PubMed · 9117666
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H Mori. 1996. [Mitral annular calcification].. https://pubmed.ncbi.nlm.nih.gov/9117666/
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Vascular calcification is a common feature in advanced atherosclerosis and also a predictor of future cardiovascular events such as unstable angina and myocardial infarction, especially in diabetes. There is a growing body of evidence that advanced glycation end products (AGEs), senescent macroprotein derivatives formed at an accelerated rate in diabetes, exist within atherosclerotic lesions, thereby being implicated in the pathogenesis of accelerated atherosclerosis in diabetes. Indeed, we have previously shown that AGE - their receptor (RAGE) interaction could induce angiogenesis through autocrine production of vascular endothelial growth factor, suggesting its role for plaque formation and enlargement in diabetes. Furthermore, we have found that AGEs have the ability to induce the osteoblatic differentiation of pericytes, thus contributing to the development of vascular calcification as well. These observations suggest that the inhibition of AGE formation or blockade of the downstream signaling of RAGE may be a novel therapeutic target for the inhibition of vascular calcification in diabetic atherosclerosis. Since we, along with others, have shown that nifedipine inhibits glycation of low-density lipoprotein in vitro and blocks the AGE-induced RAGE expression in endothelial cells through its anti-oxidative properties, nifedipine could inhibit vascular calcification by blocking the AGE formation or the downstream signaling in diabetes. In this paper, we would like to propose the possible ways of testing our hypothesis. Does nifedipine treatment slow down the progression of coronary calcification in diabetic patients? If the answer is yes, is this beneficial effect of nifedipine superior to that of other DHPs with equihypotensive properties? Does nifedipine treatment decrease expression levels of AGEs and RAGE in diabetic atherosclerosis? Is the unique effect of nifedipine on vascular calcification correlated with its AGE or RAGE-suppressing properties? These prospective studies will provide further valuable information whether nifedipine could prevent vascular calcification in diabetic atherosclerosis by blockade the AGE-RAGE signaling in vascular wall cells.
Multi-detector-row computed tomography (MDCT) has emerged as a rapidly developing method for non-invasive imaging of the heart. An understanding of ECG synchronization, contrast material administration, patient preparation and image post-processing is needed to optimize image quality. The basic technical principles and essentials of these technical basics are described here. Correctly applied cardiac MDCT allows imaging of the coronary arteries including coronary anatomy and stenosis detection. The same is true for evaluation of coronary artery bypass grafts and, to some extent, coronary artery stents. While quantification of total calcified plaque burden has been long established, coronary MDCT allows assessing plaque morphology and constitution. Recent approaches go beyond the coronaries and include evaluation of left ventricular function at rest and myocardial viability. In combination with experimental approaches for assessing aortic valve function and myocardial perfusion imaging, cardiac MDCT offers the potential for a comprehensive examination of the heart using a single breath-hold examination.
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