Intravascular ultrasound imaging in patients with acute myocardial infarction

Bocksch, Wolfgang; Schartl, M.; Beckmann, Stephan; Dreysse, Stefan; Fleck, Eckart

doi:10.1093/eurheartj/16.suppl_j.46

Cited by 32 publications

(27 citation statements)

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“…172 The Rotterdam Coronary Calcification Study, a large population-based study, showed a graded association between CAC score and stroke. 78,172 The American College of Cardiology (ACC) and American Heart Association (AHA) guidelines acknowledge the sensitivity of CAC to aid diagnosis of coronary atherosclerosis, with a similar predictive value to cardiac stress tests.…”

Section: Electron Beam Computed Tomographymentioning

confidence: 99%

Vascular Calcification

Johnson

Leopold

Loscalzo

2006

Circulation Research

817

415

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Once thought to result from passive precipitation of calcium and phosphate, it now appears that vascular calcification is a consequence of tightly regulated processes that culminate in organized extracellular matrix deposition by osteoblast-like cells. These cells may be derived from stem cells (circulating or within the vessel wall) or differentiation of existing cells, such as smooth muscle cells (SMCs) or pericytes. Several factors induce this transition, including bone morphogenetic proteins, oxidant stress, high phosphate levels, parathyroid hormone fragments, and vitamin D. Once the osteogenic phenotype is induced, cells gain a distinctive molecular fingerprint, marked by the transcription factor core binding factor alpha1. Alternatively, loss of inhibitors of mineralization, such as matrix gamma-carboxyglutamic acid Gla protein, fetuin, and osteopontin, also contribute to vascular calcification. The normal balance between promotion and inhibition of calcification becomes dysregulated in chronic kidney disease, diabetes mellitus, atherosclerosis, and as a consequence of aging. Once the physiological determinants of calcification are perturbed, calcification may occur at several sites in the cardiovascular system, including the intima and media of vessels and cardiac valves. Here, calcification may occur through overlapping yet distinct molecular mechanisms, each with different clinical ramifications. A variety of imaging techniques are available to visualize vascular calcification, including fluoroscopy, echocardiography, intravascular ultrasound, and electron beam computed tomography. These imaging modalities vary in sensitivity and specificity, as well as clinical application. Through greater understanding of both the mechanism and clinical consequences of vascular calcification, future therapeutic strategies may be more effectively designed and applied.

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Section: Electron Beam Computed Tomographymentioning

confidence: 99%

Vascular Calcification

Johnson

Leopold

Loscalzo

2006

Circulation Research

817

415

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“…This notion is based on intravascular ultrasound studies, which have shown less extensive coronary calcification in patients with acute coronary syndromes compared with patients with chronic stable angina. 82,83 In patients presenting with acute coronary syndromes, intravascular ultrasound studies show less calcification in the event-related coronary lesion than in stable plaques in other vessels. 84 These findings have been interpreted as evidence that vascular calcification is protective against acute events.…”

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confidence: 99%

Vascular Calcification

Abedin

Tintut

Demer

2004

ATVB

766

220

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Abstract-Vascular calcification, long thought to result from passive degeneration, involves a complex, regulated process of biomineralization resembling osteogenesis. Evidence indicates that proteins controlling bone mineralization are also involved in the regulation of vascular calcification. Artery wall cells grown in culture are induced to become osteogenic by inflammatory and atherogenic stimuli. Furthermore, osteoclast-like cells are found in calcified atherosclerotic plaques, and active resorption of ectopic vascular calcification has been demonstrated. In general, soft tissue calcification arises in areas of chronic inflammation, possibly functioning as a barrier limiting the spread of the inflammatory stimulus. Atherosclerotic calcification may be one example of this process, in which oxidized lipids are the inflammatory stimulus. Calcification is widely used as a clinical indicator of atherosclerosis. It progresses nonlinearly with time, following a sigmoid-shaped curve. The relationship between calcification and clinical events likely relates to mechanical instability introduced by calcified plaque at its interface with softer, noncalcified plaque. In general, as calcification proceeds, interface surface area increases initially, but eventually decreases as plaques coalesce. Key Words: calcification Ⅲ atherosclerosis Ⅲ inflammation Ⅲ bone Ⅲ vascular V ascular calcification is an important manifestation of atherosclerosis. For more than half a century, it has been associated with a poor prognosis attributable to vascular disease. 1 Its presence is a strong indicator of chronic inflammatory disease, usually atherosclerosis, and its extent directly relates to the overall burden of atherosclerotic disease. 2 Despite its clinical relevance, research on the mechanism of mineral deposition in arteries has been limited and remains at an early scientific stage relative to research on other aspects of atherosclerosis, such as lipoprotein biochemistry and inflammation. Mechanisms of Vascular CalcificationVascular calcification recapitulates embryonic osteogenesis. Pathologists in the 19th century recognized the presence of bone-like tissue within atherosclerotic arteries, with lamellar structure, osteoblast-like cells, and hematopoietic elements. 3 Yet, for most of the 20th century, vascular calcification has been regarded as a passive, unregulated, degenerative process occurring within advanced atherosclerotic plaques. The concept of regulated ossification as the mechanism behind vascular calcification has re-emerged only in the past decade. 4,5 Ossification has been identified histologically in 60% of restenotic aortic valves after balloon valvuloplasty. 6 Approximately 15% of carotid atherosclerotic plaque specimens 7 and calcified cardiac valve tissue 8 have ossification. Vascular calcification may include both osteogenic and chondrogenic differentiation. In humans, it is primarily osteogenic with bone tissue formation, whereas in mice, it is primarily chondrogenic with cartilage formation. Although osteoblas...

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“…36 Indeed, intravascular ultrasound and CT studies demonstrate that culprit coronary artery lesions in patients with acute coronary syndromes have less extensive coronary calcification in comparison with lesions associated with chronic stable angina. 37,38 This would suggest that macro-calcification of a plaque, which is measurable by the CAC score, is protective and has a role in plaque stability. However, biomechanical modelling indicates that regions of micro-calcification have the opposite effect and predispose to plaque rupture.…”

Section: Sodium Fluoride Imaging As a Biomarker Of Micro-calcificationmentioning

confidence: 99%