RESUMEN
OBJECTIVE: Effective time management is crucial for the survival of all patients, particularly those with cardiovascular conditions. This is especially true in the context of pre-hospital emergency services, where prompt intervention can significantly impact outcomes. This study delves into the timeliness of emergency services and the subsequent outcomes for hospitalized cardiovascular patients in EMS center in Fasa University of Medical Sciences, southern Iran. RESULTS: A total of 4972 emergency calls related to cardiac diagnoses were received between 2020 and 2023. The transport time was significantly correlated with age, location of the mission, and type of mission. Of the total, 86 underwent angioplasty within the standard time of less than 90 min, of which 81 were discharged and 5 died. 51 patients underwent angioplasty after more than 90 min, of which 47 were discharged and 4 died. In addition, 124 of these patients experienced cardiopulmonary resuscitation, of which 63 were successful and 61 were unsuccessful.
Asunto(s)
Servicios Médicos de Urgencia , Humanos , Irán/epidemiología , Servicios Médicos de Urgencia/estadística & datos numéricos , Masculino , Estudios Transversales , Femenino , Persona de Mediana Edad , Anciano , Adulto , Factores de Tiempo , Reanimación Cardiopulmonar , Enfermedades Cardiovasculares/terapia , Enfermedades Cardiovasculares/mortalidad , Tiempo de Tratamiento/estadística & datos numéricos , Anciano de 80 o más Años , Adulto JovenRESUMEN
Thirty percent of deaths worldwide are caused by cardiovascular disorders (CVDs). As per the WHO data, the number of fatalities due to CVDs is 17.9 million years, and it is projected to cause 22.2 million deaths by 2030. In terms of gender, women die from CVD at a rate of 51% compared to 42% for males. Most people use phytochemicals, a type of traditional medicine derived from plants, either in addition to or instead of commercially available medications to treat and prevent CVD. Phytochemicals are useful in lowering cardiovascular risks, especially for lowering blood cholesterol, lowering obesity-related factors, controlling blood sugar and the consequences of type 2 diabetes, controlling oxidative stress factors and inflammation, and preventing platelet aggregation. Medicinal plants that are widely known for treating CVD include ginseng, ginkgo biloba, ganoderma lucidum, gynostemma pentaphyllum, viridis amaranthus, etc. Plant sterol, flavonoids, polyphenols, sulphur compound and terpenoid are the active phytochemicals present in these plants. The aim of this article is to cover more and more drugs that are used for cardiovascular diseases. In this article, we will learn about the use of different herbal drugs, mechanism of action, phytochemical compounds, side effects, etc. However, more research is required to comprehend the process and particular phytochemicals found in plants that treat CVD.
RESUMEN
Background: Although the association between tuberculosis (TB) and cardiovascular disease (CVD) has been reported in several studies and is explained by mechanisms related to chronic inflammation, few studies have comprehensively evaluated the association between TB and CVD in Korea. Methods: Using the Korea National Health and Nutrition Survey, we classified individuals according to the presence or absence of previous pulmonary TB was defined as the formal reading of a chest radiograph or a previous diagnosis of pulmonary TB by a physician. Using multivariable logistic regression analyses, we evaluated the association between the 10-year atherosclerotic cardiovascular disorder (ASCVD) risk and TB exposure, as well as the 10-year ASCVD risk according to epidemiological characteristics. Results: Among the 69,331 participants, 4% (n = 3,101) had post-TB survivor group. Comparing the 10-year ASCVD risk between the post-TB survivor and control groups, the post-TB survivor group had an increased 10-year ASCVD risk in the high-risk group (40.46% vs. 24.00%, P < 0.001). Compared to the control group, the intermediate- and high-risk groups had also significantly increased 10-year ASCVD risks (odds ratio [OR] 1.14, 95% confidence interval [CI] 1.04-1.23 and OR 1.69, 95% CI 1.59-1.78, respectively) in the post-TB survivor group. In the association of CVD among post-TB survivors according to epidemiologic characteristics, age [adjusted OR (aOR) 1.10, 95% CI 1.07-1.12], current smoking (aOR 2.63, 95% CI 1.34-5.14), a high family income (aOR 2.48, 95% CI 1.33-4.62), diabetes mellitus (aOR 1.97, 95% CI 1.23-3.14), and depression (aOR 2.06, 95% CI 1.03-4.10) were associated with CVD in the post-TB survivor group. Conclusions: Our study findings suggest a higher 10-year ASCVD risk among TB survivors than healthy participants. This warrants long-term cardiovascular monitoring and management of the post-TB population.
