Journal articles: 'Medial artery calcification'

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Lehto, Seppo, Leo Niskanen, Matti Suhonen, Tapani Rönnemaa, and Markku Laakso. "Medial Artery Calcification." Arteriosclerosis, Thrombosis, and Vascular Biology 16, no. 8 (August 1996): 978–83. http://dx.doi.org/10.1161/01.atv.16.8.978.

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Arbustini, Eloisa, Antonio Bozzani, and Francesco Prati. "Medial Artery Calcification." JACC: Advances 2, no. 9 (November 2023): 100652. http://dx.doi.org/10.1016/j.jacadv.2023.100652.

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Mandalapu, Aniruddh, and Kathryn J. Stevens. "Imaging findings of arterial calcification due to deficiency of CD73: A case study." Journal of Radiology Case Reports 17, no. 12 (February 9, 2024): 27–33. http://dx.doi.org/10.3941/jrcr.v17i12.5175.

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A 52-year-old male developed right knee pain after hiking in Guatemala. On his return he underwent a knee MRI for an indication of medial knee pain, which demonstrated a medial meniscal tear. However, the MRI demonstrated marked tortuosity and dense calcification of the popliteal artery, confirmed on subsequent radiographs. Review of previous CT studies of the abdomen and lower extremities showed severe ectasia and arterial calcification in the femoral and popliteal arteries bilaterally, but no calcifications in the aorta and common iliac arteries. Dual energy CT studies of the extremities demonstrated extensive periarticular soft tissue calcification throughout the wrists, hands, ankle and feet without evidence of uric acid. Review of the electronic medical records revealed a diagnosis of Arterial Calcification due to Deficiency of CD73 (ACDC), a rare genetic disorder presenting with debilitating pain in the wrists and hands, claudication of the calves, thighs and buttocks, progressing to chronic ischemia of the feet which may be limb-threatening. The patient was enrolled in an NIH trial of bisphosphonates and dual-antiplatelet therapy with stabilization of symptoms. This case discusses the imaging findings of this rare condition, differential diagnosis to consider, and current management.

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Meer, Romain, Anna G. Hoek, Emma J. Bouman, Teddo Doesburg, Petra J. M. Elders, Pim A. de Jong, Joline Beulens, and UCC-SMART Study Group. "Association between lower extremity arterial calcification and coronary arterial calcification in a population at increased risk of cardiovascular disease." BMJ Open Diabetes Research & Care 12, no. 1 (February 2024): e003811. http://dx.doi.org/10.1136/bmjdrc-2023-003811.

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IntroductionThere is conflicting evidence whether lower extremity arterial calcification coincides with coronary arterial calcification (CAC). The aims of this study were to investigate the associations between (1) femoral and crural calcification with CAC, and (2) femoral and crural calcification pattern with CAC.Research design and methodsThis cross-sectional study included 405 individuals (74% men, 62.6±10.9 years) from the ARTEMIS cohort study at high risk of cardiovascular disease (CVD) who underwent a CT scan of the femoral, crural and coronary arteries. High CVD risk was defined as history/presence of cerebrovascular disease, coronary artery disease, abdominal aortic aneurysm, renal artery stenosis, peripheral artery disease or CVD risk factors: diabetes mellitus type 2, hypertension, hyperlipidemia. Calcification score within each arterial bed was expressed in Agatston units. Dominant calcification patterns (intimal, medial, absent/indistinguishable) were determined via a CT-guided histologically validated scoring algorithm. Multivariable-adjusted multinomial logistic regression analyses were used. Replication was performed in an independent population of individuals with diabetes mellitus type 2 (Early-HFpEF cohort study).ResultsEvery 100-point increase in femoral and crural calcification score was associated with 1.23 (95% CI=1.09 to 1.37, p<0.001) and 1.28 (95% CI=1.11 to 1.47, p=0.001) times higher odds of having CAC within tertile 3 (high) versus tertile 1 (low), respectively. The association appeared stronger for crural versus femoral arteries. Moreover, the presence of femoral intimal (OR=10.81, 95% CI=4.23 to 27.62, p<0.001), femoral medial (OR=10.37, 95% CI=3.92 to 27.38, p<0.001) and crural intimal (OR=6.70, 95% CI=2.73 to 16.43, p<0.001) calcification patterns were associated with higher odds of having CAC within tertile 3 versus tertile 1, independently from concomitant calcification score. This association appeared stronger for intimal versus medial calcification patterns. The replication analysis yielded similar results.ConclusionsHigher femoral and crural calcification scores were associated with higher CAC. Moreover, the presence of femoral intimal, femoral medial and crural intimal calcification patterns was associated with increased CAC. It appears that arterial calcification is a systemic process which occurs simultaneously in various arterial beds.

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Bobryshev, Yuri V., Reginald S. A. Lord, and Dinh Tran. "Chlamydia pneumoniaein foci of “early” calcification of the tunica media in arteriosclerotic arteries: an incidental presence?" American Journal of Physiology-Heart and Circulatory Physiology 290, no. 4 (April 2006): H1510—H1519. http://dx.doi.org/10.1152/ajpheart.01055.2005.

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Only a few previous works investigated the involvement of Chlamydia pneumoniae ( Chlamydophila pneumoniae) in arterial calcification. The present study investigated a possible association between C. pneumoniae and medial calcification. Carotid artery segments obtained by endarterectomy from 60 patients were examined by PCR and immunohistochemistry to identify the presence of C. pneumoniae. Arterial specimens showing double-positive ( n = 17), double-negative ( n = 22), and single-positive results ( n = 21) were further analyzed by a combination of histology, immunohistochemistry, and electron microscopy. Medial calcification occurred in 10 of 17 (58.8%) C. pneumoniae double-positive arterial specimens, but no medial calcification was observed in any of 22 C. pneumoniae double-negative arterial specimens. Electron microscopy indicated C. pneumoniae in smooth muscle cells (SMCs) in foci of medial calcification. Medial SMCs showing damage to the cytoplasm and basement membrane contained the structures with the appearance of elementary, reticulate, and aberrant bodies of C. pneumoniae. The presence of C. pneumoniae in SMCs was confirmed by electron-microscopic immunocytochemistry. In the extracellular matrix, calcification was observed in C. pneumoniae aberrant bodies that exited the SMCs. The findings offer a new hypothesis of arterial calcification: they suggest that C. pneumoniae infection of medial SMCs may be associated with the pathophysiological events of arteriosclerotic calcification of the tunica media.

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Liu, En-Shao, Nai-Ching Chen, Tzu-Ming Jao, and Chien-Liang Chen. "Dextromethorphan Reduces Oxidative Stress and Inhibits Uremic Artery Calcification." International Journal of Molecular Sciences 22, no. 22 (November 13, 2021): 12277. http://dx.doi.org/10.3390/ijms222212277.

