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An anomalous origin of the right coronary artery from the pulmonary artery case report. The diagnosis was made by angiotomography. Reimplantation of the right coronary artery into the ascending aorta and reconstruction of the pulmonary artery were conducted.

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BACKGROUND: Pulmonary artery trunk aneurysm (PATA) is a rare and complex vascular anomaly characterized by the abnormal dilation of the initial portion of the pulmonary artery, posing significant diagnostic and therapeutic challenges. PURPOSE: This clinical case report aims to describe the follow-up of a patient with PATA, emphasizing the role of imaging in diagnosis and monitoring, as well as discussing potential associations with other conditions. RESEARCH DESIGN: The study is designed as a clinical case report, detailing the longitudinal follow-up of a single patient with PATA. STUDY SAMPLE: The subject of this study is a 48-year-old female patient with a history of idiopathic hypertension who developed a PATA. Data Collection and/or Analysis: Since 2010, the patient underwent various imaging exams, including echocardiography, computed tomography, and catheter angiography, to detect and evaluate the aneurysm at different stages. RESULTS: The imaging results indicated a progression of the aneurysm over time, underscoring the importance of imaging in the early identification and monitoring of PATA. The report also explores the possible association of PATA with conditions such as pulmonary hypertension, Behçet's disease, and Hughes-Stovin syndrome, highlighting the diagnostic complexity. CONCLUSIONS: Imaging diagnosis is crucial for the detection, characterization, and monitoring of PATA, providing essential information for selecting appropriate treatment options and achieving a satisfactory prognosis. An individualized treatment approach, considering both medical and surgical options, is necessary based on the clinical characteristics of each patient.

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Acute pulmonary embolism (APE) is one of the leading causes of cardiovascular emergencies and the third leading cause of death. Although efforts focus on treating the acute event, patients who survive APE may develop long-term sequelae. Research reveals that approximately half of patients who have suffered an APE do not regain their previous level of function and experience a reduction in their quality of life for several years after the episode. Acute pulmonary embolism can be classified according to the risk of short-term mortality, with most mortality and morbidity concentrated in high-risk and intermediate-risk cases. The first-line treatment for APE is systemic anticoagulation. However, identifying and more aggressively treating people with intermediate to high risk, who have a more favorable risk profile for reperfusion treatments, could reduce short-term mortality and mitigate post-pulmonary embolism syndrome (PPES). Post-pulmonary embolism syndrome refers to a variety of persistent symptoms and functional limitations that occur after an APE. The presence of persistent dyspnea, functional limitations, and/or decreased quality of life after an APE has been recently termed "PPES," although this entity encompasses different manifestations. The most severe cause of persistent dyspnea is chronic thromboembolic pulmonary hypertension, where increased pulmonary artery pressure is due to the fibrotic organization of unresolved APE. Post-PE Syndrome is not always systematically addressed in management guidelines, and its prevalence may be underestimated. More research is needed to fully understand its causes and risk factors. Interventions such as cardiopulmonary rehabilitation have been suggested to improve the quality of life of patients with PPES. A comprehensive, evidence-based approach is essential to effectively prevent and manage PPES and improve the long-term outcomes and well-being of affected patients.

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Objective: . Acute myocardial infarction-related cardiogenic shock (AMI-CS) is often accompanied by tachycardia, which, in turn, increases myocardial oxygen consumption and hinders the use of ventricular assist devices, such as intra-aortic balloon pump. Evidence suggests that ivabradine may reduce heart rate (HR) without affecting other hemodynamic parameters. The aim of the present study was to determine the effect of ivabradine on reducing HR and changes in other hemodynamic parameters such as cardiac index (CI), in patients with AMI-CS and tachycardia. Materials and methods: . A single-center, open label, randomized clinical trial included patients diagnosed with AMI-CS and tachycardia with >100 beats per minute (BPM). Heart rate, cardiac index, and other hemodynamic parameters measured by pulmonary flotation catheter were compared at 0, 6, 12, 24, and 48 hours after randomization. Results: . A total of 12 patients were randomized; 6 received standard therapy, and 6 received ivabradine in addition to standard therapy. Baseline clinical characteristics were similar at randomization. A statistically significant lower heart rate was found at 12 hours (p=0.003) and 48 hours (p=0.029) after randomization, with differences of -23.3 (-8.2 to -38.4) BPM and -12.6 (-0.5 to -25.9) BPM, respectively. No differences in cardiac index, or any other evaluated hemodynamic parameters, length of hospital stay, nor mortality rate were noted between both groups. Conclusions: . The use of ivabradine in patients with AMI-CS was associated with a significant reduction in heart rate at 12 and 48 h, without affecting other hemodynamic parameters.

