases (MMPs), and tissue inhibitors of MMPs cause cardiac fibrosis. Besides, miR-21 in growth factor secretion, apoptosis, and endothelial-to-mesenchymal transition play crucial roles. miR-21 capacity regulatory function presents promising insights for cardiac fibrosis. Moreover, this review discusses numerous approaches to control miR-21 expression, including antisense oligonucleotides, anti-miR-21 compounds, and Notch signaling modulation, all novel methods of cardiac fibrosis inhibition. In summary, this narrative review aims to assess the molecular mechanisms of cardiac fibrosis and its essential miR-21 function.

Unraveling cardiac fibrosis: insights into microRNA-21's key role and promising approaches for controlCardiac fibrosis poses a significant global health threat and plays a central role in cardiovascular diseases. This examination delves into recent research revealing the participation of microRNA-21 (MiR-21) in the progression of cardiac fibrosis, providing insight into its critical function in this process. The investigation explores diverse molecular interactions, underscoring MiR-21's contribution to the development of cardiac fibrosis. Various signaling pathways, including the Renin-Angiotensin-Aldosterone System, TGF-ß, IL-6, IL-1, ERK, PI3K-Akt, and PTEN pathways, coupled with disturbances in fibroblast activity, matrix metalloproteinases (MMPs), and tissue inhibitors of MMPs (TIMPs), contribute to cardiac fibrosis. MiR-21's influence on growth factor secretion, apoptosis, and endothelial-to-mesenchymal transition further emphasizes its crucial role. What adds promise to MiR-21 is its capacity for regulation, providing potential insights into controlling cardiac fibrosis. The review also investigates various methods to modulate MiR-21 expression, such as antisense oligonucleotides, anti-miR-21 compounds, and Notch signaling modulation ­ innovative approaches showing potential in inhibiting cardiac fibrosis. In summary, this narrative review aims to dissect the complex molecular mechanisms behind cardiac fibrosis, explicitly emphasizing the indispensable role of MiR-21. By comprehending these mechanisms, researchers can lay the groundwork for inventive interventions and therapeutic strategies to hinder cardiac fibrosis, ultimately contributing to advancing cardiovascular health.

Monocyte-Derived Macrophages Aggravate Cardiac Dysfunction After Ischemic Stroke in Mice.

BACKGROUND: Cardiac damage induced by ischemic stroke, such as arrhythmia, cardiac dysfunction, and even cardiac arrest, is referred to as cerebral-cardiac syndrome (CCS). Cardiac macrophages are reported to be closely associated with stroke-induced cardiac damage. However, the role of macrophage subsets in CCS is still unclear due to their heterogeneity. Sympathetic nerves play a significant role in regulating macrophages in cardiovascular disease. However, the role of macrophage subsets and sympathetic nerves in CCS is still unclear. METHODS AND RESULTS: In this study, a middle cerebral artery occlusion mouse model was used to simulate ischemic stroke. ECG and echocardiography were used to assess cardiac function. We used Cx3cr1GFPCcr2RFP mice and NLRP3-deficient mice in combination with Smart-seq2 RNA sequencing to confirm the role of macrophage subsets in CCS. We demonstrated that ischemic stroke-induced cardiac damage is characterized by severe cardiac dysfunction and robust infiltration of monocyte-derived macrophages into the heart. Subsequently, we identified that cardiac monocyte-derived macrophages displayed a proinflammatory profile. We also observed that cardiac dysfunction was rescued in ischemic stroke mice by blocking macrophage infiltration using a CCR2 antagonist and NLRP3-deficient mice. In addition, a cardiac sympathetic nerve retrograde tracer and a sympathectomy method were used to explore the relationship between sympathetic nerves and cardiac macrophages. We found that cardiac sympathetic nerves are significantly activated after ischemic stroke, which contributes to the infiltration of monocyte-derived macrophages and subsequent cardiac dysfunction. CONCLUSIONS: Our findings suggest a potential pathogenesis of CCS involving the cardiac sympathetic nerve-monocyte-derived macrophage axis.