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Medial vascular calcification has emerged as a key factor contributing to cardiovascular mortality in patients with chronic kidney disease (CKD). Vascular smooth muscle cells (VSMCs) with osteogenic transdifferentiation play a role in vascular calcification. Nicotinamide adenine dinucleotide phosphate (NADPH) oxidase inhibitors reduce reactive oxygen species (ROS) production and calcified-medium–induced calcification of VSMCs. This study investigates the effects of dextromethorphan (DXM), an NADPH oxidase inhibitor, on vascular calcification. We used in vitro and in vivo studies to evaluate the effect of DXM on artery changes in the presence of hyperphosphatemia. The anti-vascular calcification effect of DXM was tested in adenine-fed Wistar rats. High-phosphate medium induced ROS production and calcification of VSMCs. DXM significantly attenuated the increase in ROS production, the decrease in ATP, and mitochondria membrane potential during the calcified-medium–induced VSMC calcification process (p < 0.05). The protective effect of DXM in calcified-medium–induced VSMC calcification was not further increased by NADPH oxidase inhibitors, indicating that NADPH oxidase mediates the effect of DXM. Furthermore, DXM decreased aortic calcification in Wistar rats with CKD. Our results suggest that treatment with DXM can attenuate vascular oxidative stress and ameliorate vascular calcification.

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Dogan, Omer Faruk, Musturay Karcaaltincaba, Umit Duman, Deniz Akata, Aytekin Besim, and Erkmen Boke. "Assessment of the Radial Artery and Hand Circulation by Computed Tomography Angiography: A Pilot Study." Heart Surgery Forum 8, no. 1 (February 16, 2005): 28. http://dx.doi.org/10.1532/hsf98.20041042.

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Objectives: The radial artery (RA) is increasingly being used as a coronary bypass graft. Results of a previous study using Doppler ultrasound and histopathologic examinations indicated that the RA has a higher incidence of preexisting intimal hyperplasia, medial calcification, and atherosclerosis than the internal thoracic artery. The aims of this study were to evaluate the use of computed tomographic angiography (CTA) to display hand collateral circulation, to define the criteria for an abnormal CTA test result, and to demonstrate usefulness of CTA as an alternative to conventional angiography for evaluation of the radial artery. Materials and Methods: Sixteen patients scheduled for coronary artery bypass grafting entered this study. We performed 32 examinations of forearm and hand arterial anatomy in these patients. CTA was performed in patients with a normal Allen test result, except 1 patient who had a persistent median artery. Soft tissue density forehand roentgenography was performed in all patients before the CTA evaluation. There was no selection of patients in relation to patient characteristics. As a risk factor for radial artery calcification, 6 of the patients had diabetes mellitus, 6 had aortofemoral occlusive disease, and 4 had a history of smoking. Results: Bilateral forearm arteries were visualized in all patients. Severe RA calcification was found in 1 patient, and distal occlusion was found in another patient. Focal RA calcification was noted in 2 patients. In the remaining patients no radial artery calcification or occlusion was noted. Anatomic variation of the upper limb arteries was shown in 2 patients; these variations were persistent median artery with absence of the radial and ulnar arteries and high bifurcation of the radial artery from the brachial artery. Conclusion: CTA is useful and safe for detection of radial artery calcific disease and assessment of the forehand circulation and its anatomic variations. Preoperative imaging of the RA is a means to avoid unnecessary forearm exploration or inadvertent use of a diseased conduit in coronary artery bypass candidates with multiple risk factors such as diabetes mellitus.

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Liu, Huan, Ning-Yu Ru, Yue Cai, Qiang Lyu, Chi-Hua Guo, Ying Zhou, Shao-Hua Li, et al. "The OPG/RANKL/RANK system modulates calcification of common carotid artery in simulated microgravity rats by regulating NF-κB pathway." Canadian Journal of Physiology and Pharmacology 100, no. 4 (April 2022): 324–33. http://dx.doi.org/10.1139/cjpp-2021-0329.

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Functional and structural adaptation of common carotid artery could be one of the important causes of postflight orthostatic intolerance after microgravity exposure, the mechanisms of which remain unclear. Recent evidence indicates that long-term spaceflight increases carotid artery stiffness, which might present a high risk to astronaut health and postflight working ability. Studies have suggested that vascular calcification is a common pathological change in cardiovascular diseases that is mainly manifested as an increase in vascular stiffness. Therefore, this study investigated whether simulated microgravity induces calcification of common carotid artery and to elucidate the underlying mechanisms. Four-week-old hindlimb-unweighted (HU) rats were used to simulate the deconditioning effects of microgravity on cardiovascular system. We found that simulated microgravity induced vascular smooth muscle cell (VSMC) osteogenic differentiation and medial calcification, increased receptor activator of nuclear factor κB (NF-κB) ligand (RANKL) and RANK expression, and enhanced NF-κB activation in rat common carotid artery. In vitro activation of the RANK pathway with exogenous RANKL, a RANK ligand, increased RANK and osteoprotegerin (OPG) expression in HU rats. Moreover, the expression of osteogenic markers and activation of NF-κB in HU rats were further enhanced by exogenous RANKL but suppressed by the RANK inhibitor osteoprotegerin fusion protein (OPG-Fc). These results indicated that the OPG/RANKL/RANK system modulates VSMC osteogenic differentiation and medial calcification of common carotid artery in simulated microgravity rats by regulating the NF-kB pathway.

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Happy, Happy, S. M. Ear E-Mahabub, Nazir Uddin Mollah, Md Emran Hossain, Dr Halima Khatun, and Md Magfur Rahman. "Breast Arterial Calcification on Mammography and Risk of Coronary Artery Disease." Scholars Journal of Applied Medical Sciences 10, no. 5 (May 24, 2022): 810–15. http://dx.doi.org/10.36347/sjams.2022.v10i05.023.

