The intended audience for this activity consists of medical directors, pharmacy directors, pharmacy benefit managers, and other managed care professionals who are involved with the treatment of patients with acute coronary syndrome.
Acute coronary syndrome (ACS) encompasses life-threatening cardiac disease states that include unstable angina (UA) and acute myocardial infarction (AMI). A person with AMI may present with ST-segment elevation MI (STEMI) or non-ST-segment elevation MI (NSTEMI) on electrocardiogram findings. The pathophysiology of UA, STEMI, and NSTEMI are similar in their initial courses in that there is plaque progression that may lead to incomplete or complete occlusion of the artery after thrombus formation. The typical symptoms with which patients often present include chest pain that radiates with increasing severity. Despite many recent advances in therapy, ACS continues to place substantial clinical and economic burdens on patients, the US healthcare system, and society as a whole. The estimated number of hospital discharges for patients with ACS was approximately 625,000 in 2010, with 58% of them men.1 In the United States, it is estimated that approximately 40% of the adult population (18 years and older) will have some form of cardiovascular disease (CVD) by the year 2030. In addition, the direct costs are projected to increase from $273 to $818 billion, with over 61% attributed to hospital costs, and indirect costs growing from $172 to $276 billion—the combination equaling approximately $1 trillion by 2030. Conversely, if appropriate prevention methods are implemented, it is projected that a 61% reduction in myocardial infarctions could occur over the next 30 years.2
According to the Guidelines
The most recent joint guidelines include recommendations regarding the use of the different P2Y12 inhibitors, and mainly recommend that dual antiplatelet therapies be utilized in patients with ACS. According to the 2014 American Heart Association/American College of Cardiology (AHA/ACC) guidelines, in patients with NSTEMI, clopidogrel or ticagrelor should be chosen over prasugrel as first-line agents, unless contraindicated, and patients undergoing percutaneous coronary intervention (PCI) with stenting can use any of the 3 agents.3 According to the 2013 American College of Cardiology Foundation (ACCF)/AHA guidelines, in patients presenting with STEMI in whom reperfusion therapy with primary PCI method will be required, any of the 3 antiplatelet agents—clopidogrel, prasugrel, or ticagrelor—can be utilized. In contrast, those with STEMI undergoing reperfusion with fibrinolytic therapy should only utilize clopidogrel. After fibrinolytic therapy, clopidogrel or prasugrel can be used. Since patients are at risk for subsequent cardiovascular events in the months following an AMI, secondary prevention with dual antiplatelet agents for up to a year post event is equally important. It should be noted that for post MI patients, the recommendation for therapy longer than 1 year remains unclear.4
Antiplatelet Therapy for ACS
An integral component of the appropriate management of ACS is the use of antiplatelet agents, and several novel antiplatelet agents have dramatically improved the therapy for ACS; however, the accurate and optimal use of available agents is necessary. The longest used antiplatelet still in use today in combination with other agents is acetylsalicylic acid (ASA), or aspirin. Aspirin inhibits the thromboxane A2-mediated pathway of platelet aggregation, thereby decreasing the risk of thrombus formation that may lead to a coronary event. Clopidogrel and ticlopidine were the first thienopyridine derivatives on the market, inhibiting the P2Y12 receptor that causes platelet aggregation; however, ticlopidine is rarely utilized due to its associated increased risk of hematologic adverse effects such as agranulocytosis, neutropenia, and thrombotic thrombocytopenic purpura.5,6 Prasugrel was the subsequent thienopyridine derivative and has been shown to be more potent and have a more rapid onset of action than clopidogrel.7 Ticagrelor is different in its mechanism of action since it is a reversible agent and it does not require metabolic activation, unlike clopidogrel and prasugrel, as it is not a prodrug. On the other hand, ticagrelor has a shorter half-life of 7 to 8 hours, and therefore requires twice-daily dosing versus once daily for clopidogrel and prasugrel.8 The introduction of vorapaxar is unique, because the agent is a potent and selective inhibitor of protease-activated receptor 1 (PAR-1), which provides an additional pathway of platelet inhibition.9-12
