Advances in cardiology (Adv Cardiol )

Publisher: Blackwell Publishing

Description

This series is devoted to current problems in clinical and preventive cardiology. Edited or authored by renowned specialists, volumes in this series are designed to provide up-to-date and comprehensive coverage of a particular subject. Some volumes record the proceedings of important symposia. Special emphasis is given to new findings relating to diagnostic and therapeutic measures, cardiac pharmacology, and drug-disease interactions, and to the fundamental cellular and molecular pathophysiology underlying cardiovascular disease processes. Areas of interest range throughout the field of cardiology to include coronary artery disease, congenital and acquired valvular and other structural heart diseases, primary myocardial diseases and primary and secondary electrophysiological dysfunction.

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  • Website
    Advances in Cardiology website
  • Other titles
    Advances in cardiology
  • ISSN
    0065-2326
  • OCLC
    3490010
  • Material type
    Periodical
  • Document type
    Journal / Magazine / Newspaper

Publisher details

Blackwell Publishing

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    • Articles in some journals can be made Open Access on payment of additional charge
    • 'Blackwell Publishing' is an imprint of 'Wiley'
  • Classification
    ​ yellow

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: Atrial fibrillation (AF) is an extremely prevalent dynamic chronic disease often associated with underlying heart disease, making the management of AF challenging. The antithrombotic management - and in particular the use of antiplatelet agents herein - is challenging as it depends on the (adequate) assessment of the risk of stroke and major bleeding. We therefore focus on the current (recommended) use of antiplatelet agents, address the caveats, and provide clinical tools to assess risk of stroke and major bleeding. Furthermore, we discuss novel antithrombotic agents to provide a future perspective of the role of antiplatelet agents in the antithrombotic management of AF patients.
    Advances in cardiology 01/2012; 47:155-64.
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    ABSTRACT: For many years clopidogrel was the 'gold standard' ADP receptor antagonist in patients with coronary artery disease in combination with acetylsalicylic acid, i.e. in elective/stable patients after coronary stent implantation and in patients with acute coronary syndromes with/without percutaneous coronary intervention. For the latter group, in which the risk of atherothrombotic events is increased, the new ADP receptor-antagonists, e.g. prasugrel and ticagrelor, have shown their superiority over clopidogrel. This is mainly based on the fact that up to 30% of patients with acute coronary syndromes tend to be low- or non-responders to therapy due to non-genetic and/or genetic causes. Nevertheless, there is still room for the use of clopidogrel in the majority of patients with coronary artery disease. This review summarizes the latest knowledge of clopidogrel and its current indications.
    Advances in cardiology 01/2012; 47:31-8.
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    ABSTRACT: 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.
    Advances in cardiology 01/2012; 47:64-77.
  • [Show abstract] [Hide abstract]
    ABSTRACT: The antithrombotic activity of dipyridamole was initially discovered in an in vivo experiment about half a century ago. At that time science had not appreciated the complexity of the regulation of local thrombus formation. Inhibition of platelets has been the main focus for the prevention of arterial thrombus formation. Unfortunately, established in vitro test systems have to take away several important components of the hemostatic system. Rather than directly inhibiting platelet aggregation, dipyridamole amplifies endogenous antithrombotic systems and modulates or downregulates prothrombotic processes. While for many years the main focus had been on preventing acute thrombus formation in the case of a rupture of an atherosclerotic plaque in large coronary arteries, it now has been appreciated that perfusion of tissue and patency of small vessels and capillaries is equally important for preventing further damage to the tissue. Here dipyridamole was experimentally shown to improve perfusion and function in chronic hypoperfused tissue unrelated to its vasodilatory properties. Recently, several clinical trials have shown the benefit of dipyridamole when given in a formulation that assures a sufficient plasma concentration. Its potential to scavenge particularly peroxy radicals, its direct reduction of innate inflammation, and a chronic elevation of interstitial adenosine seems to be of more importance for the prevention of vascular and tissue damage than its adenosine- and prostacyclin-mediated antithrombotic effect. In its extended-release preparation with the tartaric acid nucleus, not only does it not seem to add significantly to the risk of bleeding, but seems to hold potential for protecting tissue from oxidative and metabolic stress.
    Advances in cardiology 01/2012; 47:78-86.
