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Volume 2: No. 3, July 2005
ORIGINAL RESEARCH
Cholesterol Levels and
Statin Use in Patients With Coronary Heart Disease Treated in
Primary Care Settings
Patrick J. O’Connor, MD, MPH, Richard J. Gray, MD, Michael V. Maciosek,
PhD, Kelly M. Fillbrandt, Terese A. DeFor, MS, Charles M. Alexander, MD,
Thomas W. Weiss, DrPH, Steven M. Teutsch, MD, MPH
Suggested citation for this article: O’Connor PJ, Gray RJ, Maciosek
MV, Fillbrandt KM, DeFor TA, Alexander CM, et al. Cholesterol
levels and statin use in patients with coronary heart disease treated in primary care
settings. Prev Chronic Dis [serial online] 2005 Jul [date cited]. Available
from: URL: http://www.cdc.gov/pcd/issues/2005/
jul/04_0146.htm.
PEER REVIEWED
Abstract
Introduction
Therapy with 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors, or statins,
has proven to be effective in the
treatment of lipid disorders. However, statin therapy continues to be underused,
even though statins are a relatively safe and well-tolerated class of agents. In
this study, we assessed trends in lipid control in patients with heart disease
who receive most of their health care in primary care clinics. The objective was
to determine whether systems of care implemented within a large medical group
are associated with improved treatment and control of dyslipidemia in a
high-risk group of coronary heart disease patients.
Methods
All adults with heart disease in a Minnesota medical group (N = 2947) were
identified using diagnosis and procedure codes related to coronary heart disease
(sensitivity = 0.85; positive predictive value = 0.89) in 1996. Study subjects
were observed from 1995 to 1998. Subjects had a baseline and follow-up test for
low-density lipoprotein cholesterol and high-density lipoprotein cholesterol.
Changes between baseline and follow-up measurements and trends in the use of statins and other lipid-active agents among the study subjects were analyzed.
Results
Among 1388 subjects with two or more eligible lipid measurements, mean
low-density lipoprotein cholesterol improved from 137.6 mg/dL to 111.0 mg/dL (P
< .001), and mean high-density lipoprotein cholesterol improved from 42.3 mg/dL
to 46.3 mg/dL (P < .001). The percentage of patients with low-density
lipoprotein cholesterol ≤100 mg/dL rose from 12.5% to 39.8% (P <
.001), and the percentage with high-density lipoprotein cholesterol ≥40 mg/dL rose from 52.5% to 67.6% (P < .001). In multivariate models,
statin use was identified as the main factor that
contributed to the improvement in low-density lipoprotein cholesterol (P
< .001). Men had greater decreases in low-density lipoprotein cholesterol than
women after adjusting for other variables (P < .001). Statin use rose from 24.3% at
baseline to 69.6% at follow-up. The statin discontinuation rate was 8.3% for
baseline statin users and 12.2% for subjects who used statins at any time during
the study period.
Conclusion
Investment in better heart disease care for patients in primary care clinics led
to major improvement in lipid control over 30 months, primarily due to
increased statin use. Improvements in low-density lipoprotein cholesterol and
high-density lipoprotein cholesterol were sufficient to substantially reduce
risk of subsequent major cardiovascular events.
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Introduction
Clinical trials provide strong support for using 3-hydroxy-3-methylglutaryl
coenzyme A (HMG-CoA) reductase inhibitor
(statin) therapy in patients with coronary heart disease (CHD) (1-7). Statins
are a relatively safe and well-tolerated class of agents that have proven to be
effective in treating lipid disorders. Recent data suggest, however, that statin
therapy remains underused in the treatment of lipid disorders, or dyslipidemia.
Reasons for this underuse of statins include inadequate physician titration of
medications to reach the goal level of low-density lipoprotein cholesterol (LDL-C)
recommended by the National Cholesterol Education Program (NCEP) and inadequate
long-term patient adherence to prescribed drug therapy (8-10).
In this study, we assessed trends in the use of statin therapy and changes in
LDL-C levels in a well-defined population of adults with CHD receiving their care at a single large multispecialty medical group. During the 4-year study
period, the medical group emphasized the importance of lipid control in CHD
patients. Primary care physicians had unrestricted access to several statins
through the medical group’s drug formulary. Clinical guidelines for lipid
control emphasized aggressive pharmacotherapy, and patients received messages on
the importance of lipid control through periodic medical group publications sent
to their homes. Our study objective was to determine whether systems of care
implemented within a large medical group are associated with improved treatment
and control of dyslipidemia in a high-risk group of CHD patients.