Cangrelor is the first intravenous (IV) P2Y12 inhibitor that was studied in the acute care setting post ACS event in 3 phase 3 randomized controlled trials.13-15 And most recently, elinogrel emerged in a phase 2b trial as an IV and oral P2Y12 inhibitor; the formulations are identical in nature for a theoretically seamless transition from in- to outpatient care.16 The FDA has not yet approved cangrelor or elinogrel, so their respective roles in therapy for patients with ACS have not yet been established. The following is a summary of the pivotal trials conducted on each of the agents noted above. Additionally, the cost of each antiplatelet is outlined in the
The Clopidogrel in Unstable angina to prevent Recurrent Events (CURE) was a randomized, double-blind, placebo-controlled trial conducted from 1998 to 2000 to establish the efficacy and safety of clopidogrel. The study compared early—within 24 hours of symptom onset—and long-term use of clopidogrel plus aspirin with aspirin alone in patients with UA and NSTEMI. The first primary outcome was the composite of death from CV causes, nonfatal MI, or stroke, and the second was refractory ischemia or the composite of the first primary outcome. Subjects were followed for a mean of 9 months. Clopidogrel was administered as a 300 mg loading dose and then 75 mg daily thereafter. There were 6259 subjects in the clopidogrel group and 6303 in the placebo group, with primary outcome results of 9.3% versus 11.4%, respectively (P <.001). Moreover, there was a lower percentage of subjects in the clopidgrel treatment group versus the placebo group who met the second primary outcome (16.5% vs 18.8%, respectively, P <.001). In addition, secondary outcomes such as severe ischemia (2.8% vs 3.8%, P = .003) and recurrent angina (20.9 vs 22.9, P = .01) were significantly fewer in the clopidogrel group. There was no statistical difference between the rates of stroke in either group. Regarding safety, there was a significantly higher percentage of major bleeding in the clopidogrel treatment group compared with the placebo group (3.7% vs 2.7%, P = .001).5 This study was the first to highlight the utility of clopidogrel in addition to aspirin, which is now used extensively in practice and recommended by the ACCF/AHA guidelines.3,4 To achieve a more rapid onset action of with clopidogrel, the CURRENT- OASIS 7 study was conducted from 2006 to 2009 comparing double-dose (600 mg on day 1, 150 mg on days 2 to 7, then 75 mg daily) versus standard-dose (300 mg on day 1, then 75 mg daily) clopidogrel, and high-dose (300 to 325 mg) versus standard-dose (75 to 100 mg) aspirin in patients undergoing PCI. The primary outcome was CV death, MI, or stroke within a 30- day time frame, with 25,086 subjects randomly assigned into 4 groups to test each combination of drugs. The study showed that the double dose of clopidogrel was superior to standard dosing, and there was no benefit or risk to using a higher dose of aspirin during PCI.6
Prasugrel (TRITON-TIMI 38)
The subsequent major oral antiplatelet that came to market was prasugrel, which drew attention after the Trial to Assess Improvement in Therapeutic Outcomes by Optimizing Platelet Inhibition with Prasugrel — Thrombolysis in Myocardial Infarction 38 (TRITON-TIMI 38), a randomized, double-blind, double-dummy, parallel-group trial conducted to test the superiority of prasugrel compared with clopidogrel in addition to aspirin. Prasugrel was dosed as a 60 mg loading dose followed by 10 mg daily, and clopidogrel as a 300 mg loading dose followed by 75 mg daily. The difference in this trial was that it not only included patients with UA and NSTEMI, but also those with STEMI, all of whom required PCI. The primary outcome was the time to the composite of CV death, nonfatal MI, or nonfatal stroke. Similar bleeding rates were hypothesized regarding the safety end points. The patients were then maintained on the antiplatelet they were randomized to and followed for a mean of 12 months. There were 13,608 patients included in the study and prasugrel had a significantly reduced primary efficacy end point compared with clopidogrel of 9.9% versus 12.1% (P <.001), in addition to secondary end points including target vessel revascularization (2.5% vs 3.7%; P <.001) and stent thrombosis (1.1% vs 2.4%; P <.001). However, the safety outcome showed that prasugrel significantly increased the risk of major (2.4% vs 1.8%; P = .03), life-threatening (1.4% vs 0.9%; P = .01), and fatal (0.4% vs 0.1%; P = .002) bleeding. The groups at higher risk of negative safety outcomes were those aged more than 75 years, or who weighed less than 60 kg, or who had a history of stroke.7
