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Готові списки джерел за темами / Premature coronary atherosclerosis

Добірка наукової літератури з теми "Premature coronary atherosclerosis"

Автор: Grafiati

Опубліковано: 23 вересня 2022

Оновлено: 28 вересня 2022

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Статті в журналах з теми "Premature coronary atherosclerosis":

1

Turek, Łukasz, Anna Polewczyk, Marianna Janion, and Marcin Sadowski. "Coronary artery fistula and premature coronary atherosclerosis." Cardiology Journal 26, no. 3 (June 27, 2019): 296–97. http://dx.doi.org/10.5603/cj.2019.0059.

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2

Kaplan, Mehmet, Ozge Ozcan Abacýoglu, Fethi Yavuz, Gizem Ilgýn Kaplan, Betül Düzen, Nurbanu Bursa, and Ferhat Zorlu. "Intraocular pressure predicts premature coronary atherosclerosis." Revista da Associação Médica Brasileira 66, no. 12 (December 2020): 1707–11. http://dx.doi.org/10.1590/1806-9282.66.12.1707.

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SUMMARY OBJECTIVE: The aim of this study was to investigate the association between intraocular pressure (IOP) and premature atherosclerotic coronary artery disease (PACAD) by comparing central corneal thicknesses (CCTs) measurements. METHODS: One hundred-eighty-six subjects were enrolled in this cross-sectional study, 100 in the PACAD group and 86 in the control group. All participants underwent a physical examination and routine biochemical tests. Ophthalmological examinations, including IOP and CCTs measurements, were performed for each subject. Additionally, pulse wave velocity measurements were obtained and recorded. RESULTS: Participants with PACAD showed significantly higher IOP values than those without atherosclerosis (p = 0.001), and there was no statistically significant difference between the groups in terms of CCT (p = 0.343). Also, pulse wave velocity (PWV) values were statistically significantly higher in the PACAD group (p = 0.001). High IOP was not significantly associated with metabolic syndrome parameters (p > 0.05). CONCLUSIONS: A relationship was found between PACAD and IOP, but CCTs were not associated with PACAD. The IOP measurement is affected by CCT; therefore, CCT is used to correct IOP values. To our knowledge, this is the first study to report a positive relationship between PACAD and IOP based on CCTs measurements.

3

van den Handel Vestergaard, Majken, Ann Bovin, and Erik Lerkevang Grove. "Coronary Atherosclerosis and Aortic Valve Disease as Long-Term Sequelae of Radiation Therapy in Childhood." Case Reports in Cardiology 2021 (November 30, 2021): 1–2. http://dx.doi.org/10.1155/2021/9324573.

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Coronary atherosclerosis and valvular heart disease are rare, but potentially severe sequelae following mediastinal radiation therapy. We present a case of premature ischemic heart disease and severe aortic stenosis in a 40-year-old woman following radiation therapy in childhood. We stress the awareness of prior mediastinal radiation therapy as an important risk factor for premature coronary atherosclerosis and valvular heart disease, particularly in younger patients without classical risk factors for coronary artery disease.

4

Culebras, C., M. Irurita, J. Irurita, J. Fuentes, L. Lopez, C. Deniz, M. Martinez Saavedra, R. Chirino, and V. Nievo. "W01.15 Interleukin inflammatory phenotypes in premature coronary atherosclerosis." Atherosclerosis Supplements 5, no. 1 (April 2004): 4. http://dx.doi.org/10.1016/s1567-5688(04)90015-9.

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5

CULEBRAS, C. "W01.15 Interleukin inflammatory phenotypes in premature coronary atherosclerosis." Atherosclerosis 5, no. 1 (April 2004): 4. http://dx.doi.org/10.1016/s0021-9150(04)90015-9.

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6

Asanuma, Yu, Annette Oeser, Ayumi K. Shintani, Elizabeth Turner, Nancy Olsen, Sergio Fazio, MacRae F. Linton, Paolo Raggi, and C. Michael Stein. "Premature Coronary-Artery Atherosclerosis in Systemic Lupus Erythematosus." New England Journal of Medicine 349, no. 25 (December 18, 2003): 2407–15. http://dx.doi.org/10.1056/nejmoa035611.

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7

Rho, Young Hee, Cecilia P. Chung, Annette Oeser, Joseph Solus, Yu Asanuma, Tuulikki Sokka, Theodore Pincus, et al. "Inflammatory mediators and premature coronary atherosclerosis in rheumatoid arthritis." Arthritis & Rheumatism 61, no. 11 (November 15, 2009): 1580–85. http://dx.doi.org/10.1002/art.25009.