RESUMEN
Platelet dysregulation is drastically increased with advanced age and contributes to making cardiovascular disorders the leading cause of death of elderly humans. Here, we reveal a direct differentiation pathway from hematopoietic stem cells into platelets that is progressively propagated upon aging. Remarkably, the aging-enriched platelet path is decoupled from all other hematopoietic lineages, including erythropoiesis, and operates as an additional layer in parallel with canonical platelet production. This results in two molecularly and functionally distinct populations of megakaryocyte progenitors. The age-induced megakaryocyte progenitors have a profoundly enhanced capacity to engraft, expand, restore, and reconstitute platelets in situ and upon transplantation and produce an additional platelet population in old mice. The two pools of co-existing platelets cause age-related thrombocytosis and dramatically increased thrombosis in vivo. Strikingly, aging-enriched platelets are functionally hyper-reactive compared with the canonical platelet populations. These findings reveal stem cell-based aging as a mechanism for platelet dysregulation and age-induced thrombosis.
Asunto(s)
Envejecimiento , Plaquetas , Diferenciación Celular , Células Madre Hematopoyéticas , Trombosis , Animales , Células Madre Hematopoyéticas/metabolismo , Plaquetas/metabolismo , Trombosis/patología , Trombosis/metabolismo , Ratones , Humanos , Megacariocitos/metabolismo , Ratones Endogámicos C57BL , Células Progenitoras de Megacariocitos/metabolismo , MasculinoRESUMEN
BACKGROUND: Patients with hidradenitis suppurativa (HS) often suffer from comorbid diabetes, metabolic syndrome, and hyperlipidemia and, therefore, are susceptible to the development of cardiovascular diseases (CVDs). Moreover, systemic inflammation plays a vital role in the development of atherosclerosis. The creation of atherosclerotic plaque is characterized by endothelial dysfunction driven by elevated concentrations of interleukin (IL)-1, IL-6, and IL-18 among others, as well as tumor necrosis factor (TNF) alpha. METHODS: This study aimed to assess the risk of HS patients developing CVDs. We performed a large-scale, propensity-matched global retrospective cohort study analyzing the risk of development of CVDs in patients suffering from HS. The analysis included 144,100 HS patients with 144,100 healthy controls (HC). The cohorts were matched regarding demographics and history of diseases relevant to CVDs, e.g., diabetes, obesity, and nicotine dependence. A total of 90 cardiovascular disorders were identified. The identification of cardiovascular disorders was based on ≥1% appearance of the event, based on absolute numbers, in both cohorts. RESULTS: Before the matching, HS patients displayed a higher frequency in excess weight or obesity (25 vs. 14.4%, respectively), nicotine dependence, and diabetes mellitus, but lower odds of primary hypertension in comparison to healthy controls. A total of 47 CVDs are associated with an increased risk of onset in HS patients. Although the highest hazard ratio (HR; 2.1; 95% CI: 1.95-2.269) was found for unspecified heart failure, the HS cohort was exceptionally predisposed to developing myocardial infarction (HR: 2.06; 95% CI: 1.88-2.27) and an acute embolism and deep vein thrombosis of the lower extremity (HR: 1.93; 95% CI: 1.74-2.14). CONCLUSIONS: This is the most extensive study on the association of HS with CVDs. We demonstrated that HS patients are at significantly greater risk of developing various CVDs compared to matched controls, with heart failure being the most common one.
