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Improving Lipid Evaluation and Management in Medicare Patients Hospitalized for Acute Myocardial Infarction
Monte Malach, MD, MACP, FACC;
John Quinley, MD, MPH;
Pascal James Imperato, MD, MACP, MPH & ; TM;
Marcia Wallen, MPH
Arch Intern Med. 2001;161:839-844.
ABSTRACT
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Background The control of low-density lipoprotein cholesterol (LDL-C) levels in
patients with known coronary artery disease, particularly in those with acute
myocardial infarction, has been shown to reduce the rates of disease progression,
recurrent events, and mortality.
Objectives To evaluate and improve hospital-based processes for measuring and treating,
when necessary, LDL-C levels above 3.36 mmol/L (>130 mg/dL) in patients with
an acute myocardial infarction.
Design A nonrandomized retrospective baseline study followed by a collaborative
educational intervention with participating hospitals and a second nonrandomized
postintervention study.
Patients Four hundred six preintervention patients discharged from the hospital
alive after a confirmed acute myocardial infarction in 1996, and 498 postintervention
patients discharged from the hospital in 1999.
Interventions Performance of lipid profiles on admission to the hospital and during
hospitalization and drug and dietary interventions.
Results The measurement of LDL-C level on admission to the hospital increased
from 8% preintervention in 1996 to 32% postintervention in 1999. The measurement
during hospitalization increased from 14% preintervention to 48% postintervention.
Hospitals that initiated programs to ensure early lipid evaluations through
preprinted orders and policy changes achieved an average patient LDL-C measurement
rate of 70% in 1999. Hospitals lacking standard policies averaged only 23%
at the same time. Of the patients with a measured LDL-C level greater than
3.36 mmol/L (>130 mg/dL) who were not undergoing drug therapy on admission
to the hospital, 46% were given lipid-lowering agents by discharge from the
hospital during the postintervention period. During this same period, only
11% of the patients were prescribed this therapy if they had either a lower
measured level or no LDL-C measurement at all.
Conclusion Active hospital-based programs to ensure routine LDL-C measurements
in patients admitted for acute myocardial infarction increased the use of
appropriate lipid-lowering therapy in these high-risk individuals and could
contribute to reducing the incidence of recurrent coronary artery disease.
INTRODUCTION
ACUTE MYOCARDIAL infarction (AMI) is a leading cause of morbidity and
mortality among Medicare patients. In recent years, the management of patients
with AMI has emphasized the use of aspirin, ß-blockers, and thrombolytic
agents or percutaneous transluminal coronary angioplasty during the first
hours of onset.1 Despite the existence of clear
guidelines, not all hospitals have processes in place to ensure their timely
implementation.2
Lowering serum lipid levels to normal levels has been shown to be a
major contributor to reducing the rate of disease progression, recurrent events,
and mortality among patients with documented coronary artery disease (CAD).
Practice guidelines that address the management of lipids in these patients
have been established by the American College of Cardiology/American Heart
Association1 and by the National Institutes
of Health's National Cholesterol Education Program.3
Screening and intervention for the secondary prevention of recurrent
coronary events, including dietary education and therapy for lipemia, can
significantly improve the long-term prognosis for patients with an AMI. It
is suggested that these measures be implemented during the predischarge phase
of hospitalization.4 Despite such recommendations,
patients with an AMI often do not undergo lipid screening and appropriate
interventions while hospitalized. Frolkis5
recently reported that at 1 major tertiary care institution, a measurement
of the low-density lipoprotein cholesterol (LDL-C) level was ordered in only
50% of hospitalized patients with an AMI.
The total cholesterol level has been shown to be a risk factor for older
patients (aged  65 years) with CAD, even after adjustment for other comorbid
conditions.6 Despite this evidence, Medicare
patients who experience an AMI and have lipemia are as a group undertreated
for the latter.7 Overall, there is significant
evidence that more patients with AMI and lipemia are not achieving ideal lipid
levels as recommended by the National Cholesterol Education Program guidelines.8
Randomized clinical trials, a meta-analysis of previous clinical trials,
and angiographic studies have documented the benefits of LDL-C lowering in
patients with CAD.9 The Scandinavian Simvastatin
Survival Study10 found that, compared with
patients who received routine medical care, patients who received a cholesterol-lowering
agent had a nearly 70% reduction in major cardiac events. A meta-analysis9 of secondary cholesterol intervention trials found
that aggressive cholesterol lowering resulted in a 31% reduction in rates
of fatal and nonfatal reinfarction and a 21% reduction in all causes of mortality.