Assessment of Native Myocardial T1 Mapping for Early Detection of Anthracycline-Induced Cardiotoxicity in Patients with Cancer: a Systematic Review and Meta-analysis.

Anthracycline antibiotic is one of the most effective anti-tumor drugs used to manage certain types of breast cancers, lymphomas, and leukemias. However, anthracyclines induce a dose-dependent cardiotoxicity that may progress to heart failure. Thus, using a sensitive predictor of early cardiac dysfunction in patients treated with anthracyclines can help detect subclinical cardiac dysfunction early and help initiate interventions to protect these patients. Among parameters of myocardial measure, cardiac magnetic resonance (CMR)-measured native myocardial T1 mapping is considered a sensitive and accurate quantitative measure of early subclinical cardiac changes, particularly cardiac inflammation and fibrosis. However, to understand the quality and the validity of the current evidence supporting the use of these measures in patients treated with anthracyclines, we aimed to conduct a systematic review of clinical studies of this measure to detect early myocardial changes in cancer patients treated with anthracyclines. The primary outcome was the level of native T1 mapping. We performed fixed-effects meta-analyses and assessed certainty in effect estimates. Of the 1780 publications reviewed (till 2022), 23 were retrieved, and 9 articles met the inclusion criteria. Our study showed that exposure to anthracycline was associated with a significant elevation of native myocardial T1 mapping from baseline (95% CI 0.1121 to 0.5802; p = 0.0037) as well as compared to healthy control patients (95% CI 0.2925 to 0.7448; p < 0.0001). No significant publication bias was noted on the assessment of the funnel plot and Egger's test. According to the Q test, there was no significant heterogeneity in the included studies (I2 = 0.0000% versus healthy controls and I2 = 14.0666% versus baseline). Overall, our study suggests that native myocardial T1 mapping is useful for detecting anthracycline-induced cardiotoxicity in patients with cancer.

Role of Early Left Atrial Functional Decline in Predicting Cardiotoxicity in HER2 Positive Breast Cancer Patients Treated With Trastuzumab.

Trastuzumab is widely used in HER2 breast cancer. However, it may cause left ventricular (LV) dysfunction. A decrease in LV global longitudinal strain (GLS) has been previously demonstrated to be a good predictor of subsequent cancer therapy related dysfunction (CTRCD). Left atrial morphological remodeling during Trastuzumab therapy has also been shown. The aim of this study is exploring the relationship between early changes in left atrial function and the development of Trastuzumab-induced cardiotoxicity. Consecutive patients with diagnosis of HER2+non-metastatic breast cancer treated with Trastuzumab were prospectively enrolled. A clinical, conventional, and advanced echocardiographic assessment was performed at baseline and every three months, until a one-year follow-up was reached. One-hundred-sixteen patients completed the 12 months follow-up, 10 (9%) cases of CTRCD were observed, all after the sixth month. GLS and LVEF significantly decreased in the CTRCD group at 6 months of follow-up, with an earlier (3 months) significant worsening in left atrial morpho-functional parameters. Systolic blood pressure, early peak atrial longitudinal strain (PALS), peak atrial contraction (PACS) and left atrial volume (LAVI) changes resulted independent predictors of CTRCD at multivariable logistic regression analysis. Moreover, early changes in PALS and PACS resulted good predictors of CTRCD development (AUC 0.85; p = 0.008, p < 0.001 and 0.77; p = 0.008, respectively). This prospective study emphasizes that the decline in PALS and PACS among trastuzumab-treated patients could possibly increase the accuracy in identifying future CTRCD in non-metastatic HER2 breast cancer cases, adding predictive value to conventional echocardiographic assessment.

Impact of left atrial appendage flow velocity on thrombus resolution and clinical outcomes in patients with atrial fibrillation and silent left atrial thrombi: insights from the LAT study.