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Methods
Study site
The study was conducted at HealthPartners Medical Group (HPMG), a large
multispecialty group practice in Minnesota established in 1957 that in 1998 provided care to
220,000 patients insured by HealthPartners. Patients received clinical care at
one of 18 primary care clinics staffed by internal medicine and family practice
physicians.
About 75% of CHD patients at HPMG have pharmaceutical benefits as part of
their health insurance. Most patients with such benefits had a copayment of $10
to $15 for each 30-day supply of a prescription medication during the study
period. Most patients without pharmaceutical benefits were aged 65 years or
older and chose not to have such coverage because of the additional monthly
premium required. There were no other out-of-pocket costs to plan members or
disincentives to physicians for measuring serum lipids or prescribing lipid
treatment as desired. The medical group formulary included unrestricted
physician prescribing of statins. During the study period, lovastatin (Mevacor),
fluvastatin (Lescol), pravastatin (Pravachol), simvastatin (Zocor), and atorvastatin (Lipitor), along with a wide selection of other lipid active agents — including gemfibrozil (Lopid), niacin preparations, and cholestyramine — were available
for unrestricted use.
Local clinical practice guidelines for lipid screening and treatment were
implemented in 1995 and updated annually through the Institute for Clinical
Systems Improvement (ICSI), a collaborative health improvement organization
organized and supported by HealthPartners and many other Minnesota health care
organizations, including the Park Nicollet Clinic, Allina Medical Clinic, and
the Mayo Clinic. ICSI lipid treatment guidelines (11) are similar to those of
NCEP (12) and, at the time of the study, emphasized aggressive pharmacotherapy
for patients with CHD to reduce LDL-C levels to <100 mg/dL.
Study subjects
Study subjects were adult patients identified as having CHD in 1996. A
diagnosis of CHD was assigned to any patient meeting at least one of the
following criteria in 1996: at least two diagnoses from among codes 410.xx–414.xx
or 429.2 in the International Classification of Diseases, Ninth Revision, Clinical Modification (ICD-9-CM); at least one procedure from among codes
33510–33545 and 36822 in Current Procedural Terminology (CPT); or at least one
procedure from among codes 36.0–36.29 and 36.9–36.99 in the International
Classification of Diseases, Ninth Revision
(ICD-9). This
process of identifying study subjects has been formally assessed and has an
estimated sensitivity of 0.85, specificity of 0.99, and positive predictive
value of 0.89 (13). Each eligible study subject was aged 19 years or
older on January 1, 1996, and was continuously enrolled for care at HPMG during
the 1996 calendar year. This process identified 2947 eligible patients with
heart disease in 1996. The study was reviewed, approved, and monitored by the
HealthPartners Institutional Review Board.
Definition and measurement of variables
Trends in lipid control were necessarily based on change in LDL-C levels from
a baseline test to a follow-up test. The baseline test was defined as the first
LDL-C test done on or after January 1, 1995. The follow-up test was defined as
the most recent LDL-C test done before December 31, 1998. Furthermore, the
follow-up LDL-C test must have been done at least 365 days after the
baseline measurement. Thus, for eligible baseline and follow-up data, a study subject must have had at least two LDL-C measures at least 365
days apart between January 1, 1995, and December 31, 1998. Of 2947 eligible study
subjects aged 19 years or older with CHD, a total of 1388 (47%) had two
qualifying LDL-C measurements recorded during the specified time period.
Among the 1559 without two qualifying LDL-C measures, 155 died or disenrolled by
December 31, 1998. Changes in high-density lipoprotein cholesterol (HDL-C) were
also measured using the same definition of test dates and period between tests.
To explore associations between changes in LDL-C and statin use from
administrative data, we defined a second subpopulation. We analyzed data on
individuals with two qualifying LDL-C measurements and pharmacy
coverage provided by HealthPartners. There were 1038 in this subpopulation (75%
of study subjects with two LDL-C measurements). Pharmacy coverage was defined as
present from baseline to follow-up LDL-C tests, allowing for a gap in coverage
of up to 60 days during that period.