Objetivo: . El choque cardiogénico relacionado con el infarto agudo de miocardio (AMI-CS, por sus siglas en inglés) suele ir acompañado de taquicardia, lo que, a su vez, aumenta el consumo de oxígeno miocárdico y dificulta el uso de dispositivos de asistencia ventricular, como la bomba de balón intraaórtico. La evidencia sugiere que la ivabradina puede reducir la frecuencia cardíaca (FC) sin afectar otros parámetros hemodinámicos. El objetivo del presente estudio fue determinar el efecto de la ivabradina en la reducción de la FC y los cambios en otros parámetros hemodinámicos como el índice cardíaco (CI) en pacientes con AMI-CS y taquicardia. Materiales y métodos: Se incluyeron pacientes diagnosticados con AMI-CS y taquicardia con >100 latidos por minuto (LPM) en un ensayo clínico aleatorizado de un solo centro. La frecuencia cardíaca, el índice cardíaco y otros parámetros hemodinámicos medidos mediante catéter de flotación pulmonar se compararon a las 0, 6, 12, 24 y 48 h después de la aleatorización. Resultados: Se aleatorizaron un total de 12 pacientes; 6 recibieron terapia estándar y 6 recibieron ivabradina además de la terapia estándar. Las características clínicas basales fueron similares en la aleatorización. Se encontró una frecuencia cardíaca significativamente más baja a las 12 h (p=0,003) y a las 48 h (p=0,029) después de la aleatorización, con diferencias de -23,3 (-8,2 a -38,4) LPM y -12,6 (-0,5 a -25,9) LPM, respectivamente. No se observaron diferencias en el índice cardíaco, en ningún otro parámetro hemodinámico evaluado; tampoco en la duración de la estancia hospitalaria, ni en la tasa de mortalidad entre ambos grupos. Conclusiones: El uso de ivabradina en pacientes con AMI-CS se asoció con una reducción significativa en la frecuencia cardíaca a las 12 y 48 h, sin afectar otros parámetros hemodinámicos.

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CLINICAL DATA: A nine-month-old female infant diagnosed with transposition of the great arteries with symptoms of heart failure associated with cyanosis and difficulty in gaining weight was referred to our center with late diagnosis (at nine months of age). CHEST RADIOGRAPHY: Cardiomegaly; attenuated peripheral vascular markings.Electrocardiography: Sinus rhythm with biventricular overload and aberrantly conducted supraventricular extra systoles. ECHOCARDIOGRAPHY: Wide atrial septal defect, ventricular axis torsion with concordant atrioventricular connection and discordant ventriculoarterial connection. COMPUTED TOMOGRAPHY ANGIOGRAPHY: Concordant atrioventricular connection, right ventricle positioned superiorly and left ventricle positioned inferiorly; discordant ventriculoarterial connection with right ventricle connected to the aorta and left ventricle connected to pulmonary artery. DIAGNOSIS: Crisscross heart is a rare congenital heart defect, accounting for 0.1% of congenital heart diseases. It consists of the 90º rotation of ventricles' axis in relation to their normal position; therefore, ventricles are positioned in the superior-inferior direction rather than anterior-posterior. Most cases have associated cardiac anomalies, and in this case, it is associated with transposition of the great arteries. The complexity and rarity of its occurrence make diagnosis and surgical treatment challenging. OPERATION: Modified Senning procedure using the pericardial sac in the construction of a tunnel from pulmonary veins to the right atrium. Cardiopulmonary bypass time of 147 minutes with nine minutes of total circulatory arrest.