AIMS: Blood stasis is crucial in developing left atrial (LA) thrombi. LA appendage peak flow velocity (LAAFV) is a quantitative parameter for estimating thromboembolic risk. However, its impact on LA thrombus resolution and clinical outcomes remains unclear. METHODS AND RESULTS: The LAT study was a multicentre observational study investigating patients with atrial fibrillation (AF) and silent LA thrombi detected by transoesophageal echocardiography (TEE). Among 17 436 TEE procedures for patients with AF, 297 patients (1.7%) had silent LA thrombi. Excluding patients without follow-up examinations, we enrolled 169 whose baseline LAAFV was available. Oral anticoagulation use increased from 85.7% at baseline to 97.0% at the final follow-up (P < 0.001). During 1 year, LA thrombus resolution was confirmed in 130 (76.9%) patients within 76 (34-138) days. Conversely, 26 had residual LA thrombi, 8 had thromboembolisms, and 5 required surgical removal. These patients with failed thrombus resolution had lower baseline LAAFV than those with successful resolution (18.0 [15.8-22.0] vs. 22.2 [17.0-35.0], P = 0.003). Despite limited predictive power (area under the curve, 0.659; P = 0.001), LAAFV ≤ 20.0 cm/s (best cut-off) significantly predicted failed LA thrombus resolution, even after adjusting for potential confounders (odds ratio, 2.72; 95% confidence interval, 1.22-6.09; P = 0.015). The incidence of adverse outcomes including ischaemic stroke/systemic embolism, major bleeding, or all-cause death was significantly higher in patients with reduced LAAFV than in those with preserved LAAFV (28.4% vs. 11.6%, log-rank P = 0.005). CONCLUSION: Failed LA thrombus resolution was not rare in patients with AF and silent LA thrombi. Reduced LAAFV was associated with failed LA thrombus resolution and adverse clinical outcomes.

Role of the Lymphatics in Cardiac Disease.

Cardiovascular diseases remain the largest cause of death worldwide with recent evidence increasingly attributing the development and progression of these diseases to an exacerbated inflammatory response. As a result, significant research is now focused on modifying the immune environment to prevent the disease progression. This in turn has highlighted the lymphatic system in the pathophysiology of cardiovascular diseases owing, in part, to its established function in immune cell surveillance and trafficking. In this review, we highlight the role of the cardiac lymphatic system and its potential as an immunomodulatory therapeutic target in selected cardiovascular diseases.

Cardiac manifestations in inherited metabolic diseases.

Inherited metabolic diseases (IMD) are caused by the functional defect of an enzyme, of genetic origin, that provokes a blockage in a specific metabolic pathway. Individually, IMD are considered rare diseases, with an incidence of less than 1/100,000 births. The symptoms are usually multisystemic, but frequently include cardiac manifestations. Of these, the most common are cardiomyopathies, especially hypertrophic cardiomyopathy. In addition, they can cause dilated or restrictive cardiomyopathy and non-compacted cardiomyopathy of the left ventricle. Characteristic signs also include rhythm alterations (atrio-ventricular conduction disturbances, Wolff-Parkinson-White syndrome or ventricular arrhythmias), valvular pathology and ischaemic coronary pathologies. The aim of this study is to present a narrative review of the IMD that may produce cardiac involvement. We describe both the specific cardiac manifestations of each disease and the systemic symptoms that guide diagnosis.

Cardiac evaluation in pregnant patients with dyspnea and palpitations.