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    ABSTRACT: The unifying basis of acute coronary syndrome (ACS) is the complication of a vulnerable coronary plaque, an event primarily mediated by platelet activation. Three major pathways are predominantly involved in this process: thromboxane A(2) via the thromboxane A(2) receptor, adenosine diphosphate via the P2Y(12) receptor, and thrombin via the protease-activated receptor (PAR)-1, with the latter being the most potent platelet activator. Despite the effective inhibition of the first two pathways with aspirin and an expanding family of P2Y(12) inhibitors, respectively, the recurrence of ischemic events in patients with ACS remains high. There is also a growing concern regarding the safety profile in terms of bleeding with more powerful antiplatelet agents, which has tempered expectations of newly developed compounds. PAR-1 inhibitors are a novel class of antiplatelet agents that inhibit thrombin-mediated platelet activation. Preliminary data indicate that these compounds have the potential to improve ischemic prognosis without increasing the bleeding risk. In this chapter we will discuss the rationale for developing this novel class of antiplatelet agents and specifically, the two compounds in most advanced clinical development, vorapaxar and atopaxar.
    Advances in cardiology 01/2012; 47:87-99.
  • Advances in cardiology 01/2012; 47:1-4.
  • [Show abstract] [Hide abstract]
    ABSTRACT: Dual antiplatelet therapy with aspirin and a P2Y(12) receptor antagonist improves outcomes in patients with acute coronary syndrome and in those treated with percutaneous coronary intervention (PCI) and a coronary stent. Candidate gene and genome-wide association studies have found that common genetic polymorphisms of the cytochrome P450 (CYP) 2C19 isoenzyme that result in a loss of functional activity are associated with less exposure of clopidogrel active metabolite and a diminished antiplatelet effect. Meta-analyses of registries and genetic substudies of randomized clinical trials demonstrate that carriers of these polymorphisms who are treated with clopidogrel are at an increased risk of cardiovascular events, particularly stent thrombosis, compared with noncarriers. This deleterious effect appears to be attenuated in patients not treated with PCI. The influence of polymorphisms of other genes, such as ABCB1, is inconsistent across clinical studies. The clinical efficacy of the newer P2Y(12) antagonists prasugrel and ticagrelor do not appear to be affected by the CYP2C19 genotype, but these agents increase major bleeding not related to coronary artery bypass surgery. Although data from randomized clinical trials are currently lacking, these observations suggest that a pharmacogenomic-guided approach to antiplatelet therapy in acute coronary syndrome could potentially maximize ischemic benefit while minimizing bleeding risk.
    Advances in cardiology 01/2012; 47:100-13.
  • [Show abstract] [Hide abstract]
    ABSTRACT: Because platelet activation plays an important pathophysiological role in acute coronary syndromes, antiplatelet agents are a mainstay of cardiovascular therapy, both in high-risk primary prevention and in secondary prevention. This is usually done with aspirin in all such cases, and adding a P2Y(12) inhibitor in secondary prevention usually for 1 year after an acute coronary syndrome, especially after stent implantation. P2Y(12) inhibitors include ticlopidine (now rarely used), clopidogrel, prasugrel, and ticagrelor. In the setting of high-risk acute coronary syndromes treated with percutaneous coronary interventions, the addition of a glycoprotein IIb/IIIa antagonist, especially abciximab, is contemplated. Conversely, the role of antiplatelet therapy in preventing stroke after atrial fibrillation has been recently downgraded in most risk classes, in favor of anticoagulants. This chapter provides a general overview of the use of antiplatelet agents in heart disease.
    Advances in cardiology 01/2012; 47:5-19.
  • Article: Conclusion.
    Advances in cardiology 01/2012; 47:165.
  • [Show abstract] [Hide abstract]
    ABSTRACT: Ischemic stroke is a major cause of death and disability worldwide. Determination of the underlying stroke mechanism is critical for the optimization of treatment. The role of antiplatelet therapy in primary and secondary stroke prevention is of major significance. Antiplatelet agents predominantly in use are aspirin, clopidogrel, and combination regimens. Novel antiplatelet agents either in use or in advance clinical development seek an indication in the management of stroke patients; yet data are limited. The present review focuses on the optimization of antithrombotic therapy in the field of primary and secondary prevention of stroke, based on data obtained from randomized controlled trials and systemic reviews of the literature.
    Advances in cardiology 01/2012; 47:141-54.
