Search

Introduction: This post hoc subanalysis of the randomized Japanese Primary Prevention Project investigated whether once-daily low-dose aspirin versus no aspirin reduced the risk of cardiovascular events (CVEs) in patients aged ≥ 70 years with atherosclerotic risk factors. Methods: Patients aged < 70 years (young-old) or ≥ 70 years (old) with hypertension, dyslipidemia, or diabetes participated between 2005 and 2007. Patients were randomized 1:1 to receive 100 mg enteric-coated aspirin once daily or no aspirin plus standard of care. The primary outcome was a composite of death from cardiovascular causes plus nonfatal stroke and nonfatal myocardial infarction. The secondary outcome was a composite of the primary outcome plus transient ischemic attack, angina pectoris, and arteriosclerotic disease requiring medical or surgical intervention. Old (n = 7971) and young-old (n = 6493) patients were followed up for a median 5.02 years. Results: Aspirin did not reduce the risk of primary (hazard ratio [HR] 0.92 [95% confidence interval {CI} 0.74–1.16]; P = 0.50) or secondary (0.85 [0.70–1.04]; P = 0.11) outcomes in patients aged ≥ 70 years. In old men with high-density lipoprotein < 40 mg/dL, treatment with low-dose aspirin was associated with a reduction in the incidence of the primary endpoint compared with the group not receiving aspirin (10/260 vs 22/250; HR 0.44 [95% CI 0.20–0.93]; P = 0.03). This subgroup was also found to contain significant larger proportions of patients with elevated body mass index, patients with diabetes mellitus, and smokers (P < 0.001). Old patients also showed differences in bleeding outcomes. Serious extracranial hemorrhage requiring transfusion or hospitalization occurred significantly more frequently in the aspirin-treated group than in the non–aspirin-treated group (35 [0.88%] vs 18 [0.45%]; HR 1.96 [1.11–3.46]; P = 0.020). Gastrointestinal hemorrhage occurred significantly more frequently in the aspirin-treated group than the non–aspirin-treated group (63 [1.58%] vs 18 [0.45%]; relative risk [RR] 3.5 [2.08–5.90]; P < 0.0001). Cerebral hemorrhage (intracranial hemorrhage) tended to occur more frequently in the aspirin-treated group than the non–aspirin-treated group (22 [0.55%] vs 11 [0.28%]; RR 2.01 [0.97–4.14]; P = 0.058). Cerebral hemorrhage occurred significantly more frequently in old patients than in young-old patients (33 [0.41%] vs 10 [0.15%]; HR 2.7 [1.34–5.53]; P = 0.0055). Gastrointestinal hemorrhage occurred in a slightly higher proportion of old patients compared with young-old patients (81 [1.02%] vs 53 [0.82%]; RR 1.2 [0.88–1.76]; P = 0.21). Discussion/Conclusions: Aspirin did not reduce the risk of the primary or secondary outcomes in old patients. Aspirin treatment may have reduced CVEs within a high CVE risk elderly population subgroup. Aspirin treatment in such a group requires caution, because of the increased risk of intracranial hemorrhage, severe extracranial hemorrhage requiring hospitalization or transfusion, and gastrointestinal bleeding in old patients receiving aspirin therapy. Clinical Trial Registration: The study is registered at ClinicalTrials.gov [NCT00225849]. [ABSTRACT FROM AUTHOR]

Background: Residual risk of cardiovascular disease from increased small dense low-density lipoprotein (sdLDL)-cholesterol levels and low n-3 polyunsaturated fatty acid (PUFA) levels is a considerable therapeutic issue. The purpose of this study was to evaluate the effect of ezetimibe as an add-on to statins and supplemental eicosapentaenoic acid (EPA) on sdLDL cholesterol and absorption of EPA in patients with coronary artery disease. Methods: The study population consisted of ten male patients who were concurrently receiving statins and EPA 1,800 mg/day. Serum lipids and PUFAs, including EPA and arachidonic acid, were measured in blood samples collected before ezetimibe (baseline), 4 weeks after starting 10-mg/day ezetimibe, and 4 weeks after discontinuing ezetimibe. Results: Ezetimibe significantly decreased sdLDL-cholesterol levels after 4 weeks of treatment (baseline 35 ± 13 mg/dl; treatment 27 ± 9 mg/dl), but the levels returned to baseline after discontinuation of ezetimibe (37 ± 13 mg/dl). The concentration of EPA did not significantly change during the study. Conclusion: Ezetimibe shows great promise as an add-on therapy to statins to reduce sdLDL-cholesterol-related residual risk of cardiovascular disease without affecting absorption of supplemental EPA in patients with coronary artery disease. [ABSTRACT FROM AUTHOR]

Background: The change (Δ) in the low-density lipoprotein cholesterol (LDL-C) / high-density lipoprotein cholesterol (HDL-C) ratio ( ΔLDL-C/HDL-C) and obesity are known to play important roles in the progression of coronary atherosclerosis. We hypothesized that a reasonable predictive model of coronary plaque regression could be constructed using ΔLDL-C/HDL-C and the body mass index (BMI). Objective: The purpose of this study was to establish a predictive model of coronary plaque regression using ΔLDL-C/HDL-C and BMI. Methods and Results: A 6-month prospective observational study was conducted among 114 patients with coronary artery disease (CAD) who were treated with pravastatin. The plaque volume, as assessed using volumetric intravascular ultrasound, decreased significantly by 9.9 % (p < 0.0001 vs baseline). In a multi-variate regression analysis with traditional risk factors, ΔLDL-C/HDL-C (β: 0.473, p = 0.0001) and the baseline BMI (β : 0.249, p= 0.004) were identified as independent predictors of the Δplaque volume. The patients were divided using the 50th percentile of the baseline BMI and the 50th percentile of the ΔLDL-C/HDL-C ratio as cutoffs, and a model for predicting coronary atherosclerotic regression was prepared using a combination of the two variables. The Δplaque volumes were -18.3 %, -14.1 %, -4.8%, and - 2.2% for the groups with ΔLDL-C/HDL-C≤-22.2 % and a BMI ≤ 24.1 kg /m², ΔLDL-C/HDL-C≤-22.2 % and ΔBMI >24.1 kg /m², ΔLDL-C/HDL-C>-22.2 % and BMI ≤ 24.1 kg /m² and ΔLDL-C/HDL-C>-22.2 % and BMI >24.1 kg /m², respectively (p = 0.003). Conclusion: A predictive model for coronary plaque regression based on a combination of ΔLDL-C/HDL-C and the baseline BMI may be a useful clinical tool in patients with CAD. [ABSTRACT FROM AUTHOR]