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The American Journal of Medicine (2007) 120, 734.e11-734.e17

LINICAL RESEARCH STUDY

ctive Lipid Management In Coronary Artery DiseaseALMICAD) Study

anjaya Khanal, MD, Omar Obeidat, MD, Michael P. Hudson, MD, Mouaz Al-Mallah, MD, Mary Bloome, PharmD,ei Lu, PhD, Adam B. Greenbaum, MD, Aaron D. Kugelmass, MD, W. Douglas Weaver, MD
enry Ford Hea
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ABSTRACT

URPOSE: Many providers have implemented specialized lipid clinics to more effectively identify,onitor, and treat hyperlipidemia in patients with coronary artery disease. The effectiveness of such a

trategy is not known. We sought to investigate whether a specialized clinic achieves better lipid resultsnd clinical outcomes than standard care.UBJECTS AND METHODS: A total of 1233 patients who had coronary disease documented by coronaryngiography were randomized to lipid clinic or standard care groups by their providers and followed for 2 years.he primary end point was a composite of death, myocardial infarction, repeat revascularization, and stroke.ESULTS: Lipid clinic (n � 617) and standard care (n � 616) groups had no significant baseline differ-nces. After 2 years, the lipid clinic group had similar total cholesterol (166 � 42 mg/dL vs 166 � 41g/dL, P � .83), low-density lipoprotein cholesterol levels (84 � 32 vs 85 � 32, P � .28), and percentage

f patients with low-density lipoprotein cholesterol less than 100 mg/dL (77.5% vs 77.6%, P � .97). Thereere no significant differences in the primary end point (12.3% vs 11.4%, P � .60) and mortality (7.6%s 7.3%, P � .80) between the lipid clinic and standard care groups.ONCLUSIONS: In patients identified by diagnostic coronary angiography and managed within aingle health care system, implementation of a specialized lipid clinic did not achieve greaterttainment of hyperlipidemia treatment goals or improved cardiac outcomes. © 2007 Elsevier Inc. Allights reserved.

KEYWORDS: Lipid clinic; Outcomes; Secondary prevention

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reatment of hyperlipidemia in patients with risk factorsor cardiovascular disease or established atherosclerosiseduces adverse cardiovascular outcomes.1-7 Secondaryrevention of coronary artery disease with 3-hydroxy-3-ethylglutaryl-CoA reductase inhibitors (statins) is both

fficacious and cost-effective.8 Although statins haveevolutionized lipid-lowering therapy and have been aajor advance in primary and secondary coronary artery

isease prevention, there is still controversy concerning

Supported in part by unrestricted grants from Merck and Co,ew Jersey, and Henry Ford Heart and Vascular Institute, Detroit,ichigan.

Correspondence should be addressed to Sanjaya Khanal, MD, K-2,ardiac Catheterization Laboratory, Henry Ford Hospital, 2799 W Grandlvd, Detroit, MI 48202.

a: [email protected]

ront matter © 2007 Elsevier Inc. All rights reserved.ed.2006.06.048

arget lipid levels, risk-stratified dose adjustment, andptimal systems of patient management and monitoring.9

ften the highest risk patients are not treated to theecommended target levels according to randomized clin-cal trials.10,11 Some health care systems and providersse specialized lipid clinics in an attempt to more effec-ively identify, monitor, and treat patients with hyperlip-demia, often at significant expense. There are no datahether patients with coronary artery disease treated foryperlipidemia by specialized lipid clinics have betterutcomes than conventional treatment and follow-up. Weherefore conducted the Active Lipid Management Inoronary Artery Disease (ALMICAD) trial to testhether a specialized lipid clinic achieves better results

nd clinical outcomes than standard care in patients with
ngiographically documented coronary artery disease.

