BJU Int. 2005 Jan;95(1):110-6.
Vardenafil is effective and well-tolerated for treating erectile
dysfunction in a broad population of men, irrespective of age.
Giuliano F, Donatucci C, Montorsi F, Auerbach S, Karlin G, Norenberg
C, Homering M, Segerson T, Eardley I; Vardenafil Study Group.
Department of Urology, CHU de Bicetre, AP-HP, 78 rue du General
Leclerc, 94272 Le Kremlin Bicetre Cedex, France.
OBJECTIVES: To assess the efficacy and safety of vardenafil in
the treatment of erectile dysfunction (ED) in men of different
age groups. PATIENTS AND METHODS: In a retrospective pooled subgroup
analysis of randomized, double-blind, placebo-controlled studies,
men from the general population with ED received either placebo
or vardenafil 5, 10 or 20 mg over 12 weeks. Efficacy variables
included the erectile function (EF) domain score from The International
Index of Erectile Function, diary response rates to questions
on vaginal penetration and maintenance of erection, and positive
responses to the Global Assessment Question (GAQ) "Has the
treatment you have been taking over the past 4 weeks improved
your erections?'. The 1385 men were grouped by age (< 45, 45-64
and > or =65 years). RESULTS: At 12 weeks the EF domain scores
approached 20 with vardenafil and 14 with placebo in men aged
> or = 65 years (P < 0.03 vardenafil 5 mg vs placebo, P
< 0.001 vardenafil 10 and 20 mg vs placebo). The corresponding
scores were 22 and 14 in men aged 45-64 years and up to 24 and
16 in those aged <45 years (P < 0.03 vardenafil 5 mg vs
placebo, P < 0.001 vardenafil 10 and 20 mg vs placebo). Vardenafil
generated positive GAQ responses in approximately 71%, 76% and
85% of men aged <45, 45-64 and > or = 65 years (P < or
= 0.001 vardenafil vs placebo). The corresponding placebo rates
were 23%, 25% and 34%. The most common treatment-emergent adverse
events were headache, rhinitis, flushing and dyspepsia, which
were mild to moderate, transient and unrelated to age. CONCLUSION:
Vardenafil is an effective and generally well-tolerated treatment
for ED, irrespective of age.
Am J Cardiol. 2004 Jun 1;93(11):1419-21, A10.
Effect of fluvastatin therapy on coronary flow reserve in patients
with hypercholesterolemia.
Fujimoto K, Hozumi T, Watanabe H, Shimada K, Takeuchi M, Sakanoue
Y, Shimizu N, Ostuka R, Kawase Y, Sakamoto K, Yoshiyama M, Baba
Y, Haze K, Yoshikawa J.
Department of Internal Medicine and Cardiology, Osaka City University
Medical School, 1-4-3 Asahi-machi, Abeno-ku, Osaka 545-8585, Japan.
Coronary flow reserve was evaluated using transthoracic Doppler
echocardiography before and after 3 months of fluvastatin therapy
in patients with hypercholesterolemia. Coronary flow reserve increased
significantly after lipid-lowering therapy, and coronary microcirculation
was improved in patients with hypercholesterolemia.
Metabolism. 2004 Jun;53(6):733-9.
Fluvastatin improves endothelial dysfunction in overweight postmenopausal
women through small dense low-density lipoprotein reduction.
Shimabukuro M, Higa N, Asahi T, Oshiro Y, Takasu N.
Second Department of Internal Medicine, Faculty of Medicine, University
of the Ryukyus, Okinawa, Japan.
Small dense low-density lipoprotein (sdLDL), which are often associated
with obesity, are considered as the most atherogenic and have
been shown to impair endothelial function. It is not known whether
reduction of sdLDL by pharmacological intervention can improve
endothelial function. Thirty-four consecutive postmenopausal women
with >/=5.70 mmol/L total cholesterol were placed into either
an overweight (body mass index [BMI] >/= 25.0, n = 22) or a
normal-weight (BMI < 25.0, n = 12) group, and forearm blood
flow (FBF) was measured using strain-gauge plethysmography during
reactive hyperemia before and after fluvastatin treatment. At
baseline, the peak FBF during reactive hyperemia in the overweight
group was less than that in the normal-weight group (mean +/-
SD, 13.6 +/- 4.4 v 22.2 +/- 4.0 mL/min/100 mL, P <.01). The
maximal FBF after nitroglycerin was similar in both groups. In
the stepwise multiple regression analysis, only the concentration
of sdLDL was the predictor for peak FBF (standard coefficient
= -0.517, P =.0115). The nonsignificant parameters for the correlations
in the model were age, BMI, systolic blood pressure, the homeostasis
model assessment of insulin resistance (HOMA-IR), hemoglobin A(1c)
(HbA(1c)), and LDL-cholesterol. Fluvastatin treatment was associated
with the recovery of the peak FBF in the overweight group but
it did not influence that of the normal-weight group. Changes
in sdLDL fractions by fluvastatin correlated well with the peak
FBF recovery. These results suggested that an increased sdLDL
was linked to endothelial dysfunction in overweight postmenopausal
women and fluvastatin treatment improved endothelial dysfunction
by decreasing the atherogenic sdLDL fraction in this population.