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8

Welson, GeorgeM, and AhmedA Reda. "Premature coronary atherosclerosis and its relation to familial hypercholesterolemia." Menoufia Medical Journal 35, no. 2 (2022): 331. http://dx.doi.org/10.4103/mmj.mmj_182_21.

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9

Farhat, Nada, Nathalie Thorin-Trescases, Guillaume Voghel, Louis Villeneuve, Maya Mamarbachi, Louis P. Perrault, Michel Carrier, and Eric Thorin. "Stress-induced senescence predominates in endothelial cells isolated from atherosclerotic chronic smokers." Canadian Journal of Physiology and Pharmacology 86, no. 11 (November 2008): 761–69. http://dx.doi.org/10.1139/y08-082.

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Age-associated telomere shortening leads to replicative senescence of human endothelial cells (EC). Risk factors for cardiovascular disease (CVD) accelerate ageing, while there is a concomitant rise in oxidative stress known to promote stress-induced senescence (SIS) in vitro. Of all risk factors for CVD, smoking is most associated with the development of inflammation and accelerated atherosclerosis due to a prooxidant–antioxidant imbalance. We tested the hypothesis that SIS predominates in EC isolated from chronic smokers with premature atherosclerosis undergoing coronary artery bypass graft surgery (CABG). We isolated and cultured EC from segments of internal mammary arteries from smoker, former smoker, and nonsmoker coronary patients. Senescence of EC was induced by serial passage and quantified by the measurement of telomere length and senescence-associated β-galactosidase activity. Compared with nonsmokers, smoker patients were 10 years younger at the time of CABG, evidence of premature atherosclerosis. Cellular senescence was independent of telomere length and directly related to oxidative damage. EC exhibited higher expression levels of markers of oxidative stress (lipid peroxydation level and caveolin-1 mRNA), inflammation (angiopoietin-like 2 mRNA), hypoxia (vascular endothelial growth factor (VEGF)-A mRNA), and cell damage (p53 mRNA). In conclusion, a high oxidative stress environment in EC isolated from atherosclerotic chronic smokers predisposes to SIS rather than replicative senescence.

10

Juneja, Manish, Pankaj Raut, Milind Lohkare, and Harshawardhan Dhanraj Ramteke. "Systemic Lupus Erythematosus and Atherosclerosis." Vidarbha Journal of Internal Medicine 32 (August 10, 2022): 129–31. http://dx.doi.org/10.25259/vjim_20_2022.

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Disorders likely ‘inflammatory’ in nature are known to be linked to accelerated atherosclerotic processes that increase the chances of cardiovascular disease. Systemic lupus erythematosus (SLE) is a well-known autoimmune disease for its ability to affect any organ and cause morbidity. One such major cause of morbidity and mortality in SLE is premature coronary heart disease. Inflammation is considered to be the main pathogenesis of atherosclerosis and an important risk factor for vascular disease. Many clinical trials and studies of epidemiological and pathogenesis-related factors revealed that there is a common link between the pathogenesis of autoimmune diseases such as SLE, causing inflammatory responses similar to those seen in atherosclerosis. In the following review article, we will describe how SLE, inflammation and its traditional risk factors, promotes atherosclerosis.

Більше джерел

Дисертації з теми "Premature coronary atherosclerosis":

1

Zeitouni, Michel. "Athérosclérose coronaire prématurée : facteurs de risque, pronostic, prévention et nouvelles approches mécanistiques." Thesis, Sorbonne université, 2021. http://www.theses.fr/2021SORUS526.