Asunto(s)
Enfermedades Cardiovasculares , Hidradenitis Supurativa , Puntaje de Propensión , Humanos , Hidradenitis Supurativa/complicaciones , Hidradenitis Supurativa/epidemiología , Hidradenitis Supurativa/sangre , Estudios Retrospectivos , Masculino , Femenino , Adulto , Enfermedades Cardiovasculares/epidemiología , Enfermedades Cardiovasculares/etiología , Persona de Mediana Edad , Obesidad/complicaciones , Obesidad/epidemiología , Estudios de Casos y Controles , Diabetes Mellitus/epidemiología , Comorbilidad , Hipertensión/epidemiología , Hipertensión/complicaciones , Adulto Joven , Medición de Riesgo/estadística & datos numéricos , Infarto del Miocardio/epidemiología , Infarto del Miocardio/etiología , Factores de Riesgo , Insuficiencia Cardíaca/epidemiología , Insuficiencia Cardíaca/etiologíaRESUMEN
Diabetes is a major risk factor for cardiovascular disease. However, the exact mechanism by which diabetes contributes to vascular damage is not fully understood. The aim of this study was to investigate the role of SUMO-1 mediated SERCA2a SUMOylation in the development of atherosclerotic vascular injury associated with diabetes mellitus. ApoE-/- mice were treated with streptozotocin (STZ) injection combined with high-fat feeding to simulate diabetic atherosclerosis and vascular injury. Human aortic vascular smooth muscle cells (HAVSMCs) were treated with high glucose (HG, 33.3 mM) and palmitic acid (PA, 200 µM) for 24 h to mimic a model of diabetes-induced vascular injury in vitro. Aortic vascular function, phenotypic conversion, migration, proliferation, intracellular Ca2+ concentration, the levels of small ubiquitin-like modifier type 1 (SUMO1), SERCA2a and SUMOylated SERCA2a were detected. Diabetes-induced atherosclerotic mice presented obvious atherosclerotic plaques and vascular injury, companied by significantly lower levels of SUMO1 and SERCA2a in aorta. HG and PA treatment in HAVSMCs reduced the expressions of SUMO1, SERCA2a and SUMOylated SERCA2a, facilitated the HAVSMCs phenotypic transformation, proliferation and migration, attenuated the Ca2+ transport, and increased the resting intracellular Ca2+ concentration. We also confirmed that SUMO1 directly bound to SERCA2a in HAVSMCs. Overexpression of SUMO1 restored the function and phenotypic contractile ability of HAVSMCs by upregulating SERCA2a SUMOylation, thereby alleviating HG and PA-induced vascular injury. These observations suggest an essential role of SUMO1 to protect diabetes-induced atherosclerosis and aortic vascular injury by the regulation of SERCA2a-SUMOylation and calcium homeostasis.
RESUMEN
Objective: We aimed to investigate antiplatelet drug resistance utilizing light transmission-lumiaggregometry (LT-LA) and the Platelet Function Analyzer-100 (PFA-100) in patients undergoing cardiovascular surgery. Materials and Methods: The study included 60 patients diagnosed with stable coronary artery disease and peripheral vascular diseases that required surgery. Participants were divided into three groups: patients receiving aspirin (ASA) (n=21), patients receiving clopidogrel (CLO) (n=19), and patients receiving dual therapy (ASA+CLO) (n=20). Aggregation and secretion tests by LT-LA and closure time by the PFA-100 were used to measure antiplatelet drug resistance. Results: Based on the adenosine diphosphate (ADP)-induced aggregation test, 43% of patients were resistant to ASA, 22% to CLO, and 15% to dual therapy. Diabetes, hypertension, and hyperlipidemia were the most commonly identified comorbid disorders. In patients with comorbid risk factors, the median value of platelet aggregation response to ADP was significantly higher in the ASA group than in the CLO and dual therapy groups (p=0.0001). In patients receiving ASA monotherapy, the maximum amplitude of aggregation response to platelet agonists was ≥70% in 43% of patients for ADP and 28% for collagen by LT-LA. Elevated ADP (≥0.29 nmol) and collagen (≥0.41 nmol)-induced adenosine triphosphate release were found by LT-LA in 66% of patients utilizing an ADP agonist and 80% of patients using a collagen agonist undergoing ASA therapy. Closure times obtained with the PFA-100 were normal in 28% of patients using collagen-ADP cartridges and 62% of patients using collagen-epinephrine (CEPI) cartridges who received ASA. Recurrent thrombosis and bleeding were observed in 12 (20%) patients with cardiovascular disease. Three of these individuals (25%) showed ASA resistance with normal responses to ADP-induced aggregation (≥70%) and secretion (≥0.29 nmol), as well as normal CEPI closure times. Conclusion: Our findings suggest that antiplatelet drug monitoring by LT-LA and PFA-100 may be useful for high-risk and complicated cardiovascular patients.