Cleve Clin J Med. 2003 Jun;70(6):561-6.
The Lescol Intervention Prevention Study (LIPS): start all patients
on statins early after PCI.
Messerli AW, Aronow HD, Sprecher DL.
Department of Cardiovascular Medicine, The Cleveland Clinic Foundation,
OH 44195, USA.
The Lescol Intervention Prevention Study (LIPS) was the first
randomized trial to show a significant reduction in the risk of
cardiac events in patients started on fluvastatin immediately
after a successful percutaneous coronary intervention. The benefit
was independent of baseline cholesterol levels. The results suggest
that all patients should be discharged on lipid-lowering therapy
after a percutaneous coronary intervention. Currently, this is
seldom done.
Clin Ther. 2003 Mar;25(3):904-18.
Comparison of treatment with fluvastatin extended-release 80-mg
tablets and immediate-release 40-mg capsules in patients with
primary hypercholesterolemia.
Isaacsohn JL, LaSalle J, Chao G, Gonasun L.
Metabolic and Atherosclerosis Research Center, Cincinnati, Ohio,
USA.
BACKGROUND: According to the National Cholesterol Education Program
(NCEP) Adult Treatment Panel (ATP) III guidelines, hypercholesterolemic
patients with greater risk for cardiovascular heart disease require
more aggressive lowering of low-density lipoprotein cholesterol
(LDL-C) levels. Numerous studies have demonstrated that despite
these guidelines, patients often do not reach their target levels,
and that physicians frequently do not titrate the drug beyond
the starting dose. For these patients, it may be more suitable
to initiate treatment with a higher starting dose of statin. With
the immediate-release (IR) formulation of fluvastatin, the maximal
dose of 80 mg is recommended to be administered in divided doses
(40 mg BID). An extended-release (ER) formulation of fluvastatin
at a higher dose (fluvastatin ER 80 mg) was designed to provide
greater LDL-C lowering with QD dosing. Use of this formulation
should bring more patients into compliance with target LDL-C levels.
OBJECTIVE: This analysis compared the efficacy and tolerability
of fluvastatin ER 80 mg QD and fluvastatin IR 40 mg QD in lowering
total cholesterol, LDL-C, triglyceride, and apolipoprotein (apo)
B levels and raising high-density lipoprotein cholesterol (HDL-C)
and apo A-I levels in patients with hypercholesterolemia over
a 12-week treatment period. METHODS: This was a prospective, multicenter,
double-blind, double-dummy, randomized, parallel-group, active-controlled
study Patients with primary hypercholesterolemia who qualified
for lipid-lowering drug therapy based on NCEP ATP II guidelines
were randomized to fluvastatin ER 80 mg QD or fluvastatin IR 40
mg QD, and treated for 12 weeks. RESULTS: A total of 173 patients
were randomized to treatment: 86 to the fluvastatin ER 80-mg group
and 87 to the fluvastatin IR 40-mg group. Compared with fluvastatin
IR 40 mg, fluvastatin ER 80 mg produced greater mean reductions
in LDL-C (32% vs 22%, respectively; P < 0.001). For each of
the 3 coronary heart disease (CHD) risk groups (defined by the
NCEP), as well as for the total population studied, more patients
from the fluvastatin ER 80-mg group than the IR 40 group achieved
NCEP ATP II target LDL-C levels (79% vs 47%, respectively [P =
NS], for patients with < 2 risk factors; 58% vs 15%, respectively
[P < 0.001], for patients with > or = 2 risk factors; and
40% vs 14%, respectively [P = 0.012], for patients with CHD).
