1,721,217 research outputs found

    Is it possible that angioplasty does not improve the quality of life in patients with stable angina?

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    The scientific evidence in favour of percutaneous transcatheter coronary angioplasty (PTCA) in chronic ischaemic heart disease in terms of reduction of myocardial infarction and mortality is very scarce and controversial. However, for many years, the cardiology community has believed in the dogma that PTCA in chronic ischaemic heart disease could improve symptoms, especially when combined with effective medical therapy. A recent randomized controlled trial (ORBIT) has completely overturned this dogma, questioning much of what we have been taught about revascularization procedures in patients with stable coronary artery disease. In this article, the ORBITA study is discussed in depth, highlighting the lights and shadows of the study itself

    Free radicals and antioxidants in cardiovascular diseases

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    It has been demonstrated that redox homeostasis is important in the pathophysiology of several human diseases, including cardiovascular diseases. In this respect, genetic polymorphism, nutritional and environmental factors, age, lifestyle and physical activity may account for variable antioxidant defenses, which may be more or less effective at counteracting oxidative damage. Since accumulating oxidative damage may be associated with several pathologic conditions, including different cardiovascular diseases, prevention of oxidative stress appears to be a promising approach to improve such diseases. Exercise training, diets rich in antioxidants and a good control of blood glucose and lipid levels help to strengthen the physiologic antioxidant defense system, perhaps coupled to drugs capable of increasing the nitric oxide bioavailability and decreasing superoxide production. Within the next few years other therapeutic approaches will be available, such as gene therapy, which will prove to be even more effective but devoid of several important systemic side effects. © 2005 Future Drugs Ltd

    Inhibition of the tissue factor coagulation pathway

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    It is widely accepted that blood coagulation in vivo is initiated during normal hemostasis, as well as during intravascular thrombus formation, when the cell-surface protein, tissue factor, is exposed to the blood as a consequence of vascular injury. In addition to its essential role in hemostasis, tissue factor may be also implicated in several pathophysiological processes, such as intracellular signaling, cell proliferation, and inflammation. For these reasons, the tissue factor:factor VIIa complex has been the subject of intense research focus. Many experimental studies have demonstrated that inhibition of tissue factor:factor VIIa procoagulant activity are powerful inhibitors of in vivo thrombosis and that this approach usually results in less pronounced bleeding tendency, as compared to other "more classical" antithrombotic interventions. Alternative approaches may be represented by transfecting the arterial wall with natural inhibitors of tissue factor:factor VIIa complex, such as tissue factor pathway inhibitor, which may result in complete inhibition of local thrombosis without incurring in potentially harmful systemic effects. Additional studies are warranted to determine the efficacy and safety of such approaches in patients. © 2004 Bentham Science Publishers Ltd

    A systolic murmur late after infective endocarditis: Looking for the guilty

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    Aortic location of infective endocarditis is a risk factor for perivalvular extension of infection, even when a native valve is involved. We report the case of a 50-year-old man with a systolic murmur and a history of previous aortic valve infective endocarditis requiring cardiac surgery. A thorough echocardiographic assessment, including three-dimensional transesophageal echocardiography, clearly demonstrated the presence of two distinct postinfective complications, i.e., a fistula of the mitral-aortic intervalvular curtain communicating in systole with the left atrium and an acquired Gerbode-type ventricular septal defect. Our case highlights the pivotal role of echocardiography for a correct and comprehensive diagnostic assessment in the complex scenarios frequently encountered after infective endocarditis

    Beneficial effects of one-month sacubitril/valsartan treatment in a patient affected by end-stage dystrophinopathic cardiomyopathy

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    Dystrophinopathic cardiomyopathy (DCM) is an almost constant manifestation in Becker muscular dystrophy (BMD) patients significantly contributing to morbidity and mortality. The nearly complete replacement of the myocardium by fibrous and fatty connective tissue results in an irreversible cardiac failure, characterized by progressive reduction of the ejection fraction. According to PARADIGM-HF trial results, the European Society of Cardiology (ESC) guidelines recommend the use of sacubitril/valsartan in ambulatory patients with heart failure and reduced ejection fraction, who remain symptomatic despite an optimal medical therapy. To date, little is still known about the use of sacubitril/valsartan in DCM. We report the case of a patient with dystrophinopathic end stage dilated cardiomyopathy with reduced ejection fraction who successfully responded to sacubitril/valsartan treatment
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