Because clopidogrel and prasugrel are both nonreversible thienopyridines with different pharmacokinetic properties, the introduction of ticagrelor presented a unique antiplatelet in the class, as it is reversible, with a shorter half-life. The study that established ticagrelor was the Platelet Inhibition and Patient Outcomes (PLATO) trial, a multicenter, randomized, double-blind trial that compared ticagrelor with clopidogrel in addition to aspirin. This trial was conducted from 2006 to 2009 and included patients with NSTEMI or STEMI with an estimated follow-up period of 12 months. The primary outcome was similar to the previous trials with composite CV death, MI, or stroke, in addition to several related secondary outcomes. The safety outcome was the time to an event of any major bleeding. The ticagrelor group received a loading dose of 180 mg followed by 90 mg twice daily thereafter, and the clopidogrel group received a 300 mg loading dose then 75mg daily thereafter. There were 18,624 subjects randomized to either study drug or active control with significantly reduced rates of the primary end point with ticagrelor compared with clopidogrel (9.8% vs 11.7%; P <.001). The primary endpoint rate was also significantly lower in patients on ticagrelor compared with clopidogrel who were planned for invasive strategy (8.9% vs 10.6%; P = .003), as well as for stent thrombosis (1.3% vs 1.9%; P = .009). The bleeding rates in both groups were comparable (11.6% and 11.2%, respectively; P = .43); however, there was a higher rate of noncoronary artery bypass graft (non—CABG)-related bleeding in the ticagrelor group (4.5% vs 3.8%; P = .03). There was also higher rate of patients experiencing dyspnea in the ticagrelor arm (13.8% vs 7.8%; P <.001).8
Vorapaxar (TRACER and TRA 2°P-TIMI 50)
The antiplatelet with the newest mechanism of action is vorapaxar, a reversible thrombin receptor antagonist by inhibition of PAR-1. The first study that focused on its use in ACS was the Thrombin Receptor Antagonist for Clinical Event Reduction in Acute Coronary Syndrome (TRACER) trial, conducted from 2007 to 2010, which was a multinational, double-blind, randomized, and placebo-controlled. The trial included patients with UA or NSTEMI with an estimated minimum follow-up of 12 months. The primary efficacy end point was a composite of CV-related death including MI, stroke, recurrent ischemia, or urgent revascularization with similar key secondary end points of death from CV causes, MI, or stroke. The safety end point was a composite of moderate or severe bleeding, based on the Global Use of Strategies to Open Occluded Coronary Arteries (GUSTO) criteria. There were 12,944 patients enrolled in the study; however, after a safety review was conducted, the trial was prematurely terminated in January 2011 due to the unacceptable rates of bleeding. There was adequate enrollment for data to be analyzed for the prespecified end points, although the trial was stopped early. No difference was seen in the primary efficacy end point with vorapaxar and placebo (18.5% vs 19.9%; P = .07). The composite of the secondary end point for 2-year Kaplan-Meier estimates occurred in more patients in the vorapaxar group, with more significance seen in the reduction in rate of MI (11.1% vs 12.5%; P = .02). Regarding the bleeding outcomes, vorapaxar increased the rate of moderate to severe bleeding compared with placebo (7.2% vs 5.2%; P <.001). Additionally, the vorapaxar group had a greater number of intracranial hemorrhages (1.1% vs 0.2%; P <.001).9 Overall, this study was associated with an increased risk of bleeding without demonstrating a strong enough benefit. There was a follow-up study published in 2014 analyzing the use of vorapaxar specifically in patients who underwent non-CABG after randomization. This was a subgroup analysis from the TRACER trial; therefore, the end points are the same. Of the 1312 who underwent non-CABG surgery, the primary end point occurred in 43 patients in the vorapaxar group and 70 patients in the placebo group (8.2% vs 12.9%; P = .005). Moreover, the difference between the groups in the major non—CABG-related bleeding rates were not statistically significant, although bleeding rates did increase in the vorapaxar group post discharge. This analysis showed that there may be a benefit of vorapaxar use in this specific patient population, but additional randomized, prospective trials are warranted to further confirm this finding.10