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Cette thèse s’est intéressée à la question de l’athérosclérose coronaire prématurée, du profil clinique et biologique des individus qui en sont touchés, avec une approche physiopathologique permettant d’évaluer la contribution de l’inflammation et l’âge vasculaire. Les études 1 et 2 ont décrit le profil cardiovasculaire à très haut risque de ces patients et les facteurs d’évolution péjorative sur le long-terme. Ces études ont démontré que l’athérosclérose coronaire est une maladie évolutive avec une atteinte multi artérielle rapide, menant à un taux de mortalité de 20 % sur 10 ans. L’étude 3 a démontré la contribution importante de l’inflammation infraclinique dans la genèse de l’athérosclérose coronaire chez les individus les plus jeunes, en comparaison avec les populations plus âgées. Cette observation a pu être effectuée grâce à l’utilisation d’un nouveau biomarqueur de l’inflammation chronique le GlycA, signal composite de la glycosylation des protéines de phase aiguë. L’étude 4 a mis en avant l’importante implication de l’ IL-1β dans la cascade inflammatoire post infarctus du myocarde, et son association avec la mortalité à court et long terme. L’étude 5 a évalué la rigidité de la racine de l’aorte mesurée en IRM comme nouveau marqueur de risque de la maladie coronaire prématurée, en ouvrant la voie vers une mesure intégrative du vieillissement vasculaire. Les études 6 et 7 ont mis en évidence la difficulté qu’ont les recommandations internationales américaines et européennes à détecter et traiter les individus à haut risque d’athérosclérose prématurés, et les opportunités manquées de traitement intensif après un premier infarctus du myocarde prématuré
This thesis focused on premature coronary atherosclerosis, the clinical and biological profile of affected individuals, with a pathophysiological approach aiming to assess the contribution of inflammation and vascular age. Studies 1 and 2 described the very high-risk cardiovascular profile of these patients and the factors of poor long-term outcomes. These studies have demonstrated that premature coronary atherosclerosis is a progressive disease with a rapid multi-arterial involvement, leading to a mortality rate of 20% over 10 years. Study 3 demonstrated the significant contribution of subclinical inflammation to the genesis of coronary atherosclerosis in younger individuals, compared with older populations. This observation relied on the use of a new biomarker of chronic inflammation, GlycA, a composite signal of the glycosylation of proteins in the acute phase. Study 4 demonstrated the significant involvement of IL-1β in the post-myocardial infarction inflammatory cascade, and its association with short and long-term death. Study 5 evaluated the stiffness of the aortic root measured by MRI as a new risk marker for premature coronary artery disease, introduction a new tool for an integrative measure of vascular aging. Studies 6 and 7 have highlighted the lack of performance of American and European international guidelines in detecting and treating individuals at high risk of premature atherosclerosis, and the missed opportunities for intensive treatment after a first myocardial infarction. premature

2

Ribeiro, Giovana Gomes. "Calcificação prematura de artérias coronárias no lúpus eritematoso sistêmico: associação com duração de doença e densidade mineral óssea." Universidade de São Paulo, 2009. http://www.teses.usp.br/teses/disponiveis/5/5145/tde-16062009-164313/.

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Objetivo: Avaliar a relevância de fatores de risco tradicionais para doença cardiovascular (FRC), fatores relacionados ao lúpus e densidade mineral óssea (DMO) na calcificação prematura de artérias coronárias (CAC) em mulheres jovens com lúpus eritematoso sistêmico (LES). Métodos: Noventa e quatro pacientes lúpicas do sexo feminino com duração de doença 5 anos e idade menor que 45 anos foram selecionadas consecutivamente para este estudo. Os fatores de risco cardiovascular analisados foram: diabetes mellitus, hipertensão arterial sistêmica, dislipoproteinemia, fumo, índice de massa corpórea (IMC), insuficiência ovariana e renal. Fatores de risco relacionados ao LES estudados foram: duração de doença, critérios ACR, SLICC/ACR modificado (excluindo escores relacionados à aterosclerose), SLEDAI, tratamento com glicocorticóide e ciclofosfamida. A densidade mineral óssea de corpo inteiro, coluna lombar e colo do fêmur foram realizadas por densitometria de dupla emissão de fontes de raios-X (DXA). Calcificação de artérias coronárias foi determinada usando tomografia computadorizada com 16 multidetectores. Resultados: Calcificação prematura de artérias coronárias foi identificada em 12 (12,7%) dos pacientes, havendo associação com maior freqüência de pacientes com FRC (p=0,008), maior número de FCR (p=0,003), idade (p=0,025), duração de doença (p=0,011) e SLICC (p=0,011). A análise individual dos FRC demonstrou que a presença de menopausa (p=0,036), dislipidemia (p=0,003) e hipertensão (p=0,006) foram significativamente associados com calcificação coronariana. Análise de regressão logística múltipla usando FRC, idade, duração de doença, SLICC e DMO de corpo inteiro revelou que apenas duração de doença (p=0,042) e DMO de corpo inteiro (p=0,023) permaneceram fatores significantes para calcificação coronariana. Conclusão: Identificamos que duração de doença e DMO reduzida são preditores independentes para calcificação coronariana prematura em mulheres jovens com LES, sugerindo um mecanismo subjacente comum
Objective: To evaluate the relevance of traditional cardiovascular risk factors (CVR), disease-related risk factors and bone mineral density (BMD) for premature coronary artery calcification (CAC) in young female systemic lupus erythematosus (SLE). Methods: Ninety-four female SLE patients 5 years disease duration and age <45 years were consecutively selected for this study. Cardiovascular risks (CVR) analyzed were: diabetes mellitus, arterial hypertension, dyslipoproteinemia, smoking, body mass index (BMI), ovarian and renal insufficiency. SLE-related risk factors evaluated were: disease duration, ACR criteria, modified SLICC/ACR (excluding atherosclerosis-related scores), SLEDAI, glucocorticoid and cyclophosphamide treatment. Bone mineral density (BMD) in whole body, lumbar spine and femoral neck was assessed by dual X ray absorptiometry (DXA). Coronary artery calcification was determined using the 16-slice multidetector computed tomography. Results: Premature coronary artery calcification was identified in 12 (12.7%) patients and was associated with a higher frequency of patients with CVR (p=0.008), a higher mean number of CVR (p=0.003), mean age (p= 0.025), mean disease duration (p=0.011) and mean SLICC (p=0.011). Individual analysis of CVR demonstrated that the presence of menopause (p= 0.036), dyslipidemia (p= 0.003) and hypertension (p=0.006) were significantly associated with coronary calcification. Additionally, premature calcification was associated with a lower whole body BMD (p=0.013). Multiple logistic regression analysis using CVR, age, disease duration, SLICC and whole body BMD revealed that only disease duration (p=0.042) and whole body BMD (p=0.023) remained significant factors for coronary calcification. Conclusion: We have identified that disease duration and decreased BMD are independent predictors for premature coronary calcification in young women with SLE, suggesting a common underlying mechanism