Asunto(s)
Aspirina , Clopidogrel , Resistencia a Medicamentos , Inhibidores de Agregación Plaquetaria , Agregación Plaquetaria , Pruebas de Función Plaquetaria , Humanos , Clopidogrel/uso terapéutico , Clopidogrel/farmacología , Aspirina/uso terapéutico , Aspirina/farmacología , Femenino , Masculino , Inhibidores de Agregación Plaquetaria/uso terapéutico , Inhibidores de Agregación Plaquetaria/farmacología , Estudios Transversales , Anciano , Persona de Mediana Edad , Agregación Plaquetaria/efectos de los fármacos , Procedimientos Quirúrgicos Cardiovasculares/efectos adversos , Enfermedad de la Arteria Coronaria/cirugía , Enfermedad de la Arteria Coronaria/tratamiento farmacológicoRESUMEN
Cardiovascular disorders (CVD) are the primary cause of death worldwide. Multiple factors have been accepted to cause cardiovascular diseases; among them, smoking, physical inactivity, unhealthy eating habits, age, and family history are flag-bearers. Individuals at risk of developing CVD are suggested to make drastic habitual changes as the primary intervention to prevent CVD; however, over time, the disease is bound to worsen. This is when secondary interventions come into play, including antihypertensive, anti-lipidemic, anti-anginal, and inotropic drugs. These drugs usually undergo surgical intervention in patients with a much higher risk of heart failure. These therapeutic agents increase the survival rate, decrease the severity of symptoms and the discomfort that comes with them, and increase the overall quality of life. However, most individuals succumb to this disease. None of these treatments address the molecular mechanism of the disease and hence are unable to halt the pathological worsening of the disease. Gene therapy offers a more efficient, potent, and important novel approach to counter the disease, as it has the potential to permanently eradicate the disease from the patients and even in the upcoming generations. However, this therapy is associated with significant risks and ethical considerations that pose noteworthy resistance. In this review, we discuss various methods of gene therapy for cardiovascular disorders and address the ethical conundrum surrounding it.
Asunto(s)
Enfermedades Cardiovasculares , Terapia Genética , Humanos , Terapia Genética/métodos , Enfermedades Cardiovasculares/terapia , Enfermedades Cardiovasculares/genética , Vectores Genéticos , Animales , Calidad de VidaRESUMEN
Increased medical attention is needed as the prevalence of autism spectrum disorder (ASD) rises. Both cardiovascular disorder (CVD) and hyperlipidemia are closely associated with adult ASD. Shank3 plays a key genetic role in ASD. We hypothesized that Shank3 contributes to CVD development in young adults with ASD. In this study, we investigated whether Shank3 facilitates the development of atherosclerosis. Using Gene Set Enrichment Analysis software (Version No.: GSEA-4.0.3), we analyzed the data obtained from Shank3 knockout mice (Gene Expression Omnibus database), a human population-based study cohort (from Taiwan's National Health Insurance Research Database), and a Shank3 knockdown cellular model. Shank3 knockout upregulated the expression of genes of cholesterol homeostasis and fatty acid metabolism but downregulated the expression of genes associated with inflammatory responses. Individuals with autism had higher risks of hyperlipidemia (adjusted hazard ratio (aHR): 1.39; p < 0.001), major adverse cardiac events (aHR: 2.67; p < 0.001), and stroke (aHR: 3.55; p < 0.001) than age- and sex-matched individuals without autism did. Shank3 downregulation suppressed tumor necrosis factor-α-induced fatty acid synthase expression; vascular cell adhesion molecule 1 expression; and downstream signaling pathways involving p38, Jun N-terminal kinase, and nuclear factor-κB. Thus, Shank3 may influence the development of early-onset atherosclerosis and CVD in ASD. Furthermore, regulating Shank3 expression may reduce inflammation-related disorders, such as atherosclerosis, by inhibiting tumor necrosis factor-alpha-mediated inflammatory cascades.