Thus, it is clear that secondary prevention strategies can reduce morbidity
and mortality. Despite the evidence supporting secondary prevention, it is
often not implemented. A recent cross-sectional analysis by Majumdar et al11 demonstrated that lipid-lowering drugs were used
in only 37% of patients with established CAD and lipemia who were hospitalized
with an AMI.
Given the importance of evaluating lipid levels in patients hospitalized
with an AMI and of initiating appropriate therapy when indicated, we sought
to assess hospital-based processes for achieving these goals. We also implemented
a collaborative educational intervention program with 20 hospitals to improve
these processes and conducted a postintervention assessment to measure its
outcomes. This project was undertaken by IPRO, the peer review agent for Medicare
in the state of New York, as part of the federal Health Care Financing Administration's
Health Care Quality Improvement Program.
PATIENTS AND METHODS
Hospitals in the state of New York interested in improving the level
of measurement and management of elevated lipid levels in Medicare patients
who experienced an AMI were recruited into this study during the second quarter
of 1998. Twenty hospitals eventually agreed to participate.
Four hundred twenty-eight Medicare patients from the 20 participating
hospitals were included in the baseline phase of the study. These patients
had been discharged alive from these hospitals in July, August, November,
and December of 1996. Discontinuous months were chosen to account for possible
variations in seasonality for AMI.12 The medical
records of these patients had been included in the Health Care Financing Administration's
Cooperative Cardiovascular Project remeasurement phase of 1996.13
Following a 4-month collaborative educational intervention in the latter half
of 1998, the medical records of 498 Medicare patients discharged from the
hospital with a diagnosis of AMI from January 1, 1999, through April 30, 1999,
were studied. These 498 patients were treated at the 20 hospitals in the study.
Consecutive months were used for the remeasurement group since no seasonal
variation was found on the baseline medical records.
Eligible participants for this study included Medicare patients discharged
from the hospital with a principal diagnosis of AMI (International
Classification of Diseases, Ninth Revision [ICD-9]),14
code 410.x1) in whom the AMI was confirmed on medical record review by an
elevated creatine phosphokinase of muscle band or an elevated lactate dehydrogenase
level (with the level of lactate dehydrogenase isoenzyme LD1>LD2) or by 2 of the following criteria: chest pain, a 2-fold elevation
of the creatine phosphokinase level, or evidence of an AMI on an electrocardiogram.
These participants also had to be discharged alive, as part of the Cooperative
Cardiovascular Project.
The quality indicators chosen for this study are presented in Table 1. These indicators were based on
existing national guidelines, which stress the importance of total cholesterol
and LDL-C measurements to assess lipid status. Because of an anticipated initial
decrease in cholesterol and LDL-C levels associated with an AMI, separate
quality indicators were developed for cholesterol and LDL-C measurements within
24 hours of arrival and later in the hospitalization. Although statins are
the most common form of drug therapy, fibrates, bile acid resins, and nicotinic
acid were included as drug treatment. Dietary intervention was measured as
any documentation of the patient receiving education on or a copy of a lipid-lowering
diet.
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Baseline and Postintervention Results for Medicare Patients Discharged
From 20 New York State Hospitals Following an Acute Myocardial Infarction*
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Care was taken to abstract the data completely and reliably from the
patient medical records supplied by the collaborating hospitals. The data
collection instrument was developed by the IPRO project team (M.M., J.Q.,
and P.J.I.) and pretested on a sample of patient medical records. Nurse abstractors
were trained using "gold standard" medical records with agreed values. An
initial set of medical records was reabstracted by all abstractors, and interrater
reliability was shown to be high for all variables ( >0.6) before abstracting
the full set. Because of the large variety of multichannel chemistry tests
and panels, which may or may not include measurement of the cholesterol level
in individual hospitals, it was decided that the presence of a cholesterol
value on the medical record would be accepted as evidence that a cholesterol
measurement was ordered, in addition to specific orders. The same rule was
applied to LDL-C measurements, since some LDL-C values were found in the absence
of a clear order while some medical records with clear orders did not have
the LDL-C values recorded.
Twenty hospitals volunteered to participate in the project during the
first half of 1998. Nearly all project interventions took place between September
and December 1998 and consisted of the following activities:
1. Collaborating hospitals were requested to form multidisciplinary
teams to identify gaps in their process of care for AMI that led to failure
to evaluate LDL-C status early and failure to initiate treatment through either
dietary or, when indicated, drug therapy. Each team was to work on 3 tasks.
