Academic literature on the topic 'Uveitis treatment; statins (cardiovascular agents)'
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Journal articles on the topic "Uveitis treatment; statins (cardiovascular agents)"
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Shevko, V. G., M. A. Galas, T. L. Galankin, and A. S. Kolbin. "Evaluation of the effectiveness of lipid-lowering agents." Scientific Notes of the Pavlov University 26, no. 3 (February 4, 2020): 78–85. http://dx.doi.org/10.24884/1607-4181-2019-26-3-78-85.
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Introduction. Nowadays, lipid-lowering therapy is considered an essential strategy for primary and secondary prevention of cardiovascular outcomes, which is confirmed by numerous studies. Nevertheless, researches are often guided by analysis of surrogate endpoints, which becomes not just everyday practice, but also an actual problem. Surrogate endpoints are wellknown sources of bias that can distort the risk-benefit analysis.The objective of the study was to assess the significance of lipid-lowering therapy with statins in relation to mortality.Methods and materials. The analysis of prospective controlled trials was carried out with a sample of 2000 patients and more, in which mortality rate was assessed for 2 or more years of statin therapy, as well as systematic literature reviews with a meta-analysis of mortality rates. The search was carried out on websites of the Russian scientific electronic libraries eLibrary and сyberleninka , English-language works – on the PubMed website.Results. An increase in survival during treatment with statins in case of secondary prevention of cardiovascular diseases reached about 2 % after five years’ treatment and was absent after ten years’ treatment. The average increase in life expectancy was only 4.1 days. Primary prevention with statins has not been shown to increase survival significantly.Conclusion. Effectiveness of lipid-lowering therapy with statins as a part of secondary prevention of cardiovascular outcomes assessed by surrogate endpoints could be greatly exaggerated. A biased approach to selecting surrogate endpoints can lead to incorrect results. Similarly, the encouraging results of therapy with statins in the prevention of cardiovascular mortality may be biased when the effect of statins on other causes of death is not considered. Mortality refers to a universal endpoint that characterizes both the effectiveness and safety of a drug.
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Kim, Kyuho, Henry N. Ginsberg, and Sung Hee Choi. "New, Novel Lipid-Lowering Agents for Reducing Cardiovascular Risk: Beyond Statins." Diabetes & Metabolism Journal 46, no. 4 (July 31, 2022): 517–32. http://dx.doi.org/10.4093/dmj.2022.0198.
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Statins are the cornerstone of the prevention and treatment of atherosclerotic cardiovascular disease (ASCVD). However, even under optimal statin therapy, a significant residual ASCVD risk remains. Therefore, there has been an unmet clinical need for novel lipid-lowering agents that can target low-density lipoprotein cholesterol (LDL-C) and other atherogenic particles. During the past decade, several drugs have been developed for the treatment of dyslipidemia. Inclisiran, a small interfering RNA that targets proprotein convertase subtilisin/kexin type 9 (PCSK9), shows comparable effects to that of PCSK9 monoclonal antibodies. Bempedoic acid, an ATP citrate lyase inhibitor, is a valuable treatment option for the patients with statin intolerance. Pemafibrate, the first selective peroxisome proliferator-activated receptor alpha modulator, showed a favorable benefit-risk balance but the large clinical phase 3 trial (Pemafibrate to Reduce Cardiovascular OutcoMes by Reducing Triglycerides IN patiENts With diabe- Tes [PROMINENT]) was recently stopped due to the underperformance from interim analysis. High dose icosapent ethyl, a modified eicosapentaenoic acid preparation, shows cardiovascular benefits. Evinacumab, an angiopoietin-like 3 (ANGPTL3) monoclonal antibody, reduces plasma LDL-C levels in patients with refractory hypercholesterolemia. Novel antisense oligonucleotides targeting apolipoprotein C3 (apoC3), ANGPTL3, and lipoprotein(a) have significantly attenuated the levels of their target molecules with beneficial effects on associated dyslipidemias. Apolipoprotein A1 (apoA1) is considered as a potential treatment to exploit the athero-protective effects of high-density lipoprotein cholesterol (HDL-C), but solid clinical evidence is necessary. In this review, we discuss the mode of action and clinical outcomes of these novel lipid-lowering agents beyond statins.
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Mostovoy, Y. M., and T. D. Danilevych. "PULMONARY ADVERSE REACTIONS OF CARDIOVASCULAR DRUGS." Ukrainian Pulmonology Journal 30, no. 1 (2022): 15–24. http://dx.doi.org/10.31215/2306-4927-2022-30-1-15-24.
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PULMONARY ADVERSE REACTIONS OF CARDIOVASCULAR DRUGS Y. M. Mostovoy, T. D. Danilevych Abstract Diagnosis and treatment of chronic obstructive pulmonary disease, bronchial asthma, pneumonia, idiopathic pulmonary fibrosis is an actual problem in medicine and pulmonology. These diseases are quite often combined with common diseases of the cardiovascular system, in particular, coronary artery disease, hypertension, and heart failure. The supervision of such patients is a difficult problem for the physicians. This review focuses on published data regarding the use of common drugs for the treatment of the cardiovascular diseases, such as angiotensin converting enzyme inhibitors, angiotensin II receptor blockers, calcium channel blockers, antiplatelet agents, statins, antiarrhythmic drugs, etc. Special emphasis has been made on pulmonary adverse reaction of these medications. Key words: amiodarone, angiotensin-converting enzyme inhibitors, beta-blockers, acetylsalicylic acid, statins, pulmonary adverse reactions.
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Ginsberg, Henry N. "REVIEW: Efficacy and Mechanisms of Action of Statins in the Treatment of Diabetic Dyslipidemia." Journal of Clinical Endocrinology & Metabolism 91, no. 2 (February 1, 2006): 383–92. http://dx.doi.org/10.1210/jc.2005-2084.
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Context: The Adult Treatment Panel III recommends 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors, or statins, as first-line lipid-altering therapy for all adult patients with diabetes mellitus. This is based on the well-characterized efficacy and safety profiles of this class of agents as well as several clinical trials demonstrating that statin treatment reduces the risk of cardiovascular events. Evidence Acquisition: This review provides an overview of the effectiveness and mechanisms of action of statins in patients with diabetes mellitus using small efficacy trials and large clinical outcomes trials as well as studies of the effects of statins on apolipoprotein B (apoB) metabolism. Evidence Synthesis: The major findings presented are a review of mechanistic studies of selected subjects with diabetes mellitus and dyslipidemia and a compilation of results from large-scale clinical trials of patients with diabetes. Conclusions: Statins are highly efficacious as low-density lipoprotein cholesterol-lowering agents and have more modest effects on very low-density lipoprotein triglyceride and high-density lipoprotein cholesterol levels. The effects of statins on plasma lipids and lipoproteins result from their ability to both increase the efficiency with which very low-density lipoprotein and low-density lipoprotein are cleared from the circulation and reduce the production of apoB-containing lipoproteins by the liver. Additional investigations are needed to clarify the mechanisms by which statins reduce apoB secretion from the liver.