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The diameter (mPAD) of the main pulmonary artery (pulmonary artery trunk) is a crucial indicator for cardiovascular health and prognoses in various conditions. Its enlargement is associated with increased mortality and severity in COVID-19-related pneumonia. However, its relevance to non-COVID pneumonia remains uncertain. The aim of this study was to establish an association between mPAD and the severity of non-COVID pneumonia. Eligible participants with qualified Chest Computed Tomography scans from November 2019 to February 2023 were recruited to a cross-sectional retrospective study. They were stratified into pneumonia and non-pneumonia cohorts. Exclusion criteria included pulmonary hypertension, polytrauma, lung neoplasia, or a history of pulmonary stenosis repair. The mPAD was measured in both groups, and medical records were reviewed to identify comorbidities. Pulmonary CT data were classified by pattern and severity, and the mPAD was measured perpendicularly to the long axis of the artery at the point of bifurcation on an axial slice. Analysis of 380 CT scans (52.6% men, 47.4% women; mean age 52.88 ± 17.58) revealed a significant difference in mPAD between pneumonia and non-pneumonia cases (mean difference: 1.19 mm, 95% CI [0.46, 1.92], p = 0.001). Age correlated positively with mPAD (r = 0.231, 95% CI [0.028, 0.069], p < 0.0001), and this correlation persisted after adjusting for confounders (r = 0.220, 95% CI [0.019, 0.073], p = 0.001). Ordinal logistic regression indicated 1.28 times higher odds of severe pneumonia with a larger diameter. The study highlights associations between mPAD, pneumonia, and severity, suggesting clinical relevance. Furthermore, the mPAD should be carefully considered in defining severity criteria for adverse outcomes in pneumonia patients. Further research is needed to refine clinical criteria on the basis of these findings.

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Loeys-Dietz syndrome (LDS) is an autosomal-dominant connective tissue disorder associated with mutations in the transforming growth factor ß receptor. It is characterized by distinctive craniofacial changes, skeletal features, and cardiovascular complications. We present a case of a 24-year-old male with development delay and a one-year history of progressively worsening dyspnea on moderate exertion and orthopnea. Echocardiography revealed right atrial and right ventricle dilation, right ventricle hypertrophy, atrial septal defect, and aneurysmal dilation of the pulmonary artery trunk. This case underscores the importance of early detection and comprehensive imaging in patients suspected of having LDS, particularly considering the potential for atypical vascular manifestations.

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Idiopathic pulmonary arterial hypertension is a serious condition that carries a poor prognosis. While exertional dyspnea is the most common symptom, angina like chest pain, most often due to right ventricle ischemia, may occur at advanced stages. We present a patient with pulmonary hypertension symptomatic for dyspnea and angina in whom computed coronary tomography angiography showed compression of the left main coronary artery by a large pulmonary artery aneurysm. Percutaneous coronary intervention and stenting was performed resulting in significant clinical improvement. This case emphasizes the role of different cardiovascular imaging modalities for the diagnosis of rare conditions.

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This clinical vignette describes the first case of a woman in his 40s with a set of congenital anomalies given by tetralogy of Fallot associated with aortic origin of the left pulmonary artery and uncorrected right aortic arch. All of these entities have a poor probability of survival in adulthood.

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Objetivo: Evaluar la utilidad de la estimación de la presión de la arteria pulmonar fetal obtenida por ecografía doppler como indicador de madurez fetal y su correlación con los resultados neonatales en un grupo de pacientes que asistan al área de sala de parto del Hospital Central de San Cristóbal, entre marzo y julio de 2023. Métodos: Se trata de un estudio observacional, descriptivo, correlacional. La muestra fue de 90 mujeres (90 fetos) con embarazo simple entre 34 y 40 semanas de gestación. Resultados: De las variables doppler analizadas, se evidenció que la presión de la arteria pulmonar fetal disminuyó significativamente (p < 0,001) con el avance de la edad gestacional. Se determinó que existe una asociación significativa inversa entre la presión de la arteria pulmonar fetal y la madurez fetal (p < 0,001), de manera que a menor valor de la presión de la arteria pulmonar fetal se tiene un mayor porcentaje de madurez fetal. Un punto de corte de la presión de la arteria pulmonar fetal ubicado en 55,9 mm Hg determinó la sensibilidad y especificidad más alta conjuntamente para el diagnóstico de madurez pulmonar fetal, siendo su sensibilidad de 93,75 % y especificidad de 80,77 %. Con un valor predictivo positivo de 92,31 % y un valor predictivo negativo de 84 %. Conclusión: La estimación de la presión de la arteria pulmonar fetal obtenida mediante ecografía doppler es útil como indicador de madurez fetal(AU)

