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INTRODUCTION: Antiplatelet therapy is the cornerstone of treatment for patients with acute coronary syndromes in the acute phase and in long-term management. Over the last few years, new antiplatelet drugs have been developed and the therapeutic landscape has rapidly evolved. AREAS COVERED: We review the available evidence and most recent data concerning all of the principal classes of antiplatelet agents, including aspirin, thienopyridines and glycoprotein IIb/IIIa inhibitors, as well the impact of the new drugs prasugrel and ticagrelor and the available data concerning cangrelor, elinogrel and PAR-1 inhibitors (still under development). EXPERT OPINION: This review considers the management of antiplatelet therapy in the light of recent advances, highlighting how to identify patients who will receive the greatest benefit from the older and newer agents, and underscoring the importance of carefully balancing the risks of ischaemia and bleeding in order to improve clinical outcomes. Finally, the paper discusses the potential role of functional and genetic tests in guiding the choice of antiplatelet therapy in a future perspective of 'personalised medicine'.

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Adenosine is widely used for the treatment of supraventricular tachycardias for its efficacy and excellent safety, but it has been reported to precipitate severe bronchospasm in patients with pulmonary disease. The drug is therefore contraindicated in asthmatic subjects and should be used with caution in patients with chronic obstructive pulmonary disease. Nevertheless, true bronchospasm is rare and should be distinguished from the much more common occurrence of dyspnea, only as a symptom and without respiratory compromise, which is benign and transient. We describe the occurrence of severe bronchospasm following adenosine administration for a supraventricular tachycardia in a young male without any history of pulmonary disease. To our knowledge, this is the first time such complication is reported in a subject without lung disease. The patient arrived at the emergency department for palpitations with a regular wide QRS tachycardia with a left bundle-branch block morphology. Sinus carotid massage was unsuccessful, and 2 intravenous adenosine boluses were given without effect. A further 12-mg bolus cardioverted the patient, who became increasingly dyspneic and hypoxic, with diffuse bronchospasm. An urgent chest radiograph had normal results. He was treated with oxygen and inhaled and intravenous steroids, but dyspnea and bronchospasm resolved only after intravenous aminophylline. The arrhythmia recurred and was finally terminated by intravenous flecainide. Although dyspnea after adenosine administration is usually a transient, benign phenomenon, physicians should be alert to the presence of objective signs of respiratory distress, which should prompt immediate treatment, even in subjects without previous history of pulmonary disease.

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The antiplatelet agent clopidogrel is an effective drug for the prevention of thrombotic events in patients with acute coronary syndrome and in those undergoing percutaneous coronary intervention with the deployment of a coronary stent. However, it has been reported that, despite adequate treatment, about 30% of patients continue to show the high degree of platelet reactivity that is central to the development of atherothrombotic complications and poorer clinical outcomes. Up to 13% of those taking clopidogrel experience a recurrent ischemic event during the first year after acute coronary syndrome, 1-3% experience subacute stent thrombosis after percutaneous coronary intervention probably due to a poor drug response, and about 1.5% experience major bleeding mainly due to an enhanced response. Recent research findings have highlighted the role of genetic variations in determining antiplatelet response variability, and this has aroused interest in genotyping all thienopyridine-eligible patients in order to identify those who would be at increased risk of harm if treated with clopidogrel. However, it remains to be determined whether this information is necessary or sufficient for risk stratification. Only when there are clinical data to support the hypothesis that genotype-guided therapy reduces the rate of ischemic and bleeding events will it be possible to justify the use of genetic testing in all potential patients. When that happens, genotype-guided antiplatelet therapy will also be available in the field of cardiovascular medicine.

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Atherosclerotic plaque instability is directly involved in triggering acute coronary syndromes, including unstable angina, acute myocardial infarction, and sudden coronary death. Different and not completely unknown mechanisms are involved in the pathogenesis of the destabilisation of the vulnerable plaque; currently three mechanisms are considered to play a causal role in this process: embolization, vasoconstriction and plaque rupture that only in a few cases lead to thrombosis; in most cases it is repaired spontaneously. Therefore only some plaques lead to clinical manifestations whereas many others remain asymptomatic. It is possible formulate two hypothesis: in the first case there are different types of plaques, some with strong thrombogenic stimulus; in the second case all the plaques are considered to be equal and instead is the patient who in particular situations has an hypercoagulable state that leads to an high risk of acute coronary syndromes. The aim of this review is to analyze the complex mechanisms leading to plaque and patient vulnerability.

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