Asunto(s)
Aterosclerosis , Trastorno del Espectro Autista , Trastorno Autístico , Enfermedades Cardiovasculares , Hiperlipidemias , Animales , Humanos , Ratones , Adulto Joven , Aterosclerosis/genética , Trastorno del Espectro Autista/genética , Trastorno Autístico/genética , Macrodatos , Proteínas de Microfilamentos , Proteínas del Tejido Nervioso/genética , Factor de Necrosis Tumoral alfaRESUMEN
Hypertrophic Cardiomyopathy (HCM) is a common inherited disorder that can lead to heart failure and sudden cardiac death, characterized at the histological level by focal areas of myocyte disarray, hypertrophy and fibrosis, and only a few disease-targeted therapies exist. To identify the focal and spatially restricted alterations in the transcriptional pathways and reveal novel therapeutic targets, we performed a spatial transcriptomic analysis of the areas of focal myocyte disarray compared to areas of normal tissue using a commercially available platform (GeoMx, nanoString). We analyzed surgical myectomy tissue from four patients with HCM and the control interventricular septum tissue from two unused organ donor hearts that were free of cardiovascular disease. Histological sections were reviewed by an expert pathologist, and 72 focal areas with varying degrees of myocyte disarray (normal, mild, moderate, severe) were chosen for analysis. Areas of interest were interrogated with the Human Cancer Transcriptome Atlas designed to profile 1800 transcripts. Differential expression analysis revealed significant changes in gene expression between HCM and the control tissue, and functional enrichment analysis indicated that these genes were primarily involved in interferon production and mitochondrial energetics. Within the HCM tissue, differentially expressed genes between areas of normal and severe disarray were enriched for genes related to mitochondrial energetics and the extracellular matrix in severe disarray. An analysis of the gene expression of the ligand-receptor pair revealed that the HCM tissue exhibited downregulation of platelet-derived growth factor (PDGF), NOTCH, junctional adhesion molecule, and CD46 signaling while showing upregulation of fibronectin, CD99, cadherin, and amyloid precursor protein signaling. A deconvolution analysis utilizing the matched single nuclei RNA-sequencing (snRNA-seq) data to determine cell type composition in areas of interest revealed significant differences in fibroblast and vascular cell composition in areas of severe disarray when compared to normal areas in HCM samples. Cell composition in the normal areas of the control tissue was also divergent from the normal areas in HCM samples, which was consistent with the differential expression results. Overall, our data identify novel and potential disease-modifying targets for therapy in HCM.
Asunto(s)
Cardiomiopatía Hipertrófica , Trasplante de Corazón , Humanos , Transcriptoma , Donantes de Tejidos , Cardiomiopatía Hipertrófica/genética , Células MuscularesRESUMEN
Background: Serum levels of branched-chain amino acids (BCAAs) are associated with various vital physiological functions and thus elevation in circulating levels results in several metabolic disturbances. Serum levels of BCAAs are strong predictors of various metabolic disorders. Their association with cardiovascular health is uncertain. The study aimed to investigate the association of BCAAs with circulating levels of vital cardiovascular and hepatic markers. Methods: The study population of 714 individuals was included from the population tested for the vital cardio and hepatic biomarkers at the Vibrant America Clinical Laboratories. The subjects were stratified into four quartiles based on the serum levels of BCAAs, and their association with vital markers was studied using the Kruskal-Wallis test. Pearson's correlation analyzed the univariant relationship of BCAAs with selected cardio and hepatic markers. Results: BCAAs exhibited a strong negative correlation with serum HDL. Serum triglycerides were found to have a positive correlation with serum levels of leucine and valine. Univariant analysis exhibited a strong negative correlation between serum levels of BCAAs and HDL, and a positive correlation was observed between triglycerides and amino acids isoleucine and leucine. Among analyzed hepatic markers, alanine transaminase exhibited a considerable association with BCAAs. Conclusions: The elevated levels of serum BCAAs are strongly associated with serum HDL and triglycerides. Consumption of these supplements must be in coordination with healthcare providers to avoid metabolic and cardiovascular risk.
RESUMEN
Large animal models of cardiac ischemia-reperfusion are critical for evaluation of the efficacy of cardioprotective interventions prior to clinical translation. Nonetheless, current cardioprotective strategies/interventions formulated in preclinical cardiovascular research are often limited to small animal models, which are not transferable or reproducible in large animal models due to different factors such as: (i) complex and varied features of human ischemic cardiac disease (ICD), which are challenging to mimic in animal models, (ii) significant differences in surgical techniques applied, and (iii) differences in cardiovascular anatomy and physiology between small versus large animals. This article highlights the advantages and disadvantages of different large animal models of preclinical cardiac ischemic reperfusion injury (IRI), as well as the different methods used to induce and assess IRI, and the obstacles faced in using large animals for translational research in the settings of cardiac IR.