Objective: To evaluate the usefulness of the estimation of fetal pulmonary artery pressure obtained by doppler ultrasound as an indicator of fetal maturity and its correlation with neonatal outcomes in a group of patients attending the delivery room area of the Hospital Central de San Cristobal, between March and July 2023. Methods: This is an observational, descriptive, correlational study. The sample consisted of 90 women (90 fetuses) with a single pregnancy between 34 and 40 weeks of gestation. Results: From the doppler variables analyzed, it was evidenced that the fetal pulmonary artery pressure decreased significantly (p < 0.001) with advancing gestational age. It was determined that there is a significant inverse association between fetal pulmonary artery pressure and fetal maturity (p < 0.001), such that the lower the fetal pulmonary artery pressure value, the higher the percentage of fetal maturity. A fetal pulmonary artery pressure cut-off point located at 55.9 mm Hg jointly determined the highest sensitivity and specificity for the diagnosis of fetal lung maturity, its sensitivity being 93.75% and specificity being 80.77%. With a positive predictive value of 92.31% and a negative predictive value of 84%. Conclusion: The estimation of fetal pulmonary artery pressure obtained by doppler ultrasound is useful as an indicator of fetal maturity(AU)

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Structural variants (SVs) pose a challenge to detect and interpret, but their study provides novel biological insights and molecular diagnosis underlying rare diseases. The aim of this study was to resolve a 9p24 rearrangement segregating in a family through five generations with a congenital heart defect (congenital pulmonary and aortic valvular stenosis and pulmonary artery stenosis), by applying a combined genomic analysis. The analysis involved multiple techniques, including karyotype, chromosomal microarray analysis (CMA), FISH, genome sequencing (GS), RNA-seq, and optical genome mapping (OGM). A complex 9p24 SV was hinted at by CMA results, showing three interspersed duplicated segments. Combined GS and OGM analyses revealed that the 9p24 duplications constitute a complex SV, on which a set of breakpoints matches the boundaries of the CMA duplicated sequences. The proposed structure for this complex rearrangement implies three duplications associated with an inversion of ~ 2 Mb region on chromosome 9 and a SINE element insertion at the more distal breakpoint. Interestingly, this genomic structure of rearrangement forms a chimeric transcript of the KANK1/DMRT1 loci, which was confirmed by both RNA-seq and Sanger sequencing on blood samples from 9p24 rearrangement carriers. Altogether with breakpoint amplification and FISH analysis, this combined approach allowed a deep characterization of this complex rearrangement. Although the genotype-phenotype correlation remains elusive from the molecular mechanism point of view, this study identified a large genomic rearrangement at 9p24 segregating with a familial congenital heart defect, revealing a genetic biomarker that was successfully applied for embryo selection, changing the reproductive perspective of affected individuals.

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We present the case of a 14-year-old adolescent boy with a history of poorly controlled asthma and a final diagnosis of a bridge bronchus associated with sling of the left pulmonary artery. Regarding the case report, we describe the characteristic findings in computerized tomography multidetector of the thorax, its classification, and the most relevant information about this malformation. Congenital malformations of the tracheobronchial tree may occur in the context of asymptomatic or symptomatic respiratory patients. These malformations may be associated with other vascular, tracheal, and syndromes with multiorgan involvement. Although most patients are asymptomatic, some of them will have nonspecific symptoms without a clear etiology or will be diagnosed incidentally during the diagnostic evaluation of other pathologies. It is important to know and recognize the normal anatomy and its variations, since radiology undoubtedly plays a fundamental role in the diagnosis and preoperative assessment of these malformations, which although they have low incidence, must be identified in a timely manner by the specialist in diagnostic images.

