Advances in Cardiology最新文献

{"title":"Antiplatelet therapy in acute coronary syndromes: ticagrelor.","authors":"Steen Husted","doi":"10.1159/000338055","DOIUrl":"https://doi.org/10.1159/000338055","url":null,"abstract":"<p><p>Ticagrelor is a direct-acting, oral, reversibly binding P2Y(12) receptor antagonist. As a cyclopentyltriazolopyrimidine, ticagrelor represents a new chemical class of agents that do not require metabolic activation and have consistent ability to inhibit platelet aggregation. The phase III PLATO study evaluated ticagrelor compared with clopidogrel in 18,624 patients with acute coronary syndromes, and demonstrated a significant reduction in the risk of death from vascular causes/myocardial infarction (MI)/stroke with ticagrelor (9.8 vs. 11.7% with clopidogrel; HR: 0.84; 95% CI: 0.77-0.92; p < 0.001) without a significant increase in PLATO-defined major bleeding (11.6 vs. 11.2%, respectively; p = 0.43). MI and death from vascular causes were separately significantly reduced, and death from any cause and stent thrombosis reductions achieved nominal statistical significance. Ticagrelor showed benefit over clopidogrel in almost all patient subgroups, including patients who had received clopidogrel at randomization, patients with both planned invasive or noninvasive treatment; patients with ST elevation myocardial infarction (STEMI) referred for primary percutaneous coronary intervention, patients with non-STEMI, and patients who underwent bypass surgery. Hence, the PLATO population reflected specifically those patients who would ordinarily receive thienopyridine-based antiplatelet therapy in a clinical setting.</p>","PeriodicalId":50954,"journal":{"name":"Advances in Cardiology","volume":"47 ","pages":"64-77"},"PeriodicalIF":0.0,"publicationDate":"2012-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000338055","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"30846002","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Stents and antiplatelet therapy.","authors":"Amir-Ali Fassa,&nbsp;Philip Urban","doi":"10.1159/000338054","DOIUrl":"https://doi.org/10.1159/000338054","url":null,"abstract":"<p><p>Coronary stents are used during the majority of percutaneous coronary interventions. When compared to medical therapy, they have been shown to decrease mortality for patients with acute coronary syndromes, and to improve symptom control in patients with stable angina. Their use, however, may be complicated by stent thrombosis (ST), a potentially fatal event. Early ST, which occurs during the first month following device implantation, is usually linked to procedural factors, with similar frequencies for bare metal stents and drug-eluting stents (DES). Late and very late (between 1 month and 1 year, respectively, and >1 year after the procedure) ST, which appear to be more frequent with DES, are due to factors such as incomplete stent apposition, delayed or dysfunctional endothelialization, and chronic inflammation. Furthermore, discontinuation of antiplatelet therapy (which includes the association of aspirin and thienopyridines) or resistance to these molecules may also lead to ST. New stent designs as well as the use of more potent antiplatelet therapies should contribute to reducing the incidence of ST in the future.</p>","PeriodicalId":50954,"journal":{"name":"Advances in Cardiology","volume":"47 ","pages":"114-24"},"PeriodicalIF":0.0,"publicationDate":"2012-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000338054","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"30846006","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Introduction. Antiplatelet therapy in ACS and A-Fib.","authors":"Victor L Serebruany,&nbsp;Dan Atar","doi":"10.1159/000338206","DOIUrl":"https://doi.org/10.1159/000338206","url":null,"abstract":"","PeriodicalId":50954,"journal":{"name":"Advances in Cardiology","volume":"47 ","pages":"1-4"},"PeriodicalIF":0.0,"publicationDate":"2012-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000338206","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"30846596","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The relationship between obstructive sleep apnea and cardiovascular and metabolic diseases is a topical subject of concern to a wide range of specialists and general practitioners. Introduction.","authors":"","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":50954,"journal":{"name":"Advances in Cardiology","volume":"46 ","pages":"XV"},"PeriodicalIF":0.0,"publicationDate":"2011-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"30291952","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Endothelial dysfunction in adults with obstructive sleep apnea.","authors":"","doi":"10.1159/000325108","DOIUrl":"https://doi.org/10.1159/000325108","url":null,"abstract":"<p><p>Vascular endothelial dysfunction refers to a loss of normal homeostatic functions in the blood vessels. It is characterized by reduced vasodilation and enhanced vasoconstriction functions and chronic prothrombotic and inflammatory activity. There is convincing evidence for endothelial dysfunction in obstructive sleep apnea (OSA): OSA is associated with alterations in vascular structures and their elastic properties, increased circulating cell-derived microparticles, reduced endothelial repair capacity, and vascular reactivity. These alterations may be related to the reduced availability of nitric oxide, which has major vasoprotective effects including vasodilation, inhibition of platelet adhesion and aggregation, inhibition of leukocyte-endothelial adhesion and inhibition of smooth muscle cell proliferation. It is unknown whether endothelial dysfunction in OSA is due to alterations in vasoconstriction mechanisms related to angiotensin II or endothelin 1. In OSA, endothelial dysfunction may be related to chronic intermittent hypoxia and to sleep loss and fragmentation. These conditions may increase the levels of various markers of inflammation and oxidative stress, as well as those of increased procoagulant and thrombotic activity. In addition, they may produce an imbalance of vasomotor function. Endothelial dysfunction contributes to the development of atherosclerosis and cardiovascular disorders associated with OSA. However, other diseases that are also associated with endothelial dysfunction are OSA comorbidities, e.g. obesity, insulin resistance, smoking habits and cardiovascular diseases such as hypertension and coronary artery disease. This makes it difficult to demonstrate a causal link between OSA and endothelial dysfunction; nevertheless, evidence for such a link has been produced by therapeutic studies. The administration of continuous positive airway pressure may reverse changes associated with endothelial dysfunction and, therefore, may decrease the risk of cardiovascular disease in OSA patients.