Asunto(s)
Daño por Reperfusión Miocárdica , Humanos , Animales , Daño por Reperfusión Miocárdica/veterinaria , Modelos Animales de EnfermedadRESUMEN
Vitamin D deficiency and inadequate calcium intake are supposed to be potentially related to cardiovascular outcomes, however, their combined association with hypertension remains unclear. In this cross-sectional study among 2,352 subjects, dietary calcium intake was assessed by using a valid food frequency questionnaire, and serum 25-hydroxyvitamin D (25OHD) was measured by the Ultra Performance Liquid Chromatography system. Hypertension was defined as a level of systolic pressure ≥140 mmHg or diastolic pressure ≥90 mmHg, or both, or administration of antihypertensive medications. Vitamin D status was classified into deficiency (25OHD<20 ng/mL), insufficiency (20 ng/mL≤25OHD<30 ng/mL) and sufficiency (25OHD≥30 ng/mL), while dietary calcium intake was divided into tertiles as low, medium, and high. Two-way analysis of variance (ANOVA) and multivariable logistic regression models were adopted. A significant interaction between vitamin D status and dietary calcium intake in relations to systolic blood pressure (p=0.042) and hypertension (p=0.029) indicates the associations of dietary calcium intake with systolic blood pressure and hypertension depend on the vitamin D status, and vice versa. Only in the vitamin D deficiency group, dietary calcium intake was significantly associated with systolic blood pressure level (ß=-0.162, p<0.001) and prevalence of hypertension (odd ratio=2.20, p<0.001). The significance was not substantially compromised after further adjustment for confounding factors. In conclusion, the combination of vitamin D deficiency and low dietary calcium intake, rather than alone, is associated with hypertension.
Asunto(s)
Hipertensión , Deficiencia de Vitamina D , Humanos , Presión Sanguínea , Calcio , Calcio de la Dieta , Estudios Transversales , Vitamina D , Hipertensión/epidemiología , Hipertensión/etiología , Deficiencia de Vitamina D/complicaciones , Deficiencia de Vitamina D/epidemiología , VitaminasRESUMEN
BACKGROUND: The anion gap (AG) has been linked to the prognosis of many cardiovascular disorders. However, the correlation between albumin-corrected anion gap (ACAG) and 30 d all-cause mortality of intensive care patients with acute myocardial infarction (AMI) is unclear. Furthermore, owing to the lack of studies, it is also unknown whether ACAG is more accurate than AG in predicting the mortality of AMI. METHODS: The Medical Information Mart for Intensive Care IV (MIMIC IV) dataset was used to provide patient data in this retrospective cohort study. ACAG is computed using the formulae: [4.4-{albumin (g/dl)}] × 2.5 + AG. The primary outcome was 30 d all-cause mortality intensive care patients with AMI. To explore the prognostic worthiness of ACAG, the receiver operating characteristic curve, smooth curve fitting, Cox regression model, and Kaplan survival analysis was performed. RESULTS: We enrolled 2,160 patients in this study. ACAG had a better predictive value for 30 d all-cause mortality than AG, with an area under the curve of 0.66. The association between ACAG levels and overall mortality was nonlinear. In our model, after correcting for confounding factors, the ACAG was the independent predictor for 30 d all-cause mortality (HR 1.75, 95%CI 1.24, 2.47). ACAG K-M estimator curve analyses revealed that the group with ACAG ≥ 21.75 mmol/l had poor survival rate than the other group. CONCLUSIONS: High serum ACAG levels were a significant risk factor for 30 d all-cause mortality in critically ill patients with AMI. ACAG concentration and 30 d all-cause mortality had a nonlinear relationship. ACAG had better predictive value in identifying 30 d all-cause mortality of patients with AMI in ICU than the AG.
Asunto(s)
Equilibrio Ácido-Base , Infarto del Miocardio , Humanos , Estudios Retrospectivos , Enfermedad Crítica , Albúminas , Infarto del Miocardio/diagnóstico , Infarto del Miocardio/terapiaRESUMEN
The pressure exerted on the heart and blood vessels because of blood flow is considered an essential parameter for cardiovascular function. It determines sufficient blood perfusion, and transportation of nutrition, oxygen, and other essential factors to every organ. Pressure in the primary arteries near the heart and the brain is known as central blood pressure (CBP), while that in the peripheral arteries is known as peripheral blood pressure (PBP). Usually, CBP and PBP are correlated; however, various types of shocks and cardiovascular disorders interfere with their regulation and differently affect the blood flow in vital and accessory organs. Therefore, understanding blood pressure in normal and disease conditions is essential for managing shock-related cardiovascular implications and improving treatment outcomes. In this review, we have described the control systems (neural, hormonal, osmotic, and cellular) of blood pressure and their regulation in hemorrhagic/hypovolemic shock using centhaquine (Lyfaquin®) as a resuscitative agent.
