Faculty Bibliography

OBJECTIVES/OBJECTIVE:The purpose of this study was to determine whether state-mandated continuing medical education (CME) requirements affect the use of evidence-based therapies and outcomes in patients with acute myocardial infarction (AMI). BACKGROUND:The Institute of Medicine recommends that educational programs demonstrate their effect through process and outcome measures. METHODS:We analyzed 134,609 patients according to whether or not CME was mandated in the state of physician practice. A hierarchical multivariable model was developed that controlled for state, hospital, physician, and patient level characteristics to determine the association between state CME requirements and the use of evidence-based therapies. Primary outcome measures were admission aspirin use and reperfusion therapy, and discharge aspirin and beta-blocker prescription. Thirty-day and one-year mortality were secondary outcome measures. RESULTS:States with and without CME requirements had similar rates of aspirin use at admission and discharge (79.9% vs. 79.4% and 72.5% vs. 72.5%, respectively) and beta-blocker prescription at discharge (53.6% vs. 55.3%). The rate of reperfusion therapy at admission was significantly higher in states requiring CME (53.1%) compared with states without CME (47.9%) (p < 0.0001). After adjustment, patients admitted in CME-requiring states were significantly more likely to receive reperfusion therapy, mainly owing to "patented" thrombolytic therapy (odds ratio 1.15; p = 0.016). There was no association between CME requirements and one-year mortality. CONCLUSIONS:State-mandated CME had little association with AMI care or outcome, other than an increased use of patented thrombolytic therapy. Further research is needed to maximize the measurable effect of CME on the use of proven therapies irrespective of whether patented or generic medications are involved.

BACKGROUND:Although the Medicare entitlement provides universal hospital care coverage for elderly Americans, disparities in care processes after acute myocardial infarction still exist. Whether these disparities account for increased mortality among elderly poor patients is not known. METHODS:To determine the association between socioeconomic status and acute myocardial infarction treatment, procedure use, and 30-day and 1-year mortality, we analyzed data from 132 130 elderly Medicare beneficiaries hospitalized for acute myocardial infarction between January 1994 and February 1996. Patients were categorized into 10 groups of increasing income using the median income of the ZIP code of residence. RESULTS:The highest-income beneficiaries received higher rates of evidence-based medical therapy and had lower adjusted 30-day and 1-year mortality rates compared with the middle-income beneficiaries (30-day relative risk, 0.89 [95% confidence interval, 0.85-0.94]; and 1-year relative risk, 0.92 [95% confidence interval, 0.88-0.97]). Conversely, the lowest-income beneficiaries received lower rates of evidence-based medical treatment and had higher adjusted 30-day and 1-year mortality rates relative to the middle-income beneficiaries (30-day relative risk, 1.09 [95% confidence interval, 1.04-1.13]; and 1-year relative risk, 1.05 [95% confidence interval, 1.00-1.10]). Coronary revascularization rates were similar among income groups. CONCLUSIONS:Despite the Medicare entitlement, there remain significant socioeconomic disparities in medical treatment and mortality among elderly patients following acute myocardial infarction. Income was independently associated with short- and long-term mortality. More research is required to determine the mechanisms contributing to adverse outcomes among poor elderly patients and to determine whether expansion of Medicare coverage will alleviate these disparities.

It is widely accepted that proteinuria reduction is an appropriate therapeutic goal in chronic proteinuric kidney disease. Based on large randomized controlled clinical trials (RCT), ACE inhibitor (ACEI) and angiotensin receptor blocker (ARB) therapy have emerged as the most important antiproteinuric and renal protective interventions. However, there are numerous other interventions that have been shown to be antiproteinuric and, therefore, likely to be renoprotective. Unfortunately testing each of these antiproteinuric therapies in RCT is not feasible. The nephrologist has two choices: restrict antiproteinuric therapies to those shown to be effective in RCT or expand the use of antiproteinuric therapies to include those that, although unproven, are plausibly effective and prudent to use. The goal of this work is to provide the documentation needed for the nephrologist to choose between these strategies. This work describes 25 separate interventions that are either antiproteinuric or may block injurious mechanisms of proteinuria. Each intervention is assigned a level of recommendation (Level 1 is the highest; Level 3 is the lowest) according to the strength of the evidence supporting its antiproteinuric and renoprotective efficacy. Pathophysiologic mechanisms possibly involved are also discussed. The number of interventions at each level of recommendation are: Level 1, n = 7; Level 2, n = 9; Level 3, n = 9. Our experience indicates that we can achieve in most patients the majority of Level 1 and many of the Level 2 and 3 recommendations. We suggest that, until better information becomes available, a broad-based, multiple-risk factor intervention to reduce proteinuria can be justified in those with progressive nephropathies. This work is intended primarily for clinical nephrologists; therefore, each antiproteinuria intervention is described in practical detail.

