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Serruys PWJC, de Feyter P, Macaya C, et al. Fluvastatin for Prevention of Cardiac Events Following Successful First Percutaneous Coronary Intervention: A Randomized Controlled Trial. JAMA. 2002;287(24):3215–3222. doi:10.1001/jama.287.24.3215
Author Affiliations: Interventional Cardiology, Thoraxcenter, Academic Hospital, Rotterdam, the Netherlands (Drs Serruys and de Feyter); Cardiology Department, Hospital San Carlos, Madrid, Spain (Dr Macaya); Cardiology Department, Hopital Purpan, Toulouse, France (Dr Puel); Cardiology Department, St Jan Hospital, Genk, Belgium (Dr Vrolix); Cardiology Department, Ospedale Santa Orsola, Bologna, Italy (Dr Branzi); Institute Dante Pazzanese of Cardiology, Sao Paulo, Brazil (Dr Bertolami); Cardiology Department, Guys Hospital, London, England (Dr Jackson); Division of Cardiology, St Michaels Hospital, Toronto, Ontario (Dr Strauss); Medical Department, Cardiology, University Hospital Insel, Bern, Switzerland (Dr Meier). Dr Kokott is in cardiological private practice affiliated with Koepenick Hospital, Berlin, Germany.
Context Percutaneous coronary intervention (PCI) is associated with excellent
short-term improvements in ischemic symptoms, yet only three fifths of PCI
patients at 5 years and one third of patients at 10 years remain free of major
adverse cardiac events (MACE).
Objective To determine whether treatment with fluvastatin reduces MACE in patients
who have undergone PCI.
Design and Setting Randomized, double-blind, placebo-controlled trial conducted at 77 referral
centers in Europe, Canada, and Brazil.
Patients A total of 1677 patients (aged 18-80 years) recruited between April
1996 and October 1998 with stable or unstable angina or silent ischemia following
successful completion of their first PCI who had baseline total cholesterol
levels between 135 and 270 mg/dL (3.5-7.0 mmol/L), with fasting triglyceride
levels of less than 400 mg/dL (4.5 mmol/L).
Interventions Patients were randomly assigned to receive treatment with fluvastatin,
80 mg/d (n = 844), or matching placebo (n = 833) at hospital discharge for
3 to 4 years.
Main Outcome Measure Survival time free of MACE, defined as cardiac death, nonfatal myocardial
infarction, or reintervention procedure, compared between the treatment and
Results Median time between PCI and first dose of study medication was 2.0 days,
and median follow-up was 3.9 years. MACE-free survival time was significantly
longer in the fluvastatin group (P = .01). One hundred
eighty-one (21.4%) of 844 patients in the fluvastatin group and 222 (26.7%)
of 833 patients in the placebo group had at least 1 MACE (relative risk [RR],
0.78; 95% confidence interval [CI], 0.64-0.95; P
= .01). This result was independent of baseline total cholesterol levels (above
[RR, 0.76; 95% CI, 0.56-1.04] vs below [RR, 0.77; 95% CI, 0.57-1.02] the median).
In subgroup analysis, the risk of MACE was reduced in patients with diabetes
(n = 202; RR, 0.53; 95% CI, 0.29-0.97; P = .04) and
in those with multivessel disease (n = 614; RR, 0.66; 95% CI, 0.48-0.91; P = .01) who received fluvastatin compared with those who
received placebo. There were no instances of creatine phosphokinase elevations
10 or more times the upper limit of normal or rhabdomyolysis in the fluvastatin
Conclusion Fluvastatin treatment in patients with average cholesterol levels undergoing
their first successful PCI significantly reduces the risk of major adverse
Percutaneous coronary intervention (PCI) comprises a group of procedures
that are used to relieve ischemic symptoms due to coronary atherosclerotic
narrowing in patients with increasingly earlier stages of coronary heart disease
(CHD). The most frequently performed PCI procedure is balloon angioplasty
with or without stenting. In the United States, balloon angioplasty procedures
increased nearly 4-fold between 1987 and 1999, and in 1999, 1.1 million angioplasty
procedures, both with and without stent placement, were performed in the United
Percutaneous coronary intervention has been demonstrated to be at least
as effective as coronary artery bypass grafting (CABG) in terms of survival
and prevention of myocardial infarction (MI) in appropriately selected patients
with either single-vessel or multivessel disease.2,3
Although PCI achieves short-term improvements in ischemic symptoms in 9 of
10 patients who undergo the procedure, patients continue to have high rates
of postprocedure cardiovascular events. Approximately 3 of 5 patients at 5
years and only 1 of 3 patients at 10 years remain free of major adverse cardiac
Lipid-lowering treatment with 3-hydroxy-3-methylglutaryl coenzyme A
reductase inhibitors (statins) has been shown to significantly reduce the
incidence of cardiovascular events in patients with CHD5-8
but not to reduce the 6-month restenosis rate after PCI.9-11
Data supporting the benefit of these treatments following PCI are currently
limited to retrospective analyses and to patients at relatively advanced stages
of cardiac disease, with average or high pretreatment cholesterol values,
and with statin treatment initiated 6 months or later following PCI.