</p>","PeriodicalId":50954,"journal":{"name":"Advances in Cardiology","volume":"46 ","pages":"139-170"},"PeriodicalIF":0.0,"publicationDate":"2011-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000325108","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"30214266","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hemodynamic and autonomic changes in adults with obstructive sleep apnea.","authors":"","doi":"10.1159/000325109","DOIUrl":"https://doi.org/10.1159/000325109","url":null,"abstract":"<p><p>Obstructive sleep apnea (OSA) is characterized by repetitive episodes of complete or partial obstruction of the upper airway during sleep that lead to an increase in airway resistance and respiratory effort. This may produce oxygen desaturation, hypercapnia and central nervous system arousal that restore airflow. OSA is associated with hemodynamic changes that are related to alterations in the activity of the autonomic nervous system. During the course of an apnea, the heart rate may slow down, increase or remain stable. The blood pressure decreases at the start of the apnea and increases at its terminal portion. When ventilation resumes, heart rate, blood pressure and ventilation reach a peak accompanied by an abrupt reduction in left ventricular stroke volume. During the early phase of apnea, sympathetic nerve activity (SNA) is suppressed; it then increases constantly and reaches a peak at the end of apnea and on arousal. As soon as ventilation resumes, there is an abrupt inhibition of SNA in the peripheral blood vessels. The resumption of ventilation occurs in the context of peripheral vasoconstriction and increased peripheral resistance. This situation persists for several seconds after the SNA has ceased, due to the kinetics of norepinephrine uptake, release and washout at the neurovascular junction. Hypoxemia, hypercapnia, lung inflation and blood pressure are important factors that may modulate these autonomic changes. The alterations in the autonomic nervous system are carried over into wakefulness and may contribute to the development of the cardiovascular disorders associated with OSA, including sympathovagal imbalance accompanied with changes in the baroreflex and chemoreflex. The hemodynamic and autonomic dysfunction associated with OSA is improved following treatment with continuous positive airway pressure.</p>","PeriodicalId":50954,"journal":{"name":"Advances in Cardiology","volume":"46 ","pages":"171-195"},"PeriodicalIF":0.0,"publicationDate":"2011-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000325109","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"30214267","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cardiovascular disorders associated with obstructive sleep apnea.","authors":"","doi":"10.1159/000325110","DOIUrl":"https://doi.org/10.1159/000325110","url":null,"abstract":"<p><p>Epidemiological, longitudinal and therapeutic studies have produced convincing evidence that obstructive sleep apnea (OSA) is associated with an increased risk of cardiovascular morbidity and mortality. The strongest evidence supports an independent causal link between OSA and arterial hypertension. OSA may be independently associated with an increased risk for ischemic heart disease, stroke, arrhythmias and mortality. It remains to be determined whether OSA is an independent cause of congestive heart failure and pulmonary hypertension. Confounders and methodological biases are the main reasons for the lack of definitive conclusions in causality studies. Longitudinal studies, adequately powered randomized controlled studies and therapeutic studies involving well-defined participants are all needed to definitively answer the questions surrounding the relationship between OSA and clinical cardiovascular outcomes, comorbidities and intermediate pathogenic mechanisms. OSA is a modifiable risk factor: continuous positive airway pressure administration, the gold standard treatment of OSA, may reduce the early signs of endothelial dysfunction and atherosclerosis, and improve cardiovascular outcomes, such as the mortality related to cardiovascular events, blood pressure, nonfatal coronary events and cardiac function in heart failure patients. However, cardiac patients may not display the typical signs and symptoms of OSA, such as an excessive body mass index and sleepiness. This fact, and the cardiovascular risk associated with OSA, underlines the need for collaborative guidelines to define a diagnostic strategy specifically oriented toward the evaluation of OSA in cardiovascular patients.