The use of glycoprotein IIb/IIIa inhibitors reduces morbidity and mortality in patients with acute coronary syndromes and patients undergoing percutaneous coronary intervention. Despite the sound body of evidence that supports the use of these agents, registry data indicate that there is substantial underuse in eligible patients. This may be due to their modest treatment effect, controversy over the significance of reductions in recurrent myocardial infarction, or confusion over appropriate combinations of antiplatelet and antithrombin agents. The challenge for clinicians is to identify patients that receive the most benefit from the use of glycoprotein IIb/IIIa inhibitors. Until the results of ongoing trials become available, the American College of Cardiology/American Heart Association guidelines provide reasonable recommendations on the use of these agents in clinical practice.

OBJECTIVES: We sought to determine whether income-based disparities in care processes and outcome exist in patients with acute coronary syndromes. BACKGROUND: Using income proxies and limited clinical data, some observational studies have shown income disparities in outcome after acute myocardial infarction (MI). METHODS: Using annual household income from the economic substudy of the PURSUIT (Platelet Glycoprotein IIB/IIIA In Unstable Angina: Receptor Suppression Using Integrilin Therapy) trial, patients were grouped into low-, middle-, and high-income categories based on the U.S. Census Bureau definition of poverty. Logistic regression analysis was used to examine the association between income category and the use of cardiac procedures and the prescription of evidence-based medications at hospital discharge. Cox regression analysis was used to examine the hazard of 30-day and six-month death or recurrent MI across income categories, after adjusting for baseline characteristics. RESULTS: Low-income patients had more chronic medical conditions and were sicker at presentation. Among low-income patients, the use of some evidence-based medications and cardiac procedures was lower and the unadjusted rates of 30-day death and six-month death or MI was higher. After multivariable adjustment, there was no consistent pattern for disparity in care processes, but the trend for higher short and intermediate-term death or MI persisted for low-income patients. CONCLUSIONS: Income level is associated with a trend toward worse outcome among patients with acute coronary syndromes. The disparity in 30-day and six-month death or MI between low and high-income patients could not be readily explained by differences in in-hospital medical or invasive treatment, suggesting that the poor outcomes may be due to differences occurring after hospital discharge

The risk of death or recurrent myocardial infarction (MI) in patients with chest pain and baseline isolated troponin elevation is unclear. To determine the early and short-term risk of death or MI associated with isolated troponin elevation across a spectrum of chest pain syndromes, we used baseline creatine kinase (CK)-MB and troponin data from the Platelet IIb/IIIa Antagonism for the Reduction of Acute Coronary Syndrome Events in a Global Organization Network (PARAGON) B troponin substudy, the Global Utilization of Strategies To Open Occluded Coronary Arteries (GUSTO) IIa troponin substudy, and the Chest Pain Evaluation by Creatine Kinase-MB, Myoglobin, and Troponin I (CHECKMATE) study. Patients were grouped into 1 of 4 categories based on marker status (troponin-positive/CK-MB-positive, troponin-positive/CK-MB-negative, troponin-negative/CK-MB-positive, or troponin-negative/CK-MB-negative). The adjusted odds of death or MI occurring at 24 hours and 30 days was assessed by baseline marker status using multivariable logistic regression, with the group negative for both markers used as the reference. Patients who were positive for both markers had the highest odds of the 24-hour and 30-day end point. The adjusted odds of the 30-day end point for patients with isolated troponin elevation were 1.3 (95% confidence interval 0.7 to 2.3) and 4.8 (95% confidence interval 1.4 to 16.0) for high- and low-risk patients, respectively. The risk for 24-hour and 30-day death or MI with isolated positive CK-MB results was lower than with isolated positive troponin results, and it was not significantly greater than if the 2 markers were negative. For patients with high- and low-risk chest pain, baseline troponin elevation without CK-MB elevation was associated with increased risk for early and short-term adverse outcomes. This suggests that these patients should be admitted to the hospital and monitored in either an intensive care or step-down unit.

Quality assurance and improvement have increasingly been the focus of health care providers, third-party payers, and patients. Because cardiovascular procedures are common, easily identifiable with claims data, and account for a relatively large proportion of health care expenditures, particular attention has been paid to quality assurance in the setting of the diagnostic and interventional cardiac catheterization laboratory. The structure, process, and outcomes domains of quality measurement in the interventional laboratory involve the maintenance of volume standards, the availability of surgical backup, consistent tracking of procedural outcomes and complications so they can be compared with national standards, and the application of evidence-based therapy. Quality assurance i the diagnostic laboratory revolves around the clinical proficiency of the operators, the maintenance and management of catheterization laboratory equipment, and the presence of a continuous quality improvement program. The evolution of interventional equipment and techniques along with the establishment of national registries has led to a gradual improvement in the quality of percutaneous coronary intervention. Given the dynamic nature of cardiology, adaptable quality assurance and quality improvement programs will remain the foundation of successful catheterization labs.