Until recently, lipid-lowering treatment with statins was a neglected
therapeutic approach in patients undergoing PCI. In a European study assessing
the relation between serum cholesterol and long-term restenosis following
coronary angioplasty in 2753 patients, only 9.7% of patients with total cholesterol
levels of less than 301 mg/dL (7.8 mmol/L) and 17.2% of those with a level
of 301 mg/dL (7.8 mmol/L) or greater were receiving lipid-lowering treatment
at trial entry. Less than 25% were taking lipid-lowering drugs at 6-month
follow-up.12 In a recently published survey
conducted in 1 center in the United States,13
only 26.5% of 5052 patients undergoing PCI between 1993 and 1999 were receiving
statin treatment at the time of the procedure.
The Lescol Intervention Prevention Study (LIPS) was designed to investigate
whether cholesterol lowering with fluvastatin, initiated within days following
successful completion of first PCI (with or without stenting), would prolong
cardiac disease–free survival time compared with placebo.
A detailed description of the study design of LIPS has been reported.14 The study was a double-blind, randomized placebo-controlled
trial. Men and women aged 18 to 80 years were recruited from 57 interventional
centers in 10 countries (Belgium, France, Germany, Italy, United Kingdom,
the Netherlands, Spain, Switzerland, Canada, and Brazil). All patients had
successfully undergone their first PCI (index procedure) of 1 or more lesions
in the native coronary arteries. Successful PCI was defined as a reduction
of the stenosis diameter to less than 50% in the target lesion without evidence
of myocardial necrosis, need for repeat PCI or CABG, or death before hospital
discharge. Any type of PCI was allowed and included balloon angioplasty with
or without stent placement, rotational or directional atherectomy, laser ablation,
transluminal extraction catheter, or cutting balloon. The procedure was performed
during 1 hospital stay at one of the 57 recruiting interventional centers,
and patients were followed up after hospital discharge at the same clinic
or at a referral center, with a total of 77 sites participating in the study.
Patients were eligible for enrollment in the study if they had a total
cholesterol level between 135 and 270 mg/dL (3.5-7.0 mmol/L), with fasting
triglyceride levels of less than 400 mg/dL (4.5 mmol/L) before the index procedure.
The upper total cholesterol limit for eligibility was 212 mg/dL (5.5 mmol/L)
for patients whose baseline lipids were measured from blood drawn 24 hours
to 4 weeks following MI and 232 mg/dL (6.0 mmol/L) for patients with type
1 or 2 diabetes mellitus. Exclusion criteria included sustained systolic blood
pressure of more than 180 mm Hg and diastolic blood pressure of more than
100 mm Hg despite medical therapy, left ventricular ejection fraction of less
than 30%, a history of previous PCI or CABG, severe valvular disease, idiopathic
cardiomyopathy or congenital heart disease, severe renal dysfunction (defined
as serum creatinine level >1.8 mg/dL [160 µmol/L]), obesity (defined
as a body mass index >35 kg/m2), and the presence of malignant
or other disease with a life expectancy of less than 4 years. All patients
provided written informed consent, and the ethics committee at each participating
center approved the trial.
After inclusion, patients were randomly assigned to receive either fluvastatin,
40 mg twice per day (Lescol, Novartis Pharma AG, Basel, Switzerland) or matching
placebo for a period of at least 3 years and no longer than 4 years. Patients
were to be allocated to treatment in the order in which they were enrolled
into the study at each center according to medication pack numbers using block
randomization, with each interventional center receiving multiple blocks.
All patients received dietary and lifestyle counseling at hospital discharge.