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734.e12 The American Journal of Medicine, Vol 120, No 8, August 2007

ETHODS

atient Populationetween April 2002 and February 2004, 1233 patientsere enrolled in the study from a single center (Figure 1).ritten informed consent was ob-

ained from all patients. Patientsho were more than 18 years of

ge and had angiographic coro-ary artery disease during diag-ostic coronary angiography wereandomized to either the lipidlinic or standard care. Coronaryrtery disease was defined as anyuminal diameter stenosis of 20%r more in an epicardial coronaryrtery with a diameter of 2 mm orore. Patients were excluded if

hey had participated in any othernvestigational study within 30ays, were pregnant or breastfeed-ng, or were already being fol-owed by a lipid clinic at the timef enrollment. Patients were notxcluded on the basis of currentipid levels or statin use at the timef enrollment. The study enrollment was stopped in Oc-ober of 2004 when it was determined by a monitoringommittee that there was little likelihood of showing alinical difference between the 2 treatment groups. Clin-cal follow-up was obtained for 24 months in all enrolledatients. Some 6% of patients (79/1233) were lost toollow-up at 24 months (Figure 1). Mortality was con-rmed in all enrolled patients using the national death

CLINICAL SIGNIF

● Follow-up in aresulted in simiment of targetoutcomes compaby patient care p

● Educating providment and emphdose statin uselished coronaryequally approprcompared withspecialized lipid

Figure 1 Screening, enroll

egistries. Only 13 patients had less than a 6-monthlinical follow-up, and 4 patients had no clinical fol-ow-up since enrollment. All analyses were done on anntention-to-treat basis.

Study Design and ProtocolThis was a single-center, prospec-tive, open-label, outpatient, ran-domized study to compare activelipid management in the lipidclinic versus usual care by the pa-tients’ care providers. Patientspresenting to the cardiac catheter-ization laboratory were asked toparticipate in the study, sign in-formed consent form, and providefasting blood samples. Patientswere randomly assigned in a 1:1ratio to the lipid clinic or theirusual caregivers (standard ther-apy) for lipid management. All pa-tients had assigned primary careproviders within the health sys-tem, and nearly all patients hadprecatheterization evaluation by acardiologist. Patient demographics

nd clinical, angiographic, and fasting lipid profiles wereollected at the time of enrollment. Primary care and car-iology providers of both patient groups were notified of thengiography results and had electronic medical record ac-ess to baseline and all subsequent lipid testing results.atients randomized to the lipid clinic were managed in apecialized telephone-based computerized clinic staffed byrained nonphysician health care professionals using a pro-

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734.e13Khanal et al Active Lipid Management In Coronary Artery Disease Study

rietary lipid workflow program. The lipid clinic followed atandard lipid management algorithm based on patients’ipid levels and response to therapy (Figure 2). Delegatedhysician authority was given to the lipid clinic staff toptimize drug therapy by escalating doses of statins tochieve target lipid levels, provide lifestyle counseling,anage medication side effects, monitor laboratory results,

nd ensure patient medication and laboratory compliance byail or telephone. The aim was to maximize statin therapy

nd achieve a low-density lipoprotein (LDL) cholesterolevel less than 100 mg/dL (Figure 2). All changes in treat-ent were electronically communicated to their physician.ll patients enrolled in the study were scheduled to have a

asting serum lipid profile and alanine aminotransferaseALT) measured at 6 months and 2 years. Clinical data werelso collected at the same intervals through telephone inter-iews and chart reviews.

nd Pointshe primary end point of this study was to compare the

ncidence of major adverse cardiac events (MACE), defineds the composite of death, nonfatal myocardial infarction,troke, percutaneous coronary intervention, and coronaryrtery bypass surgery at 2 years follow-up between the lipid

igure 2 Lipid clinic algorithm. FLPP � fasting lipid profile; Aerol. %Statins: May substitute simvastatin with atorvastatin or prand increase as tolerated to 3 g/d. �Fibrates: fenofibrate 67 mg/dBile acids: colesevelam 625 mg, 3 tablets twice per day with meaith meals.

linic group and the standard care group. Secondary end (

oints included individual components of the primary endoint and target LDL cholesterol level of less than 100g/dL at 6 months and 2 years. Death was defined as death

ue to any cause. Myocardial infarction was defined as theresence of either 2 of the 3 following criteria: chest pain ofnginal character lasting more than 30 minutes, biochemicalarker of myocardial damage (troponin or creatine phos-

hokinase MB-fraction), or new Q-waves in a standard2-lead electrocardiogram in 2 or more contiguous leads.troke was defined as any permanent, documented (clini-ally and/or by neurologic imaging) neurologic impairment.ercutaneous coronary intervention was defined as any cor-nary balloon angioplasty, stent implantation, and atherec-omy or thrombus removal other than in the index enroll-ent period. Coronary artery bypass surgery included any

oronary bypass procedure in the follow-up period. Rehos-italization was defined as admission to the hospital withardiac symptoms requiring 1 day or more in the hospital.ll analysis was done as intention to treat.

