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CBT showed a reduction in insomnia and improvements in sleep quality. However, there is insufficient evidence to draw conclusions on the effects of CBT on insomnia. These results suggest that further investigation into insomnia outcomes is needed.

There is strong evidence to suggest that CBT is associated with improvements in anxiety, depression, and quality of life in persons with mild cognitive impairment and dementia. CBT showed a reduction in insomnia and improvements in sleep quality. However, there is insufficient evidence to draw conclusions on the effects of CBT on insomnia. These results suggest that further investigation into insomnia outcomes is needed.

Hypercholesterolemia is a major risk factor for cardiovascular diseases. Administration of statins represents the cornerstone of the prevention and treatment of cardiovascular disease, with demonstrated long-term safety and efficacy. This review aims to revisit statin intolerance mechanisms, as well as to discuss new data and therapeutic options.

Although statins are well tolerated, myopathy and other adverse effects are a challenging problem, being the main reason for poor adherence to treatment and failure in lowering cardiovascular risk. Statin intolerance is the subject of ongoing research, as these drugs are widely used. There are alternative options of treatment if statin intolerance emerges, that is, lowering the dose, intermittent dosages, and/or combining a statin with other drugs, such as ezetimibe, proprotein convertase subtilisin-kexin type 9 inhibitors, bempedoic acid, angiopoietin-like 3 protein inhibitors, and nutraceuticals. If even the lowest statin dose cannot be tolerated, a nonstatin regimen is recommended to reduce LDL cholesterol levels.

Treatment options in statin intolerance include combinations of a lower dose of statin with other lipid-lowering regimens or only nonstatin drugs in the presence of complete intolerance. New hypolipidemic therapies that address gene editing are emerging, and may prove useful in the future.

Treatment options in statin intolerance include combinations of a lower dose of statin with other lipid-lowering regimens or only nonstatin drugs in the presence of complete intolerance. New hypolipidemic therapies that address gene editing are emerging, and may prove useful in the future.

Elevated levels of triglycerides, independent of low-density lipoprotein cholesterol (LDL-C) levels and statin therapy, are associated with heightened cardiovascular risk.

Mixed omega-3 fatty acid formulations, which contain varying amounts of docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA), lower triglycerides levels but trial results with omega-3 fatty acids combinations have generally been neutral for cardiovascular outcomes. In contrast, the REDUCE-IT trial with icosapent ethyl (IPE), a highly purified ethyl ester of EPA, demonstrated reduced cardiovascular risk in individuals with established atherosclerotic cardiovascular disease or diabetes with at least one additional risk factor, despite having relatively well controlled LDL-C levels but triglycerides at least 135 mg/dl while on statin therapy. Linsitinib ic50 IPE offers an important new avenue for cardiovascular risk management in statin-treated individuals with elevated triglycerides.

This review summarizes the results from outcome trials conducted with omega-3 fatty acids, differentiating between those with combinations of EPA/DHA and those with pure EPA, as well as imaging and preclinical data that help explain the different cardiovascular efficacy observed. A list of frequently asked questions with evidence-based responses is provided to assist our colleagues and their patients in the shared-decision process when considering if IPE is appropriate for cardiovascular risk reduction.

This review summarizes the results from outcome trials conducted with omega-3 fatty acids, differentiating between those with combinations of EPA/DHA and those with pure EPA, as well as imaging and preclinical data that help explain the different cardiovascular efficacy observed. A list of frequently asked questions with evidence-based responses is provided to assist our colleagues and their patients in the shared-decision process when considering if IPE is appropriate for cardiovascular risk reduction.

Coronary artery calcification (CAC) predisposes to suboptimal revascularization outcomes after percutaneous coronary intervention (PCI). Despite the availability of several plaque modification devices, their rates of use remain low despite the prevalence of CAC encountered in clinical practice. It is important to understand how each device can be utilized in clinical practice in order to improve outcomes after PCI.

This article summarizes the most recent clinical evidence for each plaque modification device. Although rotational atherectomy is the most frequently used device for plaque modification, the use of orbital atherectomy (OA) has been increasing. Balloon-based strategies including recent studies evaluating a novel intravascular lithotripsy balloon have shed light on the benefits of nonablative devices in modifying CAC during PCI.

CAC poses significant technical challenges in achieving optimal stent results. Several intracoronary plaque modification devices are currently available and understanding the technical aspects, indications and contraindications to the use of each device is essential. Although rotational and OA are most commonly used, laser atherectomy and balloon-based devices may offer an advantage in certain lesion subsets.

CAC poses significant technical challenges in achieving optimal stent results. Several intracoronary plaque modification devices are currently available and understanding the technical aspects, indications and contraindications to the use of each device is essential. Although rotational and OA are most commonly used, laser atherectomy and balloon-based devices may offer an advantage in certain lesion subsets.

Hypertension (HTN) and obesity are major risk factors for cardiac remodeling and dysfunction, leading to left ventricular hypertrophy (LVH) and heart failure (HF). In this review, we discuss the complex mechanisms and effects of HTN and obesity, and their treatments in LVH, ventricular function, and HF.

Obesity and HTN impact the heart through overlapping neurohormonal pathways. However, the relationship between obesity and cardiomyopathy is more complex, and additional metabolic and hemodynamic pathways seem to contribute to cardiac dysfunction in these patients. Weight loss and blood pressure (BP) control help to prevent and reverse at least some of the damage caused by obesity and HTN even beyond what would be expected from solely the hemodynamic changes.

Obesity and HTN cause maladaptive changes in the heart that can lead to LVH and HF. Weight loss and BP control help to, at least partially, reverse some of these changes and improve clinical outcomes in patients with HF.

Obesity and HTN cause maladaptive changes in the heart that can lead to LVH and HF.

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