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Živanović, Željko. "Hypolipidemic agents in the secondary prevention of the stroke." Galenika Medical Journal 1, no. 4 (2022): 96–102. http://dx.doi.org/10.5937/galmed2204109z.
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Stroke is one of the leading causes of morbidity, mortality and disability in the world, and fat metabolism disorder is one of the most significant risk factors for its occurrence. Numerous studies have confirmed that lowering LDL cholesterol with the use of statins significantly reduces the risk of ischemic stroke (AIS). Therefore, their use is advised in all patients who have survived IMU or transient ischemic attack (TIA). Although in these patients the use of statins may increase the risk for intracerebral hemorrhage (ICH), the overall clinical benefit of reducing ischemic cardiovascular risks and mortality is far greater. The significance of the use of statins is greatest if atherosclerosis of the large arteries is the basis of AIS or TIA. Treatment should most often be started with high-intensity statins aiming to achieve an LDL cholesterol level of <1.8 mmol/l. If this goal is not achieved with statins, ezetimibe should be added to the therapy, which lowers the LDL cholesterol level more effectively, which at the same time further reduces the ischemic risk. PCSK9 inhibitors are a new therapeutic option for lowering LDL cholesterol if even the previous combination does not achieve the target result. The importance of treating hypertriglyceridemia in the prevention of stroke is still not completely clear, but the recommendations clearly state that after adequate treatment of hypercholesterolemia this residual atherogenic risk must also be actively treated. Despite the lack of sufficient evidence to restrict the use of statins after a hemorrhagic stroke, in these patients, the therapeutic approach must be individualized and carefully evaluated, due to the risk-benefit ratio of long-term statin use.
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Pereverzeva, К. G., and S. S. Yakushin. "Aspirin and statins: possibilities for joint improvement of prognosis in cardiovascular disease." Medical Council, no. 21 (January 20, 2019): 28–33. http://dx.doi.org/10.21518/2079-701x-2018-21-28-33.
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Today, cardiovascular diseases (CVDs) are the main cause of death in all countries of the world, which is largely due to the low adherence of patients with CVDs to treatment. According to the RECVASA register, the average adherence of patients of one of the polyclinics in the city of Ryazan to treatment (n = 1,165) in 2012 was 62.4%, adherence to beta-adrenergic blocking agent (BABs) was 70.8%, to angiotensin-converting enzyme inhibitors (ACEs) – 62.2%, to angiotensin II (ARB) receptor blockers – 57.1%, to statins – 46.8%, and to antiplate agents – 70.0%. The average adherence to treatment in survivors of the same group (n = 918) in 4 years in 2016 was significantly lower (p<0.001) and amounted to 47.8%. Patient adherence to BABs, ACEs also became statistically significantly lower (p<0.0001), at 43.8% and 50.0%, respectively; adherence to ARB was statistically insignificantly lower by 3.6% compared to the original level. The highest level of adherence to the use of antiplatelet agents was 63.9%, although it was significantly lower compared to the initial data (p = 0.0037), and the initially low adherence to the use of statins for 4 years has statistically significantly decreased (p<0.0001) and amounted to only 28.2%. The data obtained determine one of the possible ways to increase adherence to statins a fixed combination of them with other drugs affecting the prognosis, such as antiplatelet drugs.
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Markowska, Anna, Michał Antoszczak, Janina Markowska, and Adam Huczyński. "Statins: HMG-CoA Reductase Inhibitors as Potential Anticancer Agents against Malignant Neoplasms in Women." Pharmaceuticals 13, no. 12 (November 25, 2020): 422. http://dx.doi.org/10.3390/ph13120422.
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Statins, also known as HMG-CoA inhibitors, are a class of bioactive small molecules that efficiently reduce the levels of cholesterol, and therefore are commonly used to manage and prevent various cardiovascular diseases. With respect to their original medical indications, statins are currently in the group of the most prescribed drugs worldwide. Of note is that statins are perceived actually rather as agents that have pleiotropic activities; in addition to their inhibitory activity on the production of endogenous cholesterol. Statins may also affect cell proliferation, angiogenesis and/or migration (metastasis) of different cancer cells, and play a positive role in the chemoprevention of cancer, thus being the excellent candidates to be repurposed in oncology. Particularly intriguing in this context seems to be the promising role of statins on both the incidence and course of common malignant neoplasms in women. In this article, we review and discuss the effect of the use of statins in the treatment of three types of cancer, i.e., breast, endometrial and ovarian cancer, with the highest mortality among gynecological cancers.
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Vavuranakis, Manolis, Maria Kariori, Gerasimos Siasos, Konstantinos Kalogeras, and Dimitris Tousoulis. "Statins in Acute Coronary Syndromes." Current Pharmaceutical Design 23, no. 46 (February 1, 2018): 7086–98. http://dx.doi.org/10.2174/1381612823666170816114403.
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Background: Patients with acute coronary syndrome (ACS) frequently experience recurrent adverse events from the cardiovascular system comparing to either healthy individuals or individuals with stable coronary artery disease. This is attributed to the inflammatory cascade that is activated during ACS resulting in increased risk for rupture of vulnerable plaques. </P><P> Objective: Therefore, it is of great importance to avoid recurrent events with treatment aiming at secondary prevention which includes the management of lipid profile besides alteration in the lifestyle and habits. </P><P> Methods: This review will present current data concerning present status of treatment with statins, and refer to non-statin strategies as well as novel and promising agents for the secondary prevention therapy after ACS. A thorough search of PubMed and the Cochrane Database was conducted in order to identify the majority of trials, studies, current guidelines and novel articles related to the subject. </P><P> Results: Statins have been proved to play very significant role in the part of secondary prevention since they decrease the burden of atherosclerotic plaques, the risk of adverse events and the need for revascularization in symptomatic patients with CAD. Therefore, they were established and suggested by both European and American guidelines as first-line treatment option for lipid-lowering management. Several clinical trials, meta- analyses and randomized trials strongly recommended the application of early and intensive treatment with statins in patients with ACS. Nevertheless, a vast majority of individuals neither tolerated statins nor achieved the optimal value for LDL-C with the highest tolerated dose of statins resulting in poor clinical outcome. Furthermore, recent clinical trials indicated further benefit of combined treatment of statins with non-statins drugs on the decrease of cardiovascular events as well as progress of coronary artery plaque. Finally, novel agents that are still evaluated with ongoing clinical trials have been turned into a very promising treatment option. </P><P> Conclusion: In conclusion, statins are established as the first-line treatment for the secondary prevention after acute coronary syndromes in order to avoid the recurrence of thrombotic events. However, the research field on the field of lipid-lowering therapies is still ongoing and very promising for the future.