</p>","PeriodicalId":50954,"journal":{"name":"Advances in Cardiology","volume":"46 ","pages":"197-266"},"PeriodicalIF":0.0,"publicationDate":"2011-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000325110","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"30214268","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Metabolic disorders associated with obstructive sleep apnea in adults.","authors":"","doi":"10.1159/000325106","DOIUrl":"https://doi.org/10.1159/000325106","url":null,"abstract":"<p><p>The relationship between metabolic disorders and obstructive sleep apnea (OSA) is multidirectional. Obesity is recognized as the strongest risk factor for OSA. It is unknown whether metabolic syndrome and insulin resistance/type 2 diabetes mellitus contribute to the development or aggravation of OSA, although this is likely. Conversely, OSA may be a risk factor for metabolic disorders. Strong evidence suggests that OSA may increase the risk of developing insulin resistance, glucose intolerance and type 2 diabetes mellitus. OSA has also been associated with the development and/or aggravation of obesity, dyslipidemia, metabolic syndrome and nonalcoholic fatty liver disease - a liver manifestation of metabolic syndrome. In addition, metabolic disorders are confounding factors in OSA. Metabolic disorders and OSA share common intermediate pathogenic pathways, including alterations in autonomic nervous system regulation, increased inflammatory activity, and alterations in adipokine levels and endothelial dysfunction, which may be involved in the interplay between these conditions. Overall, this complexity makes it especially difficult to reveal and understand the links between OSA and metabolic and cardiovascular disorders. The International Diabetes Federation has recently published clinical practice recommendations suggesting that OSA patients should be routinely screened for markers of metabolic disturbance and cardiovascular risk, such as waist circumference, blood pressure, and fasting lipid and glucose levels. It also recommends that the possibility of OSA should be considered in the assessment of all patients with type 2 diabetes mellitus and metabolic syndrome.</p>","PeriodicalId":50954,"journal":{"name":"Advances in Cardiology","volume":"46 ","pages":"67-138"},"PeriodicalIF":0.0,"publicationDate":"2011-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000325106","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"30214265","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Impact of metabolic syndrome in patients with acute coronary syndrome.","authors":"M. Feinberg, R. Schwartz, S. Behar","doi":"10.1159/0000115191","DOIUrl":"https://doi.org/10.1159/0000115191","url":null,"abstract":"The reported incidence of metabolic syndrome among patients with an acute coronary syndrome varies between 29 and 46%. The standard fasting cut-off levels for glucose and blood pressure cannot be applied on admission in patients with acute coronary syndrome and therefore modified criteria were used to define the metabolic syndrome. Patients with metabolic syndrome and acute coronary syndrome had increased incidence of heart failure, and worse long-term mortality compared to those without metabolic syndrome. However, they had less heart failure than those with known diabetes mellitus. Hyperglycemia as a risk factor for poor outcome is particularly significant in patients with metabolic syndrome. De novo identification of the metabolic syndrome on admission has the potential to improve risk stratification and management of patients with an acute coronary syndrome.","PeriodicalId":50954,"journal":{"name":"Advances in Cardiology","volume":"45 1","pages":"114-26"},"PeriodicalIF":0.0,"publicationDate":"2008-02-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"64394264","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hyperglycemia and the pathobiology of diabetic complications.","authors":"D. Aronson","doi":"10.1159/0000115118","DOIUrl":"https://doi.org/10.1159/0000115118","url":null,"abstract":"Both type I and type II diabetes are powerful and independent risk factors for coronary artery disease (CAD), stroke, and peripheral arterial disease. Atherosclerosis accounts for virtually 80% of all deaths among diabetic patients. Prolonged exposure to hyperglycemia is now recognized as a major factor in the pathogenesis of diabetic complications, including atherosclerosis. Hyperglycemia induces a large number of alterations at the cellular level of vascular tissue that potentially accelerates the atherosclerotic process. Animal and human studies have elucidated several major mechanisms that encompass most of the pathological alterations observed in the diabetic vasculture. These include: (1) Nonenzymatic glycosylation of proteins and lipids which can interfere with their normal function by disrupting molecular conformation, alter enzymatic activity, reduce degradative capacity, and interfere with receptor recognition. In addition, glycosylated proteins interact with a specific receptor present on all cells relevant to the atherosclerotic process, including monocyte-derived macrophages, endothelial cells, and smooth muscle cells. The interaction of glycosylated proteins with their receptor results in the induction of oxidative stress and proinflammatory responses. (2) Protein kinase C (PKC) activation with subsequent alteration in growth factor expression. (3) Shunting of excess intracellular glucose into the hexosamine pathway leads to O-linked glycosylation of various enzymes with perturbations in normal enzyme function. (4) Hyperglycemia increases oxidative stress through several pathways. A major mechanism appears to be the overproduction of the superoxide anion (O-2 ) by the mitochondrial electron transport chain. (5) Hyperglycemia promotes inflammation through the induction of cytokine secretion by several cell types including monocytes and adipocytes. Importantly, there appears to be a tight pathogenic link between hyperglycemia-induced oxidant stress and other hyperglycemia-dependent mechanisms of vascular damage described above, namely AGEs formation, PKC activation, and increased flux through the hexosamine pathway. For example, hyperglycemia-induced oxidative stress promotes both the formation of advanced glycosylation end products and PKC activation.","PeriodicalId":50954,"journal":{"name":"Advances in Cardiology","volume":"45 1","pages":"1-16"},"PeriodicalIF":0.0,"publicationDate":"2008-02-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/0000115118","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"64394167","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}