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Background: Breast arterial calcification (BAC) is generally detected on screening mammography which shows medial calcification of the mammary arteries. On the other hand, CAD is an important cause of morbidity and mortality worldwide. BAC is associated with risk factors for cardiovascular disease specially in patients who underwent screening mammography. Methods: This study was a cross-sectional observational study that was conducted at Bangabandhu Sheik Mujib Medical University. Dhaka. Bangladesh during the period of January 2018- December 2022. The sample size for this study was 70. Result: The mean ±SD age of the respondents who underwent mammography was 58± 8 years where who had breast arterial calcification it was 62±7 years. Total cholesterol was 5.1±1.9 and 5.2±2.0, ASSIGN score was in 15±10.8 and 18.1±11.0, coronary artery calcium score was in 0(0,52) and 13 (0, 107), any coronary artery disease on CCTA was in 35(50%) and 7(58.3%), obstructive coronary artery disease on CCTA was in 10(14.3%) and 2(16.7%) cases. Coronary artery calcification 5 was found in TP, 14 was in TN, 3 was in FP, 14 was in FN, 2 was in sensitivity, 7 was in specificity, 6 was in PPV, 5 was in NPV and .545 was in AUC and followed by coronary artery calcification (>400 AU) was in 1, 27, 8, 1, 3, 6, 1, 9 and 0.554, any coronary artery disease on CCTA was in 5, 14, 3, 14, 2, 7, 6, 5 and 0.546, obstructive coronary artery disease on CCTA was in 2, 25, 7, 4, 3, 7, 2, 8 and 0.556. Conclusion: BAC on mammography is a potential woman-specific risk predictor for CAD and is also related to the growth of coronary atherosclerosis proven by CCTA having important clinical implications. BAC is also strongly associated with the development of CAC and CAP.

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Niskanen, L., O. Siitonen, M. Suhonen, and M. I. Uusitupa. "Medial Artery Calcification Predicts Cardiovascular Mortality in Patients With NIDDM." Diabetes Care 17, no. 11 (November 1, 1994): 1252–56. http://dx.doi.org/10.2337/diacare.17.11.1252.

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He, Pengcheng, Hongjiao Yu, Lei Jiang, Ziying Chen, Siying Wang, Vicky E. Macrae, Xiaodong Fu, and Dongxing Zhu. "Hdac9 inhibits medial artery calcification through down-regulation of Osterix." Vascular Pharmacology 132 (September 2020): 106775. http://dx.doi.org/10.1016/j.vph.2020.106775.

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Zhou, Ye-bo, Jing Zhang, Yan Cai, Xu Teng, Xiao-hui Duan, Jun-qiu Song, Jie Du, Chao-shu Tang, and Yong-fen Qi. "Insulin resistance induces medial artery calcification in fructose-fed rats." Experimental Biology and Medicine 237, no. 1 (January 2012): 50–57. http://dx.doi.org/10.1258/ebm.2011.011252.

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Nicoll, Rachel. "Correlation between coronary and valve calcification: Review of current evidence." International Cardiovascular Forum Journal 1, no. 1 (March 29, 2015): 19. http://dx.doi.org/10.17987/icfj.v1i1.10.

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We carried out a review of the correlation between calcification of different arteries and valves and their risk factors to determine the extent of the association. We found a strong correlation between calcification presence, extent and progression between different arterial beds and the aortic valve, suggesting that calcification is a systemic diffuse disease, affecting the arterial tree as a whole. Despite this strong association, a comparison between coronary artery calcification (CAC) and calcification of other arteries may not be strictly valid, since only intimal calcification is seen in the coronary artery while other arteries may also contain medial calcification, with current scanning modalities being incapable of detecting the difference. Furthermore the pathogenesis of each type may be different.Calcification seems to appear first in the coronary artery in younger adults but may be more prevalent in the aorta in the elderly, although the incidence is notably higher in the abdominal aorta among women. Mitral annulus calcification (MAC) occurs less frequently than aortic valve calcification (AVC) in asymptomatic subjects only. MAC is correlated with calcification of the aorta and advanced MAC is found with higher CAC but there is little relationship with AVC and calcification of other arterial beds. As with the coronary artery, in the aorta and aortic valve, calcium begets calcium. Although age, male gender and possibly systolic hypertension are most frequently associated with arterial calcification, there is little consistency for other conventional risk factors and MAC andabdominal aortic calcification may be more prevalent among postmenopausal women. When the presence of CAC is factored in as a risk factor for calcification of the other arteries, multivariate analysis shows no additional significant risk factors except age.Although AVC has been viewed as a cardiac manifestation of atherosclerosis, we found little evidence to suggest that this is also true of MAC.

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Sekulic, Miroslav, and Alexander M. Truskinovsky. "Metaplastic Ossification of the Temporal Artery with Osteoclast-Like Giant Cells: A Mimicker of Giant Cell (Temporal) Arteritis." European Journal of Ophthalmology 27, no. 3 (May 2017): e99-e103. http://dx.doi.org/10.5301/ejo.5000941.

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Purpose To describe a patient presenting with suspected giant cell (temporal) arteritis (GCA) in whom subsequent temporal artery biopsy showed luminal narrowing by medial calcification, metaplastic ossification, and fibrointimal proliferation, consistent with calciphylaxis. Methods A 55-year-old man with end-stage renal disease presented with unilateral loss of vision and elevated erythrocyte sedimentation rate and was initially treated as though he had GCA; however, a subsequent temporal artery biopsy showed marked luminal narrowing by medial calcification, metaplastic ossification, and fibrointimal proliferation, consistent with calciphylaxis. In addition, the tunica media of the affected artery contained multinucleate giant cells, but these represented osteoclasts and foreign body giant cells reacting to calcium, rather than a part of GCA. Results This is a rare report of metaplastic ossification and the finding of non-GCA-related giant cells in the tunica media of the temporal artery, thus representing a clinical and histopathologic mimicker of GCA. Conclusions The clinical differential diagnosis of GCA includes other etiologies that can present similarly; however, temporal artery biopsy can discern the underlying pathology. Importantly, the identification of giant cells is not required for the diagnosis of GCA, and likewise, as our case shows, the finding of giant cells in the wall of a temporal artery does not always imply a diagnosis of GCA.

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Nakano-Kurimoto, Ritsuko, Koji Ikeda, Maki Uraoka, Yusuke Nakagawa, Kotaro Yutaka, Masahiro Koide, Tomosaburo Takahashi, et al. "Replicative senescence of vascular smooth muscle cells enhances the calcification through initiating the osteoblastic transition." American Journal of Physiology-Heart and Circulatory Physiology 297, no. 5 (November 2009): H1673—H1684. http://dx.doi.org/10.1152/ajpheart.00455.2009.