BACKGROUND: Symptoms of underlying cardiac disease in pregnancy can often be mistaken for common complaints because of normal physiological changes in pregnancy. Echocardiographic evaluation of patients with symptoms of palpitations and dyspnea can detect structural changes and identify high-risk features. OBJECTIVE: This study aimed to examine transthoracic echocardiograms of perinatal individuals completed for palpitations or dyspnea to determine the frequency of identifying structural changes. STUDY DESIGN: This was a retrospective cohort study of all perinatal individuals with a transthoracic echocardiogram at a single academic center between October 1, 2017, and May 1, 2022. The indication for the echocardiogram, demographics, and clinical characteristics were recorded. Transthoracic echocardiograms with any abnormal findings noted in the transthoracic echocardiogram report were reviewed and categorized into findings of congenital heart disease, valvular disease, pericardial effusion, evidence of ischemia or wall motion abnormalities, abnormal diastolic or systolic function, and other. RESULTS: Of 539 transthoracic echocardiograms completed on 478 individuals who were pregnant or in the 12-week postpartum period, 96 (17.8%) had an indication of palpitations, and 32 (5.9%) had an indication of dyspnea. Abnormal findings were seen in 21.9% of patients with palpitations and in 34.4% of patients with dyspnea. In patients with palpitations who had abnormal findings, 33.3% had congenital heart disease; 33.3% had mild valvular disease, including mitral valve prolapse; 19.0% had a pericardial effusion; and 14.3% had evidence of ischemia or wall motion defects. Abnormal transthoracic echocardiogram findings in the dyspnea cohort included ischemia or wall motion defects (27.3%), mild valvular disease or mitral valve prolapse (36.4%), and abnormal systolic or diastolic function (36.4%). CONCLUSION: Many of the transthoracic echocardiograms completed for patients with dyspnea or palpitations identified no structural abnormality; however, in 1 of 3 to 1 of 4 patients, underlying structural heart disease was identified. Although some of these abnormalities were unlikely to change delivery plans, such as mild valvular disease or small effusions, other abnormalities, such as ischemia, congenital abnormalities, and abnormal systolic or diastolic function, were likely to have implications for pregnancy and postpartum management.

Sex-based differences in short- and longer-term diet-induced metabolic heart disease.

Sex-based differences in the development of obesity-induced cardiometabolic dysfunction are well documented, however, the specific mechanisms are not completely understood. Obesity has been linked to dysregulation of the epitranscriptome, but the role of N6-methyladenosine (m6A) RNA methylation has not been investigated in relation to the sex differences during obesity-induced cardiac dysfunction. In the current study, male and female C57BL/6J mice were subjected to short- and long-term high-fat/high-sucrose (HFHS) diet to induce obesogenic stress. Cardiac echocardiography showed males developed systolic and diastolic dysfunction after 4 mo of diet, but females maintained normal cardiac function despite both sexes being metabolically dysfunctional. Cardiac m6A machinery gene expression was differentially regulated by duration of HFHS diet in male, but not female mice, and left ventricular ejection fraction correlated with RNA machinery gene levels in a sex- and age-dependent manner. RNA-sequencing of cardiac transcriptome revealed that females, but not males may undergo protective cardiac remodeling early in the course of obesogenic stress. Taken together, our study demonstrates for the first time that cardiac RNA methylation machinery genes are regulated early during obesogenic stress in a sex-dependent manner and may play a role in the sex differences observed in cardiometabolic dysfunction.NEW & NOTEWORTHY Sex differences in obesity-associated cardiomyopathy are well documented but incompletely understood. We show for the first time that RNA methylation machinery genes may be regulated in response to obesogenic diet in a sex- and age-dependent manner and levels may correspond to cardiac systolic function. Our cardiac RNA-seq analysis suggests female, but not male mice may be protected from cardiac dysfunction by a protective cardiac remodeling response early during obesogenic stress.

Preclinical Models of Cardiac Disease: A Comprehensive Overview for Clinical Scientists.

For recent decades, cardiac diseases have been the leading cause of death and morbidity worldwide. Despite significant achievements in their management, profound understanding of disease progression is limited. The lack of biologically relevant and robust preclinical disease models that truly grasp the molecular underpinnings of cardiac disease and its pathophysiology attributes to this stagnation, as well as the insufficiency of platforms that effectively explore novel therapeutic avenues. The area of fundamental and translational cardiac research has therefore gained wide interest of scientists in the clinical field, while the landscape has rapidly evolved towards an elaborate array of research modalities, characterized by diverse and distinctive traits. As a consequence, current literature lacks an intelligible and complete overview aimed at clinical scientists that focuses on selecting the optimal platform for translational research questions. In this review, we present an elaborate overview of current in vitro, ex vivo, in vivo and in silico platforms that model cardiac health and disease, delineating their main benefits and drawbacks, innovative prospects, and foremost fields of application in the scope of clinical research incentives.