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Ferreira, Carlos Eduardo dos Santos, Francisco Antônio Helfenstein Fonseca, and Cristóvão Luis Pitangueira Mangueira. "PCSK9 and its clinical importance with the new therapeutic targets against dyslipidemia." Einstein (São Paulo) 10, no. 4 (December 2012): 526–27. http://dx.doi.org/10.1590/s1679-45082012000400024.
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This is a remarkable progress; since the finding of statins, there was no new way of reducing, significantly, cholesterol and LDL fraction. It is also clear that this decrease, by statins, is related to future cardiovascular lesions, being useful in its primary and secondary prophylaxis. The authors presented studies on research to promote the falling of blood cholesterol by means of antibodies, which inhibit the pro-protein PCSK9, as well as agents that act performing the RNA interference. We had two advantages immediately: for patients with myopathy associated with statins, and the fact of being injected every 15 days, that may contribute to better treatment adherence.
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Burnett, John R., and Samuel D. Vasikaran. "Cardiovascular disease and osteoporosis: is there a link between lipids and bone?" Annals of Clinical Biochemistry: International Journal of Laboratory Medicine 39, no. 3 (May 1, 2002): 203–10. http://dx.doi.org/10.1258/0004563021902134.
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Atherosclerotic heart disease and osteoporosis are both diseases of old age. Evidence is accumulating for a link between vascular and bone disease. Calcification is a common feature of atherosclerotic plaques, and osteoporosis is associated with both atherosclerosis and vascular calcification. However, the relationship of vascular calcification to the pathogenesis of atherosclerosis remains incompletely understood. Hormone replacement therapy has beneficial effects in the prevention of both atherosclerosis and osteoporosis. Bisphosphonates inhibit bone resorption and are used in the treatment of osteoporosis, whereas the statins inhibit cholesterol biosynthesis and are used for the treatment of atherosclerosis. We have reviewed recent advances in the knowledge of the actions of bisphosphonates and statins at the cellular, molecular and end-organ levels in order to examine the relationship between cardiovascular disease and osteoporosis and to explore the link between lipids and bones. These studies suggest that the mechanism of actions of these two classes of drugs at the cellular level may not be mutually exclusive. There are some early clinical data to complement these findings, suggesting that statins increase bone density and bisphosphonates may have a beneficial effect in vivo on plasma lipid levels and on the atherosclerotic process. Properly designed prospective studies that examine the effect of statins on bone density and fractures, as well as the effects of bisphosphonates on lipid profiles, atherosclerotic progression and cardiovascular morbidity and mortality are needed to define clearly the clinical effects and potential new roles for these agents.
Dissertations / Theses on the topic "Uveitis treatment; statins (cardiovascular agents)"
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Burns, Erin M. "Simvastatin treatment modulates the immune response, increasing the survival of mice infected with Staphylococcus aureus." Muncie, Ind. : Ball State University, 2009. http://cardinalscholar.bsu.edu/612.
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Horn, Mary P. "The effects of simvastatin on Staphyloccus aureus infection in endothelial cells." Virtual Press, 2007. http://liblink.bsu.edu/uhtbin/catkey/1366299.
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Simvastatin, a commonly prescribed statin, has exhibited several unexpected non-cholesterol lowering benefits. For example, patients taking statins have a decreased mortality rate due to bactereamia, a systemic bacterial infection commonly caused by Staphylococcus aureus (S. aureus). To investigate statin protection during bactereamia, human umbilical vein endothelial cells (HUVEC) were pre-treated with simvastatin followed by infection with S. aureus, and infection was significantly decreased. Simvastatin inhibits the cholesterol biosynthesis pathway. Therefore, the protective effect of simvastatin may be due to isoprenoid inhibition, specifically, farnesyl pyrophosphate (Fpp) and geranylgeranyl pyrophosphate (GGpp). Fpp and GGpp prenylate small G-proteins that function in cytoskeletal rearrangement and endocytosis. When Fpp and GGpp were replenished, infection was not significantly reduced. Furthermore, when farnesyl transferase and geranylgeranyl transferase, enzymes essential to transfer isoprenoid group during prenylation, were inhibited a significant decrease in infection was observed. The data indicates that Fpp and GGpp are essential for S. aureus infection.Department of Biology
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Ooi, Esther M. M. "Regulation of lipoprotein transport in the metabolic syndrome : impact of statin therapy." University of Western Australia. School of Medicine and Pharmacology, 2007. http://theses.library.uwa.edu.au/adt-WU2007.0125.
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[Truncated abstract] The metabolic syndrome is characterized by cardiovascular risk factors including dyslipidemia, insulin resistance, visceral obesity, hypertension and diabetes. The dyslipidemia of the metabolic syndrome includes elevated plasma triglyceride and apolipoprotein (apo) B levels, accumulation of small, dense low-density lipoprotein (LDL) particles and low high-density lipoprotein (HDL) cholesterol concentration. However, the precise mechanisms for this dyslipoproteinemia, specifically low plasma HDL cholesterol, are not well understood. This thesis therefore, focuses on HDL, its structure, function and metabolism. However, lipoprotein metabolism is a complex interconnected system, which includes forward and reverse cholesterol transport pathways. Hence, this thesis also examines and discusses the metabolism of apoB-containing lipoproteins. This thesis tests the general hypothesis that apolipoprotein kinetics are altered in the metabolic syndrome, and that lipid regulating therapies can improve these kinetic abnormalities. The aims were first, to compare and establish the clinical, metabolic and kinetic differences between metabolic syndrome and lean subjects; and second, to determine the regulatory effects of statin therapy, specifically, rosuvastatin on lipoprotein transport in the metabolic syndrome. Five observation statements were derived from the general hypothesis and examined in the studies described below. The findings are presented separately as a series of original publications. Study 1 Twelve men with the metabolic syndrome and ten lean men were studied in a case-control setting. ... These findings explain the HDL raising effects of rosuvastatin in the metabolic syndrome. Collectively, these studies suggest that the dyslipidemia of the metabolic syndrome results from increased production rates of VLDL and LDL particles, reduced fractional catabolic rates of these lipoproteins, together with accelerated catabolism of HDL particles. Treatment with rosuvastatin increases the catabolic rates of all apoB-containing lipoproteins and at a higher dose, decreases LDL apoB production. These effects are consistent with inhibition of cholesterol synthesis leading to an upregulation of LDL receptors. Rosuvastatin decreases the fractional catabolism of HDL particles. The effects of rosuvastatin on HDL kinetics may be related to a reduction in triglyceride concentration and cholesterol ester transfer protein activity. These findings are consistent with the general hypothesis that apolipoprotein kinetics are altered in the metabolic syndrome, and that statin therapy improves these kinetic abnormalities.