Investigators remained blinded to all lipid values unless total cholesterol
exceeded 278 mg/dL (7.2 mmol/L); in that case, the central laboratory informed
the appropriate clinical investigators. If the total cholesterol level remained
higher than 278 mg/dL (7.2 mmol/L) for 3 months or more, patients were to
discontinue study medication at the discretion of the study investigator and
receive an open-label statin or other lipid-lowering therapy. Investigators
were requested not to perform any determination of serum lipid levels in the
local laboratory during the course of the study. The protocol did not restrict
or specify any other diagnostic or therapeutic measures except as indicated
in the exclusion criteria.
Patients were assessed at the referral trial centers at week 6 after
randomization and every 6 months thereafter. All attempts were made to retain
patients in the study regardless of trial medication intake.
Laboratory measures, including serum total cholesterol, low-density
lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C),
and fasting triglyceride levels, were assessed at a central laboratory (Analytico
Medinet, Breda, the Netherlands) from fasting blood samples.
The primary clinical composite end point was development of a MACE,
defined as cardiac death (any death unless an unequivocal noncardiac cause
could be established); nonfatal MI (appearance of pathological Q waves that
were absent at baseline or a total creatine kinase level >2 times the upper
limit of normal [ULN] with presence of CK isoenzyme MB higher than the ULN);
or a reintervention procedure (CABG, repeat PCI, or PCI for a new lesion).
Angiographic assessments without interventions were not included.
Prespecified secondary clinical end points were MACE, excluding reintervention
procedures (surgical or PCI) occurring in the first 6 months of follow-up
for lesions treated at the index procedure, cardiac mortality, noncardiac
mortality, all-cause mortality, combined cardiac mortality and MI, and combined
all-cause mortality and MI. Secondary end points also included treatment effects
on measured lipid levels throughout the trial, as well as the safety and tolerability
An independent critical events committee blinded to treatment assignment
reviewed all deaths and suspected nonfatal MIs for adjudication, and all analyses
were based on the committee's classification of the end points.
All analyses of the primary and secondary end points were performed
with results stratified by treatment center. All randomized patients constituted
the intent-to-treat population. This was the primary efficacy analysis population
and was used for both the primary end-point and secondary end-point analyses.
All patients were analyzed according to their original treatment allocation.
All primary and secondary end-point data were collected for the entire duration
of the follow-up for all patients, whether or not they were receiving study
medication or other lipid-lowering treatments, and were used in the statistical
analyses. Patients lost to follow-up were considered at risk until the date
of last contact, at which point they were censored. The log-rank test was
used for the primary end point, and Kaplan-Meier curves were used to examine
MACE-free survival time. The Cox proportional hazards model and the Cochran-Mantel-Haenszel
test were used to assess risk reduction and to compare the incidences of the
primary and secondary clinical end points, respectively.
Study sample size was calculated to provide the study with 90% power
for a 2-sided α-level of .05, assuming a 25% MACE rate at 3 years in
the placebo group and an 18.75% MACE rate in the fluvastatin group. Because
age (≥65 vs <65 years), multivessel vs single-vessel disease, previous
MI, ejection fraction (below vs above median), high total cholesterol levels
(above vs below median), and diabetes are known risk factors that may have
an impact on the primary clinical end point, a Cox regression analysis was
performed on the primary end point using these factors as covariates.
Two interim analyses were conducted using the O'Brien-Fleming stopping
rule by an independent data safety and monitoring board at 1 and 2 years following
recruitment of the last patient. These analyses were aimed at ensuring adherence
to the study protocol, assessing the appropriateness of sample size and statistical
assumptions, and considering ethical issues that could have affected the continuation
of the study. Consequently, the significance level for the primary analysis
was adjusted to .04592. All secondary end points were tested using a .05 level
of significance. All data were analyzed using SAS software, version 6.12 (SAS
Institute Inc, Cary, NC).
Between April 1996 and October 1998, a total of 1677 patients were recruited
and were randomly assigned to receive either fluvastatin (n = 844) or placebo
(n = 833) (Figure 1). The groups
were well balanced with regard to baseline characteristics, except for a significant
between-group difference in the incidence of diabetes mellitus (14.2% vs 9.8%
for the fluvastatin and placebo groups, respectively; 95% confidence interval
[CI] of the difference between groups, 1.3-7.5) (Table 1). Balloon angioplasty with or without stent placement was
performed in 98% of patients. The mean time between index PCI and randomization
was 2.7 days in both groups (median, 2.0 days; range, 0-22 days in the fluvastatin
group and 0-21 days in the placebo group). Median time from index PCI to initiation
of study medication was 2.0 days. Median follow-up was 3.9 years in both groups.
