The response to the comment regarding our article is accurate: chronic consumption of a 6% Hibiscus sabdariffa Linnaeus (HSL) infusion for one month in healthy rats reduces reactive oxygen species (ROS) [...].

Ingestion of Hibiscus sabdariffa L. (HSL) provides antioxidants with beneficial effects for several pathologies with underlying oxidative stress. However, excessive, chronic consumption of the antioxidant-rich diet with HSL in healthy rats may possibly induce reductive stress (RS) with damaging effects. The aim of this study was to evaluate if the consumption of an infusion of 6% HSL for two months alters the function and structure of the myocardium. A total of 24 male Wistar rats were divided into three groups: Control (C), HSL infusion at 6% for two months (HSL 6%), and a washout group that received HSL 6% for two months followed by two months of natural water (HSL ± 6%). Myocardial performance during ischemia–reperfusion (I/R) was evaluated by using the isolated Langendorff heart model, accompanied by surface electrocardiography and histopathological analyses. Chronic 6% HSL intake increased systolic pressure (p ≤ 0.03), NrF2 expression, and elevated coronary vascular resistance, while it depressed mechanical performance and led to bradycardia and critical, extended asystolic/sinus pauses. Histopathology showed dense, permanent networks of interstitial and perivascular collagen encapsulating the hypertrophied cardiomyocytes. Chronic 6% HSL infusion was associated with myocardial structural, mechanical, and hemodynamic alterations, and with electrical changes during I/R. The washout group showed possible partial functional differences associated with withdrawal, although interpretation is limited by the longer study period.

Hydrogen sulfide (H2S) is essential for renal function; however, it is toxic at high concentrations. H2S is increased during reductive stress (RS). Increased antioxidant capacity and reduced/oxidized glutathione (GSH/GSSG) characterize a rat model of RS associated with chronic consumption of 6% Hibiscus sabdariffa Linnaeus (HSL). Here, we evaluate if chronic consumption of an infusion of HSL causes kidney damage associated with an increase in H2S. Twenty-one Wistar rats were divided into three groups. Group 1: rats received plain tap water ad libitum (G1); Group 2: rats received an ad libitum infusion of 6% HSL for one month (G2); and Group 3: rats consumed a 6% HSL infusion for one month and were then given natural water for another month (G3). We evaluated renal vasodilatation, cystathionine-β-synthase (CBS), cystathionine-γ-lyase (CSE), 3-mercaptopyruvate-sulfur-transferase (3-MST), γ-glutamylcysteine synthetase (GCLC), Nrf2, total OXPHOS, H2S concentration, GSH/GSSG and oxidized/reduced thiols in the kidney. Renal vasodilatation and total OXPHOS in complex IV and I and oxidized/reduced thiols were decreased (p ≤ 0.01) but H2S, CBS, SCE, GCLC, and NrF2 expression and GSH/GSSG were increased (p ≤ 0.04). The HSL infusion provided cysteine that was metabolized by CBS and CSE, elevating chronic H2S and favoring renal damage.

Introduction: Marfan syndrome is a rare disease in which different metabolic pathways and immune mediators such as transforming growth factor (31, interleukins and metalloproteinases participate. Material and methods: Thoracic aortic rings were obtained from 20 healthy male Wistar rats weighing 350-400 g to evaluate vascular reactivity in the presence of serum from healthy subjects or patients with Marfan syndrome with or without transforming growth factor (31, verapamil, sodium nitroprusside and nitro-L-arginine methyl ester. Interleukins were determined by Enzyme-Linked Immunosorbent Assay in the serum, and the nitrates and nitrites ratio was evaluated by spectrometry. Metalloproteinases and inducible nitric oxide synthase were evaluated in the thoracic aorta aneurysm from patients with Marfan syndrome and healthy subjects by immunohistochemistry. Results: There was increased vasoconstriction, (p = 0.008) and decreased vasodilation (P = 0.01) in the presence of transforming growth factor (31, in aortas incubated with serum from patients with Marfan syndrome. Aortic rings from healthy subjects or Marfan syndrome incubated in the presence or absence of the combination of verapamil, transforming growth factor (31, sodium nitroprusside and nitro-L-arginine methyl ester (P = 0.001) showed a decrease in vasoconstriction and an increase in vasorelaxation. The concentration of interleukins-6 and c reactive protein and of the nitrates and nitrites ratio was increased in serum from Marfan syndrome (p <= 0.03). The Metalloproteinases and inducible nitric oxide synthase were increase in thoracic aortic from Marfan syndrome versus healthy subjects or, (P = 0.03 and P = 0.04 respectively). Conclusion: The increase in circulating active transforming growth factor (31 and the subsequent activation of its downstream signaling pathway could be involved in the pathogenesis of aortic aneurysms in human patients with Marfan syndrome contributing to the modulation of vascular reactivity in healthy aortas.