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Volk, Catherine B. "Role of inhibition of protein prenylation in the cholesterol-dependent and cholesterol-independent effects of simvastatin." Virtual Press, 2006. http://liblink.bsu.edu/uhtbin/catkey/1339597.
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Statins are widely used to treat hypercholesterolemia. Statins inhibit cholesterol biosynthesis, thereby activating genes involved in cholesterol homeostasis, which are under the control of the Sterol Regulatory Element (SRE). Statins also have cholesterol-independent beneficial cardiovascular effects mediated through the phosphoinositide 3-kinase (PI3-K) / Akt signaling pathway and by inhibition of protein prenylation. Because statins inhibit the synthesis of isoprenoids, they can act by inhibiting the small signaling GTPases Ras and Rho, which require post-translational prenylation to become membrane-anchored and functional. We showed that simvastatin-mediated inhibition of protein prenylation does not appear to play a role in activation of SRE transcriptional activity in HepG2 cells. We also found that when isoprenoids were replenished, basal phospho-Akt decreased, suggesting that inhibition of prenylation by simvastatin mediates Akt phosphorylation. Future studies will be needed to investigate the role that inhibition of protein prenylation plays in the activation of the PI3-K/Akt pathway by simvastatin.Department of Biology
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Jayaram, Raja. "Effects of peri-operative statin treatment on atrial electrical properties, post-operative atrial fibrillation and in-hospital clinical outcomes in patients undergoing elective cardiac surgery." Thesis, University of Oxford, 2014. https://ora.ox.ac.uk/objects/uuid:224a03c7-30f5-456b-a996-0679591ea6a8.
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Surgical myocardial revascularization remains the standard of care for patients with multi-vessel coronary artery disease. A growing body of evidence indicates that systemic inflammation and myocardial oxidative stress are associated with the development of postoperative atrial fibrillation (POAF) and low cardiac output syndrome in patients undergoing cardiac surgery. Statins have been shown to exert rapid anti-inflammatory and antioxidant effects by inhibiting myocardial NOX2 oxidases and by increasing the bioavailability of nitric oxide (NO). However, whether these so-called pleiotropic effects of statins result in improved patient outcomes remains to be established. To provide further insights into the mechanisms of action and impact on clinical outcomes of peri-operative statin treatment in patients undergoing cardiac surgery, I studied the molecular mechanisms underlying the myocardial nitroso-redox balance in samples of the right atrial appendages (RAA) obtained before (PRE) and after cardiopulmonary bypass (CPB) and reperfusion (POST) and setup two double-blind randomised placebo-controlled trials: 1) STARR (Statin Treatment on Atrial Refractoriness and Reperfusion injury), which tested the effect of Atorvastatin (80 mg once daily for up to 6 days before surgery and 5 days after) on the atrial effective refractory period (AERP, over 4 post-operative days) and superoxide production in paired PRE- and POST- RAA samples from 60 patients 2) STICS (Statin Treatment In Cardiac Surgery), which assessed the effects of peri-operative treatment with Rosuvastatin (20mg od) on POAF (assessed by continuous holter ECG monitoring for 5 days postoperatively) and myocardial injury (assessed by serial troponin I measurements) in 1922 patients undergoing elective cardiac surgery. I observed that atrial superoxide production increased significantly after reperfusion due to increased mitochondrial and NOX2 oxidase activity and to uncoupling of NOS activity. NOS activity in RAA samples decreased significantly after reperfusion (by 60%), but this reduction was not prevented by BH4 supplementation (10 μM) or NOX2 inhibition. Instead, I identified increased endothelial NOS S-glutathionylation as the main mechanism responsible for NOS uncoupling after reperfusion. In STARR, atorvastatin prevented increase in RAA superoxide production, maintained the functionally coupled status of NOS and NO bioavailability after reperfusion but had no measurable effect on postoperative AERP. In STICS, treatment with rosuvastatin significantly reduced LDL-C concentration by 48 hours after surgery but had no effect on the incidence of POAF (203 (21%) of the Rosuvastatinallocated patients vs. 197 (20%) of the placebo-allocated patients) or on perioperative myocardial damage (P = 0.80). Pre-defined subgroup analyses (age, sex, prior statin use, baseline troponin concentration, duration of randomized treatment before surgery, type of cardiac surgery, and postoperative use of anti-inflammatory drugs) did not identify any category of patient who benefited from perioperative rosuvastatin treatment. Nor were there beneficial effects on any of the other in-hospital clinical outcomes that were assessed. In conclusion, cardiac surgery on CPB is associated with myocardial nitroso redox imbalance that is reversed by perioperative intensive therapy with statins. However, these effects have no beneficial effects on common in-hospital complications after elective cardiac surgery. Although the benefits of long-term statin therapy in patients requiring myocardial revascularization are well established, the work presented in this thesis does not support routine use of perioperative intensive therapy with statins for the prevention of postoperative complications in patients undergoing elective cardiac surgery.
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Fontaine, David. "Analyse pharmacologique comparative de l'action vasculaire du ramipril et d'inhibiteurs de l'HMG-COA réductase sur l'aorte isolée de rat: perspectives d'applications cliniques." Doctoral thesis, Universite Libre de Bruxelles, 2004. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/211194.
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La prévention des maladies cardiovasculaires constitue actuellement une approche capitale dans la diminution de la mortalité au sein de nos pays industrialisés. Tous les facteurs de risques étant associés à une dysfonction endothéliale, nous nous sommes intéressés à deux classes de médicaments dont l’action bénéfique se situe, du moins en partie, au niveau de l’endothélium vasculaire :les inhibiteurs de l’enzyme de conversion de l’angiotensine (IECA) et les inhibiteurs de l’hydroxy-3-méthyl-3-glutaryl-Coenzyme A (HMG-CoA) réductase (statines).Le présent travail contribue à l’étude in vitro des effets protecteurs vasculaires de l’administration chronique, chez le rat, de deux statines (la pravastatine et l’atorvastatine) vis-à-vis de la toxicité aiguë des LDL humaines oxydées et vis-à-vis de la tolérance à la nitroglycérine. Une comparaison est menée par rapport au ramipril dans ces deux modèles expérimentaux.
Les effets de ces médicaments se manifestent au niveau vasculaire par une amélioration de la disponibilité du NO. Toutefois, dans nos modèles, des mécanismes singulièrement différents ont été identifiés entre les agents étudiés :alors que le ramipril engendre une augmentation de l’expression de la eNOS, enzyme synthétisant le NO, les statines permettent une meilleure disponibilité de ce radical par un mécanisme post-traductionnel. Outre cette action, elles semblent agir directement sur des enzymes oxydatives comme les NAD(P)H oxydases.
Une action antioxydante des statines pourrait expliquer tous les effets observés, ce qui n’est pas le cas pour le ramipril. Vu que le stress oxydatif intervient dans tous les facteurs de risques cardiovasculaires, diverses perspectives cliniques sont envisagées afin d’améliorer l’approche thérapeutique de la maladie athéroscléreuse.
