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In patients who have, or are at risk for, coronary artery disease, niacin added to statin therapy resulted in regression of the carotid intima–media thickness. In contrast, ezetimibe added to statin therapy paradoxically resulted in progression of the carotid intima–media thickness. Treatment with 3-hydroxy-3-methylglutaryl–coenzyme A reductase inhibitors reduces low-density lipoprotein (LDL) cholesterol levels and results in clinically significant reductions in the relative risk of major cardiovascular events. 1 However, because of the residual cardiovascular risk seen with statin monotherapy, treatment may be intensified with the use of combination therapy, aimed at either further reducing the LDL cholesterol level or at altering levels of other lipids, such as high-density lipoprotein (HDL) cholesterol. Progressive lowering of the LDL cholesterol level through intensification of statin therapy leads to a 16% reduction in the odds of cardiovascular events and death from cardiovascular causes. 2 This approach has . . .

In a 2-year clinical trial, the addition of ezetimibe to simvastatin had no effect on the progression of atherosclerosis, as measured by carotid-artery intima–media thickness, despite the additional lowering of levels of low-density lipoprotein cholesterol and C-reactive protein by ezetimibe when added to simvastatin. However, the study was not powered to assess clinical end points. The addition of ezetimibe to simvastatin had no effect on the progression of atherosclerosis, as measured by carotid-artery intima–media thickness, despite the additional lowering of levels of low-density lipoprotein cholesterol and C-reactive protein. A reduction in levels of low-density lipoprotein (LDL) cholesterol constitutes one of the cornerstones in the prevention of cardiovascular disease. In recent trials comparing various statins or the same statin at various doses, aggressive therapy to lower LDL cholesterol levels was associated with a reduction in rates of cardiovascular events. 1 – 4 However, administration of the highest approved statin dose offers only limited additional lowering of LDL cholesterol at the expense of an increased incidence of side effects. 5 Therefore, novel compounds that further reduce LDL cholesterol levels when added to statin therapy are of interest. A recently introduced compound, ezetimibe, selectively . . .

Obstructive sleep apnea (OSA) is associated with adverse cardiovascular outcomes, including myocardial infarction and stroke. Atherosclerosis is a key mechanism for these cardiovascular events. Recent cross-sectional studies showed the presence of early signs of atherosclerosis in patients with OSA who were free of comorbidities. To determine the impact of treatment with continuous positive airway pressure (CPAP) on atherosclerosis. We randomly assigned 24 patients with severe OSA (age, 46 +/- 6 yr) who were free of comorbidities to receive no treatment (control, n = 12) or CPAP (n = 12) for 4 months. Carotid intima-media thickness, arterial stiffness (evaluated by pulse-wave velocity), carotid diameter, 24-hour blood pressure monitoring, C-reactive protein, and catecholamines were determined at baseline and after 4 months. At baseline, all measurements were similar in both groups and did not change in the control group after 4 months. In contrast, a significant decrease occurred in carotid intima-media thickness (707 +/- 105 vs. 645 +/- 95 microm, P = 0.04), pulse-wave velocity (10.4 +/- 1.0 vs. 9.3 +/- 0.9 m/s, P < 0.001), C-reactive protein (3.7 +/- 1.8 vs. 2.0 +/- 1.2 mg/L, P = 0.001), and catecholamines (365 +/- 125 vs. 205 +/- 51 ng/ml, P < 0.001) after 4 months of CPAP. Carotid diameter did not change significantly. Regarding the whole group, changes in carotid intima-media thickness were correlated with changes in catecholamines (r = 0.41, P < 0.05). Changes in pulse-wave velocity were correlated with changes in C-reactive protein (r = 0.58, P < 0.01) and catecholamines (r = 0.54, P < 0.01). The treatment of OSA significantly improves early signs of atherosclerosis, supporting the concept that OSA is an independent risk factor for atherosclerosis. Clinical trial registered with www.clinicaltrials.gov (NCT 00400543).