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Medial artery calcification, which does not accompany lipid or cholesterol deposit, preferentially occurs in elderly population, but its underlying mechanisms remain unclear. In the present study, we investigated the potential role of senescent vascular smooth muscle cells (VSMCs) in the formation of senescence-associated medial calcification. Replicative senescence was induced by the extended passages (until passages 11–13) in human primary VSMCs, and cells in early passage ( passage 6) were used as control young cells. VSMC calcification was markedly enhanced in the senescent cells compared with that in the control young cells. We identified that genes highly expressed in osteoblasts, such as alkaline phosphatase (ALP) and type I collagen, were significantly upregulated in the senescent VSMCs, suggesting their osteoblastic transition during the senescence. Knockdown of either ALP or type I collagen significantly reduced the calcification in the senescent VSMCs. Of note, runt-related transcription factor-2 (RUNX-2), a core transcriptional factor that initiates the osteoblastic differentiation, was also upregulated in the senescent VSMCs. Knockdown of RUNX-2 significantly reduced the ALP expression and calcification in the senescent VSMCs, suggesting that RUNX-2 is involved in the senescence-mediated osteoblastic transition. Furthermore, immunohistochemistry of aorta from the klotho−/− aging mouse model demonstrated in vivo emergence of osteoblast-like cells expressing RUNX-2 exclusively in the calcified media. We also found that statin and Rho-kinase inhibitor effectively reduced the VSMC calcification by inhibiting Pi-induced apoptosis and potentially enhancing matrix Gla protein expression in the senescent VSMCs. These findings strongly suggest an important role of senescent VSMCs in the pathophysiology of senescence-associated medial calcification, and the inhibition of osteoblastic transition could be a new therapeutic approach for the prevention of senescence-associated medial calcification.

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Smith, Christopher David, Jonathan Gavin Bilmen, Shehzad Iqbal, Sharon Robey, and Melwyn Pereira. "Medial Artery Calcification as an Indicator of Diabetic Peripheral Vascular Disease." Foot & Ankle International 29, no. 2 (February 2008): 185–90. http://dx.doi.org/10.3113/fai.2008.0185.

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Thakur, Manovriti, Nico Angliker, Mark Siegrist, Yvonne Jansen, Berenice Martinez, Julia Wollenhaupt, Heidi Noels, and Yvonne Döring. "Molecular drivers of medial arterial calcification in lower extremity artery disease." Atherosclerosis 395 (August 2024): 118319. http://dx.doi.org/10.1016/j.atherosclerosis.2024.118319.

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St. Hilaire, Cynthia. "Medial Arterial Calcification: A Significant and Independent Contributor of Peripheral Artery Disease." Arteriosclerosis, Thrombosis, and Vascular Biology 42, no. 3 (March 2022): 253–60. http://dx.doi.org/10.1161/atvbaha.121.316252.

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Over 200 million individuals worldwide are estimated to have peripheral artery disease (PAD). Although the term peripheral can refer to any outer branch of the vasculature, the focus of this review is on lower-extremity arteries. The initial sequelae of PAD often include movement-induced cramping pain in the hips and legs or loss of hair and thinning of the skin on the lower limbs. PAD progresses, sometimes rapidly, to cause nonhealing ulcers and critical limb ischemia which adversely affects mobility and muscle tone; acute limb ischemia is a medical emergency. PAD causes great pain and a high risk of amputation and ultimately puts patients at significant risk for major adverse cardiovascular events. The negative impact on patients’ quality of life, as well as the medical costs incurred, are huge. Atherosclerotic plaques are one cause of PAD; however, emerging clinical data now shows that nonatherosclerotic medial arterial calcification (MAC) is an equal and distinct contributor. This ATVB In Focus article will present the recent clinical findings on the prevalence and impact of MAC in PAD, discuss the known pathways that contribute specifically to MAC in the lower extremity, and highlight gaps in knowledge and tools that limit our understanding of MAC pathogenesis.

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Janda, Katarzyna, Marcin Krzanowski, Mariusz Gajda, Paulina Dumnicka, Ewa Jasek, Danuta Fedak, Agata Pietrzycka, Marek Kuźniewski, Jan A. Litwin, and Władysław Sułowicz. "Vascular Effects of Advanced Glycation End-Products: Content of Immunohistochemically Detected AGEs in Radial Artery Samples as a Predictor for Arterial Calcification and Cardiovascular Risk in Asymptomatic Patients with Chronic Kidney Disease." Disease Markers 2015 (2015): 1–9. http://dx.doi.org/10.1155/2015/153978.

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Objectives.Our aim was to determine whether vascular deposition of advanced glycation end-products (AGEs) is associated with arterial calcification and cardiovascular mortality in chronic kidney disease (CKD) patients and to assess the relationships between vascular content of AGEs and selected clinical and biochemical parameters.Materials and Methods.The study comprised 54 CKD patients (33 hemodialyzed, 21 predialyzed). Examined parameters included BMI, incidence of diabetes, plasma fasting glucose, AGEs, soluble receptor for AGEs and 2,2-diphenyl-1-picrylhydrazyl (DPPH) scavenging, serum C-reactive protein (hsCRP), plasminogen activator inhibitor-1 (PAI-1), and fetuin-A. Fragments of radial artery obtained during creation of hemodialysis access were stained for calcifications using alizarin red. AGEs deposits were identified immunohistochemically and their relative content was quantified.Results.Vascular content of AGEs was positively correlated with BMI, hsCRP, fetuin-A, PAI-1, and DPPH scavenging in simple regression; only fetuin-A was an independent predictor in multiple regression. There was a significant positive trend in the intensity of AGEs immunostaining among patients with grades 1, 2, and 3 calcifications. AGEs immunostaining intensity predicted 3-year cardiovascular mortality irrespective of patient’s age.Conclusions.The present study demonstrates an involvement of AGEs in the development of medial arterial calcification and the impact of arterial AGE deposition on cardiovascular mortality in CKD patients.

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Kato, Tsukasa, Sho Torii, Norihito Nakamura, Kazuki Aihara, Yuta Terabe, Osamu Iida, Takahiro Tokuda, et al. "Pathological Analysis of Medial and Intimal Calcification in Lower Extremity Artery Disease." JACC: Advances 2, no. 9 (November 2023): 100656. http://dx.doi.org/10.1016/j.jacadv.2023.100656.

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Sheen, Campbell R., Pia Kuss, Sonoko Narisawa, Manisha C. Yadav, Jessica Nigro, Wei Wang, T. Nicole Chhea, et al. "Pathophysiological Role of Vascular Smooth Muscle Alkaline Phosphatase in Medial Artery Calcification." Journal of Bone and Mineral Research 30, no. 5 (April 16, 2015): 824–36. http://dx.doi.org/10.1002/jbmr.2420.

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Krishnan, Prakash, Pedro R. Moreno, Irene C. Turnbull, Meerarani Purushothaman, Urooj Zafar, Arthur Tarricone, Sandeep Singla, et al. "Incremental effects of diabetes mellitus and chronic kidney disease in medial arterial calcification: Synergistic pathways for peripheral artery disease progression." Vascular Medicine 24, no. 5 (May 15, 2019): 383–94. http://dx.doi.org/10.1177/1358863x19842276.