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    ABSTRACT: Platelets play a critical role in the pathophysiology of acute coronary syndrome and thromboembolic complications associated with atrial fibrillation. Despite the development of newer and more potent antiplatelet agents, aspirin remains the cornerstone of antithrombotic therapy. Clinical trials conducted over the past decades have clearly established the safety and efficacy of aspirin therapy for the acute treatment and secondary prevention of acute myocardial infarction, ischemic stroke, and vascular death among patients at high risk for cardiovascular events. Although the absolute benefit of aspirin for primary prevention is lower than seen in secondary prevention trials, it is nevertheless an accepted preventive. This chapter provides a comprehensive overview of the clinical utility of aspirin in the setting of acute coronary syndrome and atrial fibrillation.
    Advances in cardiology 01/2012; 47:20-30.
  • [Show abstract] [Hide abstract]
    ABSTRACT: Antiplatelet therapy serves an important role in the management of acute coronary syndromes and in reducing the risk of thrombotic complications from atrial fibrillation. There has been rapid development of newer and more potent antiplatelet therapies over the last several years that have further reduced ischemic complications, but with a trade-off of increased bleeding risk. Bleeding complications associated with antiplatelet and anticoagulant therapies are associated with significantly increased risk of adverse outcomes, including death. Understanding the risk of bleeding associated with antiplatelet agents is critical to developing strategies to mitigate this risk.
    Advances in cardiology 01/2012; 47:125-40.
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    ABSTRACT: 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.
    Advances in cardiology 01/2011; 46:67-138.
  • [Show abstract] [Hide abstract]
    ABSTRACT: Obstructive sleep apnea (OSA) is currently considered to be an inflammatory disorder. Evidence suggests that the chronic intermittent hypoxia and, possibly, sleep loss and fragmentation associated with OSA increase the levels of various markers of inflammation, oxidative stress, and procoagulant and thrombotic activity. These alterations may contribute to the development of endothelial and metabolic dysfunction, atherosclerosis and cardiovascular disorders associated with OSA. However, these alterations are also associated with OSA comorbidities, making it difficult to discern which effects are attributable to OSA and/or these other conditions. Well-designed longitudinal and interventional studies that take confounding variables into account are needed to demonstrate a causal link between OSA and inflammation, to assess specific mechanisms that could explain these alterations and to address whether they may be improved by continuous positive airway pressure therapy.
    Advances in cardiology 01/2011; 46:43-66.
  • [Show abstract] [Hide abstract]
    ABSTRACT: 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.
    Advances in cardiology 01/2011; 46:197-266.
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    ABSTRACT: 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.
    Advances in cardiology 01/2011; 46:139-70.
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    ABSTRACT: 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.
    Advances in cardiology 01/2011; 46:171-95.
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    ABSTRACT: Obstructive sleep apnea (OSA) is characterized by repetitive episodes of complete and partial obstructions of the upper airway during sleep. The diagnosis of OSA requires the objective demonstration of abnormal breathing during sleep by measuring the respiratory disturbance index (RDI, events per hour of sleep), i.e. the frequency of apnea (complete upper airway obstruction), hypopnea (partial upper airway obstruction) and arousals from sleep related to respiratory efforts. OSA is defined by combining symptoms and an RDI ≥5 or by an RDI ≥15 without symptoms. The apnea-hypopnea index (AHI), the frequency of apnea and hypopnea events per hour of sleep, is widely used to define OSA (many clinical and epidemiological studies use this metric). In the general adult population, the prevalence of OSA defined by ≥5 apnea and hypopnea events per hour of sleep associated with excessive sleepiness is approximately 3-7% in men and 2-5% in women. The prevalence of OSA is much higher, e.g. ≥50%, in patients with cardiac or metabolic disorders than in the general population. Risk factors for OSA include obesity (the strongest risk factor), upper airway abnormalities, male gender, menopause and age (the prevalence of OSA associated with a higher risk of morbidity and mortality increases with age and peaks at approximately 55 years of age). OSA is associated with symptoms during sleep (snoring, choking and nocturia) and wakefulness (excessive sleepiness, fatigue and lack of energy) and with sequelae such as psychological changes, alterations in the quality of life, and social, familial and professional performance including vehicle and industrial accidents. The identification of OSA may be a difficult task for the clinician, even in populations in which OSA is highly prevalent such as patients with cardiovascular disorders because they may not present the cardinal signs of the disease, e.g. excessive sleepiness and obesity. Guidelines have been developed to tailor OSA therapy to patients according to the results of their disease evaluation and their preferences.
    Advances in cardiology 01/2011; 46:1-42.