All lipid tests during the study period were performed at a single accredited
clinical chemistry laboratory using standard assay methods (14-16) that did not
change during the study period. Values of LDL-C were calculated in milligrams
per deciliter (mg/dL) using the Friedewald formula (17). The fasting period prior to
taking the blood sample was recorded along with each test result; only LDL-C
values drawn after a minimum 12-hour fast were used in this study. Levels of HDL-C
directly measured in mg/dL using a standard assay were also
obtained from automated laboratory databases. Changes in LDL-C or HDL-C from
baseline to follow-up were calculated as the follow-up LDL-C (or HDL-C) minus
the baseline level. A negative number thus represents improvement in LDL-C over
time, and a positive number represents
improvement in HDL-C over time.
All identified CHD patients were surveyed by mail with a telephone follow-up
(18) in 1998 to assess demographic variables, such as age, sex,
height, weight, educational level, smoking status, and aspirin use; 2122 (72%) of the
2947 study-eligible members returned surveys with complete responses on these
variables.
Administrative data were used to identify patients with CHD and their age,
sex, pharmacy coverage, filled prescriptions for statins, and filled
prescriptions for other cholesterol-acting agents. For all patients with
pharmacy coverage, pharmacy databases provided name of medication, dose
per tablet, number of tablets dispensed, and the dispense date. For multivariate analysis, we measured statin use as the portion of the days
between the baseline and follow-up LDL-C measures for which the subject had a
filled statin prescription. We measured the use of other cholesterol-acting
agents (“other use”) in the same manner. These agents included fibrates,
resins, nicotinic acid, probucol, and oral estrogens. Over-the-counter niacin
formulations were not tracked on the pharmacy database. Lipid tests and results
were available from electronic databases, as was information on health plan
enrollment.
Plan of analysis
Initial analysis was done to assess the distributions of baseline LDL-C,
follow-up LDL-C, change in LDL-C, and other lipid measures. Differences in
demographic variables between participants with and without two qualifying LDL-C
measurements were analyzed using two-sample t tests for continuous
variables and chi-square tests for count variables. The Satterthwaite
adjustment for unequal variances in two-sample tests was used when appropriate.
Changes over time in continuous variables were analyzed using the single-sample t
test of the difference between baseline and follow-up for continuous variables
and the McNemar test for count variables. Multivariate linear regression was
used to estimate relationships between the difference in baseline and follow-up
LDL-C as well as the difference in HDL-C as the key dependent variables. In all
analyses, a two-tailed α of 0.05 was used to test for significant
associations.
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Results
The overall population of individuals with at least two qualifying LDL-C
measures (n = 1388) is described in
Table 1. Although baseline and follow-up
lipid measures were required to be at least 365 days apart, the median time
between the measures was 917 days, or 2.5 years.
The mean age of study subjects with two qualifying LDL-C measures was 64.9
years; 66.6% were male, and 24.1% had a college degree. Current smoking was
reported by 7.1%, and 59.4% indicated a prior history of smoking. Regular
aspirin use was reported by 82.9%. Mean body mass index (BMI) was 27.1 kg/m2,
and 24.3% were identified as having diabetes at baseline. There were
statistically significant differences between study-eligible members with and
without two qualifying LDL-C measurements for all variables other than BMI and
baseline diabetes.
Table 2 describes LDL-C and HDL-C
measures at baseline and at
follow-up. Data are presented for all patients with qualifying LDL-C
measurements (n = 1388), for patients with baseline LDL-C >100 mg/dL (n =
1214), and for patients with baseline LDL-C >130 mg/dL (n = 781). For all
patients with qualifying measurements, there was a significant decline in
mean LDL-C, from 137.6 mg/dL at baseline to 111.0 mg/dL at follow-up, a change
of −26.6 mg/dL (P < .001). Mean HDL-C also improved, with an
increase from 42.3 mg/dL at baseline to 46.3 mg/dL at follow-up, a change of +4.0 mg/dL
(P < .001). For the subgroup with baseline LDL-C >100 mg/dL, mean
LDL-C decreased from 144.7 mg/dL at baseline to 113.5 mg/dL at follow-up, a
change of −31.2
mg/dL (P < .001). Mean HDL-C in this subgroup increased from 42.8 mg/dL
to 46.6 mg/dL, a change of
+3.8 mg/dL (P = .008). For the subgroup with baseline LDL-C
>130 mg/dL, the change in mean LDL-C was −42.5 mg/dL (P < .001),
and the change in HDL-C was +3.5 mg/dL (P = .02). The percentage of patients
in the study with LDL-C ≤100 mg/dL rose from 12.5% to 39.8% (P
< .001), and the percentage of patients with HDL-C ≥40 mg/dL
rose from 52.5% to 67.6% (P < .001).