Doctorat en sciences pharmaceutiques
info:eu-repo/semantics/nonPublished
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Ooi, Kenneth Gek-Jin. "The potential immunomodulatory effects of the statins in uveitis." Thesis, 2006. http://hdl.handle.net/2440/69455.
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The aim of this study was to delineate the patterns of cytokine expression which occur in various forms of immune-mediated uveitis in order to better understand their origins. Further, the study investigated the potential immunomodulatory role of the group of compounds known as the statins as adjunctive or steroid-sparing therapy in uveitis. The data recorded provides evidence for the potential of statins in the treatment of uveitis as a steroid-sparing monotherapy or as part of combination therapy.Thesis (M.S.) -- University of Adelaide, School of Medicine, 2006
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Glassburn, Jenny E. "The effects of simvastatin pretreatment on innate immune responses to Staphylococcus aureus infection." 2011. http://liblink.bsu.edu/uhtbin/catkey/1640179.
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Sepsis is a systemic inflammatory response that causes, increased heart rate, respirations, fever, and inadequate blood flow to organs. One of the most prevalent causes of sepsis is Staphylococcus aureus (S. aureus). With increasing numbers of strains of bacteria becoming antibiotic resistant, new methods for the treatment and clearance of sepsis are needed. Studies have shown that the lipid lowering drug simvastatin is protective for incidence of sepsis, having immunomodulatory effects and anti-inflammatory properties, specifically. Thus, it may be an alternative way to prevent sepsis due to S. aureus infections. Studies in our laboratory have shown that simvastatin pretreatment increases survival of mice infected with S. aureus and alters the adaptive immune response such that levels of IgG2c are reduced to the level of uninfected controls. Our studies have demonstrated that while simvastatin does not enhance bacterial clearance, or affect serum C5a levels, it does decrease serum levels of TNF.Department of Biology
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"Pharmacogenetic and environmental determinants of response to HMG-CoA reductase inhibitors." Thesis, 2007. http://library.cuhk.edu.hk/record=b6074340.
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A total of 146 Chinese patients with various degrees of hyperlipidaemia and high cardiovascular risk, suitable for treatment with rosuvastatin 10 mg daily and in whom it was possible to obtain baseline lipid profiles measured on no lipid lowering drug, were enrolled in to the study. The drug compliance was assessed by personal interview and 9 patients were excluded from the efficacy analysis because they stated their compliance was less than 80%. From the remaining 137 subjects, 62 had a clinical diagnosis of familial hypercholesterolaemia. Data for dietary intake were available in 121 of the 137 subjects. The average reduction in LDL-cholesterol in these subjects was 48.8 +/- 12.8% and as anticipated there was a wide range between individuals. The percentage reductions in LDL-cholesterol were significantly greater in the female than in the male subjects (-51.35 +/-10.89% vs. -46.38 +/-13.96%; p = 0.025), but this was no longer significant after adjustment for body weight. In patients with familial hypercholesterolaemia the absolute reductions in total cholesterol and LDL-cholesterol were significantly greater (p<0.001) than in those without familial hypercholesterolaemia, but the percentage reductions were not significantly different in the two groups. The increases in HDL-cholesterol and the decreases in triglycerides were significantly greater in the subjects with familial hypercholesterolaemia than in those without familial hypercholesterolaemia, both for the absolute changes and for the percentage changes. There were no significant effects on the percentage changes in lipids with rosuvastatin treatment due to age, measurements of body fatness, smoking or alcohol drinking status, or having hypertension or diabetes.Polymorphisms in the CYP2D6 gene were analyzed and the subjects were divided into 4 groups as wild-type or extensive metabolisers, heterozygotes for CYP2D6*10 and wild-type, homozygotes for CYP2D6*10, and subjects with one allele for poor metaboliser status. The groups in this order would be expected to have decreasing activity of the CYP2D6 enzyme. There was a tendency for greater reduction in LDL-cholesterol in groups with lower CYP2D6 activity, most obvious in male subjects and this was significant in the patients with familial hypercholesterolaemia comparing the first 3 groups. The fourth group had a low number of subjects, which may have biased that result. In the subjects without familial hypercholesterolaemia, the % change in LDL-cholesterol was similar in all genotype groups, but the % reduction in triglycerides was numerically higher in the wild-type group than in groups with CYP2D6*10 alleles and the group with poor metaboliser status showed a lower % reduction. These differences were not significant and may be influenced by the baseline levels of triglycerides, which were not corrected for in this analysis.
The daily calorie intake and percentage of different macronutrient intake was obtained by using seven days food recall records. Dietary intake of most nutrients with higher in male than in female patients and was higher in the patients compared to gender-matched population data. Higher intake of most nutrients was associated with higher baseline triglyceride levels, but not LDL-cholesterol levels in all patients, and in lower HDL-cholesterol levels in the patients without familial hypercholesterolaemia. Higher intake of total calories was associated with less percentage reduction in LDL-cholesterol with rosuvastatin in the patients without familial hypercholesterolaemia and a similar non-significant tendency was seen with higher intake of total fat, saturated fat and cholesterol.
The study described in this thesis examined the role of the CYP2D6*10 polymorphism on the lipid response to rosuvastatin in addition to a number of phenotypic factors such as diet, gender, measures of obesity and other medical conditions.
These findings suggest that the CYP2D6 genotype may have some influence on the lipid response to rosuvastatin, but it appears to interact with other factors including, gender, diet and the presence of familial hypercholesterolaemia. (Abstract shortened by UMI.)
Lui, Siu Hung.
"February 2007."
Adviser: Brian Tomlinson.
Source: Dissertation Abstracts International, Volume: 69-01, Section: B, page: 0248.
Thesis (Ph.D.)--Chinese University of Hong Kong, 2007.
Includes bibliographical references (p. 165-190).
Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web.
Electronic reproduction. [Ann Arbor, MI] : ProQuest Information and Learning, [200-] System requirements: Adobe Acrobat Reader. Available via World Wide Web.
Abstracts in English and Chinese.
School code: 1307.
10
"Modulation of porcine coronary artery BKCa and IKATP channels gatings by 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase inhibitor." Thesis, 2008. http://library.cuhk.edu.hk/record=b6074588.