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Diabetes mellitus (DM) and chronic kidney disease (CKD) separately are known to facilitate the progression of medial arterial calcification (MAC) in patients with symptomatic peripheral artery disease (PAD), but their combined effect on MAC and associated mediators of calcification is not well studied. The association of MAC and calcification inducer bone morphogenetic protein (BMP-2) and inhibitor fetuin-A, with PAD, is well known. Our aim was to investigate the association of MAC with alterations in BMP-2 and fetuin-A protein expression in patients with PAD with DM and/or CKD. Peripheral artery plaques (50) collected during directional atherectomy from symptomatic patients with PAD were evaluated, grouped into no-DM/no-CKD ( n = 14), DM alone ( n = 10), CKD alone ( n = 12), and DM+CKD ( n = 14). MAC density was evaluated using hematoxylin and eosin, and alizarin red stain. Analysis of inflammation, neovascularization, BMP-2 and fetuin-A protein density was performed by immunohistochemistry. MAC density, inflammation grade and neovessel content were significantly higher in DM+CKD versus no-DM/no-CKD and CKD ( p < 0.01). BMP-2 protein density was significantly higher in DM+CKD versus all other groups ( p < 0.01), whereas fetuin-A protein density was significantly lower in DM+CKD versus all other groups ( p < 0.001). The combined presence of DM+CKD may be associated with MAC severity in PAD plaques more so than DM or CKD alone, as illustrated in this study, where levels of calcification mediators BMP-2 and fetuin-A protein were related most robustly to DM+CKD. Further understanding of mechanisms involved in mediating calcification and their association with DM and CKD may be useful in improving management and developing therapeutic interventions.

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Zhu, Jie, Qiping Liu, Yuzhong Zhuang, Ran Wei, Yi Sun, Hao Wang, and Bin Song. "Intracranial Carotid Artery Calcification Subtype in Patients with Anterior Circulation Acute Ischemic Stroke Undergoing Intravenous Thrombolysis." Neurology India 71, no. 6 (2023): 1205–10. http://dx.doi.org/10.4103/0028-3886.391400.

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Background and Aim: The aim of this study was to investigate the potential value of intracranial carotid artery calcification (ICAC) in therapeutic efficacy and functional outcomes in patients with anterior circulation acute ischemic stroke (AIS) undergoing intravenous thrombolysis. Materials and Methods: A total of 207 patients with anterior circulation AIS who underwent intravenous thrombolysis were enrolled in this retrospective study. We divided them into three groups according to thin-slice head noncontrast computed tomography as follows: no ICAC, medial ICAC, and intimal ICAC. The differences in risk factors of different ICAC subtypes were compared, and the effect of ICAC subtype on hemorrhage transformation (HT) after intravenous thrombolysis was also evaluated. Functional outcomes were assessed at 90 days using the modified Rankin Scale. Results: Compared to the no and intimal ICAC, patients with the medial ICAC were older and more likely to have diabetes mellitus, hyperlipidemia, previous stroke, and atrial fibrillation. Moreover, the medial ICAC group had a high baseline National Institute of Health Stroke Scale (NIHSS) score and a high incidence of HT. Multivariate logistic regression analysis showed that baseline NIHSS score (odds ratio [OR]: 1.121, 95% confidence interval [CI]: 1.027–1.224) was independently associated with HT. Medial ICAC (OR: 7.418, 95% CI: 1.190–46.231) and baseline NIHSS score (OR: 1.141, 95% CI: 1.042–1.250) were independent risk factors of poor functional outcome at 90 days. Conclusions: Medial ICAC could be a new imaging biomarker for predicting functional outcomes in patients with anterior circulation AIS undergoing intravenous thrombolysis. Medial ICAC and baseline NIHSS score were independently associated with poor prognosis at 90 days.

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Bas, Alicia, Ignacio Lopez, Jose Perez, Mariano Rodriguez, and Escolastico Aguilera-Tejero. "Reversibility of Calcitriol-Induced Medial Artery Calcification in Rats With Intact Renal Function." Journal of Bone and Mineral Research 21, no. 3 (December 19, 2005): 484–90. http://dx.doi.org/10.1359/jbmr.051211.

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Kumric, Marko, Josip A. Borovac, Tina Ticinovic Kurir, Dinko Martinovic, Ivan Frka Separovic, Ljupka Baric, and Josko Bozic. "Role of Matrix Gla Protein in the Complex Network of Coronary Artery Disease: A Comprehensive Review." Life 11, no. 8 (July 24, 2021): 737. http://dx.doi.org/10.3390/life11080737.

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Coronary artery disease (CAD) is widely recognized as one of the most important clinical entities. In recent years, a large body of accumulated data suggest that coronary artery calcification, a process highly prevalent in patients with CAD, occurs via well-organized biologic processes, rather than passively, as previously regarded. Matrix Gla protein (MGP), a vitamin K-dependent protein, emerged as an important inhibitor of both intimal and medial vascular calcification. The functionality of MGP hinges on two post-translational modifications: phosphorylation and carboxylation. Depending on the above-noted modifications, various species of MGP may exist in circulation, each with their respective level of functionality. Emerging data suggest that dysfunctional species of MGP, markedly, dephosphorylated-uncarboxylated MGP, might find its application as biomarkers of microvascular health, and assist in clinical decision making with regard to initiation of vitamin K supplementation. Hence, in this review we summarized the current knowledge with respect to the role of MGP in the complex network of vascular calcification with concurrent inferences to CAD. In addition, we discussed the effects of warfarin use on MGP functionality, with concomitant implications to coronary plaque stability.

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OKYAR, Burak, Bekir TORUN, Fatih ALBAYRAK, Sezen KOÇARSLAN, Fatih YILDIZ, and Gözde YILDIRIM ÇETİN. "Dev hücreli arteriti taklit eden nadir bir Mönckeberg medial kalsifik skleroz olgusu." Cukurova Medical Journal 47, no. 2 (June 30, 2022): 901–4. http://dx.doi.org/10.17826/cumj.1063305.

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Background: Mönckeberg Medial Calcific Sclerosis (MMCS) is a rare condition that can mimic giant cell arteritis (GCA). It may be misinterpreted as giant cell arteritis by the clinician and cause unnecessary treatments. Therefore, it is a disease that should be differentiated from giant cell arteritis with its clinical, radiological, and pathological findings. Case Presentation: A 56-year-old female patient was admitted to our clinic with sudden unilateral vision loss on the right, pain in the right temporal artery trace, scalp sensitivity in the section corresponding to that area, difficulty chewing, and temporal artery sensitivity. He had a history of hemodialysis for 13 years due to hypertension, osteoporosis, a history of renal stones, and end-stage renal failure. In routine blood tests, White Blood Cell: 7.86X109/L, Hemoglobulin: 10.9 g/dL, C-reactive protein: 3.03 mg/L, Erythrocyte sedimentation rate: 53 mm/hour came. As a result of temporal artery biopsy performed for GCA, absence of giant cells, absence of epithelioid histiocytes, absence of pathological findings in the internal elastic lamina, diffuse calcification in the tunica media, and sclerosis was diagnosed as MMCS. Conclusions: In the literature, 4 case reports resemble giant cell arteritis and are diagnosed as MMCS. This case report is a rare case report showing that MMCS can completely mimic GCA findings.

