PMID- 22152283
OWN - NLM
STAT- MEDLINE
DCOM- 20120416
LR  - 20221207
IS  - 1878-5050 (Electronic)
IS  - 1567-5688 (Linking)
VI  - 12
IP  - 3
DP  - 2011 Nov
TI  - Pitavastatin: clinical effects from the LIVES Study.
PG  - 285-8
LID - 10.1016/S1567-5688(11)70888-1 [doi]
AB  - Although clinical trials provide useful information on drug safety and efficacy, 
      results do not always reflect those observed in the real world. The Japanese 
      long-term prospective post-marketing surveillance LIVALO Effectiveness and Safety 
      (LIVES) Study was designed to assess the efficacy and safety of pitavastatin in 
      clinical practice in ~20,000 patients. After 104 weeks, pitavastatin was 
      associated with significant reductions in low-density lipoprotein-cholesterol 
      (LDL-C) (29.1%) that largely occurred within 4 weeks of treatment initiation. In 
      patients with abnormal triglyceride (TG) and high-density lipoprotein-cholesterol 
      (HDL-C) levels at baseline, pitavastatin reduced TG and increased HDL-C by 22.7% 
      and 19.9%, respectively. Overall, 88.2% of the primary prevention low-risk 
      patients attained their Japan Atherosclerosis Society LDL-C target, compared with 
      82.7% of intermediate-risk patients, 66.5% of high-risk patients and 50.3% of 
      secondary prevention patients. Only 10.4% of pitavastatin-treated patients 
      experienced adverse events (AEs), of which approximately 84% were mild and around 
      1% was severe. Increases in blood creatine phosphokinase (2.7%), alanine 
      aminotransferase (1.8%), myalgia (1.1%), aspartate aminotransferase (1.5%) and 
      gamma-glutamyltransferase (1.0%) were the most common AEs and only 7.4% of 
      patients discontinued pitavastatin due to AEs. Regression analysis demonstrated 
      that age was not a significant factor for the incidence of any AE or 
      myopathy-associated events. A subanalysis of initial LIVES data focussing on the 
      effects of pitavastatin on HDL-C levels showed that HDL-C was elevated by 5.9% in 
      all patients and by 24.6% in those with low (<l mmol/L; 40 mg/dL) HDL-C levels at 
      baseline (P < 0.0001). A time-course analysis showed that the elevation in HDL-C 
      in the low-HDL-C group was enhanced by 14.0% and 24.9% at 12 weeks and 104 weeks, 
      respectively. In contrast, previous studies have shown that other statins have 
      inconsistent effects on HDL-C levels, with elevations ranging from 0% to 12%. 
      According to a LIVES subanalysis, pitavastatin produced a significant increase in 
      HDL-C levels in patients switching from other statins, suggesting that patients 
      with an unacceptably low level of HDL-C might benefit from switching to 
      pitavastatin. Further analyses showed an improvement in HbA1c in patients with 
      type 2 diabetes after long-term pitavastatin treatment and a significant increase 
      in eGRF in patients with chronic kidney disease. Results from the 5-year LIVES 
      extension study (N = 6,582) showed that long-term treatment with pitavastatin was 
      well tolerated and that the reduction in LDL-C achieved after 104 weeks was 
      maintained for the duration of treatment, whereas levels of HDL-C continued to 
      rise. Importantly, multivariate analysis of the 5-year data showed that, in 
      addition to advanced age (>/= 65 years), male gender, hypertension, diabetes, and a 
      history of ischemic heart disease, on-treatment levels of HDL-C and LDL-C were 
      significant predictors for cardiovascular (CV) and cerebrovascular risk. In this 
      study, the greatest reduction in CV and cerebrovascular risk was achieved by 
      patients achieving both their LDL-C and HDL-C targets. Overall, results from the 
      LIVES study show that pitavastatin is well tolerated and effectively modifies 
      atherogenic lipid profiles, thereby reducing CV and cerebrovascular risk in 
      Japanese patients with hypercholesterolemia. Pitavastatin's ability to 
      significantly and continually increase HDL-C levels over time suggests a 
      particular benefit for patients with low baseline levels of HDL-C and/or those 
      that fail to increase their HDL-C levels using alternative statins.
CI  - Copyright (c) 2011 Elsevier Ireland Ltd. All rights reserved.
FAU - Teramoto, Tamio
AU  - Teramoto T
AD  - Department of Internal Medicine, Teikyo University School of Medicine, Kaga 
      2-11-1, Itabashi-ku, Tokyo 173-8605, Japan. ttera@med.teikyo-u.ac.jp
LA  - eng
PT  - Journal Article
PT  - Review
PL  - Netherlands
TA  - Atheroscler Suppl
JT  - Atherosclerosis. Supplements
JID - 100973461
RN  - 0 (Biomarkers)
RN  - 0 (Cholesterol, HDL)
RN  - 0 (Cholesterol, LDL)
RN  - 0 (Glycated Hemoglobin A)
RN  - 0 (Heptanoic Acids)
RN  - 0 (Hydroxymethylglutaryl-CoA Reductase Inhibitors)
RN  - 0 (Pyrroles)
RN  - 0 (Quinolines)
RN  - 0 (Triglycerides)
RN  - A0JWA85V8F (Atorvastatin)
RN  - AGG2FN16EV (Simvastatin)
RN  - M5681Q5F9P (pitavastatin)
SB  - IM
MH  - Atorvastatin
MH  - Biomarkers
MH  - Cardiovascular Diseases/epidemiology/prevention & control
MH  - Cerebrovascular Disorders/epidemiology/prevention & control
MH  - Cholesterol, HDL/blood
MH  - Cholesterol, LDL/blood
MH  - Clinical Trials, Phase IV as Topic/methods/*statistics & numerical data
MH  - Comorbidity
MH  - Diabetes Mellitus, Type 2/blood
MH  - Dyslipidemias/blood/*drug therapy
MH  - Glomerular Filtration Rate/drug effects
MH  - Glycated Hemoglobin/analysis
MH  - Heptanoic Acids/therapeutic use
MH  - Humans
MH  - Hydroxymethylglutaryl-CoA Reductase Inhibitors/adverse 
      effects/pharmacology/*therapeutic use
MH  - Japan/epidemiology
MH  - Kidney Diseases/blood
MH  - Multicenter Studies as Topic/methods/*statistics & numerical data
MH  - Muscular Diseases/chemically induced
MH  - Prospective Studies
MH  - Pyrroles/therapeutic use
MH  - Quinolines/adverse effects/pharmacology/*therapeutic use
MH  - Risk
MH  - Simvastatin/therapeutic use
MH  - Treatment Outcome
MH  - Triglycerides/blood
EDAT- 2011/12/14 06:00
MHDA- 2012/04/17 06:00
CRDT- 2011/12/14 06:00
PHST- 2011/12/14 06:00 [entrez]
PHST- 2011/12/14 06:00 [pubmed]
PHST- 2012/04/17 06:00 [medline]
AID - S1567-5688(11)70888-1 [pii]
AID - 10.1016/S1567-5688(11)70888-1 [doi]
PST - ppublish
SO  - Atheroscler Suppl. 2011 Nov;12(3):285-8. doi: 10.1016/S1567-5688(11)70888-1.