Atorvastatin for Anthracycline-Associated Cardiac Dysfunction: The STOP-CA Randomized Clinical Trial.

Importance: Anthracyclines treat a broad range of cancers. Basic and retrospective clinical data have suggested that use of atorvastatin may be associated with a reduction in cardiac dysfunction due to anthracycline use. Objective: To test whether atorvastatin is associated with a reduction in the proportion of patients with lymphoma receiving anthracyclines who develop cardiac dysfunction. Design, Setting, and Participants: Double-blind randomized clinical trial conducted at 9 academic medical centers in the US and Canada among 300 patients with lymphoma who were scheduled to receive anthracycline-based chemotherapy. Enrollment occurred between January 25, 2017, and September 10, 2021, with final follow-up on October 10, 2022. Interventions: Participants were randomized to receive atorvastatin, 40 mg/d (n = 150), or placebo (n = 150) for 12 months. Main Outcomes and Measures: The primary outcome was the proportion of participants with an absolute decline in left ventricular ejection fraction (LVEF) of ≥10% from prior to chemotherapy to a final value of <55% over 12 months. A secondary outcome was the proportion of participants with an absolute decline in LVEF of ≥5% from prior to chemotherapy to a final value of <55% over 12 months. Results: Of the 300 participants randomized (mean age, 50 [SD, 17] years; 142 women [47%]), 286 (95%) completed the trial. Among the entire cohort, the baseline mean LVEF was 63% (SD, 4.6%) and the follow-up LVEF was 58% (SD, 5.7%). Study drug adherence was noted in 91% of participants. At 12-month follow-up, 46 (15%) had a decline in LVEF of 10% or greater from prior to chemotherapy to a final value of less than 55%. The incidence of the primary end point was 9% (13/150) in the atorvastatin group and 22% (33/150) in the placebo group (P = .002). The odds of a 10% or greater decline in LVEF to a final value of less than 55% after anthracycline treatment was almost 3 times greater for participants randomized to placebo compared with those randomized to atorvastatin (odds ratio, 2.9; 95% CI, 1.4-6.4). Compared with placebo, atorvastatin also reduced the incidence of the secondary end point (13% vs 29%; P = .001). There were 13 adjudicated heart failure events (4%) over 24 months of follow-up. There was no difference in the rates of incident heart failure between study groups (3% with atorvastatin, 6% with placebo; P = .26). The number of serious related adverse events was low and similar between groups. Conclusions and Relevance: Among patients with lymphoma treated with anthracycline-based chemotherapy, atorvastatin reduced the incidence of cardiac dysfunction. This finding may support the use of atorvastatin in patients with lymphoma at high risk of cardiac dysfunction due to anthracycline use. Trial Registration: ClinicalTrials.gov Identifier: NCT02943590.

Immune-mediated denervation of the pineal gland underlies sleep disturbance in cardiac disease.

Disruption of the physiologic sleep-wake cycle and low melatonin levels frequently accompany cardiac disease, yet the underlying mechanism has remained enigmatic. Immunostaining of sympathetic axons in optically cleared pineal glands from humans and mice with cardiac disease revealed their substantial denervation compared with controls. Spatial, single-cell, nuclear, and bulk RNA sequencing traced this defect back to the superior cervical ganglia (SCG), which responded to cardiac disease with accumulation of inflammatory macrophages, fibrosis, and the selective loss of pineal gland-innervating neurons. Depletion of macrophages in the SCG prevented disease-associated denervation of the pineal gland and restored physiological melatonin secretion. Our data identify the mechanism by which diurnal rhythmicity in cardiac disease is disturbed and suggest a target for therapeutic intervention.

Cognitive Impairment in Patients With Cardiac Disease: Implications for Clinical Practice.