3

Lo, Man-Soi, та 羅文帥. "Variant of the β1-Adrenergic Receptor Gene and Risk Factors of Premature Coronary Atherosclerosis in Taiwanese Subjects". Thesis, 2001. http://ndltd.ncl.edu.tw/handle/38907055824502091928.

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Книги з теми "Premature coronary atherosclerosis":

1

Raggi, Paolo, and Luis D’Marco. Imaging for detection of vascular disease in chronic kidney disease patients. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0116.

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The well-known severity of cardiovascular disease in patients suffering from chronic kidney disease (CKD) requires an accurate risk stratification of these patients in several clinical situations. Imaging has been used successfully for such purpose in the general population and it has demonstrated excellent potential among CKD patients as well. Two main forms of arterial pathology develop in patients with CKD: atherosclerosis, with accumulation of inflammatory cells, lipids, fibrous tissue and calcium in the subintimal space, and arteriosclerosis. The latter is characterized by accumulation of deposits of hydroxyapatite and amorphous calcium crystals in the muscular media of the vessel wall, and is believed to be more closely associated with alterations of mineral metabolism than with traditional atherosclerosis risk factors. The result is the development of what appears to be premature arterial ageing, with loss of elastic properties, increased stiffness, and increased overall fragility of the arterial system. Despite intensifying research and increasing awareness of these issues, the underlying pathophysiology of the aggressive vasculopathy of CKD remains largely unknown. As a consequence, there are currently very limited pathways to prevent progression of vascular damage in CKD. The indications, strengths and weaknesses of several imaging modalities employed to evaluate vascular disease in CKD are described, focusing on coronary arterial circulation and the peripheral arteries, with the exclusion of the intracranial arteries.

Частини книг з теми "Premature coronary atherosclerosis":

1

Elliott, Perry, Pier D. Lambiase, and Dhavendra Kumar. "Familial hypercholesterolaemia." In Inherited Cardiac Disease, 343–48. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198829126.003.0012.

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Familial hypercholesterolaemia (FH) is an inborn error of metabolism that leads to accumulation of low-density lipoprotein cholesterol (LDL-C) particles in the blood and premature coronary artery atherosclerosis. This chapter covers the clinical criteria for the diagnosis of FH, the genetics that underpins the condition, cascade testing, premature coronary heart disease, and treatment methods.

2

Xia, Xiujuan, Linfang Zhang, Canxia Xu, Hao Hong, and Zhenguo Liu. "Helicobacter pyloriInfection and Endothelial Dysfunction." In Helicobacter pylori - From First Isolation to 2020 [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.97260.