Marfan syndrome (MFS) results from heterogeneous mutations in fibrillin-1. This releases TGF-β1 contributing to thoracic aneurysms formation (TAA). Vit D might participate in this process. Here we evaluate whether vit D deficiency and alteration of the SERCA/IP3 axis result in increased Ca 2+ and lead to of vascular smooth muscle cell (VSMC) remodeling. We evaluated Vit D, Ca 2+ , β-Actin, laminin-𝛾-1, SERCA2, TGF-β1, fibronectin, COL IV, α-SMA, TGF-β1, troponin, IP3, MMPs expressions and activities, in homogenate from the TAA in 13 MFS patients versus 16 control subjects (CS). The results show that Vit D (p = 0.01) and SERCA2 (p = 0.01) were decreased (p = 0.1) but the MMP-1 (p = 0.03), -9 (p = 0.009), Ca 2+ (p = 0.005), β-actin (p = 0.01), myosin-p (p = 0.01), TGF-β1 (0.002), troponin (p = 0.03), IP3 (p = 0.03), α-SMA (p = 0.005), laminin-𝛾-1, (p = 0.01), fibronectin (p = 0.03) and Col IV (p = 0.03) were increased in MFS. MFS is an active cellular process in which the VSMCs of the aorta attempt to compensate for the instability of the extracellular matrix by increasing the contractile machinery. However, the attempt is disorganized due to inefficient Ca 2+ handling caused by decreased Vit D associated with increased TGF-β1. Therefore, VSMCs shift from a contractile to a secretory state and the condition evolves with fatal consequences for the patient.

Objetivo: El objetivo principal de este estudio es conocer los niveles de OPG y OPN, junto con la ORR, y evaluar su asociación con la puntuación SYNTAX y conocer el potencial de estas moléculas como marcadores predictivos de riesgo, ayudando en la estratificación del riesgo. Con el tiempo, podrían emplearse incluso antes de la angiografía para medir la gravedad de las lesiones coronarias. Métodos: Estudio prospectivo con 147 participantes, 101 (69%) eran hombres, con una edad promedio de 60 años. Se incluyeron tres grupos (1) pacientes con SCA sometidos a ICP (SCA-ICP), (2); pacientes sin SCA sometidos a angiografía coronaria por una indicación distinta a la isquemia y no sometidos a ICP (sin SCA sin) (3) un sujeto asintomático. Se midieron OPG, OPN. Se calcularon las puntuaciones ORR y SYNTAX. Se investigó la asociación entre los niveles de OPG y OPN y variables clínicas importantes. Resultados: Los niveles de OPG en el Grupo 1 fueron más bajos en comparación con los Grupos 2 y 3 (controles). Grupo 1 (490 pg/mL) versus Grupo 2 (829 pg/mL) versus Grupo 3 (845 pg/mL) [p = 0.001]). La OPG tuvo niveles más bajos en pacientes con estenosis de la arteria coronaria versus sin estenosis. Se mostró una disminución en la ORR en todos los grupos y no hubo asociación con la puntuación SYNTAX. Conclusiones: Los niveles de OPG OPN (y ORR) están disminuidos en pacientes con SCA y no muestran correlación con la puntuación SYNTAX. Como estudio exploratorio, nuestro trabajo sugiere que los niveles elevados de OPG y OPN en pacientes sin SCA pueden tener, de hecho, un efecto protector. Este estudio es uno de los pocos con un control adecuado en SCA y la reproducibilidad es necesaria principalmente con estudios multicéntricos.

