Explore chapters and articles related to this topic
Rosuvastatin to Prevent Vascular Events in Men and Women with Elevated C-Reactive Protein
Published in Juan Carlos Jimenez, Samuel Eric Wilson, 50 Landmark Papers Every Vascular and Endovascular Surgeon Should Know, 2020
Juan Carlos Jimenez, Samuel Eric Wilson
Results The study was terminated after a median follow-up of 1.9 years. At the 12-month visit, the rosuvastatin group, as compared with the placebo group, had a 50% lower median LDL cholesterol level (mean difference, 47 mg per dL [1.2 mmol per liter]), a 37% lower median hsCRP level, and a 17% lower median triglyceride level (P < 0.001 for all three comparisons). There were 142 first major cardiovascular events in the rosuvastatin group compared with 251 in the placebo group. The rates of the primary endpoint were 0.77 and 1.36 per 100 person-years of follow-up in the rosuvastatin and placebo groups, respectively (hazard ratio for rosuvastatin, 0.56; 95% confidence interval [CI], 0.46 to 0.69; P < 0.00001). Rosuvastatin was also associated with statistically significant reductions in fatal or nonfatal MI, fatal or nonfatal stroke, arterial revascularization, unstable angina, deep venous thrombosis, pulmonary embolism, and rates of death from any cause. There were no differences reported adverse events in both groups. Physician-reported diabetes was higher in the rosuvastatin group (p = 0.01).
Cardiovascular Drugs
Published in Radhwan Nidal Al-Zidan, Drugs in Pregnancy, 2020
Risk Summary: The use of Rosuvastatin is contraindicated during pregnancy due to the fact that Cholesterol and products synthesized by cholesterol are essential during fetal development. Moreover, the discontinuation of Rosuvastatin during pregnancy should have no influence on the long-term treatment of hyperlipidemia.
Compatibility of commonly used drugs in lactation
Published in Amy Brown, Wendy Jones, A Guide to Supporting Breastfeeding for the Medical Profession, 2019
There is no research on the use of statins during breastfeeding. Cholesterol is important to the development of the baby and the long-term effects of lowered levels are unknown. Simvastatin – oral bioavailability 5%, PPB 95%, no studies. Atorvastatin – oral bioavailability 14%, PPB >98%, no studies. Pravastatin – oral bioavailability 17%, PPB 50%, no studies. Rosuvastatin – oral bioavailability 20%, PPB 88%, RID 0.6–0.77%. Study of one patient but baby was not breastfed so no outcome data.
Rosuvastatin exposure in female Wistar rats alters uterine contractility and do not show evident (anti)estrogenic effects
Published in Drug and Chemical Toxicology, 2022
Jorge Willian Franco de Barros, Patrícia Villela e Silva, Gustavo Venâncio da Silva, Katiussia Pinho da Silva, Cibele dos Santos Borges, André Mueller, Lethícia Valencise, André Sampaio Pupo, Wilma De Grava Kempinas
This study provides information on the effects of rosuvastatin upon the rat uterus. The founds in this study indicate that rosuvastatin might not cross efficiently the tissues, once the results of in vivo and ex vivo exposures to rosuvastatin showed different responses of uterine contractility. Uterine physiology may be affected by this statin, not by the estrogenic or antiestrogenic mechanisms, but by indirect effects on the tissue and smooth muscle cells, as observed with both in vivo and ex vivo exposure assays, which could be influenced by the statin pleiotropic effects, and consequently affect female reproductive parameters, as reported previously by our group (Barros et al. 2020). Furthermore, it is noteworthy that rosuvastatin may interact with different pathways that regulate myometrial contraction throughout different female reproductive phases. Thus, the direct effects promoted by rosuvastatin in the uterus should be analyzed in greater detail to elucidate whether this drug can impair female fertility or might serve as a future adjuvant in the treatment of uterine pathological conditions that affect female reproductive health.
Progression of a supra-valvular aortic stenosis in adulthood during 13 years
Published in Acta Cardiologica, 2021
G. Clermont, A. Friart, C.-H. Huynh, M. Antoine
A 27-year-old woman presented for the first time to the Cardiology department in 2006 for an asymptomatic heart murmur since the childhood and familial hypercholesterolaemia. Cholesterol level was 161 mg/dL under rosuvastatin 40 mg, compared to 317 mg/dL before treatment. Physical examination revealed an aortic midsystolic heart murmur of 2/6 intensity. No signs of hypercholesterolaemia were identified. The EKG was normal. The transthoracic echocardiography (TTE) showed a tricuspid aortic valve, with a mean and maximum transaortic gradient of 16/20 mmHg respectively and a maximal velocity (Vmax) of 2.73 m/s. A supra-valvular aortic narrowing is seen at the sino-tubular junction, reducing the diameter of the aorta to 1.5 cm (Figure 1). The diagnosis of supra-valvular stenosis is established and further confirmed by cardiac magnetic resonance (cMR) (Figure 2) and cardiac scan (cCT). Other heart defects, such as pulmonary artery stenosis which is frequently associated, have been excluded. Stress echography showed no increase in the mean gradient. CoroCT revealed normal coronary arteries.
Fixed-dose combination of rosuvastatin and ezetimibe: treating hypercholesteremia according to cardiovascular risk
Published in Expert Review of Clinical Pharmacology, 2021
Vivencio Barrios, Carlos Escobar
Rosuvastatin is a relatively hydrophilic, potent, and highly selective 3-hydroxy-3-methylglutaryl-CoA reductase inhibitor that significantly reduces the generation of cholesterol. The absolute bioavailability of rosuvastatin is around 20%. Approximately 90% of the drug is bound to plasma proteins, mainly to albumin. Of note, rosuvastatin undergoes limited metabolism, as it is a poor substrate for cytochrome P450–based metabolism (~10%), which translates into a low risk of drug–drug interactions. Around 90% of rosuvastatin is excreted unchanged in feces and the remaining 10% in urine. The plasma elimination half-life is approximately 19 hours. Age does not have a relevant impact on the pharmacokinetics of rosuvastatin. Although mild to moderate renal insufficiency does not affect plasma concentrations, severe renal impairment markedly increases exposure to rosuvastatin [8–10].