ABSTRACT
BACKGROUND: Statins play an important role in the care of patients with cardiovascular disease and have a good safety record in clinical practice. Hepatotoxicity is a barrier that limits the ability of primary care physicians to prescribe statins for patients with elevated liver transaminase values and/or underlying liver disease. However, limited population-based data are available on the use of statin therapy and on the hepatotoxicity of statins in very elderly patients. This prospective study evaluated the liver enzyme elevation during statin therapy in very elderly patients (≥80 years old). METHODS: Patients with hypercholesterolemia (LDL-C levels ≥3.4 and < 5.7 mmol/L), atherosclerosis, coronary heart disease (CHD), or a CHD-risk equivalent were enrolled and received once-daily statin treatment. Multivariate logistic regression models were used to study the impact of age, gender, hepatitis B infection, fatty liver disease, biliary calculus, other chronic diseases, drug kinds, alcohol abuse, statin variety, and statin dose variables. RESULTS: A total of 515 consecutive patients ranging from 80 to 98 years old were included in the analysis. These patients were treated with simvastatin, fluvastatin, pravastatin, rosuvastatin, or atorvastatin. Twenty-four patients (4.7, 95% CI 2.7-6.6) showed an increase in their hepatic aminotransferase levels. No significant difference of hepatic aminotransferase elevation rates was observed in different statin treatment groups. The incidence of mild, moderate, and severe elevation of aminotransferase levels was 62.5% (15/24), 29.2% (7/24), and 8.3% (2/24), respectively. None of the patients developed hepatic failure. Nine patients with moderate or severe aminotransferase elevations discontinued therapy. The time of onset of hepatic aminotransferase elevation ranged from 2 weeks to 6 months after statin treatment. The onset of hepatic aminotransferase elevation was within 1 month for 70.8% of patients. The patients took 2 weeks to 3 months to recover their liver function after statin therapy cessation. Multivariate analysis identified chronic hepatitis B infection and alcohol consumption as independent factors associated with the hepatic response to statins: OR, 12.83; 95% CI (4.36-37.759) and OR, 2.736; 95% CI (1.373-5.454), respectively. CONCLUSION: The prevalence of elevated transaminases was higher than published data in very elderly patients. Overall, statin treatment is safe for patients ≥80 years old.
Subject(s)
Hydroxymethylglutaryl-CoA Reductase Inhibitors/adverse effects , Hydroxymethylglutaryl-CoA Reductase Inhibitors/therapeutic use , Liver/drug effects , Liver/enzymology , Transaminases/blood , Aged, 80 and over , Coronary Disease/blood , Coronary Disease/drug therapy , Female , Humans , Hypercholesterolemia/blood , Hypercholesterolemia/drug therapy , Male , Prospective StudiesABSTRACT
We assessed the relation between different fasting plasma glucose (FPG) levels of 5.6 to 6.9 mmol/L and the prevalence and severity of angiographic coronary artery disease (CAD) in high-risk Chinese patients. Among 512 subjects who were to undergo coronary angiography for the confirmation of suspected myocardial ischemia, 409 subjects were enrolled and categorized into 3 groups based on FPG levels: (1) =5.5 mmol/L, (2) 5.6 to 6.0 mmol/L, and (3) 6.1 to 6.9 mmol/L. Each of these groups was further divided into subgroups by sex; the second and third groups were combined as an additional group according to the 2003 definition of impaired fasting glucose (FPG at 5.6-6.9 mmol/L). We analyzed the coronary artery stenosis score, the prevalence of angiographic CAD, and the percentage of stenosis in the 3 main arteries among the groups and examined the risk factors for angiographic CAD prevalence by logistic regression analysis. A higher correlation was observed between angiographic CAD prevalence and FPG levels of 6.1 to 6.9 mmol/L as compared with FPG levels =5.5 mmol/L (adjusted odds ratio [OR], 2.67; 95% confidence interval [CI], 1.72-4.10; P = .011). The FPG levels of 5.6 to 6.9 mmol/L (adjusted OR, 2.57; 95% CI, 1.65-4.02; P < .001) and 5.6 to 6.0 mmol/L (adjusted OR, 2.33; 95% CI, 1.58-3.49; P = .008) were modestly correlated with angiographic CAD prevalence. The angiographic CAD prevalence, coronary artery stenosis score, and the percentage of stenosis in the left anterior descending branch increased corresponding to increasing FPG levels from =5.5 mmol/L to 5.6 to 6.0 mmol/L to 6.1 to 6.9 mmol/L. We concluded that FPG levels of 5.6 to 6.9 mmol/L as well as of 6.1 to 6.9 mmol/L may be an independent risk factor for angiographic CAD; furthermore, there was a progressive and graded relation between FPG levels of 5.6 to 6.9 mmol/L and angiographic CAD prevalence and severity in high-risk Chinese patients.