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Qureshi, Abdul Rashid, Hannes Olauson, Anna Witasp, Mathias Haarhaus, Vincent Brandenburg, Annika Wernerson, Bengt Lindholm, et al. "Increased circulating sclerostin levels in end-stage renal disease predict biopsy-verified vascular medial calcification and coronary artery calcification." Kidney International 88, no. 6 (December 2015): 1356–64. http://dx.doi.org/10.1038/ki.2015.194.

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Choi, Justin Chin-Bong, Jorge Miranda, Erin Greenleaf, Michael S. Conte, Marie D. Gerhard-Herman, Joseph L. Mills, and Neal R. Barshes. "Lower-extremity pressure, staging, and grading thresholds to identify chronic limb-threatening ischemia." Vascular Medicine 28, no. 1 (February 2023): 45–53. http://dx.doi.org/10.1177/1358863x221147945.

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Introduction: The Society for Vascular Surgery Threatened Limb Classification System (‘WIfI’) is used to predict risk of limb loss and identify peripheral artery disease in patients with foot ulcers or gangrene. We estimated the diagnostic sensitivity of multiple clinical and noninvasive arterial parameters to identify chronic limb-threatening ischemia (CLTI). Methods: We performed a single-center review of 100 consecutive patients who underwent angiography for foot gangrene or ulcers. WIfI stages and grades were determined for each patient. Toe, ankle, and brachial pressure measurements were performed by registered vascular technologists. CLTI severity was characterized using Global Limb Anatomic Staging System (GLASS stages) and angiosomes. Medial artery calcification in the foot was quantified on foot radiographs. Results: GLASS NA (not applicable), I, II, and III angiographic findings were seen in 21, 21, 23, and 35 patients, respectively. A toe–brachial index < 0.7 and minimum ipsilateral ankle–brachial index < 0.9 performed well in identifying GLASS II and III angiographic findings, with sensitivity rates 97.8% and 91.5%, respectively. The diagnostic accuracy rates of noninvasive measures peaked at 74.7% and 89.3% for identifying GLASS II/III and GLASS I+ angiographic findings, respectively. The presence of medial artery calcification significantly diminished the sensitivity of most noninvasive parameters. Conclusions: The use of alternative noninvasive arterial testing parameters improves sensitivity for detecting PAD. Abnormal noninvasive results should suggest the need for diagnostic angiography to further characterize arterial anatomy of the affected limb. Testing strategies with better accuracy are needed.

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Ortega, Miguel A., Diego De Leon-Oliva, Maria José Gimeno-Longas, Diego Liviu Boaru, Oscar Fraile-Martinez, Cielo García-Montero, Amador Velazquez de Castro, et al. "Vascular Calcification: Molecular Networking, Pathological Implications and Translational Opportunities." Biomolecules 14, no. 3 (February 25, 2024): 275. http://dx.doi.org/10.3390/biom14030275.

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Calcification is a process of accumulation of calcium in tissues and deposition of calcium salts by the crystallization of PO43− and ionized calcium (Ca2+). It is a crucial process in the development of bones and teeth. However, pathological calcification can occur in almost any soft tissue of the organism. The better studied is vascular calcification, where calcium salts can accumulate in the intima or medial layer or in aortic valves, and it is associated with higher mortality and cardiovascular events, including myocardial infarction, stroke, aortic and peripheral artery disease (PAD), and diabetes or chronic kidney disease (CKD), among others. The process involves an intricate interplay of different cellular components, endothelial cells (ECs), vascular smooth muscle cells (VSMCs), fibroblasts, and pericytes, concurrent with the activation of several signaling pathways, calcium, Wnt, BMP/Smad, and Notch, and the regulation by different molecular mediators, growth factors (GFs), osteogenic factors and matrix vesicles (MVs). In the present review, we aim to explore the cellular players, molecular pathways, biomarkers, and clinical treatment strategies associated with vascular calcification to provide a current and comprehensive overview of the topic.

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Silva, Gonçalo Teixeira de Almeida, Bruce B. Guest, Diego E. Gomez, Martine McGregor, Laurent Viel, M. Lynne O’Sullivan, John Runciman, and Luis G. Arroyo. "Development of a technique for determination of pulmonary artery pulse wave velocity in horses." Journal of Applied Physiology 122, no. 5 (May 1, 2017): 1088–94. http://dx.doi.org/10.1152/japplphysiol.00962.2016.

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Calcification of the tunica media of the axial pulmonary arteries (PA) has been reported in a large proportion of racehorses. In humans, medial calcification is a significant cause of arterial stiffening and is implicated in the pathogenesis of cardiac, cerebral, and renal microvascular diseases. Pulse wave velocity (PWV) provides a measure of arterial stiffness. This study aimed to develop a technique to determine PA-PWV in horses and, secondarily, to investigate a potential association between PA-PWV and arterial fibro-calcification. A dual-pressure sensor catheter (PSC) was placed in the main PA of 10 sedated horses. The pressure waves were used to determine PWV along the PA, using the statistical phase offset method. Histological analysis of the PA was performed to investigate the presence of fibro-calcified lesions. The mean (±SD) PWV was 2.3 ± 0.7 m/s in the proximal PA trunk and 1.1 ± 0.1 m/s further distal (15 cm) in a main PA branch. The mean (±SD) of mean arterial pressures in the proximal PA trunk was 30.1 ± 5.2 mmHg, and 22.0 ± 6.0 mmHg further distal (15 cm) within the main PA branch. The mean (±SD) pulse pressure in the proximal PA trunk was 15.0 ± 4.7 mmHg, and 13.5 ± 3.3 mmHg further distal (15 cm) within the main PA branch. Moderate to severe lesions of the tunica media of the PAs were observed in seven horses, but a correlation with PWV could not be established yet. Pulmonary artery PWV may be determined in standing horses. The technique described may allow further investigation of the effect of calcification of large PAs in the pathogenesis of equine pulmonary circulatory disorders. NEW & NOTEWORTHY Pulmonary artery pulse wave velocity was determined safely in standing sedated horses. The technique described may allow further investigation of the effect of calcification of large pulmonary arteries in the pathogenesis of pulmonary circulatory disorders in horses.

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Jinnouchi, Hiroyuki, Yu Sato, Rahul R. Bhoite, Salome H. Kuntz, Atsushi Sakamoto, Matthew Kutyna, Sho Torii, et al. "Intravascular imaging and histological correlates of medial and intimal calcification in peripheral artery disease." EuroIntervention 17, no. 8 (October 2021): e688-e698. http://dx.doi.org/10.4244/eij-d-20-01336.

