DISCUSSION AROUND STATIN DISCONTINUATION IN OLDER ADULTS AND PATIENTS WITH WASTING DISEASES
Maciej Banach1*, Maria-Corina Serban2,3
1
Department of Hypertension, Chair of Nephrology and Hypertension, Medical University of
Lodz, Lodz, Poland; 2Department of Epidemiology, University of Alabama at Birmingham, Birmingham, AL, USA; 3Department of Functional Sciences, Discipline of Pathophysiology, “Victor Babes” University of Medicine and Pharmacy, Timisoara, Romania.
*Corresponding author: Prof. Maciej Banach, MD, PhD, FNLA, FAHA, FESC, FASA, Head, Department of Hypertension, WAM University Hospital in Lodz, Medical University of Lodz, Zeromskiego 113; 90-549 Lodz, Poland. Phone: +48 42 639 37 71; Fax: +48 42 639 37 71; E-mail:
[email protected]
Conflict of interest: None Number of words: 1882
Statins – where are we now? Statins are usually selected as the first-line therapy to lower plasma levels of low-density lipoprotein cholesterol (LDL-C) and cardiovascular disease (CVD) morbidity and mortality [1]. They reduce the risk of myocardial infarction (MI), stroke and CVD mortality by about 25-30% [2]. That is one of the reasons why all current clinical guidelines "virtually mandate" lifetime use of statins once they are started, thus becoming a challenge for the patients due to their possible side-effects [3]. Furthermore, there has been recently a tendency towards maximizing the strength of statin treatment, sometimes with greater doses or potent forms [3,4]. The IMProved Reduction of Outcomes: Vytorin Efficacy International Trial (IMPROVE-IT) showed that the combination with ezetimibe/simvastatin 10 mg/40 mg let to an absolute 2.0% reduction (relative risk reduction: 6.4%) of the risk of CV events in contrast to simvastatin 40 mg alone [4,5]. The trial also demonstrated that the patients with obtained very low LDL-C levels < 30 mg/dl experienced no discrepancies in adverse effects than those with higher LDL-C levels [5]. ODYSSEY LONG-TERM and the Open-Label Study of LongTerm Evaluation Against LDL-C (OSLER) trials with proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors also supported the hypothesis ‘the lower the better’ for LDL-C levels, generating more arguments for lower LDL-C targets