RESUMEN
BACKGROUND: Individuals with mental health problems have been shown to have an increased risk of cardiovascular disorder (CVD), but little is known about the risk of early-onset CVD among those with intellectual disability. We aimed to investigate the association between intellectual disability and subsequent CVD, taking into consideration the severity of intellectual disability and neurodevelopmental and neurologic comorbidity. METHODS: This population-based cohort study used individual-level linked data from Danish national health registries. Participants were all live-born singletons born in Denmark during 1978-2016 (n = 2,288,393). Follow-up began from birth and continued until the onset of CVD, death, emigration, or December 31, 2018, whichever came first. Clinical diagnosis of any CVD or type-specific CVDs was identified in the Danish National Patient Register. Time-varying Cox regression analyses were used to estimate the hazard ratio (HR) of intellectual disability associated with overall and type-specific CVDs. RESULTS: A total of 11,954 individuals received a diagnosis of intellectual disability (7434 males and 4520 females). During a median follow-up time of 18.5 years (interquartile range, 18.1 years), 652 individuals with intellectual disability (5.5%) received a diagnosis of CVD (incidence rate, 2.4 per 1000 person-years), compared with 78,088 (3.4%) CVD cases in individuals without intellectual disability (incidence rate, 1.9 per 1000 person-years), corresponding to a HR of 1.24 (95% CI, 1.15-1.34). Increased risks of CVD were similar in both childhood (HR, 1.24; 95% CI, 1.08-1.43) and early adulthood (HR, 1.25; 95% CI, 1.14-1.38). For type-specific CVDs, intellectual disability was significantly associated with cerebrovascular disease (HR, 2.50; 95% CI, 2.02-3.10), stroke (HR, 2.20; 95% CI, 1.69-2.86), heart failure (HR, 3.56; 95% CI, 2.37-5.35), hypertensive disease (HR, 1.30; 95% CI, 1.22-1.39), and deep vein thrombosis (HR, 2.10; 95% CI, 1.60-2.75). Stratified HRs of overall CVD were 1.14 (95% CI, 1.01-1.30) for borderline/mild intellectual disability, 1.25 (95% CI, 1.01-1.54) for moderate intellectual disability, and 1.91 (95% CI, 1.47-2.48) for severe/profound intellectual disability. After the exclusion of individuals with neurodevelopmental and neurologic comorbidity, intellectual disability remained significantly associated with increased risks of CVD. CONCLUSIONS: Individuals with intellectual disability had increased risks of early-onset CVD, in particular, for cerebrovascular disease, stroke, heart failure, and deep vein thrombosis, and the risks also increased with the severity of intellectual disability. Our findings highlight the awareness of increased risks of CVD in intellectual disability patients.
Asunto(s)
Enfermedades Cardiovasculares , Trastornos Cerebrovasculares , Insuficiencia Cardíaca , Discapacidad Intelectual , Accidente Cerebrovascular , Trombosis de la Vena , Masculino , Femenino , Humanos , Adulto , Niño , Enfermedades Cardiovasculares/etiología , Estudios de Cohortes , Discapacidad Intelectual/epidemiología , Discapacidad Intelectual/complicaciones , Trastornos Cerebrovasculares/complicaciones , Insuficiencia Cardíaca/complicaciones , Accidente Cerebrovascular/complicaciones , Dinamarca/epidemiologíaRESUMEN
OBJECTIVES: Based on the angiogenetic, transcriptional profile of non-diseased and arteriosclerotic vessels, we aim to identify the leucocytic markers as a potential, minimal invasive tool supporting diagnosis of vascular pathology. METHODS: Transcriptional profiling was performed with Angiogenesis RT2 Profiler PCR (Polymerase Chain Reaction) array on three non-pathological and three arteriosclerotic vessels, followed by immunohistochemical staining. Based on these screening results, selected transcripts were employed for qPCR with specific primers and investigated on the blood RNA (RiboNucleic Acid) obtained from nine healthy controls and 29 patients with cardiovascular disorders. Thereafter, expression of these transcripts was investigated in vitro in human monocytes under calcification-mimicking conditions. RESULTS AND CONCLUSIONS: Transcriptional profiling on the vessels revealed that out of 84 targets investigated two were up-regulated more than 100-fold, 18 more than 30 and 15 more than 10, while the most noticeable down-regulation was observed by ephrin-A3 and platelet-derived growth factor alpha (PDGFA) genes. Based on the vessel results, investigations of the selected blood transcripts revealed that thrombospondin 1 (THBS1), thrombospondin 3 (THBS3), transforming growth factor, beta receptor 1 (TGFBR1), platelet-derived growth factor alpha, plasminogen activator, urokinase (PLAU) and platelet/endothelial cell adhesion molecule 1 (PECAM-1) were significantly elevated in cardiovascular blood as compared to corresponding controls. Induction of calcification-related conditions in vitro to human THP-1 monocytes led to noticeable modulation of these transcripts. Taken together, these data demonstrate that leucocytic THBS1, THBS3, TGFBR1, platelet-derived growth factor alpha, PLAU and PECAM-1 have a correlation with cardiovascular disorders and could be used as a supportive tool predicting development of this pathological condition.