Until the time of the first MACE or up to completion of follow-up for
patients without MACE, 19.3% of the patients in the fluvastatin group were
taking less than 80% of the study treatment regimen while not taking other
lipid-lowering drugs. On the other hand, 10.7% of patients in the fluvastatin
group and 24% of patients in the placebo group were taking other lipid-lowering
drugs (primarily statins).
During the study, 97% of patients in the fluvastatin group and 98% in
the placebo group were taking aspirin. The proportion of patients taking other
cardiovascular drugs during the study, such as β-blockers, calcium antagonists,
nitrates, angiotensin-converting enzyme inhibitors, and diuretics, was similar
between groups (Table 1).
During the follow-up period, MACE-free survival time was significantly
longer in the fluvastatin group (first quartile of time to first MACE, 1558
days; 95% lower confidence bound, 1470 days) compared with the placebo group
(1227 days; 95% lower confidence bound, 858 days; P
= .01). For the primary end point, the Kaplan-Meier curves for the fluvastatin
and placebo groups begin to separate at approximately 1.5 years and continue
to diverge up to study termination (Figure
2). One hundred eighty-one (21.4%) of the 844 patients in the fluvastatin
group and 222 (26.7%) of the 833 placebo controls had at least 1 MACE, resulting
in a statistically significant reduction in risk of MACE for fluvastatin compared
with placebo (relative risk [RR], 0.78; 95% CI, 0.64-0.95; P = .01 by the Cox proportional hazards model) (Table 2) and a significant relative reduction of 20% (P = .006 by the Cochran-Mantel-Haenszel test) (Table 2). During the follow-up period, 13 patients in the fluvastatin
group (1.5%) and 24 placebo controls (2.9%) died from cardiac causes, 30 patients
in the fluvastatin group (3.6%) and 38 placebo controls (4.6%) had a nonfatal
MI, and 167 in the fluvastatin group (19.8%) compared with 193 placebo controls
(23.2%) underwent CABG or PCI.
The Cox regression analysis performed on the primary end point using
predefined risk factors as covariates revealed significant effects for multivessel
vs single-vessel disease and presence vs absence of diabetes at baseline.
The risk of MACE was lower in the subgroup of patients with multivessel disease
(23% vs 33.9%; RR, 0.66; 95% CI, 0.48-0.91; P = .01)
and lower in the subgroup of patients with diabetes (21.7% vs 37.8%; RR, 0.53;
95% CI, 0.29-0.97; P = .04) in the fluvastatin group
compared with the placebo group (Table 3). The risk of MACE among those with baseline cholesterol levels
below the group median (200 mg/dL [5.2 mmol/L]; interquartile range, 162.4-189.5
mg/dL [4.2-4.9 mmol/L]) was 20.9% for those taking fluvastatin and 25.3% for
those receiving placebo (RR, 0.77; 95% CI, 0.57-1.02) whereas for those with
baseline levels above the group median (200 mg/dL [5.2 mmol/L]; interquartile
range, 208.8-235.9 mg/dL [5.4-6.1 mmol/L]), the risk of MACE was 20.5% for
fluvastatin and 27.5% for placebo (RR, 0.76; 95% CI, 0.56-1.04).
The primary end point was assessed in men and women in a subset analysis.
The risk reduction achieved in the fluvastatin group was similar in both groups
(for men, RR, 0.79; 95% CI, 0.64-0.98 and for women, RR, 0.66; 95% CI, 0.38-1.14)
but was statistically significant only for the subgroup of men (P = .03), which represents 84% of the total study population.
Other subgroups of interest were assessed in a post hoc analysis by
anginal status or type of PCI treatment (ie, balloon angioplasty or stenting),
the latter excluding reinterventions (surgical or PCI) occurring in the first
6 months of follow-up and indicated to treat a lesion dilated at index procedure.