Proton pump inhibitors (PPIs) are frequently prescribed in combination with clopidogrel, but conflicting data exist as to whether PPIs diminish the efficacy of clopidogrel. We assessed the association between PPI use and clinical outcomes for patients treated with percutaneous coronary intervention (PCI) and dual-antiplatelet therapy (DAPT) with clopidogrel plus aspirin. In the PRODIGY trial, 1,970 patients were randomized to 6- or 24-month DAPT at 30 days from index procedure. Among them, 738 patients (37.5%) received PPI (mainly lansoprazole; 90.1%) at the time of randomization. Proton pump inhibitor users were older, were most likely to be woman, had a lower creatinine clearance, presented more frequently with acute coronary syndrome, and had a higher CRUSADE bleeding score. After adjustment, the primary efficacy end point (composite of all-cause death, myocardial infarction, and cerebrovascular accident) was similar between no PPI and PPI users (9.2% vs 11.5%, adjusted hazard ratio [HR] 1.051, 95% CI 0.788-1.400, P = .736). Bleeding rates did not differ between the 2 groups (Bleeding Academic Research Consortium type 2, 3, or 5: adjusted HR 0.996, 95% CI 0.672-1.474, P = .980). Net clinical adverse events were also similar in no PPI and PPI patients (12.9% vs 14.9%, adjusted HR 0.99, 95% CI 0.772-1.268, P = .93). Results remained consistent at sensitivity analysis when focusing on the 548 patients who remained on PPI for the whole study duration. The current findings suggest that the concomitant use of PPIs, when clinically indicated, in patients receiving clopidogrel is not associated with adverse clinical outcome.

Carotid intima–media thickness is considered to be a measure of atherosclerosis. This study examined intima–media thickness in participants in the Diabetes Control and Complications Trial. Six years after the trial ended, the progression of intima–media thickness was significantly less in patients who had received intensive as compared with conventional therapy. Diabetes mellitus is accompanied by a substantial increase in the risk of cardiovascular disease. 1 – 5 Most epidemiologic and clinical-trial data have derived from the study of type 2 diabetes, in which cardiovascular disease accounts for 70 percent of all deaths. 1 – 3 Much less is known about cardiovascular disease in type 1 diabetes. Although the absolute risk of cardiovascular disease is lower in patients with type 1 diabetes than in those with type 2 diabetes, owing in part to their younger age, the relative risk, as compared with that of nondiabetic persons of similar age, may be increased by a factor . . .

Patients with mixed dyslipidaemia have raised triglycerides, low high-density lipoprotein (HDL) cholesterol, and high low-density lipoprotein (LDL) cholesterol. Augmentation of HDL cholesterol by inhibition of the cholesteryl ester transfer protein (CETP) could benefit these patients. We aimed to investigate the effect of the CETP inhibitor, torcetrapib, on carotid atherosclerosis progression in patients with mixed dyslipidaemia. We did a randomised double-blind trial at 64 centres in North America and Europe. 752 eligible participants completed an atorvastatin-only run-in period for dose titration, after which they all continued to receive atorvastatin at the titrated dose. 377 of these patients were randomly assigned to receive 60 mg of torcetrapib per day and 375 to placebo. We made carotid ultrasound images at baseline and at 6-month intervals for 24 months. The primary endpoint was the yearly rate of change in the maximum intima-media thickness of 12 carotid segments. Analysis was restricted to 683 patients who had at least one dose of treatment and had at least one follow-up carotid intima-media measurement; they were analysed as randomised. Mean follow-up for these patients was 22 (SD 4·8) months. This trial is registered with ClinicalTrials.gov, number NCT00134238. The change in maximum carotid intima-media thickness was 0·025 (SD 0·005) mm per year in patients given torcetrapib with atorvastatin and 0·030 (0·005) mm per year in those given atorvastatin alone (difference −0·005 mm per year, 95% CI −0·018 to 0·008, p=0·46). Patients in the combined-treatment group had a 63·4% relative increase in HDL cholesterol (p<0·0001) and an 17·7% relative decrease in LDL cholesterol (p<0·0001), compared with controls. Systolic blood pressure increased by 6·6 mm Hg in the combined-treatment group and 1·5 mm Hg in the atorvastatin-only group (difference 5·4 mm Hg, 95% CI 4·3–6·4, p<0·0001). Although torcetrapib substantially raised HDL cholesterol and lowered LDL cholesterol, it also increased systolic blood pressure, and did not affect the yearly rate of change in the maximum intima-media thickness of 12 carotid segments. Torcetrapib showed no clinical benefit in this or other studies, and will not be developed further.