Asunto(s)
Factor de Crecimiento Derivado de Plaquetas , Activador de Plasminógeno de Tipo Uroquinasa , Humanos , Molécula-1 de Adhesión Celular Endotelial de Plaqueta/genética , Molécula-1 de Adhesión Celular Endotelial de Plaqueta/metabolismo , Receptor Tipo I de Factor de Crecimiento Transformador beta/genética , Receptor Tipo I de Factor de Crecimiento Transformador beta/metabolismo , Factor de Crecimiento Derivado de Plaquetas/genética , Factor de Crecimiento Derivado de Plaquetas/metabolismo , Regulación hacia AbajoRESUMEN
Although COVID-19 is primarily a respiratory disease, it may affect also the cardiovascular system. COVID-19 patients with cardiovascular disorder (CVD) develop a more severe disease course with a significantly higher mortality rate than non-CVD patients. A common denominator of CVD is the dysfunction of endothelial cells (ECs), increased vascular permeability, endothelial-to-mesenchymal transition, coagulation, and inflammation. It has been assumed that clinical complications in COVID-19 patients suffering from CVD are caused by SARS-CoV-2 infection of ECs through the angiotensin-converting enzyme 2 (ACE2) receptor and the cellular transmembrane protease serine 2 (TMPRSS2) and the consequent dysfunction of the infected vascular cells. Meanwhile, other factors associated with SARS-CoV-2 entry into the host cells have been described, including disintegrin and metalloproteinase domain-containing protein 17 (ADAM17), the C-type lectin CD209L or heparan sulfate proteoglycans (HSPG). Here, we discuss the current data about the putative entry of SARS-CoV-2 into endothelial and smooth muscle cells. Furthermore, we highlight the potential role of long non-coding RNAs (lncRNAs) affecting vascular permeability in CVD, a process that might exacerbate disease in COVID-19 patients.
Asunto(s)
COVID-19 , Enfermedades Cardiovasculares , ARN Largo no Codificante , Humanos , SARS-CoV-2 , ARN Largo no Codificante/genética , Células Endoteliales/metabolismo , Peptidil-Dipeptidasa A/metabolismoRESUMEN
Intestinal microflora has been associated with obesity. While visceral fat is more strongly associated with cardiovascular disorder, a complication linked to obesity, than the body mass index (BMI), the association between intestinal microflora and obesity (as defined in terms of BMI) has been studied widely. However, the link between visceral fat area (VFA) and intestinal microflora has been little studied. In this study, we investigate the association between intestinal microflora and VFA and BMI using a longitudinal study on Japanese subjects with different VFA statuses (N = 767). Principal component analysis of the changes in intestinal microflora composition over the one-year study period revealed the different associations between intestinal microflora and VFA and BMI. As determined by 16S rRNA amplicon sequencing, changes in the abundance ratio of two microbial genera-Blautia and Flavonifractor-were significantly associated with VFA changes and changes in the abundance ratio of four different microbial genera were significantly associated with BMI changes, suggesting that the associated intestinal microbes are different. Furthermore, as determined by metagenomic shotgun sequences, changes in the abundance ratios of two Blautia species-Blautia hansenii and Blautia producta-were significantly and negatively associated with VFA changes. Our findings might be used to develop a new treatment for visceral fat.