The TRPV1 receptor is expressed on various cell types, including cardiomyocytes. Activation of TRPV1 leads to regulation of Ca²⁺ flux across both cell and mitochondrial membranes, which could control the ion flux under experimental systemic arterial hypertension (SAH), particularly in mitochondria, and thus prevent heart damage. In this study, SAH was induced in male Wistar rats using L-NAME, providing a system in which the regulatory action of nitric oxide (NO) is inhibited. The animals were divided into five groups: 1) Control (C), 2) Hypertensive (H), 3) H+Capsaicin (H+CS), 4) H+Capsazepine (H+CZ), and 5) H+CS+CZ. L-NAME was added to drinking water at a concentration of 200 mg/L for 40 days. Four days before the end of the L-NAME treatment, a daily subcutaneous dose of CS (5 mg/kg in the H+CS group), CZ (6 mg/kg in the H+CZ group), or a combination of CS+CZ was administered. We analyzed mitochondrial function and the damage caused by hypertension in the heart. The activation of TRPV1 under SAH conditions improved mitochondrial respiratory control, regulated oxidative stress, and modulated pro-apoptotic proteins. The improvement in mitochondrial metabolism led to the prevention of damage and better heart function.

Reductive stress (RS) results from the overactivity of the enzymatic and non-enzymatic antioxidant systems and from excess antioxidant agents that neutralize reactive oxygen species. Hibiscus sabdariffa Linnaeus (HSL) is a natural source of antioxidant molecules that can overload the antioxidant system. Twenty-one Wistar rats were divided into three groups: group 1 (G) G1: rats that consumed a 6% HSL infusion for one month (HSL + 6%), G2: rats that consumed a 6% HSL infusion for one month and were then given natural water for another month (HSL ± 6%), and G3: rats with natural drinking water. Renal vascular resistance (RVR) was evaluated through their responses to norepinephrine (Ne), acetylcholine (Ach), super oxide (O2−), hydrogen peroxide (H2O2), and peroxynitrite (ONOO−). The activity of antioxidant enzymes and oxidative stress markers was evaluated. RVR was increased by Ne and H2O2 (p = 0.03), but it was decreased by Ach, O2−, and ONOO− (p = 0.01). The reduced glutathione / oxidized glutathione (GSH/GSSG) ratio and nitrates/nitrites ratio, the total antioxidant capacity, the activities of superoxide dismutase, catalase, peroxidases, glutathione peroxidase, glutathione reductase, glucose-6-phosphate, and the expression of phosphorylated NrF2 were increased (p ≤ 0.04). However, the thiol groups, adenochrome, and glutathione-S-transferase were decreased (p = 0.01) in G1 vs. G2 and G3. The excessive consumption of antioxidants provided by a 6% HSL infusion results in RS contributing to a decrease in ROS.

BackgroundType 4 cardiorenal syndrome (CRS) involves cardiovascular alterations caused by chronic kidney disease (CKD). Fibroblast growth factor-23 (FGF23), carboxy-terminal propeptide of procollagen type I (PIP), and parathyroid hormone (PTH) have been proposed as biomarkers of pathological cardiac remodeling in CKD. In contrast, it has been suggested that MicroRNA 221 has a cardioprotective role. Available evidence shows that, 12 months after kidney transplantation (KT), type 4 CRS reverts in only half of the patients.ObjectiveTo assess long-term cardiac reverse remodeling after KT and its association with FGF23, PIP, and PTH levels.MethodsPatients with end-stage renal disease were assessed before and 28 months after KT using FGF23, PIP, and PTH serum concentrations and transthoracic echocardiography.ResultsFifty-three patients were followed for 28 months after KT. All the patients showed cardiac abnormalities upon inclusion. A follow-up assessment showed a reduction in left ventricle (LV) mass (121 ± 48 vs. 65 ± 14 gr/m2) and left atrial volume (46 vs. 30 ml/m2). The LV ejection fraction (53 vs. 63%), LV global longitudinal strain (-15.9 vs.-19.4%), and LV diastolic function improved. miR-221 expression increased after KT (8.73 RIQ= 3.7-25 vs. 40.16 RIQ= 24-223, p=0.001) and was correlated with the Ee´ratio (r= -0.32, p= 0.02). Multivariate analysis showed that post-KT LV mass was determined by pre-KT LV mass, serum Cr level, post-KT PIP, and hypertension (R2 = 0.65, F=12.1, p=0.001).ConclusionsContrary to other evidence, this study demonstrated that type 4 CRS is reversible over the long term. This is a paramount finding because KT normalizes cardiac structure and function independently of the severity of basal cardiac abnormalities.