The first was administrative issues, including how to incorporate lipid evaluation
and treatment into hospital guidelines and pathways. The second was to educate
the medical, nursing, and laboratory staff concerning the hospital's protocol
and standards. The third was to prepare educational materials and systems
for patients to better understand lipids as related to their disease, diet,
and lifestyle and to taking medications.
2. In October 1998, IPRO sent a baseline report to all participating
hospitals, including the hospital's own 1996 performance on each indicator
and anonymous comparisons with all other project hospitals.
3. In early November 1998, IPRO staff (M.M., J.Q., and P.J.I.) conducted
a series of teleconference calls with hospital team leaders, other opinion
leaders, and cardiologists from several hospitals at a time. This provided
an opportunity to review the rationale for in-hospital lipid measurement and
therapy and increase participation by the key participants.
4. An IPRO outreach department staff member (M.M., J.Q., or P.J.I.)
conducted site visits with each collaborating hospital in December 1998 to
review each hospital's system and make recommendations for improvements.
5. Each collaborating hospital was asked to submit a plan showing how
it would improve lipid monitoring and treatment. These plans were reviewed
by outreach staff, and recommendations were made in writing to those hospitals
whose plans did not demonstrate the ability to use the quality indicators.
6. Follow-up telephone calls were made to the medical directors of hospitals
that did not have plans in place by the IPRO medical director (M.M.) in charge
of the project. These calls were educational and offered technical and professional
literature support to the hospital if the latter was having difficulty facilitating
implementation of the project.
RESULTS
The baseline study demonstrated that relatively few patients had an
LDL-C determination either at the time of admission to the hospital or during
their hospital stay (Table 1).
Only 2 of the 20 participating hospitals had processes in place for routine
LDL-C measurements during hospitalization at the time of the baseline study.
The rates documented for these hospitals were 48% and 79%. Of the remaining
18 hospitals that did not have such routine processes in place, none exceeded
an LDL-C measurement rate of 30%.
Low-density lipoprotein cholesterol measurements on admission to the
hospital and during hospitalization significantly increased to 32% and 48%,
respectively, during the postintervention period, from baseline levels of
8% and 14%, respectively (Table 1).
Despite these significant improvements, rates varied greatly between hospitals
(Figure 1).
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Frequency of a low-density lipoprotein cholesterol (LDL-C) measurement
being ordered or performed during hospitalization, postintervention (1999).
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Each participating hospital described the type of improvement program
implemented by the time of follow-up. Five hospitals (25%) either implemented
preprinted orders for LDL-C level in the cardiac care unit or emergency department
or had a strong program engaging patients in tracking their own LDL-C levels.
Eight hospitals (40%) reported adopting a lipid measurement policy, protocol,
or clinical pathway and educating staff to order lipid levels, but without
preprinted orders or a patient self-monitoring program. Seven hospitals (35%)
reported that they were not able to adopt any substantial program to improve
the ordering of the LDL-C level. The rates of LDL-C measurement during hospitalization
of these 3 groups were 70%, 53%, and 23% (P<.01
for each comparison).
The rate of total cholesterol measurement on admission to the hospital
was high (72%) at baseline, but declined in the postintervention period to
54%. The rate of total cholesterol measurement during hospitalization was
78% at baseline, but also declined to a lower level (66%) in the postintervention
period.
As shown in Table 1, 15%
of the patients in the baseline study were taking lipid-lowering agents at
the time of admission to the hospital. This increased to 17% in the postintervention
period, a difference that is not statistically significant.
Among patients who had LDL-C levels greater than 3.36 mmol/L (>130 mg/dL),
none were prescribed lipid-lowering agents in the baseline period. However,
this significantly increased to 46% during the postintervention period.
Only 50% of the patients received dietary interventions, either in terms
of personal education about lipid reduction or in the form of a printed diet.
No significant change was found during the postintervention period (49%).
Lipid-lowering therapy before admission to the hospital was much more
common for patients with a history of CAD. Of 498 patients in the postintervention
sample, 20% with a history of CAD were taking lipid-lowering medication on
admission to the hospital compared with 8% of the other patients. Therapy
was also strongly influenced by age, with 22% of the patients younger than
75 years undergoing therapy vs 13% of those aged 75 to 84 years; only 4% of
those older than 85 years were undergoing therapy. This pattern persisted
at the time of discharge from the hospital.
COMMENT
The results of this study demonstrated that hospitals that have a plan
that includes an easy-to-use protocol, a care map, and/or preprinted order
sheets are able to improve the rate at which the LDL-C level is measured in
Medicare patients with an AMI. Those hospitals that did not adopt plans cited
either internal opposition to routine LDL-C measurements in this setting or
insufficient implementation time. The fact that hospitals without plans evidenced
little change in rates between the baseline and postintervention periods speaks
against these trends being due to a secular trend.