Another major study conducted from 2007 to 2011 for the secondary prevention of atherothrombotic events was the Thrombin Receptor Antagonist in Secondary Prevention of Atherothrombotic Ischemic Events-Thrombolysis in Myocardial Infarction 50 trial (TRA 2P-TIMI 50), which was a multicenter, double-blind, and placebo-controlled trial with a median follow-up of 30 months. It looked at patients with a history of MI, stroke, and peripheral arterial disease for secondary prevention of another CV event, and randomized them to vorapaxar 2.5 mg daily or placebo in addition to current standard of care of aspirin and/or clopidogrel, as appropriate. The primary end point, which was a composite of CV death, MI, or stroke, occurred in 9.3% in the vorapaxar group versus 10.5% in the placebo group (P <.001) among a total of 26,449 participants. Moderate or severe bleeding, regarding the major safety end point, occurred in more patients in the vorapaxar (4.2%) than in the placebo (2.5%) group (P <.001). Additionally, intracranial hemorrhage was statistically significantly higher in the vorapaxar group (1% vs 0.5%; P <.001). Therefore, as seen in the TRACER trial, the efficacy of vorapaxar as an agent for secondary prevention was seen at the cost of higher bleeding rates.11 A subgroup analysis was conducted as a follow-up trial, looking specifically at the group with MI for secondary prevention. There was a reduced rate of events in the vorapaxar group versus placebo, with higher rate of moderate to severe bleeding, which echoed the other published literature. Overall, it was concluded that vorapaxar might be beneficial in patients with specific comorbidities, in those <75 years of age, weighing >60 kg, and with no history of stroke or transient ischemic attack, where the benefits of its use may outweigh the risks.12
Cangrelor is a new P2Y12 agent with a rapid onset of action since it is an IV formulation, compared with the other P2Y12 inhibitors that can take between 30 minutes to 2 hours for onset. Although this drug is not yet FDA-approved, 3 major studies thus far have been conducted for the agent. The first 2 phase 3 studies, CHAMPION PCI and CHAMPION PLATFORM, conducted from 2006 to 2009, were randomized controlled trials comparing cangrelor with standard treatment in order to optimize the management of ACS in high-risk patients undergoing PCI. Patients were either given cangrelor or clopidogrel up front in CHAMPION PCI or cangrelor up front and delayed clopidogrel in CHAMPION PLATFORM. The primary end point in both trials—death, MI, or urgent revascularization—was not reduced by cangrelor; however, the cangrelor treatment groups did not experience increased severe bleeding.13,14 The most recent study was the CHAMPION PHOENIX trial, conducted 2010 to 2012, which included patients with UA, NSTEMI, or STEMI, who would undergo PCI and were never on P2Y12 inhibitors. The primary end point was similar to the CHAMPION PCI and CHAMPION PLATFORM, with a follow-up period of 48 hours. There were 11,145 patients randomized to cangrelor (30 mcg/kg followed by 4 mcg/kg) or clopidogrel (600 mg or 300 mg followed by 75 mg) before PCI. The rate of the composite end point was significantly lower in the cangrelor group (4.7%) versus the clopidogrel group (5.9%) (P = .005), with comparable severe bleeding rates in each group (0.16% vs 0.11% respectively; P = .44). Overall, these studies show that cangrelor can be utilized in a similar fashion to the glycoprotein IIb/IIIa agents, with decreased rates of bleeding. Further studies are needed to effectively transition patients to the outpatient setting after administering this drug in the acute setting.15
Another compound currently in the pipeline is elinogrel, a potent and selective P2Y12 inhibitor available in IV as well as oral formulations. Both formulations are clinically identical with the exception of the route of administration. The INNOVATE-PCI trial is a phase 2b randomized, multicenter, controlled trial conducted to test the efficacy and safety of elinogrel versus clopidogrel in non-urgent PCI patients. Elinogrel was administered as an initial IV bolus dose of 80 mg or 120 mg in addition to 50 mg, 100 mg, or 150 mg of the oral formulation, followed by twice-daily dosing of the oral doses. Clopidogrel was given as a 300 mg or 600 mg loading dose with 75 mg administered daily thereafter. The progressive nature of this agent is that patients can be transitioned from the IV to oral formulation after PCI and continue it upon discharge to provide a true continuum of pharmacotherapy care.16
Transitions of Care
The armamentarium of antiplatelet agents, including those currently available or in the development pipeline, shows notable strides for constant improvement and innovation in treating patients with ACS. These agents are but 1 component of a host of other important medications and therapies indicated for patients following an ACS event. With this in mind, medication reconciliation is an important part of the transition of care process to the outpatient setting. Transitioning a patient from the hospital involves many complex processes that are often overlooked, perhaps due to lack of standardized protocols. The appropriate transition of patients may reduce morbidity and mortality, thereby decreasing patient readmission rates and healthcare costs. Managed care professionals can improve transitions of care through increased communication with the healthcare team, the family, and the patient. Several initiatives have been created to improve transition of care processes, and discussed below are several tools that can be utilized for effective transitions of care.