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OBJECTIVES: To characterize pulmonary artery Doppler flow profile (PAFP) patterns among infants receiving care in neonatal intensive care units and to examine the association of PAFP patterns with pulmonary and right ventricular (RV) hemodynamics. STUDY DESIGN: This is a retrospective study at 2 tertiary intensive care units over 4 years that included neonates who demonstrated a complete tricuspid regurgitation envelope on targeted neonatal echocardiography. Separate personnel reviewed TNEs to characterize PAFP patterns, divide cohort into PAFP groups, and measure quantitative indices of RV hemodynamics (RV systolic pressure, pulmonary artery acceleration time and its ratio with RV ejection time, tricuspid annular plane systolic excursion, and RV output), for intergroup comparisons. RESULTS: We evaluated TNEs from 186 neonates with median gestational age of 28.5 weeks (IQR, 25.9-35.9 weeks). Four distinct PAFP patterns were identified (A) near-isosceles triangle (22%), (B) right-angled triangle (29%), (C) notching (40%), and (D) low peak velocity (<0.4 m/s; 9%). Groups A-C demonstrated a stepwise worsening in all indices of PH, whereas pattern D was associated with lower tricuspid annular plane systolic excursion and RV output. Using common definitions of pulmonary hypertension (PH), pattern A performed best to rule out PH (sensitivity range, 81%-90%) and pattern C for diagnosing PH (specificity range, 63%-78%). CONCLUSIONS: Inspection of PAFP is a simple bedside echocardiography measure that provides clinically meaningful information on underlying RV hemodynamics and may aid in screening and monitoring of patients for PH in intensive care units.

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ABSTRACT Clinical data: A nine-month-old female infant diagnosed with transposition of the great arteries with symptoms of heart failure associated with cyanosis and difficulty in gaining weight was referred to our center with late diagnosis (at nine months of age). Chest radiography: Cardiomegaly; attenuated peripheral vascular markings. Electrocardiography: Sinus rhythm with biventricular overload and aberrantly conducted supraventricular extra systoles. Echocardiography: Wide atrial septal defect, ventricular axis torsion with concordant atrioventricular connection and discordant ventriculoarterial connection. Computed tomography angiography: Concordant atrioventricular connection, right ventricle positioned superiorly and left ventricle positioned inferiorly; discordant ventriculoarterial connection with right ventricle connected to the aorta and left ventricle connected to pulmonary artery. Diagnosis: Crisscross heart is a rare congenital heart defect, accounting for 0.1% of congenital heart diseases. It consists of the 90º rotation of ventricles' axis in relation to their normal position; therefore, ventricles are positioned in the superior-inferior direction rather than anterior-posterior. Most cases have associated cardiac anomalies, and in this case, it is associated with transposition of the great arteries. The complexity and rarity of its occurrence make diagnosis and surgical treatment challenging. Operation: Modified Senning procedure using the pericardial sac in the construction of a tunnel from pulmonary veins to the right atrium. Cardiopulmonary bypass time of 147 minutes with nine minutes of total circulatory arrest.

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BACKGROUND: Studies had previously identified three cardiogenic shock (CS) phenotypes (cardiac-only, cardiorenal, and cardiometabolic). Therefore, we aimed to understand better the hemodynamic profiles of these phenotypes in acute myocardial infarction-CS (AMI-CS) using pulmonary artery catheter (PAC) data to better understand the AMI-CS heterogeneity. METHODS: We analyzed the PAC data of 309 patients with AMI-CS. The patients were classified by SCAI shock stage, congestion profile, and phenotype. In addition, 24 h hemodynamic PAC data were obtained. RESULTS: We identified three AMI-CS phenotypes: cardiac-only (43.7%), cardiorenal (32.0%), and cardiometabolic (24.3%). The cardiometabolic phenotype had the highest mortality rate (70.7%), followed by the cardiorenal (52.5%) and cardiac-only (33.3%) phenotypes, with significant differences (p < 0.001). Right atrial pressure (p = 0.001) and pulmonary capillary wedge pressure (p = 0.01) were higher in the cardiometabolic and cardiorenal phenotypes. Cardiac output, index, power, power index, and cardiac power index normalized by right atrial pressure and left-ventricular stroke work index were lower in the cardiorenal and cardiometabolic than in the cardiac-only phenotypes. We found a hazard ratio (HR) of 2.1 for the cardiorenal and 3.3 for cardiometabolic versus the cardiac-only phenotypes (p < 0.001). Also, multi-organ failure, acute kidney injury, and ventricular tachycardia/fibrillation had a significant HR. Multivariate analysis revealed that CS phenotypes retained significance (p < 0.001) when adjusted for the Society for Cardiovascular Angiography & Interventions score (p = 0.011) and ∆congestion (p = 0.028). These scores independently predicted mortality. CONCLUSIONS: Accurate patient prognosis and treatment strategies are crucial, and phenotyping in AMI-CS can aid in this effort. PAC profiling can provide valuable prognostic information and help design new trials involving AMI-CS.