Cognitive impairment is common in patients with cardiovascular disease. One in 3 patients presenting at cardiology clinics have some degree of cognitive impairment, depending on the cardiac condition, comorbidities, and age. In up to half of these cases cognitive impairment may go unrecognized; however, it may affect self-management and treatment adherence. The high prevalence of cognitive impairment in patients with cardiac disease is likely due to shared risk factors, as well as direct consequences of cardiac dysfunction on the brain. Moreover, cardiac interventions may have beneficial as well as adverse effects on cognitive functioning. In this review, we describe prevalence and risk factors for cognitive impairment in patients with several common cardiac conditions: heart failure, coronary artery disease, and aortic valve stenosis. We discuss the potential effects of guideline-based treatments on cognition and identify open questions and unmet needs. Given the high prevalence of unrecognized cognitive impairment in cardiac patients, we recommend a stepwise approach to improve detection and management of cognitive impairment.

Perioperative Point of Care Ultrasound for Hemodynamic Assessment: A Narrative Review.

While transesophageal echocardiography (TEE) has traditionally been used in perioperative care, there is growing evidence supporting point of care ultrasound (POCUS) for the anesthesiologist in guiding patient care. It is a quick way to non-invasively evaluate hemodynamically unstable patients and ascertain their state of shock, determine volume status, and guide resuscitation in cardiac arrest. In addition, through use of POCUS, the anesthesiologist is able to identify signs of chronic heart disease to provide a more tailored and safer approach to perioperative care.

The well-developed actin cytoskeleton and Cthrc1 expression by actin-binding protein drebrin in myofibroblasts promote cardiac and hepatic fibrosis.

Fibrosis is mainly triggered by inflammation in various tissues, such as heart and liver tissues, and eventually leads to their subsequent dysfunction. Fibrosis is characterized by the excessive accumulation of extracellular matrix proteins (e.g., collagens) produced by myofibroblasts. The well-developed actin cytoskeleton of myofibroblasts, one of the main features differentiating them from resident fibroblasts in tissues under inflammatory conditions, contributes to maintaining their ability to produce excessive extracellular matrix proteins. However, the molecular mechanisms via which the actin cytoskeleton promotes the production of fibrosis-related genes in myofibroblasts remain unclear. In this study, we found, via single-cell analysis, that developmentally regulated brain protein (drebrin), an actin-binding protein, was specifically expressed in cardiac myofibroblasts with a well-developed actin cytoskeleton in fibrotic hearts. Moreover, our immunocytochemistry analysis revealed that drebrin promoted actin cytoskeleton formation and myocardin-related transcription factor-serum response factor signaling. Comprehensive single-cell analysis and RNA-Seq revealed that the expression of collagen triple helix repeat containing 1 (Cthrc1), a fibrosis-promoting secreted protein, was regulated by drebrin in cardiac myofibroblasts via myocardin-related transcription factor-serum response factor signaling. Furthermore, we observed the profibrotic effects of drebrin exerted via actin cytoskeleton formation and the Cthrc1 expression regulation by drebrin in liver myofibroblasts (hepatic stellate cells). Importantly, RNA-Seq demonstrated that drebrin expression levels increased in human fibrotic heart and liver tissues. In summary, our results indicated that the well-developed actin cytoskeleton and Cthrc1 expression due to drebrin in myofibroblasts promoted cardiac and hepatic fibrosis, suggesting that drebrin is a therapeutic target molecule for fibrosis.

The ebb and flow of cardiac lymphatics: a tidal wave of new discoveries.

The heart is imbued with a vast lymphatic network that is responsible for fluid homeostasis and immune cell trafficking. Disturbances in the forces that regulate microvascular fluid movement can result in myocardial edema, which has profibrotic and proinflammatory consequences and contributes to cardiovascular dysfunction. This review explores the complex relationship between cardiac lymphatics, myocardial edema, and cardiac disease. It covers the revised paradigm of microvascular forces and fluid movement around the capillary as well as the arsenal of preclinical tools and animal models used to model myocardial edema and cardiac disease. Clinical studies of myocardial edema and their prognostic significance are examined in parallel to the recent elegant animal studies discerning the pathophysiological role and therapeutic potential of cardiac lymphatics in different cardiovascular disease models. This review highlights the outstanding questions of interest to both basic scientists and clinicians regarding the roles of cardiac lymphatics in health and disease.