Beals-Hecht (BH) syndrome is a rare autosomal dominant disorder caused by a mutation of the FBN-2 gene that codifies for fibrillin-2 (FBN-2). Its nosology includes congenital contractural arachnodactyly. The aim of this study was to evaluate the possible breakdown of redox homeostasis in the thoracic aortic aneurysm (TAA) from patients with BH. We determined OS markers such as malondialdehyde (MDA), total antioxidant capacity (TAC), carbonyl groups, glutathione (GSH), thiols the nitrate/nitrite ratio (NO3-/NO2-) and super oxide radical (O2-) by spectrophotometry in homogenized TAA from BH and the ascending fragment of the thoracic aorta (AFTA) from control subjects (CS). We also measured the activities of some of antioxidant enzymes such as GST, GPx, GR and TrxR. The super oxide dismutase (SOD) isoforms, catalase and peroxidase activities were evaluated by native polyacrylamide gels. The activities of the antioxidant enzymes GPx, TrxR, SOD isoforms, catalase and peroxidases were decreased in the TAA from patients with BH (p ≤ 0.04) and the OS markers NO3-/NO2-, TAC and thiols were decreased(p ≤ 0.04). In addition, O2- was increased in patients with BH (p = 0.02). The results suggest a possible loss of redox homeostasis; this loss could be due to the decrease of some of the enzymatic antioxidant system´s enzymes and some antioxidants of the non-enzymatic system. In addition, the decrease in TrxR activity and the concentration of thiol groups could contribute to the alteration and instability of the FBN-2 protein.

Beals-Hecht (BH) syndrome is a rare autosomal dominant disorder caused by a mutation of the FBN2 gene that codifies for fibrillin-2 (FBN-2) and part of its nosology is congenital contractural arachnodactyly. There is no information in the literature on whether there is increased oxidative stress (OS) in these patients that could lead to a break-down in the redox balance. Therefore, the aim of this preliminary study was to evaluate the possible breakdown of redox homeostasis in the thoracic aortic aneurysm (TAA) in BH. We determinate OS markers such as malondialdehyde (MDA), total antioxidant capacity (TAC), carbonyl groups, glutathione (GSH), thiols and the nitrate/nitrite ratio (NO3−/NO2−) by spectrophotometry in homogenized TAA from controls subjects (CS) and BH. We also measured the activities of some of antioxidant enzymes such as GST, GPx, GR and TrxR. The super oxide dismutase (SOD) isoforms, catalase and peroxidase activities were evaluated by native polyacrylamide gels. The activities of the antioxidant enzymes GPx and TrxR were decreased (p≤0.04) and the OS markers NO3−/NO2−, TAC and thiols groups were decreased (p≤0.04). The results suggest an intricate system in the loss of redox homeostasis in BH syndrome patients that could contribute to the FBN2 instability.

TRPV1 regulates neuronal and vascular function mediated by NO and CGRP. Systemic arterial hypertension (SAH) induces an imbalance in vascular mediators NO and CGRP by altering the transport of Ca2+ ions through TRPV1, generating cellular damage. We studied the effect of topical capsaicin (CS) treatment on cardiac mechanical work, oxidative stress (TAC, NO, BH4, and BH2), cellular damage (MDA, MTO, and 8HO2dG), and inflammation (IL-6 and TNFα), generated by SAH, which was induced by L-NAME, in male Wistar rats. CS was added to a moisturizing cream and applied to the abdomen of animals for two weeks. Experimental groups were as follows: (1) Control, (2) Control+Cream, (3) Hypertensive, and (4) Hypertensive+Cream. Hearts were exposed to ischemia-reperfusion (I-R) using the Langendorff technique to study the potential cardioprotection of CS. Expression of SOD1, SOD2, catalase, eNOS, pNOS, TRPV1, and CGRP in cardiac tissue was evaluated. In the Hypertensive group, TRPV1 activation by CS (Hypertensive+Cream) reduced oxidative stress (OS), decreasing cellular damage and inflammation and increasing TAC, modulating biochemical and tissue alterations induced by OS generated by SAH. In parallel, an increase in tissue levels and the expression of CGRP, TRPV1, and eNOS, induced by CS, was observed. These findings indicate that pretreatment with CS attenuates cardiac I-R and SAH injury in rats. The cardioprotective mechanism may be based on TRPV1-mediated CGRP overexpression.

