Type 2 diabetes mellitus is associated with a lower fibrous cap thickness but has no impact on calcification morphology: an intracoronary optical coherence tomography study

Milzi, Andrea; Burgmaier, Mathias; Burgmaier, Kathrin; Hellmich, Martin; Marx, Nikolaus; Reith, Sebastian

doi:10.1186/s12933-017-0635-2

Cited by 50 publications

(56 citation statements)

References 40 publications

(47 reference statements)

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“…Although OCT still has difficulties in visualizing cellular-level microcalcifications, it provides the potential for investigating the clinical and morphological predictors of microcalcifications in vivo. OCT-defined microcalcifications are the calcium deposits with a maximum calcium angle <22.5 • and a maximal calcification length <1 mm (Milzi et al, 2017). OCT-defined microcalcifications have been demonstrated to be related to milder stenosis with extensive plaque inflammation (Reith et al, 2018) and a large necrotic core (Kim et al, 2016).…”

Section: Calcification Size and Plaque Vulnerability Microcalcificationsmentioning

confidence: 99%

Calcification in Atherosclerotic Plaque Vulnerability: Friend or Foe?

et al. 2020

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Calcification is a clinical marker of atherosclerosis. This review focuses on recent findings on the association between calcification and plaque vulnerability. Calcified plaques have traditionally been regarded as stable atheromas, those causing stenosis may be more stable than non-calcified plaques. With the advances in intravascular imaging technology, the detection of the calcification and its surrounding plaque components have evolved. Microcalcifications and spotty calcifications represent an active stage of vascular calcification correlated with inflammation, whereas the degree of plaque calcification is strongly inversely related to macrophage infiltration. Asymptomatic patients have a higher content of plaque calcification than that in symptomatic patients. The effect of calcification might be biphasic. Plaque rupture has been shown to correlate positively with the number of spotty calcifications, and inversely with the number of large calcifications. There may be certain stages of calcium deposition that may be more atherogenic. Moreover, superficial calcifications are independently associated with plaque rupture and intraplaque hemorrhage, which may be due to the concentrated and asymmetrical distribution of biological stress in plaques. Conclusively, calcification of differential amounts, sizes, shapes, and positions may play differential roles in plaque homeostasis. The surrounding environments around the calcification within plaques also have impacts on plaque homeostasis. The interactive effects of these important factors of calcifications and plaques still await further study.

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Section: Calcification Size and Plaque Vulnerability Microcalcificationsmentioning

confidence: 99%

Calcification in Atherosclerotic Plaque Vulnerability: Friend or Foe?

et al. 2020

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“…Unlike IVUS, OCT can penetrate plaque calcification and characterize it in detail, in terms of thickness, area, and volume. Accordingly, calcifications classified as macrocalcifications, spotty calcifications, and microcalcifications can be detected by OCT imaging [45].…”

Section: Optical Coherence Tomographymentioning

confidence: 99%

Current Advances in the Diagnostic Imaging of Atherosclerosis: Insights into the Pathophysiology of Vulnerable Plaque