The risk reduction in MACE achieved with fluvastatin treatment in these subgroups
was similar to that observed in the overall study population and other subgroups
When the MACE-free survival time was assessed, excluding reintervention
procedures (surgical or PCI) occurring in the first 6 months of follow-up
for lesions treated at the index procedure, the fluvastatin group and placebo
group curves were observed to separate earlier than in the primary analysis,
at approximately 6 months, and showed a significantly extended MACE-free survival
time in the fluvastatin group (P<.001) (Figure 3). The risk of MACE was 33% lower
(RR, 0.67; 95% CI, 0.54-0.84; P<.001) in the fluvastatin
group than in placebo controls in this analysis (Table 2).
There was also a nonsignificant trend favoring the fluvastatin group
for reduction of the end points of cardiac death and combined cardiac death
and nonfatal MI (Table 2).
By 6 weeks, fluvastatin significantly reduced LDL-C (median reduction,
27%; 95% CI, 25%-29%) compared with placebo (median increase, 11%; 95% CI,
9%-13%), and these effects continued throughout follow-up (Figure 4). Fasting triglyceride levels followed a different pattern,
with greater median reductions in the fluvastatin group than in the placebo
group observed as early as 6 weeks (−14%; 95% CI, −13% to −18%
vs 0%; 95% CI, 0%-4%) and maintained until approximately 2.5 years of follow-up
(−22%; 95% CI, −18% to −25% vs −14%; 95% CI, −9%
to −17%). At study end, however, the median reduction in fasting triglycerides
was 14% in both groups. Levels of HDL-C increased by a median of 22% in both
The population available for safety analysis included 822 patients in
the fluvastatin group and 818 placebo controls. One hundred seventy-four patients
(21.2%) in the fluvastatin group temporarily or permanently discontinued study
medication due to adverse events compared with 196 patients (24.0%) in the
placebo group. Twenty-three patients in the fluvastatin group (2.7%) and 25
in the placebo group (3.0%) died from noncardiac causes (Table 4).
There were no elevations in creatine kinase levels of 10 times the ULN
or more in the fluvastatin group, and there were 3 reported cases in the placebo
group. No rhabdomyolysis was reported in patients treated with fluvastatin
during the study. Ten patients (1.2%) in the fluvastatin group and 3 (0.4%)
in the placebo group had persistent, clinically relevant elevations in aspartate
aminotransferase or alanine aminotransferase levels, defined as levels of
at least 3 times the ULN on 2 consecutive occasions. Cancers were reported
in 95 patients during the study: 46 in the fluvastatin group and 49 in the
Secondary prevention investigations have shown that statins can decrease
the incidence of both fatal and nonfatal coronary events.5-8
However, these studies generally enrolled patients with relatively advanced
cardiac disease. In addition, as few as 8% and up to only one third of patients
enrolled in earlier trials had previously received PCI, and in these patients,
statin therapy was initiated 6 months or more after the intervention. Only
the Cholesterol and Recurrent Events (CARE) trial included a sufficient number
of post-PCI patients to show a significant reduction in ischemic events in
a retrospective analysis.15 In contrast, our
study is the first prospective trial in patients undergoing their first PCI
with clinical outcomes as the primary end point. Patients enrolled in our
study generally had an earlier CHD stage (all had unstable or stable angina
or silent ischemia, and less than half had prior MI) and statin therapy was
initiated very early after the index procedure compared with earlier trials.
Results of the LIPS study show that in patients with average cholesterol
levels, early cholesterol-lowering treatment with fluvastatin, 80 mg/d, following
first PCI with or without stenting resulted in a 5.3% absolute reduction and
a 22% relative reduction in the risk of fatal or nonfatal major adverse cardiac
events during 4 years of follow-up compared with placebo. These results suggest
that treating 19 post-PCI patients with fluvastatin for 4 years would prevent
1 fatal or nonfatal MACE (number needed to treat, 19; 95% CI, 11-82), suggesting
benefit similar to that observed in other secondary prevention trials.5-8 This
risk reduction may have been even larger, considering that ultimately, 24%
of patients in the placebo group were taking other lipid-lowering treatment
compared with 10.7% in the fluvastatin group, and that 19.3% of patients in
the fluvastatin group were not compliant with the treatment regimen. These
noncompliance figures are similar to those reported in a recently published
statin secondary prevention trial.8 The crossover
rate to active medication in the placebo group that was observed in these
trials suggests the need to reconsider the clinical and ethical aspects of
investigations that assess the benefits of cholesterol-lowering medications
The subgroup analyses showing benefit of therapy in multivessel disease
and in diabetic patients are not surprising because these factors are known
to increase CHD risk.4,16,17
In these subpopulations, fluvastatin treatment appears to stabilize CHD risk,
with an incidence of cardiac events in patients taking fluvastatin similar
to that observed in the subgroups of patients with single-vessel disease and
Previous large, randomized studies indicated that statin therapy does
not prevent restenosis as assessed by quantitative angiography at 6 months.9-11 The recent Fluvastatin
Angiographic Restenosis (FLARE) study11 showed
a significantly lower incidence of total death and MI with fluvastatin, 80
mg/d, at 40 weeks after PCI (1.4% vs 4.0%; P = .03),
although the composite clinical end point that included CABG and PCI was not
significantly different from placebo controls. In view of these findings,
the MACE end point in LIPS was assessed in a prespecified analysis excluding
reinterventions (surgical or PCI) in the first 6 months of follow-up for lesions
treated at the index PCI. In this analysis, separation of the fluvastatin
MACE-free survival curve from the placebo control curve occurred at approximately
6 months, earlier than in the primary analysis, and risk reduction was greater.
