Advances in Cardiology

No abstract text is available yet for this article.

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...

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...

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...

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)...

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...

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...

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...

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...

Prasugrel is a third-generation thienopyridine which selectively inhibits the platelet P2Y(12) receptor more rapidly, more potently, and with less interindividual response variability compared with the second-generation thienopyridine clopidogrel. Large-scale phase III clinical testing showed that in high-to moderate-risk acute coronary syndrome patients undergoing percutaneous coronary intervention, prasugrel translates into a greater reduction in ischemic events, including stent thrombosis, in the short and long term compared to clopidogrel...

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...

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...

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...

No abstract text is available yet for this article.

No abstract text is available yet for this article.

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...

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...

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...

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...

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...