The 80-mg ER dose of fluvastatin provided 9.1% greater LDL-C lowering
than the 40-mg IR dose. The incidence of elevations in transaminase
levels was low and similar for both doses, with 1 patient in each
of the treatment groups being discontinued due to repeated elevation
of transaminases > 3 x the upper limit of normal (ULN). Clinically
relevant elevations in creatine kinase (ie, > or = 10x ULN)
were not observed with either dose. Nine patients (5 in the fluvastatin
ER group and 4 in the fluvastatin IR group) discontinued because
of adverse events. CONCLUSIONS: Treatment with fluvastatin ER
80 mg resulted in greater reductions in LDL-C, total cholesterol,
and apo B levels compared with fluvastatin IR 40 mg, with clinically
equivalent reduction in triglyceride levels and elevation of HDL-C
levels. Furthermore, there were few tolerability concerns of clinical
relevance with either formulation and no clinically meaningful
difference in the tolerability parameters between the 2 formulations.
For patients with higher baseline LDL-C levels, and for patients
who require greater LDL-C lowering, it may be appropriate to initiate
therapy with fluvastatin ER 80 mg. Use of the higher starting
dose likely would bring a greater proportion of high-risk patients
into compliance with NCEP ATP II target LDL-C levels and would
provide LDL-C lowering that is in the same range that has been
proved in clinical trials to be associated with reductions in
CHD event rates.
Di Yi Jun Yi Da Xue Xue Bao. 2002 Dec;22(12):1109-11.
Effects of fluvastatin on the levels of C-reactive protein and
lipids in patients with hyperlipidemia.
Chi DS, Jin FX, Yang SG, Su YW, Ge B, Zhang J, Zhang Y, Liu YL.
Department of Cardiology, Nanfang Hospital, First Military Medical
University, Guangzhou 510515, China.
OBJECTIVE: To observe the changes of C-reactive protein (CRP)
level and its relationship with blood lipids, and the effects
of fluvastatin on CRP and the lipids in patients with hyperlipidemia.
METHODS: Serum levels of cholesterol (TC), triglycerides (TG),
high density lipoprotein cholesterol (HDL-C), low-density lipoprotein
cholesterol (LDL-C), very-low-density lipoprotein cholesterol
(VLDL-C) and lipoprotein(a)[Lp(a)] were measured by enzyme assay,
and plasma CRP level by immunonephelometry before and after fluvastatin
treatment (20 mg/d for 4 weeks) in patients with hyperlipidemia.
RESULTS: CRP levels were above normal in 90.3% hyperlipidemia
cases in spite of the various accompanying diseases. Fluvastatin
treatment significantly reduced TC (-7.49%), TG (-14.32%), LDL
(-13.88%), VLDL (-18.48%) and TC/HDL(-13.50%) levels (P<0.01),
and also brought down Lp(a) concentration (-13.81%). CRP levels
was very effectively reduced after the treatment (-15.92%, P<0.001).
No association between basal CRP levels and basal lipids and Lp(a)
concentrations was observed. Positive correlation of CRP, however,
was observed after fluvastatin treatment with TC/HDL (r=0.62,
P=0.041) and Lp(a) (r=0.320, P=0.011), while inverse relations
were noted between CRP and HDL (r=-0.288, P=0.023). CONCLUSION:
CRP levels increases markedly in patients with hyperlipidemia,
a fact that is independent of the accompanying diseases. In addition
to modulating blood lipid levels, fluvastatin also reduces CRP
level, the latter possibly serving as an independent predictive
factor for atherosclerotic cardiovascular diseases and also as
an indicator for estimating the effectiveness of the treatment.
J Clin Endocrinol Metab. 2002 Dec;87(12):5485-90.
Effect of fluvastatin slow-release on low density lipoprotein
(LDL) subfractions in patients with type 2 diabetes mellitus:
baseline LDL profile determines specific mode of action.
Winkler K, Abletshauser C, Hoffmann MM, Friedrich I, Baumstark
MW, Wieland H, Marz W.
Division of Clinical Chemistry, Department of Medicine, Albert
Ludwigs-University, D-79106 Freiburg, Germany.
The objective of this study was to determine the effect of slow-release
(XL) fluvastatin on low density lipoprotein (LDL) subfractions
in type 2 diabetes. A multicenter, double-blind, randomized, parallel-group
comparison of fluvastatin XL 80 mg (n = 42) and placebo (n = 47),
each given once-daily for 8 wk, in 89 patients with type 2 diabetes
(HbA1c: 7.2 +/- 1.0%, LDL cholesterol (LDL-C): 3.4 +/- 0.7 mmol/liter,
high density lipoprotein cholesterol: 1.1 +/- 0.3 mmol/liter,
and triglycerides (TG): 2.4 +/- 1.4 mmol/liter). At baseline and
on treatment, plasma lipoproteins were isolated and quantified.