Myocardial oxidative stress increases under conditions of hyperglycemia and ischemia/reperfusion (I/R) injury, leading to cellular damage. Inhibition of oxidative stress is involved in the cardioprotective effects of hydrogen sulfide (H2S) during I/R and diabetes, and H2S has the potential to protect the heart. However, the mechanism by which H2S regulates the level of cardiac reactive oxygen species (ROS) during I/R and hyperglycemic conditions remains unclear. Therefore, the objective of this study was to evaluate the cytoprotective effect of H2S in primary cardiomyocyte cultures subjected to hyperglycemia, hypoxia–reoxygenation (HR), or both conditions, by assessing the PPAR-α/Keap1/Nrf2/p47phox/NOX4/p-eNOS/CAT/SOD and the PPAR-γ/PGC-1α/AMPK/GLUT4 signaling pathways. Treatment with NaHS (100 μM) as an H2S donor in cardiomyocytes subjected to hyperglycemia, HR, or a combination of both increased cell viability, total antioxidant capacity, and tetrahydrobiopterin (BH4) concentrations, while reducing ROS production, malondialdehyde concentrations, 8-hydroxy-2′-deoxyguanosine, and dihydrobiopterin (BH2) concentrations. Additionally, the H2S donor treatment increased the expression and activity of PPAR-α, reversed the reduction in the expression of PPAR-γ, PGC-1α, AMPK, GLUT4, Nrf2, p-eNOS, SOD, and CAT, and decreased the expression of Keap1, p47phox and NOX4. Therefore, the treatment with the H2S donor protects cardiomyocytes from damage caused by hyperglycemia, HR, or both conditions by reducing oxidative stress markers and improving antioxidant mechanisms, thereby increasing cell viability and “cardiomyocyte ultrastructure”.

Background: Neonatal rats that receive sucrose during a critical postnatal period (CP, days 12 to 28) develop hypertension by the time they reach adulthood. Inflammation might contribute to changes during this period and could be associated with variations in the vascular smooth muscle (VSMC) phenotype. Objective: We studied changes in inflammatory pathways that could underlie the expression of the secretory phenotype in the VSMC in the thoracic aorta of rats that received sucrose during CP. Methods: We analyzed histological changes in the aorta and the expression of the COX-2, TLR4, iNOS, eNOS, MMP-2 and -9, and β- and α-actin, the quantities of TNF-α, IL-6, and IL-1β using ELISA, and the levels of fatty acids using gas chromatography. Results: The aortic wall presented disorganization, decellularization, and wavy elastic fibers and an increase in the lumen area. The α- and β-actin expressions were decreased, while COX-2, TLR4, TNF-α, and the activity of IL-6 were increased. Oleic acid was increased in CP in comparison to the control group. Conclusions: There is transient hypertension at the end of the CP that is accompanied by inflammation and a change in the phenotype of VSMC to the secretory phenotype. The inflammatory changes could act as epigenetic signals to determine the development of hypertension when animals reach adulthood.

