Disclaimer. The ESC Guidelines represent the views of the ESC and were produced after careful consideration of the scientific and medical knowledge, and the evidence available at the time of their publication. The ESC is not responsible in the event of any contradiction, discrepancy, and/or ambiguity between the ESC Guidelines and any other official recommendations or guidelines issued by the relevant public health authorities, in particular in relation to good use of healthcare or therapeutic strategies. Health professionals are encouraged to take the ESC Guidelines fully into account when exercising their clinical judgment, as well as in the determination and the implementation of preventive, diagnostic, or therapeutic medical strategies; however, the ESC Guidelines do not override, in any way whatsoever, the individual responsibility of health professionals to make appropriate and accurate decisions in consideration of each patient's health condition and in consultation with that patient and, where appropriate and/or necessary, the patient's caregiver. Nor do the ESC Guidelines exempt health professionals from taking into full and careful consideration the relevant official updated recommendations or guidelines issued by the competent public health authorities, in order to manage each patient's case in light of the scientifically accepted data pursuant to their respective ethical and professional obligations. It is also the health professional's responsibility to verify the applicable rules and regulations relating to drugs and medical devices at the time of prescription.

2022 ESC/ERS Guidelines for the diagnosis and treatment of pulmonary hypertension Developed by the task force for the diagnosis and treatment of pulmonary hypertension of the European Society of Cardiology (ESC) and the European Respiratory Society (ERS).

AstraZeneca, Biosensors, and The Medicines Company.

No abstract

Multiple studies have shown a correlation between high on-treatment platelet reactivity (HPR) and ischemic complications after percutaneous coronary interventions (PCI); however, the role of platelet reactivity testing in order to adjust clopidogrel dose is debated. We sought to determine whether a strategy incorporating platelet reactivity testing with the Multiplate analyzer to tailor the dose of clopidogrel is superior to standard clopidogrel treatment after PCI. Between May 2008 and June 2009, 192 consecutive patients undergoing PCI were randomized to a tailored treatment strategy using the Multiplate analyzer or to uniform administration of 75 mg clopidogrel. In the tailored group, platelet function was assessed 24 h after clopidogrel loading, and patients with HPR (>46 U) received an additional 600 mg loading dose and 150 mg clopidogrel thereafter for one month. The primary endpoint was the composite of cardiac death, myocardial infarction, ischemic stroke or definite/probable stent thrombosis during six months. In the tailored group, a repeated loading dose of 600 mg clopidogrel significantly decreased platelet reactivity in patients with HPR (61.0 U [IQR: 52.5-71.5] vs. 21.5 U [15.8-30.5]; P < 0.0001) that remained unchanged during the maintenance phase on 150 mg clopidogrel (25.0 U [IQR: 19.8-27.0]; P = 0.20). The incidence of the primary endpoint was significantly higher in the standard clopidogrel group as compared to the Multiplate-tailored arm (5.3% vs. 0%, P = 0.03). In parallel, MACCE-free survival significantly improved in patients with Multiplate-tailored therapy (Kaplan-Meier log-rank: P = 0.02). Increasing the dose of clopidogrel according to the Multiplate assay may reduce ischemic complications in patients on clopidogrel after PCI.