Among patients with unstable angina or myocardial infarction without ST-segment elevation, prasugrel did not significantly reduce the frequency of the primary end point, as compared with clopidogrel, and similar risks of bleeding were observed. (Funded by Eli Lilly and Daiichi Sankyo; TRILOGY ACS ClinicalTrials.gov number, NCT00699998.).

BACKGROUND AND PURPOSE:Growing evidence of the relationship between poor antiplatelet response and occurrence of clinical events elicited the need of monitoring the response which has not been part of our daily practice. We present our initial experience with a new point-of-care antiplateletfunction test (VerifyNow assay) in neurointerventional procedures.

Vasospastic angina is a diagnosis of exclusion that manifests with signs and symptoms, which overlap with obstructive coronary artery disease, most often ST-segment elevation myocardial infarction. The pharmacotherapy that is available to treat vasospastic angina can help ameliorate angina symptoms. However, the etiology of vasospastic angina is ill-defined, making targeted pharmacotherapy difficult. Most patients receive pharmacotherapy that includes calcium channel blockers and/or long-acting nitrates. This article reviews the efficacy and safety of the pharmacotherapy used to treat vasospastic angina. High-dose calcium channel blockers possess the most evidence, with respect to decreasing angina incidence, frequency, and duration. However, not all patients respond to calcium channel blockers. Nitrates and/or alpha1-adrenergic receptor antagonists can be used in patients who respond poorly to calcium channel blockers. Albeit, evidence for use of nitrates and alpha1-adrenergic receptor antagonists in vasospastic angina is not as robust as calcium channel blockers and can exacerbate adverse effects when added to calcium channel blocker therapy. Despite having a clear benefit in patients with obstructive coronary artery disease, the benefit of beta-adrenergic receptor antagonists, statins, and aspirin remains unclear. More data are needed to elucidate whether or not these agents are beneficial or harmful to patients being treated for vasospastic angina. Overall, the use of pharmacotherapy for the treatment of vasospastic angina should be guided by patient-specific factors, such as tolerability, adverse effects, drug-drug, and drug-disease interactions.

Key considerations in antidepressant selection in the context of advanced HF include HF-related changes in drug pharmacokinetics that may affect initial dosing or dosage adjustment, possible drug interactions, adverse effects that may potentiate those induced by immunosuppressants added after transplantation, and tolerability issues.

Heparin‐induced thrombocytopenia (HIT) is a rare, potentially life‐threatening condition secondary to unfractionated heparin or low molecular weight heparin exposure. This immune‐mediated drug reaction manifests as thrombocytopenia with a paradoxical hypercoagulable state that can result in life‐threatening thrombosis. It is imperative to ensure cessation of heparin‐based products as soon as HIT is identified. Traditional treatment options include argatroban, bivalirudin, fondaparinux, and danaparoid with a transition to warfarin upon platelet recovery. These anticoagulants are notwithstanding limitations including parenteral administration and routine laboratory monitoring leading to prolonged hospitalizations, emphasizing the need for new therapies. Direct oral anticoagulants (DOACs) have been increasingly investigated for the management of HIT and may overcome the aforementioned challenges of current therapies. The objective of this narrative review is to summarize the current HIT guidelines, discuss limitations to contemporary treatment options, provide insight into the emerging evidence for the DOACs rivaroxaban, apixaban, and dabigatran, and conclude with a clinical summary for their use in this setting. The PubMed, Google Scholar, and MEDLINE databases were searched for peer‐reviewed literature from January 1, 2012, to June 31, 2018. Twenty‐seven articles met inclusion criteria for review: 1 prospective trial, 5 retrospective cohort studies, and 21 case reports totaling 104 patients treated with a DOAC for HIT. The DOACs prevented new and recurrent thrombosis in 98% (n=102) of cases, and bleeding complications occurred in 3% (n=3). While current literature remains limited, it is suggestive of a potential role of DOACs for HIT, which has led to their integration into the 2018 American Society Hematology Guidelines with a conditional recommendation.

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Cardiac allograft vasculopathy (CAV) is a major risk factor influencing graft loss and patient survival following orthotopic heart transplant. Allograft vasculopathy is a multifactorial process, which includes both immunologic and non-immunologic mechanisms. Given the non-immunological risk factors for vasculopathy, particularly hyperlipidemia, it is intuitive that reducing a patient's LDL would help attenuate the disease process. Multiple studies have shown benefits with the use of statin therapy. However, current heart transplant guidelines do not give a specific recommendation as to what LDL goal should be achieved in this patient population. This study is a retrospective cohort analysis designed to determine the relative risk of developing cardiac allograft vasculopathy with respect to different LDL goals. Median LDL level of <100 mg/dL was shown to significantly reduce the risk of developing cardiac allograft vasculopathy. Twelve of 37 patients with an LDL ≥100 mg/dL (32.4%) developed CAV vs 25 of 157 patients (15.9%) with an LDL <100 mg/dL (P = .021). Furthermore, a delay in to time to cardiac allograft vasculopathy was seen when a median LDL concentration of <100 mg/dL was achieved. This benefit was not extended when a goal concentration of <70 mg/dL was targeted.

Prasugrel exhibits favorable pharmacokinetic and pharmacodynamic properties compared to clopidogrel. These effects have translated to significant clinical benefits, despite the increased bleeding risk, in the context of ACS with primary PCI. Recent clinical trial evidence does not support the use of prasugrel in other ACS settings at this time, including medical management of non-ST segment elevation myocardial infarction and routine pretreatment prior to angiography. Careful patient selection for prasugrel is also imperative, taking into account the need for maintenance dose reductions in certain patient subgroups. Antiplatelet decision making for high-risk patients in the future may be facilitated with the use of both genotypic and phenotypic characteristics, including platelet function, and should be an imperative for future research efforts.