Background Externally stenting saphenous vein grafts reduces intimal hyperplasia, improves lumen uniformity and reduces oscillatory shear stress 1 year following surgery. The present study is the first to present the longer-term (4.5 years) performance and biomechanical effects of externally stented saphenous vein grafts. Methods Thirty patients previously implanted with the VEST external stent in the randomized, within-patient-controlled VEST I study were followed up for adverse events; 21 of these were available to undergo coronary angiography and intravascular ultrasound. Results Twenty-one stented and 29 nonstented saphenous vein grafts were evaluated by angiography and ultrasound at 4.5 ± 0.3 years. Vein graft failure rates were comparable between stented and nonstented grafts (30 and 23% respectively; p  = 0.42). All failures were apparent at 1 year except for one additional nonstented failure at 4.5 years. In patent vein grafts, Fitzgibbon perfect patency remained significantly higher in the stented versus nonstented vein grafts (81 and 48% respectively, p  = 0.002), while intimal hyperplasia area (4.27 mm 2  ± 1.27 mm 2 and 5.23 mm 2  ± 1.83 mm 2 respectively, p  < 0.001) and thickness (0.36 mm ± 0.09 mm and 0.42 mm ± 0.11 mm respectively, p  < 0.001) were significantly reduced. Intimal hyperplasia proliferation correlated with lumen uniformity and with the distance between the stent and the lumen ( p  = 0.04 and p  < 0.001 respectively). Conclusions External stenting mitigates saphenous vein graft remodeling and significantly reduces diffuse intimal hyperplasia and the development of lumen irregularities 4.5 years after coronary artery bypass surgery. Close conformity of the stent to the vessel wall appears to be an important factor. Trial registration NCT01415245 . Registered 11 August 2011.

Despite advances in coronary angioplasty and stenting, restenosis remains an important problem that limits clinical success. This study compared a new coronary stent coated with sirolimus (rapamycin) with a standard (uncoated) stent in patients undergoing stenting for a single coronary lesion. At six months, the rate of restenosis was 26.6 percent in the standard-stent group and 0 percent in the sirolimus-stent group. At six months, the rate of restenosis was 26.6 percent with the standard stent and 0 percent with the sirolimus stent. The growing use of stents has improved the results of percutaneous coronary revascularization. 1 – 5 However, in-stent restenosis continues to limit the long-term success of this approach. 6 , 7 For example, in a recent randomized comparison of coronary-artery bypass surgery and stenting in patients with multivessel disease, additional revascularization procedures were performed within one year in 21.0 percent of patients who had undergone stenting, as compared with 3.8 percent of patients treated surgically. 8 In controlled trials, several pharmaceutical agents have failed to inhibit restenosis after coronary interventions. 9 In contrast, the systemic and local delivery of sirolimus (rapamycin), a macrocyclic lactone that inhibits . . .

This clinical trial compared everolimus, an immunosuppressive and antiproliferative agent, with azathioprine in patients who had undergone cardiac transplantation. Everolimus reduced the incidence of both acute rejection and coronary vasculopathy, a serious disorder that causes deterioration of the graft. A promising agent for management of rejection and vasculopathy. Among recipients of heart transplants, vasculopathy of the allograft is the main cause of illness and death after the first year. 1 , 2 Early immunologic and nonimmunologic endothelial damage may initiate pathologic remodeling, resulting in progressive luminal narrowing. 3 – 5 The development of immunosuppressive agents to prevent acute allograft rejection and the proliferation of smooth-muscle cells may reduce the frequency and severity of vasculopathy. Intravascular ultrasonography is a sensitive approach for the early detection of vasculopathy. 6 – 8 If performed at the same sites at base line and one year after transplantation, ultrasonography can be used to evaluate the progression of intimal proliferation. . . .

PurposeThe aim of this study was to compare the ultrasonographic findings of femoral puncture sites and the complications of Perclose ProGlide® and FemoSeal™ after neurointerventional procedures.MethodsIn this prospective, single-center study, we randomly assigned 155 femoral puncture sites to treatment with Perclose ProGlide® or FemoSeal™. We hypothesized that the two different types of VCD cause different vascular changes. Ultrasonography of the femoral puncture sites was performed 24 h after the procedure and at an outpatient visit after 6 months. The intima–media thickness (IMT), vessel diameter, and minimal luminal diameter of the common femoral artery were measured; the perivascular soft tissue change and absorption of the hemostatic material were observed. The device failure rate and vascular complications associated with each device were also evaluated.ResultsFollow-up ultrasonography was performed at a median follow-up time of 187.0 days (range 147–240 days) after the initial ultrasonography. The IMT on follow-up ultrasonography was significantly higher in patients who received FemoSeal™ (P = 0.0000). Intimal hyperplasia and partial absorption of the hemostatic material were significantly more frequent in patients who received FemoSeal™. The vessel diameters on initial and follow-up ultrasonography were not significantly different, but the minimal diameter on follow-up ultrasonography was significantly lower in patients who received FemoSeal™. Device failure and pseudoaneurysms occurred at 9 and 3 puncture sites in patients who received Perclose ProGlide®, respectively.ConclusionsIntimal hyperplasia was more frequently observed in patients who received FemoSeal™. However, more device failures and pseudoaneurysms occurred in patients who received Perclose ProGlide®.Level of EvidenceStep 2 (level 2).