Based on the information provided by participating hospitals, it appears
that most total cholesterol measurements during the baseline period were made
as part of multichannel chemistry panels. During the intervening years, measurement
of the total cholesterol level was removed from many admission panels, which
may explain the decline observed in the postintervention period.
The rate of dietary therapy counseling varied considerably among hospitals.
However, no appreciable change was found for this indicator in the postintervention
period. Participating hospitals believed that dietary education was poorly
captured in medical records, and none reported an active intervention to improve
performance in this area.
Lipid-lowering therapy was higher in the postintervention period for
patients with a history of CAD. Also, more patients with such a history were
already taking lipid-lowering medication on admission to the hospital compared
with other patients. Age was an important determinant of such therapy, with
rates being higher for those younger than 75 years.
The lay public's knowledge of cholesterol screening, hypercholesterolemia,
and lipid-lowering treatment greatly increased from 1980 to 1992.15 Unfortunately, most dyslipemic patients receiving
lipid-lowering therapy are not achieving National Cholesterol Education Program
LDL-C target levels.16 Thus, more aggressive
therapy is necessary to attain those goals, as demonstrated by the baseline
findings of this study.
There still appears to be a sex disparity in the use of lipid-lowering
therapy in patients with CAD, despite the greater attention that has been
recently focused on this issue. The data from 16 academic centers in the United
States and Canada over 3 years showed that lipid-lowering therapy increased
in men by 55% vs 35% in women (P = .04) and that
the target LDL-C goal of less than 3.36 mmol/L (<130 mg/dL) was reached
in 31% of men but in only 12% of women (P = .001).17
Published data have clearly shown that total cholesterol level is an
independent risk factor in patients with CAD and that lowering it reduces
the risk for subsequent AMI and death.18 Indeed,
the Cholesterol and Recurrent Events (CARE) Study,19
the Long-term Intervention With Pravastatin in Ischaemic Disease Study,20 and the Air Force/Texas Coronary Atherosclerosis
Prevention Study21 found a significant reduction
in recurring coronary events, AMI, and death. In the West of Scotland Coronary
Prevention Study22 of 6595 men with an elevated
total cholesterol level, but no clinical evidence of heart disease, pravastatin
reduced the risk of a first heart attack by 31% and the need for revascularization
by 37%. The CARE study19 and the Air Force/Texas
Coronary Atherosclerosis Prevention Study21
found reduced coronary events in patients with normal cholesterol levels.
Age is no longer considered a reason to ignore total cholesterol levels.8
The National Cholesterol Education Program report3
suggests that patients with established CAD or AMI should have the LDL-C level
decreased to less than 2.59 mmol/L (<100 mg/dL). Furthermore, managed care
organizations must have a Health Plan Employer Data Information Set performance
measurement goal of an LDL-C level of less than 3.36 mmol/L (<130 mg/dL)
to achieve National Committee for Quality Assurance endorsement.23
Individuals with diabetes have a 2- to 10-fold increased risk of coronary
events compared with those without diabetes; this risk is even higher in women
with diabetes, according to the Framingham Study.24-25
Aggressive lipid-lowering therapy in diabetic patients lowered the risk of
death and major coronary events in the Scandinavian Simvastatin Survival Study10 and in the CARE Study19
by 55% and 25%, respectively, compared with 23% in nondiabetic patients. Thus,
it appears that the prevention of major CAD events in diabetic persons without
evidence of CAD is even greater than that in nondiabetic persons with CAD.
Perhaps of greatest importance are the other, multiple benefits of statin
therapy that are unrelated to lipid lowering. These benefits significantly
enhance lipid lowering and further emphasize the importance of the evaluation
of lipid levels in all patients after AMI, which is the subject of this report.
The non–lipid-lowering actions include (1) plaque stability, (2) enhanced
endothelial activity, (3) antiplatelet and antiatherothrombotic activity,
and (4) anti-inflammatory and antimacrophage activity.26
Thus, there is an increasing and evolving role of statins in the management
of atherosclerosis.
Rupture of a vulnerable coronary artery plaque is the most frequent
cause of sudden unstable angina and AMI.27
A thin-walled fibrous cap over a liquid lipid core is subject to mechanical
stress and infiltraton with inflammatory cells. Most acute coronary artery
occlusions occur in vessels with less than 50% stenosis or with noncritical
stenoses.