Get With the Guidelines-Coronary Artery Disease (GWTG-CAD)
A hospital-based national quality improvement initiative is the Get with the Guidelines-Coronary Artery Disease (GWTG-CAD) program, created to increase adherence to guidelines for patients admitted for CAD, which would in turn improve outcomes. The program consists of multidisciplinary teams (eg, physicians, nurses, and personnel from quality improvement), who attend workshops and share ideas to enhance guideline adherence in their institutions. The members also input patient clinical information, upon admission and throughout the hospital stay, through an Internet-based tool that gathers and analyzes the information and provides real-time decision-aiding tools. Since its inception in the year 2000, it has been shown to reduce readmission rates in stroke and heart failure.18 The latest study, published in 2013, compared the rates of adherence with the guidelines between teaching hospitals (THs) and nonteaching hospitals (NTHs), with the overall goal of showing steady progression in the following core measures: (a) aspirin within 24 hours in ACS; (b) aspirin at discharge in patients with CAD; (c) angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs) in patients with left ventricular systolic dysfunction; (d) beta-blockers at discharge in patients with CAD; (e) lipid-lowering medication in CAD patients with low-density lipoprotein (LDL) >100 mg/dL; and (f) smoking cessation counseling for smokers. Hospitals participating totaled 361, with 270,902 patients admitted. The THs demonstrated higher guideline adherence, defined as being compliant to all the core measures, than the NTHs (78.4% vs 73.3%, P = .01) in the beginning; however, after 5 years, the NTHs exceeded the THs, although the difference was not statistically significant (87.5% vs 89.6%, respectively; P = .37). From 2000 to 2009, length of stay greater than 4 days decreased; however, there was no statistical difference in in-hospital mortality. One limitation of the study is that there was no post discharge data available to assess the continuum of care. Although the medications that were part of the core measurements of guideline adherence were aspirin, betablockers, ACE inhibitors, and statins—and did not include P2Y12 inhibitors—this study complements the ideal that any guideline adherence would naturally improve the quality of care for patients.19
The MISSION protocol takes the guideline adherence strategy 1 step further. This protocol is based on current guidelines and includes pre-hospital, in-hospital, and outpatient decision-making tools regarding clinical treatment up to 1 year post AMI. The pre-hospital phase focuses on rapid diagnosis and early risk stratification to be identified when the patient is on the way to the hospital. Additionally, once patients are identified as PCI-eligible in the field, the appropriate medications are administered. The in-hospital phase includes admitting patients directly to a cardiac care unit, not the emergency department (ED), in order to provide faster care. Once the acute in-hospital phase has been managed, the patient is urged to adopt secondary prevention strategies, such as lifestyle modifications and drug adherence, hopefully encouraging their “buy-in.” In the outpatient phase, the patient is given appointments to attend 4 clinic visits after the AMI event. Additional appointments are set up to include cardiac rehabilitation sessions, primary care visits, and cardiologist visits thereafter. A study is being conducted in the Netherlands—after intense collaboration with outpatient primary care physicians, ambulation services, cardiac rehabilitation centers, community hospitals, and the Leiden University Medical Center—to test this protocol with preliminary results. Patients who fit predefined criteria were included in the study as they were admitted with AMI and compared with a historical group. When the pre-hospital protocol was implemented, more patients were treated within the 90-minute door-to-balloon time (80% active vs 63% historical; P = .01). In addition, more patients were discharged earlier in the active versus historical control group (3.9 ± 2.8 vs 7.3 ± 8.2 days; P <.001).20 To implement a similar protocol in a hospital would require coordinating with key professionals in both the in- and outpatient settings, as well as investing time and budget on resources which will ultimately benefit both the patients and the hospitals.