Eight weeks of fluvastatin treatment decreased total cholesterol
(-23.0%, P < 0.001), LDL-C (-29%, P < 0.001) and TG (-18%,
P < 0.001), compared with placebo. At baseline, there was a
preponderance of dense LDL (dLDL) (apolipoprotein B in LDL-5 plus
LDL-6 > 25 mg/dl) in 79% of patients, among whom fluvastatin
decreased all LDL subfractions, reductions in dLDL being greatest
(-28%, P = 0.001; cholesterol in dLDL -29%). In patients with
low baseline dLDL (apolipoprotein B in LDL-5 plus LDL-6
Expert Opin Pharmacother. 2002 Nov;3(11):1631-41.
Fluvastatin.
Lawrence JM, Reckless JP.
Clinical Research Fellow, Diabetes and Lipid Research, Wolfson
Centre, Royal United Hospital, Bath, UK.
Fluvastatin was the first wholly synthetic statin to the market
and is effective in reducing total and low density lipoprotein
cholesterol, which translates into reductions in coronary heart
disease events. The Lescol Intervention Prevention Study has established
the effectiveness of the early use of statins in reducing recurrent
events in high-risk patients with coronary heart disease post
percutaneous coronary interventions. Fluvastatin is well-tolerated
with few side effects. The occurrence of significant abnormalities
in liver enzymes is infrequent, and the risk of myositis and rhabdomyolysis
seems to be less than with other statins. There have been no reports
of fatal rhabdomyolysis to date. The potential for drug interactions
with fluvastatin is low. It seems safe in combination with cyclosporin
and there have been few reports of rhabdomyolysis when using fluvastatin
in combination with other lipid-lowering agents. It is nevertheless
important to be vigilant for this potentially important side effect
and, as with other statins, inform patients of the potential risk
and suggestive symptoms. Fluvastatin provides a useful option
in treating hypercholesterolaemia in patients at high risk of
coronary heart disease.
Cardiovasc Drugs Ther. 2002 May;16(3):203-7.
Antioxidative effects of fluvastatin on superoxide anion activated
by angiotensin II in human aortic smooth muscle cells.
Kugi M, Matsunaga A, Ono J, Arakawa K, Sasaki J.
Department of Health and Social Welfare, Fukuoka College of Health
Sciences, 2-15-1 Tamura, Sawara-Ku 814-0193, Japan.
We examined the antioxidative effects of fluvastatin, a 3-hydroxy-3-methylglutaryl
coenzyme A reductase inhibitor (statin), on superoxide anion formation
activated by angiotensin II (Ang II) in vitro. The effects of
fluvastatin were also compared to simvastatin and a water-soluble
analog of alpha-tocopherol, trolox. Treatment of human aortic
smooth muscle cells (hASMC) with Ang II for 24 hours resulted
in a 3.2 +/- 0.5-fold increase in intracellular superoxide anion
formation as detected by lucigenin assay. hASMC treated with clinical
concentrations of fluvastatin (0-100 nM) showed a dose-dependent
decrease in Ang II-activated superoxide anion formation. The addition
of similar concentrations of trolox to hASMC inhibited Ang II-activated
superoxide anion formation in a dose-dependent manner. However,
simvastatin at similar doses failed to inhibit Ang II-activated
superoxide anion formation by hASMC. Our results indicate that
in addition to its hypocholesterolemic effect, fluvastatin may
have direct antioxidative effects, suggesting its possible protective
effect on atherosclerotic process.
Nephrol Dial Transplant. 2002 Aug;17(8):1513-7.
Fluvastatin prevents development of arterial stiffness in haemodialysis
patients with type 2 diabetes mellitus.
Ichihara A, Hayashi M, Ryuzaki M, Handa M, Furukawa T, Saruta
T.
Department of Internal Medicine, Keio University School of Medicine,
Tokyo, Japan.