Full textAbstract:
3-Hydroxy-3-Methylglutaryl Coenzyme A (HMG CoA) reductase is a 97 kDa glycoprotein located in the endoplasmic reticulum responsible for cholesterol biosynthesis in mammalian liver and intestine. HMG CoA reductase inhibitors (statins) (e.g. simvastatin, mevastatin and parvastatin) are used clinically to treat and prevent coronary artery diseases by reducing plasma LDL-cholesterol level. Recent studies have demonstrated that statins can provide beneficial effects (pleiotropic effects) beyond its lipid-lowering activity. However, the modulatory effects of statins on ion channels activities have not been fully explored. Hence, this study is designed to demonstrate the existence of the HMG CoA reductase in various human isolate cardiovascular preparations and the modulatory effect(s) of simvastatin on both large-conductance calcium-activated (BKCa) and ATP-sensitive (IKATP) potassium channels of porcine isolated coronary vascular smooth muscle cells.In conclusion, our results demonstrated the biochemical existence of HMG CoA reductase in various human isolated cardiovascular preparations and porcine isolated coronary artery. Simvastatin modulates the BKCa and IKATP channels of the porcine isolated coronary artery via different and multiple cellular mechanisms.
In this study, we demonstrated the biochemical existence of the HMG CoA reductase in various human isolated cardiovascular preparations and porcine isolated coronary artery. In addition, we demonstrated that simvastatin modulates both the BKCa channels and IKATP channels of porcine isolated coronary artery via different mechanisms. Acute application of simvastatin (100 nM) slightly enhanced whereas simvastatin (≥ 1 muM) inhibited the BKCa amplitude of porcine coronary artery smooth muscle cells. The classical HMG CoA reductase-mevalonate cascade is important in mediating the inhibitory effect of simvastatin observed at low concentrations (1 and 3 muM), whereas an increased PKC-delta protein expression and activation is important in simvastatin (10 muM)-mediated inhibition of BKCa channels. In contrast, the basal activity of the IKATP channels was not affected by simvastatin (1, 3 and 10 muM). However, acute application of simvastatin (1, 3 and 10 muM) inhibited the opening of the IKATP channels by cromakalim and pinacidil in a PP2A-dependent manner (sensitive to okadaic acid, a PP2A inhibitor). The okadaic acid-sensitive, simvastatin-mediated inhibitory effect on IKATP channel is mediated by an activation of AMPK in a Ca2+-dependent manner. Activation of AMPK probably increased the activity of the Na+/K+ ATPase and subsequently caused an influx of glucose via the SGLT1 down the Na + concentration gradient for the ouabain-sensitive, glucose-dependent activation of PP2A.
Seto, Sai Wang.
Adviser: Yiu-Wa Kwan.
Source: Dissertation Abstracts International, Volume: 70-06, Section: B, page: 3456.
Thesis (Ph.D.)--Chinese University of Hong Kong, 2008.
Includes bibliographical references (leaves 221-254).
Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web.
Electronic reproduction. [Ann Arbor, MI] : ProQuest Information and Learning, [200-] System requirements: Adobe Acrobat Reader. Available via World Wide Web.
Abstracts in English and Chinese.
School code: 1307.
Books on the topic "Uveitis treatment; statins (cardiovascular agents)"
1
Atorvastatin Global Investigators Meeting (2000 Chicago). A symposium: Addressing unanswered questions in the treatment of atherosclerosis : Atorvastatin Global Investigators Meeting 2000. Edited by Brunton Stephen A. New York: Excerpta Medica, 2001.
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2
What you must know about statin drugs & their natural alternatives: A consumer's guide to safely using lipitor, zocor, mevacor, crestor, pravachol, or natural alternatives. Garden City Park, N. Y: Square One Publishers, 2005.
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3
Cohen, Jay S. Natural Alternatives to Lipitor, Zocor & Other Statin Drugs: What to Use And Do to Help Lower Your Bad Cholesterol (Square One Health Guides). Square One Publishers, 2006.
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4
The Statin Damage Crisis. Duane Graveline MD MPH, 2009.
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5
Statin Drugs: Side Effects and the Misguided War on Cholesterol. 3rd ed. Duane Graveline, 2006.
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6
Statin nation: The ill-founded war on cholesterol, what really causes heart disease, and the truth about the most overprescribed drugs in the world. Chelsea Green Publishing, 2017.
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7
Hughes, Edward, Miles Stanford, and Dania Qatarneh. Uveitis and medical ophthalmology. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199672516.003.0007.
Full textAbstract:
This chapter focuses on uveitis and medical ophthalmology. It details uveal anatomy, before discussing anterior uveitis, intermediate uveitis, and posterior uveitis. Next, it discusses posterior uveitis and then specific non-infectious posterior uveitides before moving on to infectious uveitis (viral, parasitic, fungal, and bacterial) and HIV-related disease. It continues by examining systemic associations with uveitis, including sarcoidosis, Behcets disease, multiple sclerosis, and the seronegative arthritides ankylosing spondylitis, Reiter syndrome, psoriatic arthritis, and inflammatory bowel disease. In addition, it discusses scleritis and episcleritis, ocular inflammatory disorders (systemic treatment, biological agents and periocular treatments, intraocular treatments), rheumatological disease, vasculitis, cardiovascular disease and the eye, and endocrine, respiratory, and skin diseases in ophthalmology.
8
Hughes, Edward, and Miles Stanford. Medical ophthalmology. Oxford University Press, 2012. http://dx.doi.org/10.1093/med/9780199237593.003.0005.
Full textAbstract:
The chapter begins with an introduction to uveal anatomy. The following areas of clinical knowledge are then discussed: anterior uveitis, intermediate uveitis, posterior uveitis, specific non-infectious posterior uveitides, viral infectious uveitis, parasitic infectious uveitis, fungal infectious uveitis, bacterial infectious uveitis, HIV-related disease, the systemic associations of uveitis, scleritis and episcleritis, systemic treatment of ocular inflammatory disorders, biological agents and periocular treatments of ocular inflammatory disorders, intraocular treatments of ocular inflammatory disorders, rheumatological disease, vasculitis, cardiovascular disease and the eye, endocrine diseases in ophthalmology, and respiratory and skin diseases in ophthalmology. Practical skills are also addressed, namely orbital-floor injection, posterior sub-Tenon injection, and intravitreal injection. The chapter concludes with a case-based discussion on scleritis.
9
Levy, David. Macrovascular complications, hypertension, and lipids. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198766452.003.0008.
Full textAbstract:
Premature vascular disease is common in Type 1 diabetes, especially in women and those with long duration. Many studies have identified early vascular involvement, using carotid Doppler and coronary artery calcification. Symptoms of coronary heart disease are often absent or muted, and the best methods for identifying occult coronary heart disease in Type 1 patients are not known. The concept of ideal cardiovascular health is valuable in planning preventive lifestyle and medical interventions. ‘Essential’ hypertension in young Type 1 patients is common, and reflects increased arterial stiffness. Hypertension is invariable in patients with any degree of albuminuria or renal impairment. Statin treatment in patients over 40 years old is recommended, but the evidence base is weak. Statins and ezetimibe are the only agents of prognostic value currently available for prevention of vascular events. Primary prevention with aspirin needs individual assessment. Insulin resistance/metabolic syndrome is frequent in Type 1 diabetes.