Table 3 shows the proportion of patients receiving statins (among the 1038
subjects with pharmacy coverage and two qualifying LDL-C measures) at both
baseline and follow-up and the subsequent discontinuation rate more than 1
year later in two groups of statin users: patients who used statins at baseline
and patients who used statins at any time during the study period. Statin use among all study subjects in this group
was 24.3% at baseline and 69.6% at follow-up. In those with baseline LDL-C
>100 mg/dL, statin use was 21.0% at baseline and 70.4% at follow-up. In those
with baseline LDL-C >130 mg/dL, statin use was 16.7% at baseline and 74.2% at
follow-up. Statin discontinuation rates were 8.3% for baseline statin users,
9.5% for baseline users whose baseline LDL-C was >100 mg/dL, and 4.1% for
baseline statin users whose baseline LDL-C was >130 mg/dL. For subjects who
used statins at any time during the study period, the discontinuation rate was
12.2%.
Table 4 reports the multivariate analysis of LDL-C and HDL-C changes and
statin use for the 1038 study-eligible members with pharmacy coverage. The model
presented in Table 4 includes administrative data only. The model presented in
Table 5 adds survey data and is limited to the 804 individuals included in the
previous model who returned surveys with completed responses on variables of
interest. Residual plots showed neither excessive nonnormality in the residuals
nor heteroskedasticity.
In the models of Table 4, baseline LDL-C, sex, and statin use are significant
predictors of decreases in LDL-C. Table 5 shows that use of statins for the entire period between baseline and follow-up
measures (i.e., statin use = 1.0) was associated with an additional 17 mg/dL
decrease in LDL-C compared with no statin use. On average, men experience an
additional 7 mg/dL decrease in LDL-C compared with women. Only baseline HDL-C and
sex are significantly related to changes in HDL-C. On average, women experienced
a 1.7 mg/dL greater increase in HDL than did men. Among the variables collected
from surveys (Table 5), aspirin use was associated with a statistically
significant (6 mg/dL) decrease in LDL-C, and a 1-point decrease in BMI was associated with a 0.29 mg/dL improvement in
HDL-C.
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Discussion
We analyzed trends in LDL-C and HDL-C levels in patients with diagnosed
heart disease having two LDL-C measurements in a large medical group. Statin use
was analyzed for the subgroup of 1038 (75%) with pharmacy coverage. At baseline,
all patients had established CHD and hence would have had an NCEP-established
goal of LDL-C
<100 mg/dL at the time of the study. However, at baseline only 24.3%
were receiving statin therapy, and only 12.5% had LDL-C of ≤100 mg/dL. After a mean
follow-up period of 2.5 years, mean LDL-C and HDL-C levels had significantly
improved in the entire cohort, as well as in subgroups stratified by baseline
LDL-C of >130 mg/dL and >100mg/dL. There was a corresponding marked
increase in statin use during the follow-up period, with a significant increase
in patients achieving the study goal of LDL-C ≤100 mg/dL (12.5% at baseline vs 39.8%
at follow-up, P < .001).
These data document a significant improvement in the proportion of CHD
patients treated with statins and reaching their NCEP-established LDL-C goal in
the late 1990s (19-21). Our results favorably compare with contemporaneous data
collected on the general Minnesota population, which showed worsening
cholesterol levels in the 1990s (8). Results also favorably compare with the
survey of 48,586 individuals with coronary artery disease from practices
throughout the United States, chosen for their frequent use of cholesterol-active medications, in which 44% had annual testing of LDL-C. Of those who had
annual testing, only 25% reached the target LDL-C of ≤100 mg/dL, and only
39% were taking lipid lowering therapy (9).
The Lipid Treatment Assessment Project (L-TAP) was a comprehensive survey of
lipid therapy prescribing habits and lipid results conducted in five regions of
the United States and drawn from a group of primary care physicians, also
targeted because they wrote large numbers of prescriptions for lipid-active
drugs (10). The L-TAP study demonstrated that in a cohort of 1460 patients with CHD,
only 18% attained the NCEP-established goal of LDL-C <100 mg/dL, compared
with 39.8%
in our study who attained an LDL-C level of ≤100 mg/dL. This was despite
the fact that 84.6% received treatment with lipid lowering agents, compared with 69.6% receiving statin therapy in our study (10).