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Oxidative stress is involved in increased pulmonary vascular resistance (PVR) and right ventricular (RV) hypertrophy, characteristics of pulmonary arterial hypertension (PAH). Copaiba oil, an antioxidant compound, could attenuate PAH damage. This study's aim was to determine the effects of copaiba oil on lung oxidative stress, PVR, and mean pulmonary arterial pressure (mPAP) in the monocrotaline (MCT) model of PAH. Male Wistar rats (170 g, n = 7/group) were divided into four groups: control, MCT, copaiba oil, and MCT + copaiba oil (MCT-O). PAH was induced by MCT (60 mg/kg i.p.) and, after 1 week, the treatment with copaiba oil (400 mg/kg/day gavage) was started for 14 days. Echocardiographic and hemodynamic measurements were performed. RV was collected for morphometric evaluations and lungs and the pulmonary artery were used for biochemical analysis. Copaiba oil significantly reduced RV hypertrophy, PVR, mPAP, and antioxidant enzyme activities in the MCT-O group. Moreover, increased nitric oxide synthase and decreased NADPH oxidase activities were observed in the MCT-O group. In conclusion, copaiba oil was able to improve the balance between nitric oxide and reactive oxygen species in lungs and the pulmonary artery and to reduce PVR, which could explain a decrease in RV hypertrophy in this PAH model.

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Introduction: Right ventricular remodeling with subsequent functional impairment can occur in some clinical conditions in adults and children. The triggering factors, molecular mechanisms, and, especially, the evolution over time are still not well known. Left ventricular (LV) changes associated with right ventricular (RV) remodeling are also poorly understood. Objectives: The study aimed to evaluate RV morphological, functional, and gene expression parameters in rats submitted to pulmonary artery banding compared to control rats, with the temporal evolution of these parameters, and to analyze the influence of RV remodeling by pulmonary artery banding in rats and their controls over time on LV geometry, histology, gene expression, and functional performance. Methods: Healthy 6-week-old male Wistar-EPM rats weighing 170-200 g were included. One day after the echocardiogram, depending on the animals undergoing the pulmonary artery banding (PAB) procedure or not (control group), they were then randomly divided into subgroups according to the follow-up time: 72 h, or 2, 4, 6, or 8 weeks. In each subgroup, the following were conducted: a new echocardiogram, a hemodynamic study, the collection of material for morphological analysis (hypertrophy and fibrosis), and molecular biology (gene expression). The results were presented as the mean ± standard deviation of the mean. A two-way ANOVA and Tukey post-test compared the variables of the subgroups and evolution follow-up times. The adopted significance level was 5%. Results: There was no significant difference among the subgroups in the percentage of water in both the lungs and the liver (the percentage of water in the lungs ranged from 76% to 78% and that of the liver ranged from 67% to 71%). The weight of the right chambers was significantly higher in PAB animals in all subgroups (RV PAB weighed from 0.34 to 0.48 g, and control subjects, from 0.17 to 0.20 g; right atrium (RA) with PAB from 0.09 to 0.14 g; and control subjects from 0.02 to 0.03 g). In the RV of PAB animals, there was a significant increase in myocyte nuclear volume (97 µm3-183.6 µm3) compared to control subjects (34.2 µm3-57.2 µm3), which was more intense in subgroups with shorter PAB follow-up time, and the fibrosis percentage (5.9%-10.4% vs. 0.96%-1.18%) was higher as the PAB follow-up time was longer. In the echocardiography result, there was a significant increase in myocardial thickness in all PAB groups (0.09-0.11 cm compared to control subjects-0.04-0.05 cm), but there was no variation in RV diastolic diameter. From 2 to 8 weeks of PAB, the S-wave (S') (0.031 cm/s and 0.040 cm/s), and fractional area change (FAC) (51%-56%), RV systolic function parameters were significantly lower than those of the respective control subjects (0.040 cm/s to 0.050 cm/s and 61%-67%). Furthermore, higher expression of genes related to hypertrophy and extracellular matrix in the initial subgroups and apoptosis genes in the longer follow-up PAB subgroups were observed in RV. On the other hand, LV weight was not different between animals with and without PAB. The nuclear volume of the PAB animals was greater than that of the control subjects (74 µm3-136 µm3; 40.8 µm3-46.9 µm3), and the percentage of fibrosis was significantly higher in the 4- and 8-week PAB groups (1.2% and 2.2%) compared to the control subjects (0.4% and 0.7%). Echocardiography showed that the diastolic diameter and LV myocardial thickness were not different between PAB animals and control subjects. Measurements of isovolumetric relaxation time and E-wave deceleration time at the echocardiography were different between PAB animals and control subjects in all subgroups, but there were no changes in diastolic function in the hemodynamic study. There was also increased expression of genes related to various functions, particularly hypertrophy. Conclusion: 1) Rats submitted to pulmonary artery banding presented RV remodeling compatible with hypertrophy. Such alterations were mediated by increased gene expression and functional alterations, which coincide with the onset of fibrosis. 2) Structural changes of the RV, such as weight, myocardial thickness, myocyte nuclear volume, and degree of fibrosis, were modified according to the time of exposure to pulmonary artery banding and related to variations in gene expression, highlighting the change from an alpha to a beta pattern from early to late follow-up times. 3) The study suggests that the left ventricle developed histological alterations accompanied by gene expression modifications simultaneously with the alterations found in the right ventricle.