SARS-CoV-2 is an obligatory intracellular pathogen that requires a lipid bilayer membrane for its transport to build its nucleocapsid envelope and fuse with the host cell. The biological membranes are constituted by phospholipids (PLs), and vitamin E (Vit E) protects them from oxidative stress (OS). The aim of this study was to demonstrate if treatment with Vit E restores the modified profile of the FA in PLs in serum from patients with coronavirus disease-19 (COVID-19). We evaluated Vit E, total fatty acids (TFAs), fatty acids of the phospholipids (FAPLs), total phospholipids (TPLs), 8-isoprostane, thromboxane B2 (TXB2), prostaglandins (PGE2 and 6-keto-PGF1α), interleukin-6 (IL-6), and C-reactive protein (CRP) in serum from 22 COVID-19 patients before and after treatment with Vit E and compared the values with those from 23 healthy subjects (HSs). COVID-19 patients showed a decrease in Vit E, TPLs, FAPLs, and TFAs in serum in comparison to HSs (p ≤ 0.01), and Vit E treatment restored their levels (p ≤ 0.04). Likewise, there was an increase in IL-6 and CRP in COVID-19 patients in comparison with HSs (p ≤ 0.001), and treatment with Vit E decreased their levels (p ≤ 0.001). Treatment with Vit E as monotherapy can contribute to restoring the modified FA profile of the PLs in the SARS-CoV-2 infection, and this leads to a decrease in lipid peroxidation, OS, and the inflammatory process.

Homeostasis constitutes a key concept in physiology and refers to self-regulating processes that maintain internal stability when adjusting to changing external conditions. It diminishes internal entropy constituting a driving force behind evolution. Natural selection might act on homeostatic regulatory mechanisms and control mechanisms including homeodynamics, allostasis, hormesis and homeorhesis, where different stable stationary states are reached. Regeneration is under homeostatic control through hormesis. Damage to tissues initiates a response to restore the impaired equilibrium caused by mild stress using cell proliferation, cell differentiation and cell death to recover structure and function. Repair is a homeorhetic change leading to a new stable stationary state with decreased functionality and fibrotic scarring without reconstruction of the 3-D pattern. Mechanisms determining entrance of the tissue or organ to regeneration or repair include the balance between innate and adaptive immune cells in relation to cell plasticity and stromal stem cell responses, and redox balance. The regenerative and reparative capacities vary in different species, distinct tissues and organs, and at different stages of development including ageing. Many cell signals and pathways play crucial roles determining regeneration or repair by regulating protein synthesis, cellular growth, inflammation, proliferation, autophagy, lysosomal function, metabolism and metalloproteinase cell signalling. Attempts to favour the entrance of damaged tissues to regeneration in those with low proliferative rates have been made; however, there are evolutionary constraint mechanisms leading to poor proliferation of stem cells in unfavourable environments or tumour development. More research is required to better understand the regulatory processes of these mechanisms.

Pharmacological preconditioning is an alternative to protect the heart against the consequences of damage from ischemia/reperfusion (I/R). It is based on the administration of specific drugs that imitate the effect of ischemic preconditioning (IPC). Peroxisomal proliferator-activated receptors (PPARs) can prevent apoptosis in pathologies such as I/R and heart failure. Therefore, our objective was to determine if the stimulation of PPARα with fenofibrate (feno) decreases the apoptotic process induced by hypoxia/reoxygenation (HR), high glucose (HG), and HR/HG. For that purpose, cardiomyocyte cultures were divided into the following groups: Group 1—control (Ctrl); Group 2—HR; Group 3—HR + 10 μM feno; Group 4—HG, (25 mM glucose); Group 5—HG + feno; Group 6—HR/HG, and Group 7—HR/HG + feno. Our results indicate that cell viability decreases in neonatal cardiomyocytes undergoing HR, HG, and their combination, while feno improved cell viability. Feno treatment decreased apoptosis compared with HG-, HR-, or HG/HR-vehicle-treated. Nuclear- and mitochondrial-apoptosis markers increased in neonatal cardiomyocytes from HR, HG, and HR/HG; while the cytotoxicity decreased in cells treated with feno. In addition, the expression of Bax, Bad, and caspase 9 decreased due to feno, while 14-3-3ɛ and Bcl2 were increased. Inner mitochondrial cytochrome C increased with feno in every condition, as well as mitochondrial activity. Feno treatment prevented injury in the ultrastructure and in the mitochondrial membranes. Thus, our results suggest that feno decreases apoptosis in neonatal cardiomyocytes, improving the ultrastructure of mitochondria in the pathological conditions studied.