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Endothelial cells play a critical role in maintaining the integrity of vascular structure and function. Endothelial dysfunction is closely associated with the development and progression of cardiovascular diseases (CVDs) like hypertension (HTN) and atherosclerosis. Gut microorganisms significantly contribute to atherosclerosis and related CVDs. Helicobacter pylori (H. pylori) colonizes in human gastric epithelium in a significant portion of general population in the world. Patients with H. pylori infection have significantly increased risk for CVDs including atherosclerosis, HTN, coronary heart disease, and cerebrovascular disease especially in younger patients (< 65 years old). H. pylori infection significantly impairs vascular endothelial function through multiple mechanisms including increased reactive oxygen species production and oxidative stress, inflammation, decreased nitric oxide formation, modification of the expression of cytokines and microRNAs, abnormalities of lipid and glucose metabolisms, and exosomes-mediated pathways. Endothelial dysfunction associated with H. pylori infection is reversible in both animal model and human subjects. Accumulating data suggests that H. pylori infection is an important risk factor for endothelial dysfunction and CVDs especially in young patients. Screening young male population for H. pylori infection and treating accordingly could be an effective approach for early prevention of CVDs especially premature atherosclerosis associated with H. pylori infection.

3

Espejo Paeres, Carolina, Breda Hennessey, Manel Sabaté, and Pilar Jimenez-Quevedo. "Percutaneous Coronary Intervention in Diabetic Patients." In Interventional Cardiology [Working Title]. IntechOpen, 2020. http://dx.doi.org/10.5772/intechopen.94533.

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Cardiovascular disease (CVD) is responsible for 30% of deaths worldwide and is the leading cause of premature mortality in patients with diabetes mellitus (DM). One of the main contributors to the increased atherothrombotic risk in DM patients relates to their pro- inflammatory and prothrombotic status that involves abnormalities in endothelial and vascular smooth muscle cells, in platelet function and the coagulation cascade. The characteristics of CAD in diabetic patients is distinctive and infers an increased risk. Likewise, CAD in diabetics is characterised by being diffuse, affecting the left main stem more frequently, involving multiple vessels, and also affecting the distal coronary tree. Percutaneous coronary intervention in diabetics has been shown to have less favourable long-term clinical outcomes, compared to non-diabetics. With the advent of improved stent designs and antiplatelet drugs; the percutaneous coronary intervention (PCI) results have improved in the diabetic population. However, one of the main determinants of poorer outcomes in DM is the progression of atherosclerosis, which is more pronounced in diabetics and remains the primary cause of cardiac events at one year follow up after percutaneous revascularisation. Whilst new generation of drug-eluting stents has narrowed the gap between surgery and PCI in diabetic patients, coronary artery bypass grafting (CABG) remains the gold standard in diabetics with diffuse multivessel coronary artery disease.

4

O. Konstantinov, Vladimir. "Familial Hypercholesterolemia: Three “under” (Understood, Underdiagnosed, and Undertreated) Disease." In Cardiovascular Risk Factors in Pathology. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.93042.

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Familial hypercholesterolemia (FH) is one of the most prevalent genetic disorders leading to premature atherosclerosis and coronary heart disease. The main cause of FH is a mutation in the LDL-receptor gene that leads to loss of function of these receptors causing high levels of blood cholesterol. The diagnosis of FH is not very easy. Wide screenings are needed to reveal high levels of LDL cholesterol among “healthy” population. If the patient has MI or stroke at an early age, high levels of LDL cholesterol, and tendon xanthomas, the diagnosis of FH becomes much more clear. Genetic testing is a gold standard in the diagnosis of FH. There are several factors, influencing the time course of FH. Smoking males with low levels of HDL cholesterol have an extremely higher risk of death than nonsmoking females with high HDL cholesterol. Management of FH includes low cholesterol diet, statin and ezetimibe treatment, PCSK inhibitors, and LDL aphaeresis. Early and effective treatment influences much the prognosis in FH patients.

5

Piepoli, Massimo F. "Introduction." In ESC CardioMed, edited by Massimo Piepoli, 841–46. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0207.

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Atherosclerotic cardiovascular disease, especially coronary disease, remains the leading cause of premature death worldwide. Cardiovascular disease affects both men and women; of all deaths that occur before the age of 75 years in Europe, 49% are due to cardiovascular disease in women and 40% in men. Cardiovascular disease mortality is changing, with declining age-standardized rates in most European countries, which remain high in Eastern Europe. Prevention works: 50% of the reductions seen in coronary disease mortality relate to changes in risk factors, and 40% to improved treatments. Preventive efforts should be lifelong, from birth (if not before) to old age. Population and high-risk preventive strategies should be complementary; an approach limited to high-risk persons will be less effective; and population education programmes are still needed. Despite gaps in our understanding, there is ample evidence to justify intensive public health and individual preventive efforts. There is still substantial room for improvement in risk factor control, not only at the population level but even in individuals at very high risk.