BACKGROUND: Arterial stiffness assessed by pulse wave velocity
(PWV) predicts all-cause and cardiovascular mortality in diabetic
patients with end-stage renal disease. We studied the preventive
effects of a 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor,
fluvastatin, on arterial PWV values in this population. METHODS:
Twenty-two patients with normal serum lipid levels received fluvastatin
(20 mg/day p.o.) or a placebo for 6 months. Their serum lipid
levels, serum levels of C-reactive protein (CRP), arterial PWV,
and ankle brachial indexes (ABI) were determined before, and 3
and 6 months after taking the medication to evaluate arterial
stiffness. RESULTS: At the beginning of the follow-up, there were
no differences in age, blood pressure, body mass index, serum
haemoglobin A1c level, serum CRP level, serum lipid levels, PWV
or ABI between the placebo- (n=10) and the fluvastatin-treated
patients (n=12). After 6 months, the PWV and the serum oxidized
low-density lipoprotein cholesterol (LDL-C) level increased significantly
(from 1969+/-140 to 2326+/-190 cm/s and 70.4+/-13.8 to 91.8+/-15.5
U/l, respectively) in the placebo-treated patients. However, the
fluvastatin group had a significantly reduced PWV (from 1991+/-162
to 1709+/-134 cm/s), oxidized LDL-C serum levels (from 89.0+/-9.6
to 73.0+/-5.8 U/l) and CRP serum levels (from 0.97+/-0.32 to 0.26+/-0.16
mg/dl) compared with those in the placebo group. CONCLUSIONS:
Long-term administration of fluvastatin prevents further worsening
of arterial biomechanics in haemodialysis patients with type 2
diabetes mellitus, even in the presence of serum lipid levels
in the normal range.
J Cardiovasc Pharmacol. 2002 Jul;40(1):28-34.
Valsartan therapy has additive anti-oxidative effect to that of
fluvastatin therapy against low-density lipoprotein oxidation:
studies in hypercholesterolemic and hypertensive patients.
Hussein O, Shneider J, Rosenblat M, Aviram M.
Lipid Research Laboratory, Internal Medicine Department A, Sieff
Government Hospital, Safed, Israel.
In hypercholesterolemic and hypertensive patients, an increased
propensity of their low-density lipoprotein (LDL) to oxidative
modification has been observed. Because oxidized LDL (ox-LDL)
plays a major role in atherosclerosis, the current study analyzed
the anti-oxidative effect of valsartan (an angiotensin II receptor
antagonist) therapy in combination with fluvastatin therapy in
these patients. Administration of 40 mg/d of fluvastatin for 2
months to seven patients resulted in significant reduction in
plasma total and LDL cholesterol (by 24-28%). Valsartan administration
(80 mg/d for an additional 2-month period) in combination with
fluvastatin did not further affect plasma cholesterol levels.
Fluvastatin therapy inhibited the susceptibility of LDL to copper
ion-induced oxidation, as shown by prolongation of the lag time
by 22% and by a reduction of thiobarbituric acid-reactive substances
(TBARS) levels by 14%, as compared with the patient's LDL baseline
oxidation. The addition of valsartan to fluvastatin resulted in
a further 17% prolongation of the lag time and in an additional
reduction of 21% in TBARS levels. In a parallel study, the LDL
from eight patients who were first treated with 80 mg/d of valsartan
for 2 months demonstrated reduced susceptibility to copper ion-induced
oxidation, as observed by prolongation of lag time by 23% and
reduction in TBARS levels by 19%, compared with the baseline values.
The administration of 40 mg/d of fluvastatin for an additional
2 months in combination with valsartan, however, demonstrated
no further inhibitory effect on LDL oxidation. The anti-oxidative
properties of fluvastatin and valsartan against LDL oxidation
were also demonstrated in vitro and the combination of both drugs
was shown to have an additive effect. Valsartan therapy in hypercholesterolemic
and hypertensive patients has an additive anti-oxidative effect
to that of fluvastatin therapy. This may be related both to the
anti-oxidative properties of valsartan and to the blocking of
angiotensin II-induced oxidative stress.
J Int Med Res. 2002 Jan-Feb;30(1):21-5.
Effects of fluvastatin treatment on insulin sensitivity in patients
with hyperlipidaemia.
Cingozbay BY, Top C, Terekeci H, Keskin O, Onde ME.
Department of Cardiology, Gulhane Military Medical Academy, Haydarpasa
Training Hospital, Istanbul, Turkey.
This study aimed to determine the effects of fluvastatin treatment
on insulin sensitivity in patients with hyperlipidaemia. Non-obese,
normoglycaemic, normotensive patients with hyperlipidaemia (n
= 20) and a reference group of healthy subjects of similar age,
sex, and body mass index (n = 20) were evaluated. Patients with
other causes of peripheral insulin resistance were excluded. All
participants underwent a diagnostic protocol, which included measurements
of insulin sensitivity index and other metabolic parameters. Insulin
sensitivity was assessed by Homeostasis Model Assessment (HOMA).