The Project Re-Engineered Discharge (RED) tool kit, developed by the Boston University Medical Center, focuses more on the transition to the outpatient setting to decrease readmission rates. This quality improvement tool concentrates on coordinated care for discharge planning, written care plans, and follow-up activities to standardize the process. It has been shown to decrease ED visits and readmission rates by 30%. One rural community hospital in Southwestern Pennsylvania recently conducted a study utilizing the tool kit to decrease allcause readmission. First, a team of professionals from the hospital carried out a SWOT analysis—strengths, weaknesses, opportunities, and threats—that identified several flaws in their current discharge planning process, which included the inability to verify information for discharge, uncoordinated care, delays in relaying patient discharge information to physicians, and losing patients to follow-up. The team identified crucial steps in the admission-to-discharge process that warranted particular attention. A nurse director, pharmacist, case manager, and nursing staff collaborated to create a folder of material to be given to the patient upon discharge. In addition, a training session and a discharge checklist were created for the hospital team members to educate the staff about the program. Of the 336 patients discharged from the dedicated medical/surgical unit, 28 (8%) were readmitted, and only 5 of those (17.8%) were readmitted for the same initial diagnosis. In the 4 months of this quality improvement project, there was a 32% reduction in hospital readmissions. Additionally, the reactions from those who chose to complete the discharge and readmission questionnaires were mostly positive.21 This was the most recent study conducted where Project RED tool kit was piloted and demonstrated success.
Expanding the Pharmacist’s Role
While there are an increasing number of antiplatelet options on the market and tools available to help patients transition to the outpatient setting after an ACS event, a gap still exists when it comes to consistently incorporating these components into a plan to improve overall patient care. Pharmacists are among the most accessible healthcare providers in the community and are also experts for safe and effective medication use in the hospital setting. To that end, pharmacists are prime resources to aid in more effective transitions of care for patients after experiencing an ACS event.