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Moe, Sharon M., Kalisha D. O'Neill, Danxia Duan, Sadiq Ahmed, Neal X. Chen, Stephen B. Leapman, Naomi Fineberg, and Kenyon Kopecky. "Medial artery calcification in ESRD patients is associated with deposition of bone matrix proteins." Kidney International 61, no. 2 (February 2002): 638–47. http://dx.doi.org/10.1046/j.1523-1755.2002.00170.x.

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Kockelkoren, Remko, Annelotte Vos, Wim Van Hecke, Aryan Vink, Ronald L. A. W. Bleys, Daphne Verdoorn, Willem P. Th M. Mali, et al. "Computed Tomographic Distinction of Intimal and Medial Calcification in the Intracranial Internal Carotid Artery." PLOS ONE 12, no. 1 (January 6, 2017): e0168360. http://dx.doi.org/10.1371/journal.pone.0168360.

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Vos, Annelotte, Remko Kockelkoren, Jill B. de Vis, Yvonne T. van der Schouw, Irene C. van der Schaaf, Birgitta K. Velthuis, Willem P. T. M. Mali, et al. "Risk factors for atherosclerotic and medial arterial calcification of the intracranial internal carotid artery." Atherosclerosis 276 (September 2018): 44–49. http://dx.doi.org/10.1016/j.atherosclerosis.2018.07.008.

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35

Al-Absi, A., and B. M. Wall. "MEDIAL ARTERY CALCIFICATION MIMICKING TEMPORAL ARTERITIS IN AN END-STAGE RENAL DISEASE (ESRD) PATIENT." Journal of Investigative Medicine 52 (January 2004): S276. http://dx.doi.org/10.1097/00042871-200401001-00664.

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36

Al-Absi, A., and BM Wall. "Medial Artery Calcification Mimicking Temporal Arteritis in An End-Stage Renal Disease (Esrd) Patient." Journal of Investigative Medicine 52, no. 1_suppl_part_4 (January 2001): 276. http://dx.doi.org/10.1177/108155890105201s671.

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Narula, Nupoor, Jeffrey W. Olin, and Navneet Narula. "Pathologic Disparities Between Peripheral Artery Disease and Coronary Artery Disease." Arteriosclerosis, Thrombosis, and Vascular Biology 40, no. 9 (September 2020): 1982–89. http://dx.doi.org/10.1161/atvbaha.119.312864.

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Atherosclerosis is a systemic disease that involves multiple vascular beds. The pathological characteristics and clinical presentation, however, vary among the different vascular territories. Acute coronary syndrome is a relatively common manifestation of coronary atherosclerotic disease, wherein the thrombosis occurs secondary to disruption (65%–75%) and erosion (25%–35%) of the fibrous caps of atheromatous plaques. The plaques associated with plaque rupture have large necrotic cores and thin and inflamed fibrous caps. However, the pathological manifestations of peripheral artery disease result from thrombosis regardless of the extent of atherosclerosis. Approximately 75% of peripheral arteries with significant stenosis demonstrate presence of thrombi, of which two-thirds have thrombi associated with insignificant atherosclerosis. The presence of obliterative thrombi in peripheral arteries of patients with critical limb ischemia in the absence of coronary artery–like lesions suggests a locally thrombogenic or remotely embolic basis of disease. Extensive calcification of the medial vascular layer is commonly observed. In this review, we have described and compared the pathological basis of coronary and peripheral artery disease in patients with acute coronary syndrome and critical limb ischemia. It is expected that pathogenetic characterization would allow for definition of strategic targets for superior management of peripheral artery disease.

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Dharmshaktu, GaneshS. "Medial arterial calcification of dorsalis pedis artery in a diabetic foot: A poor prognostic feature." Journal of Diabetology 11, no. 3 (2020): 218. http://dx.doi.org/10.4103/jod.jod_21_20.

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Al-Absi, A., and B. M. Wall. "111 MEDIAL ARTERY CALCIFICATION MIMICKING TEMPORAL ARTERITIS IN AN END-STAGE RENAL DISEASE (ESRD) PATIENT." Journal of Investigative Medicine 52, Suppl 1 (January 1, 2004): S276.4—S276. http://dx.doi.org/10.1136/jim-52-suppl1-664.

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Asirvatham, S., C. Sebastian, CA Sivaram, C. Kaufman, and K. Chandrasekaran. "Aortic valve involvement in calciphylaxis: Uremic small artery disease with medial calcification and intimal hyperplasia." American Journal of Kidney Diseases 32, no. 3 (September 1998): 499–502. http://dx.doi.org/10.1053/ajkd.1998.v32.pm9740169.

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Vattikuti, Radhika, and Dwight A. Towler. "Osteogenic regulation of vascular calcification: an early perspective." American Journal of Physiology-Endocrinology and Metabolism 286, no. 5 (May 2004): E686—E696. http://dx.doi.org/10.1152/ajpendo.00552.2003.

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Cardiovascular calcification is a common consequence of aging, diabetes, hypercholesterolemia, mechanically abnormal valve function, and chronic renal insufficiency. Although vascular calcification may appear to be a uniform response to vascular insult, it is a heterogenous disorder, with overlapping yet distinct mechanisms of initiation and progression. A minimum of four histoanatomic variants—atherosclerotic (fibrotic) calcification, cardiac valve calcification, medial artery calcification, and vascular calciphylaxis—arise in response to metabolic, mechanical, infectious, and inflammatory injuries. Common to the first three variants is a variable degree of vascular infiltration by T cells and macrophages. Once thought benign, the deleterious clinical consequences of calcific vasculopathy are now becoming clear; stroke, amputation, ischemic heart disease, and increased mortality are portended by the anatomy and extent of calcific vasculopathy. Along with dystrophic calcium deposition in dying cells and lipoprotein deposits, active endochondral and intramembranous (nonendochondral) ossification processes contribute to vascular calcium load. Thus vascular calcification is subject to regulation by osteotropic hormones and skeletal morphogens in addition to key inhibitors of passive tissue mineralization. In response to oxidized lipids, inflammation, and mechanical injury, the microvascular smooth muscle cell becomes activated. Orthotopically, proliferating stromal myofibroblasts provide osteoprogenitors for skeletal growth and fracture repair; however, in valves and arteries, vascular myofibroblasts contribute to cardiovascular ossification. Current data suggest that paracrine signals are provided by bone morphogenetic protein-2, Wnts, parathyroid hormone-related polypeptide, osteopontin, osteoprotegerin, and matrix Gla protein, all entrained to endocrine, metabolic, inflammatory, and mechanical cues. In end-stage renal disease, a “perfect storm” of vascular calcification often occurs, with hyperglycemia, hyperphosphatemia, hypercholesterolemia, hypertension, parathyroid hormone resistance, and iatrogenic calcitriol excess contributing to severe calcific vasculopathy. This brief review recounts emerging themes in the pathobiology of vascular calcification and highlights some fundamental deficiencies in our understanding of vascular endocrinology and metabolism that are immediately relevant to human health and health care.