Serum insulin levels were tested by radioimmunoassay. Patients
were treated with fluvastatin 40 mg once daily for 3 months. Before
fluvastatin treatment, fasting serum insulin levels were significantly
raised in patients with hyperlipidaemia compared with subjects
from the reference group (19.1 +/- 13.4 versus 8.1 +/- 3.4 microIU/ml).
The fasting serum insulin levels and HOMA-estimated insulin sensitivity
were correlated in the whole group. Correlation analysis showed
a significant relationship between HOMA-estimated insulin resistance
and plasma cholesterol and triglyceride concentrations. Patients
with hyperlipidaemia had reduced insulin sensitivity that was
reflected by high serum fasting insulin levels. Anti-hyperlipidaemic
treatment with fluvastatin increases insulin sensitivity.
J Cardiovasc Risk. 2001 Apr;8(2):63-71.
Effects of fluvastatin on cardiac events in renal transplant patients:
ALERT (Assessment of Lescol in Renal Transplantation) study design
and baseline data.
Holdaas H, Fellstrom B, Holme I, Nyberg G, Fauchald P, Jardine
A, Gronhagen-Riska C, Madsen S, Neumayer HH, Cole E, Maes B, Weinreich
T, Olsson AG, Pedersen TR, Benghozi R, Hartmann A; ALERT Study
Group. Assessment of Lescol in Renal Transplantation.
Department of Medicine, National Hospital, N-0027 Oslo, Norway.
BACKGROUND: Recent clinical trials of primary and secondary prevention
of cardiovascular disease have demonstrated that lowering plasma
cholesterol with 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA)
reductase inhibitors ('statins') reduces morbidity and mortality
from coronary heart disease in diverse patient populations. STUDY
AIMS: The aim of the present ALERT (Assessment of Lescol in Renal
Transplantation) study is to determine whether renal transplant
recipients would also benefit from statin therapy. ALERT is a
multicentre, randomized, double-blind, placebo-controlled trial
to assess the effect of fluvastatin in renal transplant recipients
with mild-to-moderate hypercholesterolaemia. The primary objective
is to investigate the effects of fluvastatin on major adverse
cardiac events (MACE). In addition, the effects on cardiovascular
and all-cause mortality, as well as renal function, will be addressed.
STUDY POPULATION: The study population contains patients with
functioning renal allografts of more than 6 months' duration,
recruited from 75 centres in Northern Europe and Canada. Patients
of both sexes, aged 30-75 years, with a total cholesterol level
of 4.0-9.0 mmol/l (155-348 mg/dl) were included, except for those
with a history of myocardial infarction, where the upper limit
for inclusion was 7.0 mmol/l (270 mg/dl). STUDY DESIGN: A total
of 2100 patients were recruited by the end of October 1997 and
will be followed for up to 6 years. This report presents the design
features of the study (recruitment, follow-up, sample size, data
analysis and study organization), along with baseline results.
ALERT is the first large-scale prospective, randomized, double-blind
study to address the prevention of cardiovascular mortality in
renal transplant patients receiving an HMGCoA reductase inhibitor.
Ter Arkh. 1997;69(4):43-5.
The effect of a new hypolipemic preparation fluvastatin (Lescol)
on rheological indices and hemostatic parameters.
Filippova VG, Mantsurova AV, Zadionchenko VS, Zaporozhets TP.
In view of inducing action of hyperlipidemia on progression of
nephropathy and relationships between thrombogenesis, atherogenesis
and sclerosis, the authors examined fluvastatin effects on platelet-rheological
hemostasis. The 12-week course in a dose 20-40 mg/ day produced
minimal side effects while its hypolipidemic action was noticeable:
a 18, 21 and 20% fall in concentrations of total cholesterol,
LDL cholesterol, triglycerides, respectively. The platelet rheology
underwent the following changes: spontaneous platelet aggregation
went down from 2.58 +/- 0.3 to 1.64 +/- 0.27 r.units, ADP-induced
platelet aggregation rose from 6.5 +/- 0.66 to 8.08 +/- 0.77 r.units.
No marked changes were registered in hematocrit, plasma and blood
density, red cell aggregation and deformability. Thus, active
lowering of blood lipids was not associated with evident inhibition
of platelet activity. The absence of this feedback in lipid-platelet
relations probably indicates an independent significance of hemostatic
disturbances in ischemic heart disease and needs further study.
