Many patients experience adverse events after discharge; numerous are medication related and preventable. The objective of this study is to evaluate the impact of pharmacist medication counseling and disease education at discharge. Pharmacist Assisting at Routine Medical Discharge is a prospective study of English- or Spanish-speaking adults discharged from internal medicine. Control patients received usual hospital discharge care; intervention patients received usual care with discharge counseling and a follow-up phone call. Evaluated outcomes included the following: 30-day hospital reutilization (combined readmissions/emergency department visits), pharmacist interventions, predictors for hospital utilization, patient satisfaction, and primary medication adherence. In all, 279 patients were enrolled: 139 in the control and 140 in the intervention group. Pharmacists made 198 interventions. The rate of hospital reutilization was 20.7% and similar between the intervention and control groups. Patients receiving the pharmacist intervention demonstrated improved primary medication adherence and increased patient satisfaction. Pharmacist-provided discharge counseling resulted in medication interventions, improved patient satisfaction, and increased medication adherence.

Nonsteroidal anti-inflammatory drugs (NSAIDs) are ubiquitous medications used by a wide range of people from otherwise healthy normotensive patients to hypertensive patients with many significant comorbidities. Through a variety of mechanisms related to prostaglandin inhibition, including sodium retention and vasoconstriction, these agents may increase blood pressure. This leads to potentially detrimental effects. A review of the current literature regarding this topic yielded 2 meta-analyses and 10 randomized controlled trials. There is evidence of small blood pressure increases in normotensive patients taking NSAIDs approximating +1.1 mm Hg. Patients with treated hypertension show variable increases with NSAID treatment, ranging up to +14.3 mm Hg for systolic pressure and +2.3 mm Hg for diastolic blood pressure. Most antihypertensive medications seem to have decreased effects with concomitant NSAID administration, with the exception of calcium channel blockers. Given the current literature, it appears that NSAIDs increase blood pressure in patients with controlled-hypertension, but the quantity of this increase is variable. If possible, patients who have hypertension should avoid taking NSAIDs.

Ticagrelor is a novel P2Y12 receptor antagonist which, like clopidogrel and prasugrel, functions by blocking adenosine diphosphate-mediated platelet aggregation. However, unlike the aforementioned agents, the binding of ticagrelor to this receptor is reversible. Ticagrelor is also believed to mediate some of its beneficial effects by augmenting the effects of adenosine, which is another unique pharmacologic property of this drug. In terms of antiplatelet effect, ticagrelor is more potent than clopidogrel and produces a faster and stronger inhibition of platelet aggregation. This may also be an advantage of ticagrelor over prasugrel, but this has not been adequately studied. Due to the reversible nature of the binding of ticagrelor to the platelet receptor, ticagrelor has a relatively fast offset of effect, with platelet aggregation approaching pretreatment levels about 3 days after discontinuation of therapy. This has advantages in patients requiring invasive procedures, but also makes medication adherence very important in order to be able to maintain an effective antiplatelet effect. Ticagrelor has been shown to be clinically superior to clopidogrel when given to patients with an acute coronary syndrome, resulting in significantly lower rates of myocardial infarction and vascular death. However, ticagrelor is indicated to be administered with aspirin, and the clinical benefits of ticagrelor may be less when daily dosages of aspirin exceed 100 mg. As expected, bleeding is the most common adverse effect with ticagrelor, although it occurs at rates comparable with those seen for clopidogrel with the exception of noncoronary artery bypass graft-related major bleeding and fatal intracranial bleeds, the latter of which occurs only rarely. Dyspnea is another common adverse effect with ticagrelor, although this is usually not severe and resolves with drug discontinuation. Unlike clopidogrel, there are no known pharmacogenomic concerns with ticagrelor, and emerging data suggest ticagrelor to be effective in patients resistant to clopidogrel, although more study is needed on this topic. While preliminary data suggest ticagrelor to be cost effective when compared with generic clopidogrel, the acquisition cost of ticagrelor is not insignificant and this will likely be an issue for many health care organizations. Currently, ticagrelor is well positioned to assume an active role in the treatment of coronary artery disease due to an impressive efficacy profile and reasonable safety. Its ultimate role in therapy will continue to evolve as studies on this drug continue eg, (Prevention of Cardiovascular Events in Patients with Prior Heart Attack Using Ticagrelor Compared to Placebo on a Background of Aspirin, PEGASUS) and more information hopefully becomes available on its use in clopidogrel nonresponders and relative safety and efficacy compared with prasugrel.

Patients with systolic heart failure are thought to be at increased risk for thromboembolic events. Although these patients may have increased hypercoaguable markers, the incidence of stroke is thought to be relatively low. Still, oral anticoagulation with warfarin is sometimes prescribed in these patients to prevent potential thromboembolic events. Current guidelines do not recommend warfarin use in patients with systolic heart failure unless indicated for other cardiovascular conditions. Several studies that have attempted to address this controversy have, as a whole, demonstrated that the rates of thromboembolic events in patients with systolic heart failure taking warfarin are similar to those in patients taking placebo, basically showing no additional protective benefit of warfarin. In addition, these studies have shown an increased risk of bleeding with warfarin. However, these trials are of poor quality to date. The 4 post hoc analyses in this article had warfarin added at the investigators' discretion and included patients with indications for warfarin, such as atrial fibrillation. The 3 randomized trials in this article did not attain enrollment numbers to reach any calculated power and were stopped early; thus, they were unable to detect a difference. Since warfarin has shown benefit in patients with atrial fibrillation and in mechanical heart valves to decrease the risk of thromboembolism, it might stand to reason that warfarin would have the same benefit in systolic heart failure patients without the above indications. However, given the current available data, warfarin is not supported in patients with systolic heart failure in the absence of an indication for this drug.