Background: Takayasu arteritis (TA) affects medium and large caliber arteries causing stenosis, occlusion, or aneurysms. It has great predilection for the aortic arch, subclavian and extracranial arteries. The global prevalence is of 1% to 2% per million inhabitants, which varies by geographical region. The main cause of death in TA of cardiovascular origin and includes ischemic cardiomyopathy and valvular disease. The aim of this study was to evaluate the surgical experience according to the type of surgery in subjects with TA and with and without long-term inflammatory activity. Methods: This was a retrospective and descriptive, cross-sectional study, between 1969 and 2017. Patients with TA with more than 3 classification criteria according to the American College of Rheumatology were included. The type of surgery was classified as: organ preservation, cardiac, bypass, exclusion, and replacement. Inflammatory activity was evaluated. Results: A total of 41 patients were included, out of which 31 (76%) were women. The age at diagnosis was 29 +/- 10 years. The long-term survival rate according to the surgical procedure was in cardiac surgery of 15 years in 90% of cases, in organ preservation surgery of 35 years in 90%. Bypass, replacement, exclusion and other surgeries had a 100% survival at a follow-up of 48 years. Conclusions: There are different types of surgical approaches to treat the complexity of each TA patient. The surgical technique well selected by experts in cardiothoracic surgery offers an excellent long-term prognosis. Interventional management successfully resolves some arterial occlusive aspects. It is necessary to evaluate the appropriate use of surgical, interventional, and hybrid management through randomized clinical trials to evaluate their comparison with transparency.

Background/Objectives: Infective endocarditis (IE) most commonly results from infections by Gram-positive bacteria, and, in this condition, the redox homeostasis is lost due to the overproduction of H2O2, leading to the overstimulation of the immune system and the upregulation of the production of proinflammatory cytokines. The aim of this study was to evaluate the levels of oxidative biomarkers and the enzymatic and non-enzymatic antioxidant systems in subjects with IE. Methods: The study included three cases with IE that had undergone aortic valve replacement (AVR) surgery that was complicated by IE, comparing them with subjects with AVR without IE. We determined the malondialdehyde (MDA), total antioxidant capacity (TAC), carbonyl group concentration, glutathione (GSH), thiols and the nitrate/nitrite ratio (NO3−/NO2−) in homogenized tissue from the cardiac valves. We also measured the activity of glutathione-S-transferase (GST), glutathione peroxidase (GPx), glutathione reductase (GR) and thioredoxin reductase (TrxR). The superoxide dismutase (SOD) isoforms and peroxidase activity were determined using native gels. Results: There were increases in the activity of antioxidant enzymes such as GST, SOD isoforms and peroxidases (p ≤ 0.01) and decreases in oxidative stress markers such as GSH (p = 0.05); meanwhile, MDA and carbonylation were increased (p ≤ 0.05). Conclusions: The results suggest that bacterial infections favor oxidative stress in the aortic valves, which increases the SOD isoforms and peroxidase activity. This contributes to the loss of the intricate redox homeostasis system in patients with IE, causing a positive feedback loop in the oxidative background that results in damage to the heart, likely leading to a fatal outcome.

Neonatal rats that receive sucrose during a critical postnatal period (CP, days 12 to 28) develop hypertension by the time they reach adulthood. Changes during this period could contribute to inflammation and be associated with variations in the vascular smooth muscle (VSMC) phenotype. We studied changes in inflammatory pathways that could underlie the expressions of the secretory phenotype in the VSMC in the thoracic aorta of rats that received sucrose during CP. We analyzed histological changes in the aorta and expressions of the COX-2, TLR4, iNOS, eNOS, MMP-2, -9, β-, α-actin, and TNF-α, IL-6 and IL-1β expressions, and fatty acids by gas chromatography. The aortic wall presented disorganization, decellularization, wavy elastic fibers and increase in the lumen area. The COX-2, TLR4 expressions, TNF-α and IL-6 were increased, but iNOS, MMP-2 and -9 tended to increase and eNOS and arachidonic acid tended to decrease, con increase in oleic acid in CP in comparison with control group. There is a transient hypertension at the end of the CP that is accompanied by an inflammation and a change in the phenotype of VSMC to the secretory phenotype. The inflammatory changes could act as epigenetic signals to determine the hypertension development during adulthood.