This suggests that earlier benefits can be observed in post-PCI patients with
fluvastatin therapy when overlapping restenotic complications are not taken
The cholesterol level distribution observed in LIPS patients is representative
of that of an unselected patient population undergoing PCI.9
In LIPS, the benefits associated with fluvastatin, 80 mg/d, on lipid levels
and clinical outcomes were demonstrated in a population with a mean baseline
LDL-C value of 132 mg/dL (3.4 mmol/L) (range, 42-243 mg/dL [1.1-6.3 mmol/L]).
The mean baseline LDL-C level found in LIPS is in the lowest range of those
reported in 4 previous major long-term secondary prevention statin outcomes
Of these trials, only CARE and the Long-term Intervention with Pravastatin
in Ischaemic Disease (LIPID) trial suggest that the benefit of lipid lowering
with a statin is diminished in patients with baseline LDL-C values of less
than 130 mg/dL (3.4 mmol/L) recommended for initiation of drug therapy.7,18 In contrast, LIPS and the Heart Protection
Study8 suggest that the benefit is significant
and equal regardless of baseline cholesterol strata.
While elevated blood cholesterol levels are a well-established independent
risk factor for the development of cardiovascular disease, there has been
ongoing debate regarding the value of cholesterol lowering and the optimal
time for initiation of drug therapy in patients with normal or low LDL-C levels
(<130 mg/dL [3.4 mmol/L]). These 2 most recent studies suggest that the
decision to initiate cholesterol-lowering therapy should be based on risk
assessment and not on baseline cholesterol levels. The results of LIPS are
consistent with the Third Report of the National Cholesterol Education Program
Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol
in Adults guidelines, which recommend the reduction of LDL-C to less than
100 mg/dL (2.6 mmol/L) in patients with CHD or CHD risk equivalents.19
The shift to a more aggressive approach to lipid lowering comes at a
time when the typical PCI patient profile is evolving from the patient with
chronic angina to the patient experiencing his or her first anginal episode.20,21 In these patients, a more aggressive
interventional approach has been advocated.22,23
This trend toward treatment earlier in the history of angina has, in part,
fueled the dramatic growth (nearly 4-fold) in balloon angioplasty procedures
performed in the United States from 1987 to 1999.1
While initial evidence has shown that drug-eluting stents may help reduce
stent failure due to restenosis,24,25
the results of LIPS demonstrate that early postprocedure statin use reduces
the rate of fatal and nonfatal cardiac events related to progression of the
underlying disease. Thus, a combined approach of mechanical treatment and
metabolic secondary prevention involving initiation of cholesterol-lowering
treatment with a statin at the time of first PCI may be an effective strategy.
Because of the need for long-term treatment with lipid-lowering drugs,
the safety of the drug used is of paramount importance. In our study, no cases
of creatine kinase elevations to more than 10 times the ULN and no severe
muscular toxic effects were observed with fluvastatin at a dosage of 80 mg/d,
and other adverse effects were reported with similar frequency in the fluvastatin
and placebo groups.
In conclusion, LIPS is the first prospective trial to demonstrate a
significant risk reduction in fatal or nonfatal MACE as a result of statin
therapy with fluvastatin, 80 mg/d, initiated early following successful completion
of first PCI, with or without stenting. The results of LIPS support the use
of early lipid-lowering therapy with fluvastatin in post-PCI patients, regardless
of baseline lipid level.
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