tatistical Analysisll data were maintained, monitored, and analyzed by a

entral data-coordinating center. Statistical analyses wereone using SAS (SAS Institute Inc, Cary, NC) or SPSS

lanine aminotransferase; D/C � discontinue; LDL � LDL choles-in at equivalent doses. #Niacin (long acting): Start with 500 mg/dimum 200 mg/d; may substitute gemfibrozil 600 mg twice daily.

y substitute cholestyramine or colestipol 2 to 6 scoops twice daily

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SPSS Inc, Chicago, Ill) statistical software. Continuous

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ariables were reported as means and standard deviationsnd compared with a 2-sample t test. The categoric variablesere reported as proportions and compared with chi-square

nd Fisher exact tests. The primary end point was calculateds the percentage of enrolled patients between the groupsnd compared with the chi-square test. The difference invent-free survival was also evaluated with survival curvessing the Kaplan-Meier method and compared with theog-rank test. A P value of less than .05 was consideredignificant. The Henry Ford Hospital Institutional Reviewoard approved the study protocol.

On the basis of an initial pilot 100-patient data collection,e anticipated a 60% rate of statin use and a 27% MACE

ncidence over 2 years of follow-up in the control group.hus, after accounting for a 5% expected dropout rate, we

ntended to enroll 2260 patients in the trial to provide 80%r greater power to detect a 20% primary end point reduc-ion in the lipid clinic group using a 2-sided alpha � 0.05.tudy conduct, enrollment, and data collection were re-iewed throughout by a Steering Committee blinded toroup assignment. The Steering Committee recommendedarly termination of patient enrollment in October of 2004fter randomization of 1233 patients because of apparent

Table 1 Baseline Characteristics of Patients

Variable

Demographics and historyAge, y (mean � SD)Male sex, No. (%)White race, No. (%)Hypertension, No. (%)Diabetes, No. (%)Family history of CAD, No. (%)Current smoker, No. (%)History of hyperlipidemia, No. (%)Prior myocardial infarction, No. (%)Prior percutaneous coronary intervention, No. (%)Prior coronary bypass surgery, No. (%)Prior stroke, No. (%)Peripheral vascular disease, No. (%)Medications at enrollmentAspirin, No. (%)Beta-blocker, No. (%)ACE inhibitor, No. (%)Statin, No. (%)Indications for angiography and findingsUnstable angina, No. (%)ST-elevation MI, No. (%)Non ST-elevation MI, No. (%)Abnormal stress test, No. (%)Left ventricular ejection fraction (mean � SD)Severe (�70% diameter) coronary stenosis, No. (%)1-vessel disease, No. (%)2-vessel disease, No. (%)3-vessel disease, No. (%)Left main disease, No. (%)

SD � standard deviation; CAD � coronary artery disease; ACE � angio

nadequate group differences in lipid results. All enrolled L

atients were followed for at least 24 � 6 months for lipidesults and clinical end points.

ESULTSatients in the 2 groups were demographically and clinicallyell matched at baseline (Table 1). Sixty percent of 617atients in the lipid clinic group and 63% of the 616 patientsn the standard care group were receiving statin therapy athe time of enrollment (P � .59). The percentages of pa-ients with LDL cholesterol less than 100 mg/dL at studyntry were 45% and 48% (P � .59) in the lipid clinic andtandard care groups, respectively (Table 2).

rimary End Pointhere was no difference in the composite primary end pointf major cardiovascular events between the 2 groups (12.3%s 11.4%, P � .62) (Figure 3). Time-to-event analysis usingvent-free Kaplan-Meier survival curves did not show aifference in outcomes between the groups (Figure 4).