While baseline LDL-C levels were being measured for this study (median
date of October 12, 1995), a system-wide program of health-related goals was implemented at
HPMG. Among these goals was a heart-health goal that called for a
25% reduction in CHD events within 4 years (22). The importance of lipid
control in CHD patients was emphasized by medical group leaders in meetings with
primary care physicians and certain subspecialty physicians, including
cardiologists.
During the years of this study, systems of care were developed and deployed
within the medical group to support both patient and provider attention to
control of lipid disorders (22-26). Results of lipid testing were stored for
electronic retrieval via computer. Lipid test results, with an explanation
and recommendations, were mailed to patients. High-risk patient registries that
included adults with CHD or diabetes and LDL-C test results or indicated a need to obtain an LDL-C test were provided to clinics and physicians as an aid for tracking, visit
planning, and active outreach. One of the authors (RJG) gave a series of
lectures at each medical group clinic about the use and benefits of lipid-lowering therapy. Also, a specialized program known as Lifestyle Management was
added to the cardiac rehabilitation program. This program featured
one-on-one sessions with nursing staff for patients and follow-up case
management, as well as a direct review of each patient’s care plan and
progress by the medical director. During the study period, it also became
commonplace to initiate statin therapy before hospital discharge following an
acute cardiac event, such as a myocardial infarction. These programs, initiated
to aggressively reduce cardiovascular events in high-risk patients during the
study period, likely accounted for some of the observed improvement in lipid
control. It is unlikely that secular trends accounted for all the improvement,
because few other medical groups have achieved similar levels of lipid drug use
(27) or lipid control (28), and lipid trends in Minnesota during these years were
not improving (8).
Several factors limit the interpretation of the data presented here. First,
misclassification of CHD status is a possibility; however, we used a validated
method for heart disease identification with an estimated sensitivity of 0.85 and a
positive predictive value of 0.89 (13). Second, the study was limited to one
large medical group in Minnesota. Studies in a variety of other settings may be
needed to replicate and extend the findings reported here. Finally, the
requirement that each patient have at least two LDL-C measurements over an
average 30-month period may have identified a population of patients having
more active management of dyslipidemia. However, this selection strategy was
essential, given our intent to assess trends of LDL-C and statin use over time.
We were unable to compare patients with and without qualifying LDL-C measures in
relation to baseline LDL-C levels or statin use. We observed at least one LDL-C in only
a portion of those without two LDL-C measurements, and the majority of the
single LDL-C measures that exist were observed near the end of the 4-year
study period. Therefore, the available LDL-C measures for the group excluded
from the analysis do not provide an analogous baseline LDL-C measure.
Likewise, our measure of statin use is tied to LDL-C baseline and follow-up
measures and could not be computed for participants without two qualifying measures.
We conclude that substantial improvement in LDL-C and HDL-C control occurred
in adults with CHD at this practice site during the late 1990s. The main cause
of the improvement was a dramatic increase in statin use, which was
significantly related to LDL-C change. However, other factors contributed to
improved lipid control in this population, including coordination of use of
clinical guidelines among clinics, use of high-risk patient registries, and use
of automated monitoring and prioritizing of patients for special attention. As LDL-C goals become more stringent (3,4,6), the application of effective
outpatient chronic disease care strategies such as registries, active outreach,
visit planning, and coordination of care across sites will increase in
importance. These data show that primary care clinics and providers are capable
of dramatic improvements in care over a short period and suggest that
resources invested to improve outpatient care can rapidly return a sizeable
clinical return on investment.
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Acknowledgments
This study was funded by a research grant from Merck & Co, Inc to
HealthPartners Research Foundation.
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Author Information
Corresponding Author: Patrick J. O’Connor, MD, MPH, Senior Clinical
Investigator, HealthPartners Research Foundation and HealthPartners Medical
Group, PO Box 1524, Mail Stop 21111R, Minneapolis, MN 55440-1524. Telephone:
952-967-5034. E-mail: Patrick.J.Oconnor@HealthPartners.com.
Author Affiliations: Richard J. Gray, MD, Michael V. Maciosek, PhD, Kelly M.
Fillbrandt, BS, Terese A. DeFor, MS, HealthPartners Research Foundation and
HealthPartners Medical Group, Minneapolis, Minn; Charles M. Alexander, MD,
Thomas W. Weiss, DrPH, Steven M. Teutsch, MD, MPH, Merck & Co, Inc, West
Point, Pa.
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