One randomized prospective trial, conducted in 4 Veteran Affairs Medical Centers from 2010 to 2013, randomized patients to usual care (UC) or multifaceted intervention (INT). The INT consisted of medication reconciliation and tailoring led by a pharmacist; patient education; collaboration of the pharmacist and the patient’s primary care physician and/or cardiologist; and voice-messaging calls for medication reminders. The primary outcome measure was patient adherence to their medications that included beta-blocker, statin, clopidogrel, and angiotensin-converting enzyme inhibitor/ angiotensin receptor blocker (ACEI/ARB). Secondary outcome measures included reaching blood pressure and LDL goals. From a total of 253 patients, more patients in the INT group than the UC group adhered to the 4 classes of medications (89.3% vs 73.9%; P = .003). Breaking the groups down further, there were higher rates of adherence to the statin (93.2% vs 71.3%; P <.001), ACEI/ARB (93.1% vs 81.7%; P = .03), and clopidogrel (86.8% vs 70.7%; P = .03) in the INT group. Patient adherence to beta-blockers was comparable among groups (88.1% vs 84.8%, P = .59), and blood pressure and LDL goals for the secondary outcomes were also comparable. This study shows the potential benefits seen with interventions from pharmacists.22
On the other hand, another study conducted from 2008 to 2009 in 2 tertiary care academic centers, Vanderbilt University Hospital in Nashville and Brigham and Women’s Hospital in Boston, designed to assess the impact of pharmacists on medication errors post discharge, did not show overall significant results compared with usual care. This randomized controlled trial compared intervention activities, including medication reconciliation and in-patient counseling by a pharmacist, along with adherence assessments and follow-up phone calls post discharge. This was compared with UC, which was conducted by a nurse and/or physician, as discharge counseling and medication reconciliation via the electronic medical record (EMR). Although this study was not focused solely on ACS patients and antiplatelet agents, 61% of patients were diagnosed and treated inpatient for ACS. Among 851 participants in the study, with about half in the intervention group, 50.8% experienced at least 1 clinically important medication error 30 days post discharge.23 This highlights the challenges a hospital may face in conducting optimal medication reconciliation and follow-up, even with a pharmacist on board; however, this may also speak to the impact of accessibility and tools on the EMR that are useful to nurses and physicians who conduct these activities (ie, usual care as defined in the study).
A single-center retrospective study to evaluate hospital readmissions conducted in Chicago in 2011 compared UC with a pharmacist and social worker program. A one-to-one matching algorithm was used to match patients enrolled in the program to patients receiving UC, defined in this study as obtaining a medication history and reconciliation upon admission, discharge plan, instructions, and education. The program with the multidisciplinary team included UC plus daily interdisciplinary rounds, medication history and education during hospitalization by a pharmacist, medication reconciliation for discharge, and a social work follow-up phone call within 2 business days of discharge. There were 100 patients included in the analysis, with a lower rate of hospital 30-day readmissions for any cause in the multidisciplinary group versus UC (10% vs 30%, P = .012). This study not only shows the benefits of a multidisciplinary team that includes pharmacists, but it also demonstrates the value of pharmacists in helping patients transition to the next level of care with decreased readmissions.24
The Affordable Care Act
The Affordable Care Act (ACA) was enacted in 2010 to expand accessible healthcare to the uninsured population, and to increase the quality of care while reducing costs. To achieve these ends, the legislation implemented value-based purchasing (VBP) to reward high-quality healthcare with incentives and transparency. Under a specific domain, 30-day hospital readmission rates for certain health conditions are measured and scored, and may be penalized financially. VBP incentive payment will be less than, equal to, or greater than the percent reduction based on the Total Performing Scores of the hospitals. The target percent reduction for 2014 is 2, 3 for 2015, with incremental increases in subsequent years. CMS adopted the same readmission measures for AMI, pneumonia, heart failure, surgical infection, and hospital-acquired infections. Therefore, secondary prevention of another event is paramount to the patient, their family, and the hospital. Hospitals will be rewarded based on their performance or improvement and penalized if they do not meet expectations. This means that the healthcare arena is now changing to a metrics-based field, as opposed to the fee-for-service model, in which accountability and proof of better outcomes is the way hospitals can thrive.25,26
The advent of novel antiplatelet agents has progressively changed the way ACS can be treated and prevented. Despite recent therapeutic advances, significant morbidity and mortality continue to be associated with ACS. Several antiplatelet agents have proven efficacy and safety through numerous pivotal studies, most of them now incorporated in the guidelines, which will continue to evolve as the medication pipeline expands. Additionally, the substantial financial burdens associated with ACS and its optimal treatment will need to be strategically managed in light of the ACA and the VBP program. Managed care and healthcare professionals should prioritize early diagnosis, treatment, and secondary prevention for patients with ACS. These outcomes are attainable when there are clear lines of communication and standardized goals among the various departments and disciplines in the inpatient, outpatient, and community settings. Lastly, patient and family education, communication, and buy-in are key factors in preventing secondary events.