econdary Lipid End Pointshere were no differences in the proportion of patients with

pid Clinic� 617

Standard CareN � 616 P value

� 11 65 � 11 .741 (62) 386 (63) .917 (66) 386 (63) .600 (79) 505 (82) .742 (33) 221 (36) .459 (34) 207 (34) .992 (17) 119 (19) .328 (79) 475 (77) .808 (19) 127 (21) .644 (22) 124 (20) .638 (16) 86 (14) .466 (7) 39 (6) .541 (13) 66 (11) .28

1 (81) 500 (81) .998 (66) 442 (72) .386 (48) 294 (48) .999 (60) 389 (63) .59

2 (28) 176 (29) .888 (3) 21 (3) .756 (16) 86 (14) .551 (39) 255 (41) .62� 14 50 � 12 .955 (69) 438 (71) .751 (47) 220 (52) .457 (30) 91 (21) .030 (16) 94 (21) .097 (6) 24 (5) .79

-converting enzyme; MI � myocardial infarction.

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63.4% vs 58.3%, P � .10) or 2 years (77.5% vs 77.6%,� .96) between the lipid clinic and standard care groups,

espectively. At 6 months, the lipid clinic group had lowerotal cholesterol (170 � 39 mg/dL vs 177 � 40 mg/dL,� .04) and LDL cholesterol (94 � 33 mg/dL vs 98 � 33g/dL, P � .03) (Table 3). There was no difference in total

holesterol (166 � 42 mg/dL vs 166 � 41 mg/dL , P � .83)nd LDL cholesterol (84 � 32 mg/dL vs 85 � 32 mg/dL,� .28) at the 2-year follow-up (Table 3). The lipid clinic

roup had marginally higher high-density lipoprotein cho-esterol (53 � 16 mg/dL vs 51 � 15 mg/dL, P � .017). Moreatients in the lipid clinic group were receiving statins at 6onths (84% vs 79%, P � .02) and 2 years (94% vs 88%,� .001). The mean ALT was similar between the groups

t 6 months and the end of the study. Four patients in theipid clinic group and 1 patient in the standard care groupad an ALT level 3 times greater than normal values. Oneatient in the lipid clinic group developed reversible hepaticnsufficiency, which was later confirmed to be caused byiral hepatitis. There were no cases of rhabdomyolysis clin-cally reported in the study population.

ISCUSSIONn a US tertiary care setting, we showed that implementationf a lipid clinic does not improve long-term hyperlipidemiaanagement or clinical outcomes among patients with an-

iographically documented coronary artery disease.Many studies have demonstrated that secondary preven-

ion with statins in patients with established coronary arteryisease results in improved cardiovascular outcome.1-6

ore recent studies have demonstrated that statins reduce

Table 2 Baseline Lipid Profiles of Patients

VariableLipid CliniN � 617

Total cholesterol mg/dL � SD 180 � 47LDL cholesterol mg/dL � SD 107 � 38Triglycerides mg/dL � SD 153 � 125HDL cholesterol mg/dL � SD 44 � 13ALT Units/L � SD 28 � 82% with LDL �100 mg/dL 45

SD � standard deviation; LDL � low-density lipoprotein; HDL � high

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Standard Care

igure 3 Comparison of clinical outcomes at 2 years (%)etween the groups. MACE � major adverse cardiac events,I � myocardial infarction, PCI � percutaneous coronary in-

vervention, CABG � coronary bypass surgery.

ardiovascular events regardless of the pretreatment LDLholesterol level in higher risk patients.1,7 Therefore, re-ised guidelines have recommended even more aggressiveDL reduction in such patients, advocating LDL cholesterol

arget concentrations of less than 70 mg/dL in patients withcute coronary syndromes or ongoing risk factors.12

Most positive randomized studies using statins for sec-ndary therapy have generated differences of 20 to 40g/dL between treatment and control groups, leading to

ignificant difference in clinical outcome.1-7 The standardare group in the ALMICAD trial had a baseline LDLoncentration of 106 mg/dL, a 63% rate of statin use attudy entry, and an 88% rate of statin use at study end.herefore, only a modest difference of 4 mg/dL waschieved in LDL cholesterol at 6 months, which entirelyesolved at 2 years in the lipid clinic group versus standardare group. In this patient cohort, a specialized lipid clinicntervention had no clinical benefit because the majority ofhe patients in the control group were receiving high dosesf effective statin therapy throughout the study. Because aajority of patients were already receiving statin therapy

nd had relatively low LDL cholesterol enrollment, the

igure 4 Kaplan-Meier major cardiovascular event-free sur-

Standard CareN � 616 P value

181 � 47 .86106 � 37 .72162 � 188 .3643 � 12 .3223 � 16 .23

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esultant low major cardiovascular event rate made it hardero show a difference between the treatment groups.