Book chapters on the topic "Uveitis treatment; statins (cardiovascular agents)"
1
Wagner, Siegfried Karl, and Edward Hughes. "Uveitis and medical ophthalmology." In Training in Ophthalmology, C7—C7.F48. 3rd ed. Oxford University PressOxford, 2022. http://dx.doi.org/10.1093/med/9780198871590.003.0007.
Full textAbstract:
Abstract This chapter focuses on uveitis and medical ophthalmology. It details uveal anatomy, before discussing anterior uveitis, intermediate uveitis, and posterior uveitis. Next, it discusses specific non-infectious posterior uveitides before moving on to infectious uveitis (viral, parasitic, fungal, and bacterial) and HIV-related disease. It continues by examining systemic associations with uveitis, including sarcoidosis, Behçet’s disease, multiple sclerosis, and the seronegative arthritides ankylosing spondylitis, reactive arthritis, psoriatic arthritis, and inflammatory bowel disease. In addition, it discusses scleritis and episcleritis, ocular inflammatory disorders (systemic treatment, biological agents and periocular treatments, intraocular treatments), rheumatological disease, vasculitis, cardiovascular disease and the eye, and endocrine, respiratory, and skin diseases in ophthalmology.
2
Lanza, Gaetano Antonio, and Antonio De Vita. "Chronic stable angina." In The ESC Handbook on Cardiovascular Pharmacotherapy, edited by Alexander Niessner, Sven Wassmann, and Udo Sechtem, 91–106. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780198759935.003.0006.
Full textAbstract:
Treatment of patients with chronic stable angina has two main objectives: to improve clinical outcome and to reduce angina symptoms. Prognosis is mainly improved by a reduction in cardiovascular risk factor burden, which may be achieved by appropriate lifestyle changes and, for some risk factors (e.g. hypercholesterolaemia, hypertension, diabetes), appropriate pharmacological therapy (including, in particular, statins and renin–angiotensin–aldosterone system inhibitors) and use of antithrombotic agents. Symptoms can be improved by a variable combination of traditional (beta-blockers, calcium channel blockers, nitrates) and novel (e.g. ivabradine, ranolazine) anti-ischaemic drugs, which may act through reduction in myocardial oxygen consumption and/or improvement of myocardial perfusion.
3
Lanza, Gaetano Antonio, and Antonio De Vita. "Chronic stable angina." In The ESC Handbook on Cardiovascular Pharmacotherapy, edited by Alexander Niessner, Sven Wassmann, and Udo Sechtem, 91–106. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780198759935.003.0006_update_001.
Full textAbstract:
Treatment of patients with chronic stable angina has two main objectives: to improve clinical outcome and to reduce angina symptoms. Prognosis is mainly improved by a reduction in cardiovascular risk factor burden, which may be achieved by appropriate lifestyle changes and, for some risk factors (e.g. hypercholesterolaemia, hypertension, diabetes), appropriate pharmacological therapy (including, in particular, statins and renin–angiotensin–aldosterone system inhibitors) and use of antithrombotic agents. Symptoms can be improved by a variable combination of traditional (beta-blockers, calcium channel blockers, nitrates) and novel (e.g. ivabradine, ranolazine) anti-ischaemic drugs, which may act through reduction in myocardial oxygen consumption and/or improvement of myocardial perfusion.
4
Lanza, Gaetano Antonio, and Antonio De Vita. "Chronic stable angina." In The ESC Handbook on Cardiovascular Pharmacotherapy, edited by Alexander Niessner, Sven Wassmann, and Udo Sechtem, 91–106. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780198759935.003.0006_update_002.
Full textAbstract:
Treatment of patients with chronic stable angina has two main objectives: to improve clinical outcome and to reduce angina symptoms. Prognosis is mainly improved by a reduction in cardiovascular risk factor burden, which may be achieved by appropriate lifestyle changes and, for some risk factors (e.g. hypercholesterolaemia, hypertension, diabetes), appropriate pharmacological therapy (including, in particular, statins and renin–angiotensin–aldosterone system inhibitors) and use of antithrombotic agents. Symptoms can be improved by a variable combination of traditional (beta-blockers, calcium channel blockers, nitrates) and novel (e.g. ivabradine, ranolazine) anti-ischaemic drugs, which may act through reduction in myocardial oxygen consumption and/or improvement of myocardial perfusion.
5
Arai, Hidenori. "Dyslipidemias and other cardiometabolic risk factors in older adults." In Oxford Textbook of Geriatric Medicine, 737–42. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198701590.003.0096.
Full textAbstract:
Dyslipidemia is a major risk factor for atherosclerotic cardiovascular disease (ASCVD) in older people. In spite of the higher absolute risk in older patients, plasma lipids lose their ability to predict the development of ASCVD along with ageing, especially over 80 years old. However, lipid-lowering agents like statins can significantly inhibit the development of ASCVD in older patients as well as in younger patients. Current consensus about the lipid-lowering treatment in older patients is that we should treat early old patients (75 years old and younger) with or without ASCVD and in patients more than 75 years old with ASCVD as in the non-elderly by taking care of the drug-induced adverse effects. However, the treatment of the oldest patients without ASCVD with statins should be individualized and the statin treatment for those over 85 years old is under discretion of the physician.
6
Sirtori, Cesare R., and Massimiliano Ruscica. "Lipid-lowering drugs." In ESC CardioMed, 204–9. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0039.
Full textAbstract:
Hyperlipidaemias, multifactorial conditions partly genetically and partly life habit induced, are the most important underlying risk factors for cardiovascular disease. They can lead to arterial lipid deposition with a consequent increased risk of coronary events. The primary effort in hypolipidaemic drug therapy is focused on the lowering of the primary carriers of cholesterol, the low-density lipoproteins (LDLs), but more recent efforts have been placed on the lowering of triglycerides. Reduced levels of the protective high-density lipoproteins (HDLs) are generally considered a primary risk factor, ‘dysfunctional’ HDL may probably be a more important factor. Among drugs primarily reducing LDL cholesterol the most important systemic agents are statins. Non-systemic agents, such as resins, have a lesser use, whereas ezetimibe is frequently given in combination with statins. A new series of systemic compounds, the inhibitors of proprotein convertase subtilisin/kexin type 9 (PCSK9), recently available, have a higher activity on LDL cholesterol. Drugs indicated for the treatment of the homozygous forms of hypercholesterolaemia are lomitapide, an inhibitor of the microsomal transfer protein, and the antisense nucleotide mipomersen, designed to inhibit synthesis of apolipoprotein B. Treatment of hypertriglyceridaemias mainly relies on fibrates, activating the peroxisomal proliferator-activated receptor-α. They treat particularly the atherogenic dyslipidaemias (elevated triglycerides with low HDL cholesterol). Nicotinic acid is less frequently used and the omega-3 fatty acids have an as yet unclear cardiovascular protective activity.
7
Sirtori, Cesare R., and Massimiliano Ruscica. "Lipid-lowering drugs." In ESC CardioMed, 204–9. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0039_update_001.
