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Cardiovascular Medicine is published by MDPI from Volume 28 Issue 1 (2025). Previous articles were published by another publisher in Open Access under a CC-BY (or CC-BY-NC-ND) licence, and they are hosted by MDPI on mdpi.com as a courtesy and upon agreement with Editores Medicorum Helveticorum (EMH).

Cardiovasc. Med., Volume 7, Issue 10 (10 2004) – 5 articles

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2 pages, 124 KB  
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Dissolution of a Saphenous Vein Graft Thrombus with Systemic Glycoprotein IIb/IIIa Receptor Inhibitor Prior to Percutaneous Coronary Intervention
by Raban V. Jeger, Andreas W. Zutter and Peter T. Buser
Cardiovasc. Med. 2004, 7(10), 373; https://doi.org/10.4414/cvm.2004.01050 - 27 Oct 2004
Viewed by 55
Abstract
A 60-year-old man with known coronary artery disease was admitted to the hospital with severe retrosternal pain persisting over two hours [...] Full article
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6 pages, 233 KB  
Proceeding Paper
Risques Vasculaires Dans le Diabète
by Jacques Philippe
Cardiovasc. Med. 2004, 7(10), 367; https://doi.org/10.4414/cvm.2004.01053 - 27 Oct 2004
Cited by 1 | Viewed by 47
Abstract
Diabetes leads to both micro- and macrovascular complications. If the major threat to type 2 diabetic patients is ischaemic heart disease, other cardiovascular complications such as heart failure, stroke and lower extremity arterial disease are also 2 to 4 times more frequent in [...] Read more.
Diabetes leads to both micro- and macrovascular complications. If the major threat to type 2 diabetic patients is ischaemic heart disease, other cardiovascular complications such as heart failure, stroke and lower extremity arterial disease are also 2 to 4 times more frequent in diabetic patients than in the general population. Type 2 diabetic patients accumulate traditional risk factors and thus it is not necessary to search for non-traditional risk factors except for microalbuminuria which is an excellent marker of cardiovascular disease. The greater cardiovascular risk observed in diabetic patients is actually already observed in patients with glucose intolerance or the metabolic syndrome, indicating that hyperglycaemia per se just increases further an already elevated risk generated by both genetic and environmental factors, such as lack of exercise and overeating. Major developments in the mechanisms by which glucose affects blood vessels have occurred during the last few years: this understanding should allow the design of specific therapeutic modalities to halt the progression of disease. In the meantime, a rather intensive multifactorial approach directed towards the classical risk factors is warranted and effective, as indicated by the results of the STENO 2 trial. Full article
4 pages, 146 KB  
Proceeding Paper
Stumme Koronare Herzkrankheit bei Diabetes Mellitus
by Michael J. Zellweger
Cardiovasc. Med. 2004, 7(10), 362; https://doi.org/10.4414/cvm.2004.01051 - 27 Oct 2004
Viewed by 45
Abstract
Silent coronary artery disease is frequently encountered in diabetic patients. In general, the prevalence of silent myocardial ischaemia varies depending on the test used for patient screening and on the patient population screened. However, incidence rates up to 65% have been reported. The [...] Read more.
Silent coronary artery disease is frequently encountered in diabetic patients. In general, the prevalence of silent myocardial ischaemia varies depending on the test used for patient screening and on the patient population screened. However, incidence rates up to 65% have been reported. The evidence is growing that silent coronary artery disease is not different from symptomatic disease with respect to prognosis. Asymptomatic high-risk diabetic patients therefore might benefit from routine screening for silent coronary artery disease. Although specific data regarding cardiac treatment of asymptomatic diabetic patients is lacking, patients with evidence of silent coronary artery disease probably should be treated irrespective of symptomatic status. Full article
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3 pages, 169 KB  
Proceeding Paper
Special Issues in Diabetes: Nitric Oxide and Oxidants in Diabetic Vascular Complications
by Richard A. Cohen
Cardiovasc. Med. 2004, 7(10), 359; https://doi.org/10.4414/cvm.2004.01052 - 27 Oct 2004
Viewed by 54
Abstract
Vascular disease in diabetes is accompanied by decreased levels of the vasodilators, nitric oxide (NO) and prostacyclin, and increased levels of vasoconstrictor eicosanoids, which enhance the progression of the disease. The vascular dysfunction caused by short term exposure to elevated glucose and the [...] Read more.
Vascular disease in diabetes is accompanied by decreased levels of the vasodilators, nitric oxide (NO) and prostacyclin, and increased levels of vasoconstrictor eicosanoids, which enhance the progression of the disease. The vascular dysfunction caused by short term exposure to elevated glucose and the long term effects of diabetes are similar, suggesting that the alteration in endothelial factors in diabetes primarily results from exposure of endothelial cells to elevated glucose. Undoubtedly hyperlipidaemia contributes as well. Increased formation of reactive oxygen species is an important feature of the diabetic endothelial cell phenotype. This results in part from uncoupling of endothelial nitric oxide synthase such that it generates superoxide anion in addition to NO, forming peroxynitrite, a damaging molecule. Peroxynitrite inactivates prostacyclin synthase leading to the accumulation of inflammatory and prothrombotic eicosanoids. This not only helps to explain the impairment of endothelial vasodilator mechanisms, but also increased progression of vascular disease. Many of these cellular abnormalities can be prevented by adequate scavenging of oxygenderived free radicals or by blocking the actions of the eicosanoids at TP receptors. Exposure to elevated glucose also gives rise to oxidants in smooth muscle, and recent studies indicate that oxidation of cysteine thiols under these conditions may prevent physiological NO signaling. As a result the responsiveness to NO is impaired and accounts in part for abnormal endotheliumdependent vasodilatation. Full article
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8 pages, 328 KB  
Proceeding Paper
The Challenge of Vulnerable Plaque Detection in the Cardiac Catheterization Laboratory
by Pierfrancesco Agostoni, Johannes A. Schaar and Patrick W. Serruys
Cardiovasc. Med. 2004, 7(10), 349; https://doi.org/10.4414/cvm.2004.01049 - 27 Oct 2004
Cited by 3 | Viewed by 51
Abstract
Rupture of vulnerable plaques is the main cause of acute coronary syndromes and myocardial infarctions. Identification of these vulnerable plaques is therefore essential to enable the development of treatment modalities to stabilise them. Several intra-vascular technologies, investigating coronary areas that will be responsible [...] Read more.
Rupture of vulnerable plaques is the main cause of acute coronary syndromes and myocardial infarctions. Identification of these vulnerable plaques is therefore essential to enable the development of treatment modalities to stabilise them. Several intra-vascular technologies, investigating coronary areas that will be responsible for future events, are underlined in this review. The ideal technique would provide morphological, mechanical and biochemical information, however, despite several imaging techniques are currently under development, none of them provides alone such all-embracing assessment. OCT has the advantage of high resolution, thermography has the potential to measure metabolism and spectroscopy obtains information on chemical components. IVUS and IVUS-palpography are easy to perform and assess morphology and mechanical instability. Shear stress is an important mechanical parameter deeply influencing vascular biology. Nevertheless all techniques are still under investigation and at present, none of them can completely identify a vulnerable plaque and, most importantly, predict its further development. From a clinical point of view, most techniques currently assess only one feature of the vulnerable plaque. Thus the combination of several modalities will be of importance in the future to ensure a high sensitivity and specificity in detecting vulnerable plaques. Full article
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