Small sample size, a short follow-up duration, and sig-ificantly lower than expected rates of MACE also dimin-shed the opportunity for demonstrating lipid clinic benefit.his current study enrolled only half the calculated sampleize and terminated early, limiting its ability to statisticallyvaluate differences in clinical outcomes. However, it isnlikely that the minimal initial difference in cholesterolevels would have resulted in significant differences in clin-cal outcome if sample size or follow-up duration was in-reased. The rate of primary end point was significantlyower than expected because of case selection and high ratesf coronary artery disease secondary prevention efforts. It isossible that enrollment in the study may have sensitized orersuaded patients and providers toward more aggressiveipid management in this nonblinded study. It is more likelyhat the high rates of effective coronary artery disease sec-ndary prevention in both groups were due to access andxposure to cardiologists before and after coronary angiog-aphy, and to our health care system’s emphasis on modi-ying coronary artery disease prognosis using aspirin,eta-blocker, angiotensin-converting enzyme inhibitor, re-ascularization, and high-dose statin therapy in all eligibleatients. It is not clear whether a stricter treatment algorithmaim for LDL cholesterol � 70 mg/dL), upfront treatmentith potent high-dose statins, or treatment of only patientsith hyperlipidemia would have resulted in a differentutcome.

Despite robust data about secondary prevention and na-ional guidelines, hyperlipidemia is not adequately treatedn clinical practice.9 The highest risk patients with estab-ished coronary artery disease, who benefit the most fromipid-lowering therapy, historically achieve LDL cholesterolargets at low rates in practice.10,11 Treatment of theseatients in some specialized clinics has demonstrated betteripid control, but clinical efficacy studies are lacking.13,14

herefore, resources required to implement such clinicsave to be balanced with the potential benefits. A recenttudy reported that an aggressive atorvastatin treatment of

Table 3 Comparison of Lipid Profiles at Six Months and Study

Variable Lipid Clinic

6 moTotal cholesterol mg/dL 170 � 39LDL cholesterol mg/dL 94 � 33Triglycerides mg/dL 157 � 105HDL cholesterol mg/dL 45 � 132 yTotal cholesterol mg/dL 166 � 42LDL cholesterol mg/dL 84 � 32Triglycerides mg/dL 145 � 94HDL cholesterol mg/dL 53 � 16ALT Units/L � SD 24 � 18

LDL � low-density lipoprotein; HDL � high-density lipoprotein; ALT �

atients with coronary artery disease in lipid-lowering dis- d

ase-managed clinics resulted in better clinical outcomehan usual care.15 These patients, however, were treatedith the aim to achieve LDL cholesterol less than 80 mg/dLith high-dose statins and followed for an average of 51.5onths.In our health care system, implementation of a lipid

linic failed to improve clinical outcomes largely becauseatients in the control group received similar aggressiveipid-lowering therapy. Study patients were dispersedhroughout a large metropolitan area, and the lipid clinicmployed midlevel providers to manage patients’ lipidshrough telephone and mail encounters. Medication sta-us, lipid levels, and other laboratory safety parametersere monitored through proprietary computer software.ther health care systems with less cardiologist access or

oronary artery disease prevention emphasis might gen-rate more robust differences in lipid and clinical out-omes using a specialized lipid clinic or a more aggres-ive lipid management algorithm. However, experiencerom this study shows that it is likely that educating careroviders about lipid management and emphasis on uni-ersal high-dose statin use in patients with establishedoronary artery disease may be equally appropriate usesf resources compared with managing patients in special-zed lipid clinics.

ONCLUSIONShis study demonstrates that follow-up in a specialized

ipid clinic results in similar long-term achievement ofarget lipid goals and clinical outcomes compared withtandard care by patient care providers. In a health careystem with ready access to cardiovascular specialistsnd emphasis on aggressive coronary artery disease pre-ention, implementation of a lipid clinic does not im-rove clinical outcomes.