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Abstract Background: Coronavirus disease (COVID-19) can cause permanent damage to vascular structures by directly or indirectly affecting the cardiopulmonary system. Lipoprotein(a) [Lp(a)] is an important identified risk factor for vascular endothelial cell dysfunction. Objective: The aim of this study was to reveal the relationship between Lp(a) levels measured at the time of COVID-19 diagnosis and the pulmonary artery (PA) to the ascending aorta (Ao) ratio (PA:Ao ratio) in survivors evaluated by transthoracic echocardiography (TTE). Methods: The study sample consisted of 100 patients who recovered from COVID-19 in the past 3 to 6 months. The relationship between the change in the PA:Ao ratio (ΔPA:Ao) and the Lp(a) levels measured at the time of diagnosis was evaluated. Diameter measurements at baseline and follow-up were evaluated with TTE. Results: A significant increase was found in PA, Ao, and epicardial adipose tissue (EAT) thickness in TTE (p< 0.001 for all). There was a weak correlation between D-dimer and high-sensitivity cardiac troponin measured at the time of diagnosis and ΔPA:Ao and ΔEAT in survivors. However, a positive and strong correlation was observed between Lp(a) levels and ΔPa:Ao (r = 0.628, p< 0.001) and ΔEAT (r = 0.633, p< 0.001). Conclusion: There may be dysfunction in vascular structures due to COVID-19. For the first time in the literature, a strong correlation was shown between the Lp(a) levels measured at the time of diagnosis and ΔPA:Ao and ΔEAT values in patients with COVID-19.

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Left congenital diaphragmatic hernia (CDH) can lead to pulmonary arteries abnormalities in the contralateral and ipsilateral sides of the diaphragm. Nitric oxide (NO) is the main therapy used to attenuate the vascular effects of CDH, but it is not always effective. We hypothesized that the left and right pulmonary arteries do not respond similarly to NO donors during CDH. Therefore, vasorelaxant responses of the left and right pulmonary arteries to sodium nitroprusside (SNP, a NO donor) were determined in a rabbit experimental model of left CDH. CDH was surgically induced in the fetuses of rabbits on the 25th day of pregnancy. On the 30th day of pregnancy, a midline laparotomy was performed to access the fetuses. The fetuses' left and right pulmonary arteries were isolated and mounted in myograph chambers. Vasodilation was evaluated by cumulative concentration-effect curves to SNP. Protein expression of guanylate cyclase isoforms (GCα, GCß) and the α isoform of cGMP-dependent protein kinase 1 (PKG1α), and the concentration of NO and cGMP were determined in the pulmonary arteries. The left and right pulmonary arteries of newborns with CDH exhibited increased vasorelaxant responses to SNP (i.e. the potency of SNP was increased) compared to the control group. GCα, GCß, and PKG1α expression were decreased, while NO and cGMP concentrations were increased in the pulmonary arteries of newborns with CDH compared to the control group. The increased cGMP mobilization may be responsible for the increased vasorelaxant responses to the SNP in the pulmonary arteries during left CDH.

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