Repercusiones cardíacas en pacientes con pectus excavatum: puesta al día. Segunda parte / Cardiac repercussions in patients with pectus excavatum: update. Part two / Repercussões cardíacas em pacientes com pectus excavatum: atualização. Parte dois

El pectus excavatum (PEX) es una deformación de la pared torácica que obedece a una alteración de los cartílagos costales con el consiguiente hundimiento del esternón. Históricamente, se clasificaba como un defecto únicamente estético o cosmético, sin embargo, en los últimos años se han desarrollado nuevos métodos de estudio para la valoración de las repercusiones de esta patología. Existe cada vez más bibliografía que demuestra importantes repercusiones funcionales. Se realizó una puesta al día de las repercusiones cardíacas de la patología y un análisis de los artículos más relevantes de los últimos años. La evidencia actual permite afirmar que existe una afectación cardíaca por compresión esternal en la mayoría de los pacientes con PEX. Las afectaciones incluyen alteraciones anatomofuncionales (trastornos del ritmo, disminución del llenado ventricular), del volumen sistólico, aumento de la presión de la aurícula derecha, valvulopatías, compresión del ventrículo derecho, derrame pericárdico, entre otras. Todo lo cual permite concluir que el PEX puede presentar importantes alteraciones cardíacas que deben ser tenidas en cuenta a la hora de valorar los pacientes con esta patología.

Pectus excavatum (PEX) is a deformation of the chest wall caused by an alteration of the costal cartilages with the consequent collapse of the sternum. Historically, it had been classified as a solely aesthetic or cosmetic defect, however, in recent years new study methods have been developed to assess the repercussions of this pathology, with increasing bibliography showing important functional consequences. We updated the cardiac pathological repercussions and analyzed the most relevant articles of recent years. The current evidence suggests that there is cardiac involvement due to sternal compression in most patients with PEX. These affectations include anatomical functional alterations: rhythm disorders, decreased ventricular filling, decreased stroke volume, increased right atrial pressure, valve disease, right ventricular compression, pericardial effusion, among others. All of which enables us to conclude that PEX can present important cardiac alterations that must be taken into account when assessing patients with this pathology.

Pectus excavatum (PEX) é uma deformação da parede torácica decorrente de uma alteração das cartilagens costais com consequente colapso do esterno. Historicamente, foi classificado como um defeito exclusivamente estético ou cosmético, porém, nos últimos anos, novos métodos de estudo foram desenvolvidos para avaliar as repercussões dessa patologia, com crescente bibliografia mostrando importantes repercussões funcionais. Foi realizada uma atualização das repercussões cardíacas da patologia e análise dos artigos mais relevantes dos últimos anos. As evidências atuais permitem afirmar que há acometimento cardíaco por compressão esternal na maioria dos pacientes com PEX. As afecções incluem alterações anatomofuncionais: distúrbios do ritmo, diminuição do enchimento ventricular, diminuição do volume sistólico, aumento da pressão atrial direita, doença valvular, compressão do ventrículo direito, derrame pericárdico, entre outras. Tudo isso permite concluir que o PEX pode apresentar alterações cardíacas importantes que devem ser levadas em consideração na avaliação de pacientes com essa patologia.

Deep Time Growing Neural Network vs Convolutional Neural Network for Intelligent Phonocardiography.

This paper explores the capabilities of a sophisticated deep learning method, named Deep Time Growing Neural Network (DTGNN), and compares its possibilities against a generally well-known method, Convolutional Neural network (CNN). The comparison is performed by using time series of the heart sound signal, so-called Phonocardiography (PCG). The classification objective is to discriminate between healthy and patients with cardiac diseases by applying a deep machine learning method to PCGs. This approach which is called intelligent phonocardiography has received interest from the researchers toward the development of a smart stethoscope for decentralized diagnosis of heart disease. It is found that DTGNN associates further flexibility to the approach which enables the classifier to learn subtle contents of PCG, and meanwhile better copes with the complexities intrinsically that exist in the medical applications such as the imbalance training. The structural risk of the two methods is compared using the A-Test method.