Loss of endothelial activity and smooth muscle cell function results
in stasis. Statins have been shown to improve or restore endothelial function
and smooth muscle cell activity, unrelated to the effect on lipid levels.26 This activity translates into a direct clinical benefit.
Improvement in coronary vasomotor function is seen within 6 months of therapy,
and improved forearm blood flow is seen in hypercholesterolemic patients treated
with statins for only 4 weeks.26
Antiplatelet and antiatherothrombotic properties of some of the statins
have been described.28 The prothrombotic factors
affected by statins include plasma factor VII and cellular receptor VIIa,
platelet aggregation, fibrinogen level, plasma viscosity, and a fibrinolytic
factor. Platelets from patients with an elevated LDL-C level are more sensitive
to aggregation than are platelets from normolipemic patients and patients
receiving statin therapy.
Anti-inflammatory antimacrophage activity is promoted by the statins.
Oxidized LDL-C attracts macrophages directly and stimulates binding to the
endothelium via adhesion molecules. The statins simvastatin and lovastatin
inhibit oxidation of LDL-C and reduce uptake by macrophages, thus blunting
atheroma formation. Invasive macrophages promote plaque rupture by the release
of enzymes (metalloproteinases), which digest and weaken the atheroma cap.26
Aggressive medical therapy with atorvastatin (lowering the LDL-C level
to a mean of 1.99 mmol/L [77 mg/dL]), compared with percutaneous transluminal
coronary angioplasty, with or without stent use, reduced the incidence of
ischemic events, overall mortality, and the need for interventional revascularizations.29 Statin monotherapy has also been shown to reduce
the incidence of stroke in patients with CAD.30
Stroke or transient ischemic attack was prevented by 24% in the Scandinavian
Simvastatin Survival Study,10 31% in the CARE
Study,19 and 19% in the Long-term Intervention
With Pravastatin in Ischaemic Disease Study.20
The present study demonstrated that active hospital policies to ensure
the routine measurement and management of lipids in Medicare patients with
an AMI may result in a significant reduction in coronary events, mortality,
and stroke. It is essential to identify physician champions for the lipid
program who set examples and who, by virtue of the respect with which they
are held by the medical staff, can promote implementation. Those hospitals
with the best practices included lipid panels on routine cardiac care unit
admission for AMI and for chest pain protocols. These hospitals also have
educational programs in place for physicians, nursing staff, and patients.
The best-practice hospitals in this study performed ongoing monitoring of
patients.
The value of benefits from the use of statins, other than lipid lowering,
has been noted. This significantly emphasizes the need to determine lipid
values for all patients with an AMI and a coronary event. The evidence that
supports aggressive lipid modification in the secondary prevention of CAD
morbidity and mortality is compelling. It is distressing to note the failure
to use therapy that has been well documented to benefit patients with acute
coronary syndromes and AMI. This is most particularly true in the more vulnerable
Medicare population. The opportunity to dramatically affect the natural history
of CAD demands the aggressive pursuit of interventions such as lipid determinations
and lipid lowering. Indeed, it may be well stated that an individual with
acute CAD categorically needs to have a lower LDL-C level.
Attention to initiating and sustaining appropriate lipid-lowering therapy
can improve the health and longevity of the Medicare population.
AUTHOR INFORMATION
Accepted for publication October 31, 2000.
The analyses on which this article are based were performed under contract
500-P700, entitled "Utilization and Quality Control Peer Review Organization
for the State of New York," sponsored by the Health Care Financing Administration,
Department of Health and Human Services, Baltimore, Md. The content of this
article does not necessarily reflect the view or policies of the Department
of Health and Human Services, nor does mention of trade names, commercial
products, or organizations imply endorsement by the US government. The authors
assume full responsibility for the accuracy and completeness of the ideas
presented. This article is a direct result of the Health Care Quality Improvement
Program initiated by the Health Care Financing Administration, which has encouraged
identification of quality improvement projects derived from analysis of patterns
of care and, therefore, required no special funding on the part of this contractor
(IPRO). Ideas and contributions to the authors concerning experience in engaging
with issues presented are welcomed.
Corresponding author and reprints: Monte Malach, MD, MACP, FACC,
IPRO, 1979 Marcus Ave, Lake Success, NY 11042 (e-mail: nypro.mmalach{at}sdps.org).
From IPRO, Lake Success, NY (Drs Malach, Quinley, and Imperato and
Ms Wallen); the Department of Medicine, New York University Medical Center,
New York (Dr Malach); and the Departments of Medicine (Dr Malach) and Preventive
Medicine and Community Health (Dr Imperato), State University of New York,
Health Science Center at Brooklyn.
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