CKNOWLEDGMENTSe acknowledge the Henry Ford Coordinating Center, Car-

letion

Standard Care P Value

177 � 40 .00498 � 33 .03

168 � 116 .1546 � 13 .56

166 � 41 .8385 � 32 .28

147 � 95 .4751 � 15 .0223 � 14 .26

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nd study coordinators Lori Douthat, Diana Sydlowski, andebra Hochberg for study support.

eferences1. Heart Protection Study Collaborative Group. MRC/BHF heart protec-

tion study of cholesterol lowering with simvastatin in 20536 high-riskindividuals: a randomised placebo-controlled trial. Lancet. 2002;360:7-22.

2. Shepherd J, Cobbe SM, Ford I, et al., for the West of ScotlandCoronary Prevention Study Group. Prevention of coronary heart dis-ease with pravastatin in men with hypercholesterolemia. N Engl J Med.1995;333:1301-1307.

3. Downs JR, Clearfield M, Weis S, et al., for the AFCAPS/TexCAPSResearch Group. Primary prevention of acute coronary events withlovastatin in men and women with average cholesterol levels: resultsof AFCAPS/TexCAPS. JAMA. 1998;279:1615-1622.

4. Scandinavian Simvastatin Survival Study Group. Randomized trial ofcholesterol lowering in 4444 patients with coronary heart disease: TheScandinavian Simvastatin Survival Study (4S). Lancet. 1994;44:1383-1389.

5. Sacks FM, Pfeffer MA, Moye L, et al. The effect of pravastatin oncoronary events after myocardial infarction in patients with averagecholesterol levels. N Engl J Med. 1996;335:1001-1009.

6. The Long-term Intervention with Pravastatin in Ischemic Disease(LIPID) Study Group. Prevention of cardiovascular events and deathwith pravastatin in patients with coronary heart disease and a broadrange of initial cholesterol levels. N Eng J Med. 1998;339:1349-1357.

7. Cannon CP, Braumwald E, McCabe CH, et al., for the Pravastatinor Atorvastatin Evaluation and Infection Therapy-Thrombolysis in
Myocardial Infarction-22. Intensive versus moderate lipid lowering
with statins after acute coronary syndromes. N Engl J Med.2004;350:1495-1504.

8. Yusuf S, Anand S. Cost of prevention: the case of lipid lowering.Circulation. 1996;93:1774-1776.

9. Expert Panel on Detection Evaluation and Treatment of High BloodCholesterol in Adults. Executive summary of the third report of theNational Cholesterol Education Program (NCEP) expert panel ondetection, evaluation, and treatment of high blood cholesterol in adults(Adult Treatment Panel III). JAMA. 2001;285:2486-2497.

0. Pearson TA, Laurora I, Chu H, Kafonek S. The lipid treatment assess-ment project- a multicenter survey to evaluate the percentages ofdyslipidemic patients receiving lipid-lowering therapy and achievinglow-density lipoprotein cholesterol goals. Arch Intern Med. 2000;160:459-467.

1. Marcello JJ, Feingold K. Inadequate treatment with HMG-CoAreductase inhibitors by health care providers. Am J Med. 1996;100:605-610.

2. Grundy SM, Cleeman JI, Merz NB, et al., for the Coordinating Com-mittee of the National Cholesterol Education Program. Implications ofthe recent clinical trials for the National Cholesterol Education Pro-gram Adult Treatment Panel III guidelines. J Am Coll Cardiol. 2004;44:720-732.

3. Bloome M, Saier R, Bronken T, Zarowitz B. Tele health attainment oflipid goals through automated workflow technology. Pharmacother-apy. 2000;20:1259.

4. Harris DE, Record NB, Gipson GW, Pearson TA. Lipid lowering in amultidisciplinary clinic compared with primary physician manage-ment. Am J Cardiol. 1998;81:929.

5. Koren MJ, Hunninghake DB, ALLIANCE Study investigators. Clin-ical outcomes in managed-care patients with coronary heart diseasetreated aggressively in lipid-lowering disease management clinics.
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