Mushenkova¹,

Summerhill

Zhang

et al. 2020

IJMS

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Atherosclerosis is a lipoprotein-driven inflammatory disorder leading to a plaque formation at specific sites of the arterial tree. After decades of slow progression, atherosclerotic plaque rupture and formation of thrombi are the major factors responsible for the development of acute coronary syndromes (ACSs). In this regard, the detection of high-risk (vulnerable) plaques is an ultimate goal in the management of atherosclerosis and cardiovascular diseases (CVDs). Vulnerable plaques have specific morphological features that make their detection possible, hence allowing for identification of high-risk patients and the tailoring of therapy. Plaque ruptures predominantly occur amongst lesions characterized as thin-cap fibroatheromas (TCFA). Plaques without a rupture, such as plaque erosions, are also thrombi-forming lesions on the most frequent pathological intimal thickening or fibroatheromas. Many attempts to comprehensively identify vulnerable plaque constituents with different invasive and non-invasive imaging technologies have been made. In this review, advantages and limitations of invasive and non-invasive imaging modalities currently available for the identification of plaque components and morphologic features associated with plaque vulnerability, as well as their clinical diagnostic and prognostic value, were discussed. Int. J. Mol. Sci. 2020, 21, 2992 2 of 26 by the low and oscillatory endothelial shear stress [3]. According to the current understanding, lesion development involves lipid accumulation in the arterial intima, resulting in foam cell formation, a local inflammatory response, and migration and proliferation of several cell types, including macrophages, smooth muscle cells (SMCs), lymphocytes, neutrophils, and dendritic cells that play a pivotal role in its progression. Lipid accumulation is a key event in the formation of the atherosclerotic lesion, and it is determined by different classes of lipoproteins [4]. Atherosclerotic plaque tends to develop early in life [5], progressing with age; however, the progression rate is not completely predictable and varies among individuals. In general, it undergoes a prolonged asymptomatic phase (lasting many years or several decades) until the manifestation of the first clinical symptoms often at the later stages of atherosclerosis. The mechanisms of plaque progression encompass SMC apoptosis, matrix synthesis, angiogenesis, arterial remodeling, fibrous cap rupture, and thrombosis, followed by necrosis and calcification. The most acute cardiovascular events are triggered by the rupture; erosion; or, the least common, calcified nodule, the vulnerable plaque phenotypes, followed by coronary thrombosis. Ruptured lesions are responsible for the majority (73%) of all ACSs [6]. In addition, the underlying mechanism of sudden coronary death from thrombi was found from plaque erosions, in 30%-35% of cases, and rarely from calcified nodules, in 2%-7% of cases [7].The biological features of two major classes of high-risk (vulnerable) plaques, such as rupture-pron...

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“…Diabetic patients are 2–4 times more likely to develop major vascular complications as a consequence of atherosclerotic plaque build‐up within their arteries 20. Diabetic patients are additionally more prone to plaque rupture 21. It is now well established that the morphology of the diabetic plaque differs with respect to its cellularity when compared with nondiabetic patients.…”

Section: Diabetes and Cardiovascular Diseasementioning

confidence: 99%

“…20 Diabetic patients are additionally more prone to plaque rupture. 21 It is now well established that the morphology of the diabetic plaque differs with respect to its cellularity when compared with nondiabetic patients. Most noticeable is the greater macrophage and T lymphocyte infiltration into the atherosclerotic plaque, as well as larger necrotic cores compared with nondiabetic specimens.…”

Section: Diabetes and Cardiovascular Diseasementioning

confidence: 99%

Recent novel approaches to limit oxidative stress and inflammation in diabetic complications

et al. 2018

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Diabetes is considered a major burden on the healthcare system of Western and non‐Western societies with the disease reaching epidemic proportions globally. Diabetic patients are highly susceptible to developing micro‐ and macrovascular complications, which contribute significantly to morbidity and mortality rates. Over the past decade, a plethora of research has demonstrated that oxidative stress and inflammation are intricately linked and significant drivers of these diabetic complications. Thus, the focus now has been towards specific mechanism‐based strategies that can target both oxidative stress and inflammatory pathways to improve the outcome of disease burden. This review will focus on the mechanisms that drive these diabetic complications and the feasibility of emerging new therapies to combat oxidative stress and inflammation in the diabetic milieu.

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Type 2 diabetes mellitus is associated with a lower fibrous cap thickness but has no impact on calcification morphology: an intracoronary optical coherence tomography study

Cited by 50 publications

References 40 publications

Calcification in Atherosclerotic Plaque Vulnerability: Friend or Foe?

Calcification in Atherosclerotic Plaque Vulnerability: Friend or Foe?

Current Advances in the Diagnostic Imaging of Atherosclerosis: Insights into the Pathophysiology of Vulnerable Plaque

Recent novel approaches to limit oxidative stress and inflammation in diabetic complications

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