Full textAbstract:
Hyperlipidaemias, multifactorial conditions partly genetically and partly life habit induced, are the most important underlying risk factors for cardiovascular disease. They can lead to arterial lipid deposition with a consequent increased risk of coronary events. The primary effort in hypolipidaemic drug therapy is focused on the lowering of the primary carriers of cholesterol, the low-density lipoproteins (LDLs), but more recent efforts have been placed on the lowering of triglycerides. Reduced levels of the protective high-density lipoproteins (HDLs) are generally considered a primary risk factor, ‘dysfunctional’ HDL may probably be a more important factor. Among drugs primarily reducing LDL cholesterol the most important systemic agents are statins. Non-systemic agents, such as resins, have a lesser use, whereas ezetimibe is frequently given in combination with statins. A new series of systemic compounds, the inhibitors of proprotein convertase subtilisin/kexin type 9 (PCSK9), recently available, have a higher activity on LDL cholesterol. Drugs indicated for the treatment of the homozygous forms of hypercholesterolaemia are lomitapide, an inhibitor of the microsomal transfer protein, and the antisense nucleotide mipomersen, designed to inhibit synthesis of apolipoprotein B. Treatment of hypertriglyceridaemias mainly relies on fibrates, activating the peroxisomal proliferator-activated receptor-α. They treat particularly the atherogenic dyslipidaemias (elevated triglycerides with low HDL cholesterol). Nicotinic acid is less frequently used and the omega-3 fatty acids have an as yet unclear cardiovascular protective activity.
8
Sirtori, Cesare R., and Massimiliano Ruscica. "Lipid-lowering drugs." In ESC CardioMed, 204–9. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0039_update_002.
Full textAbstract:
Hyperlipidaemias, multifactorial conditions partly genetically and partly life habit induced, are the most important underlying risk factors for cardiovascular disease. They can lead to arterial lipid deposition with a consequent increased risk of coronary events. The primary effort in hypolipidaemic drug therapy is focused on the lowering of the major carriers of cholesterol, the low-density lipoproteins (LDLs), but more recent efforts have been placed on the lowering of triglycerides. Reduced levels of the protective high-density lipoproteins (HDLs) are generally considered as a primary risk factor, although risk factor is probably a more important factor. Among drugs primarily reducing LDL cholesterol (LDL-C) the most important systemic agents are statins, whereas non-systemic agents, such as resins, have a lesser use. Ezetimibe is frequently given in combination with statins. The oral bempedoic acid lowers both LDL-C and the high-sensitivity C-reactive protein and avoids muscular side effects. The inhibitors of proprotein convertase subtilisin/kexin type 9 (PCSK9), given s.c., have a higher activity on LDL-C. Drugs indicated for the treatment of the homozygous forms of hypercholesterolaemia are lomitapide, an inhibitor of the microsomal transfer protein, and the newly approved inhibitor of angiopoietin-like 3 (ANGPTL-3) evinacumab given i.v. Treatment of hypertriglyceridaemias mainly relies on fibrates, activating the peroxisomal proliferator-activated receptor-crosomal transfer protein, els of the prot dyslipidaemias (elevated triglycerides with low HDL cholesterol). The nicotinic acid derivative acipimox is less frequently used and the omega-3 fatty acid eicosapentaenoic acid (EPA), at high dosages, has provided a significant protective activity in secondary prevention. Finally, the improved understanding of the atherogenic role of elevated lipoprotein(a) has led to the development of an anti-sense nucleotide, effectively reducing this lipoprotein associated cardiovascular risk factor.
9
Sfikas, Georgios, and Ioannis Valsamidis. "Therapeutic Approach to NAFLD-NASH." In Non-alcoholic Fatty Liver Disease - New-Insight and Glance Into Disease Pathogenesis [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.107487.
Full textAbstract:
Nonalcoholic fatty liver disease (NAFLD) and its progressive form nonalcoholic steatohepatitis (NASH) are the hepatic expression of metabolic syndrome and may lead to serious injury to the liver resulting in cirrhosis and hepatocellular carcinoma (HCC). Despite its seriousness, there is no definite treatment to address this life-threatening condition. Weight loss and exercise remain the cornerstone of the therapeutic treatment but also an array of medications can be used with varying degrees on liver inflammation and cirrhosis. There is also an increased risk of cardiovascular events connected to NAFLD/NASH, which should also be addressed. Statins have been shown to reduce the lipid and the inflammatory burden of the liver as well as decrease the cardiovascular risk. Aspirin also has a beneficial effect due to its anti-inflammatory properties as well as Vitamin E in certain cases. The medications (metformin, pioglitazone, GLP-1 agonists, SGLT2 inhibitors) that interfere in glucose metabolism and the activity of insulin seem to play a vital role in the metabolism of glucose and lipids and subsequent amelioration of liver function tests and the inhibition of inflammation. The aim of this review is to highlight the efficacy of current therapeutic strategies and explore the variety of the emerging new agents which target newly discovered pathways associated with the pathogenesis of NAFLD/NASH with promising results.
10
Mueller, Thomas F., and Valerie Luyckx. "Special considerations in patients undergoing renal replacement therapy and kidney transplant patients." In ESC CardioMed, edited by Christoph Wanner, 1003–6. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0241.
Full textAbstract:
Cardiovascular disease (CVD) is the leading cause of death in patients with end-stage kidney disease (ESKD) on dialysis, peri-transplant, and after transplantation. The coexistence of traditional cardiovascular risk factors with superimposed renal disease- and transplantation-related risk factors such as uraemia, vascular calcification, inflammation, electrolyte abnormalities, volume shifts, transplant surgery, infections, and immunosuppression makes assessment and treatment more complex when compared with patients without renal disease. For coronary artery disease, evidence suggests less benefit in ESKD and renal transplant patients compared to those with milder renal dysfunction of traditional primary and secondary prevention strategies including angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, beta blockers, statins, and antiplatelet agents. Prevention of sudden cardiac death is difficult and the use of implantable cardioverter defibrillators in ESKD patients is being investigated. The diagnosis of myocardial ischaemia in patients with ESKD is challenging given the frequent lack of typical symptoms, abnormal baseline electrocardiograms, and the reduced sensitivity of troponin measurements. Screening for CVD in asymptomatic dialysis patients awaiting transplantation is controversial. Non-invasive screening is recommended for those with significant risk factors although the test of choice is unclear. Positive stress-testing is predictive of cardiac events and death and must be investigated with coronary angiography. Once significant coronary artery disease is diagnosed, the optimal choice of revascularization strategy remains unclear. Coronary artery bypass grafting may be superior to angioplasty with stenting in ESKD and transplant patients. Many questions remain unsatisfactorily answered and much research is required to develop optimal strategies to manage CVD in ESKD and kidney transplant patients.