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Sakata, Noriyuki, Kazuma Takeuchi, Keita Noda, Keijiro Saku, Yutaka Tachikawa, Tadashi Tashiro, Ryoji Nagai, and Seikoh Horiuchi. "Calcification of the Medial Layer of the Internal Thoracic Artery in Diabetic Patients: Relevance of Glycoxidation." Journal of Vascular Research 40, no. 6 (2003): 567–74. http://dx.doi.org/10.1159/000075807.

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Lin, Tonghui, Xue-Lin Wang, Sara L. Zettervall, Yujun Cai, and Raul J. Guzman. "Dorsomorphin homologue 1, a highly selective small-molecule bone morphogenetic protein inhibitor, suppresses medial artery calcification." Journal of Vascular Surgery 66, no. 2 (August 2017): 586–93. http://dx.doi.org/10.1016/j.jvs.2016.03.462.

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Dayo, A., D. Miles, and P. Corby. "IDF23-0563 Medial Arterial Calcification of the Internal Carotid Artery: A Sensitive Radiographic Marker for Diabetes." Diabetes Research and Clinical Practice 209 (March 2024): 111543. http://dx.doi.org/10.1016/j.diabres.2024.111543.

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Gandini, Roberto, Stefano Merolla, Jacopo Scaggiante, Marco Meloni, Laura Giurato, Luigi Uccioli, and Daniel Konda. "Endovascular Distal Plantar Vein Arterialization in Dialysis Patients With No-Option Critical Limb Ischemia and Posterior Tibial Artery Occlusion: A Technique for Limb Salvage in a Challenging Patient Subset." Journal of Endovascular Therapy 25, no. 1 (December 21, 2017): 127–32. http://dx.doi.org/10.1177/1526602817750211.

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Purpose: To detail a percutaneous technique for distal plantar venous arterialization in diabetic, end-stage renal disease (ESRD) patients with no-option critical limb ischemia (CLI). Technique: After failure of standard intraluminal recanalization attempts, a subintimal approach through the posterior tibial artery (PTA) is begun using a 0.014-inch, 190- or 300-cm-long guidewire supported by a 2-×20-mm, low-profile balloon catheter positioned a short distance behind the narrow “U-shaped” loop in the guidewire. Typically, heavy calcification in the distal tortuous segment of the PTA prevents reentry to the arterial true lumen; however, an entry in the distal lateral or medial plantar vein from a subintimal channel in the plantar artery can be intentionally pursued as a bailout technique, pointing the tip of the guidewire opposite to the arterial wall calcifications. Venous access is confirmed by contrast injection through the balloon catheter. Once the guidewire is advanced in the distal lateral or medial plantar vein and a plantar arteriovenous fistula (AVF) has been created, the AV anastomosis and the occluded PTA segment are dilated with 0.014-inch balloon catheters. The technique has been attempted in 9 consecutive diabetic, ESRD patients (mean age 69 years; 5 men) with no-option CLI; an AVF was created between the PTA and plantar vein in 7 patients. The mean TcPO2 at 1 month was 30±17 mm Hg (vs 7.3±2.2 at baseline). Six ulcers healed over an average of 21±4 weeks. Three of the 9 patients had below-knee amputations. Conclusion: Although further investigations are required, distal plantar venous arterialization may represent a promising technique to improve recanalization rates and limb salvage in diabetic ESRD patients with extremely calcified PTA occlusions.

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Molostvov, Guerman, Sean James, Simon Fletcher, Jeanette Bennett, Hendrik Lehnert, Rosemary Bland, and Daniel Zehnder. "Extracellular calcium-sensing receptor is functionally expressed in human artery." American Journal of Physiology-Renal Physiology 293, no. 3 (September 2007): F946—F955. http://dx.doi.org/10.1152/ajprenal.00474.2006.

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Accelerated medial calcification is a major cause of premature cardiovascular mortality in patients with chronic kidney disease (CKD). Evidence suggests that extracellular concentration of Ca2+ and vascular smooth muscle cells may play a pivotal role in the pathogenesis of vascular calcification. The calcium-sensing receptor (CaSR) is a G protein-coupled receptor that is expressed in a range of tissues, but characterization of its expression and function in the cardiovascular system is limited. Here we report the expression of CaSR mRNA (RT-PCR) and protein (Western blotting and immunocytochemistry) in human aortic smooth muscle cells (HAoSMC). Treatment of HAoSMC with Ca2+ (0–5 mM; 0–30 min) or the CaSR agonists gentamycin and neomycin (0–300 μM; 0–30 min) resulted in a dose- and time-dependent phosphorylation of ERK1/2. Gentamycin- and neomycin-mediated ERK1/2 stimulation was inhibited by pretreatment with PD-98059, an ERK-activating kinase 1 (MEK1) inhibitor, confirming specificity of the observed effects. ERK1/2 activation was inhibited in HAoSMC, with CaSR expression knocked down by transfection with specific small-interference RNA, which confirmed that the observed neomycin/gentamycin-induced MEK1/ERK1/2 activation was mediated via the CaSR. CaSR mRNA and protein were also expressed in large and small arteries from normal subjects (kidney donors) and patients with end-stage renal disease (ESRD). The CaSR was detected in smooth muscle and endothelial cells. Expression was significantly lower in arteries from ESRD patients. In conclusion, these data not only demonstrate the presence of a functional CaSR in human artery but show a correlation between CaSR expression and progression of CKD.

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Antonova, Larisa, Anton Kutikhin, Viktoriia Sevostianova, Arseniy Lobov, Egor Repkin, Evgenia Krivkina, Elena Velikanova, et al. "Controlled and Synchronised Vascular Regeneration upon the Implantation of Iloprost- and Cationic Amphiphilic Drugs-Conjugated Tissue-Engineered Vascular Grafts into the Ovine Carotid Artery: A Proteomics-Empowered Study." Polymers 14, no. 23 (November 26, 2022): 5149. http://dx.doi.org/10.3390/polym14235149.

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Implementation of small-diameter tissue-engineered vascular grafts (TEVGs) into clinical practice is still delayed due to the frequent complications, including thrombosis, aneurysms, neointimal hyperplasia, calcification, atherosclerosis, and infection. Here, we conjugated a vasodilator/platelet inhibitor, iloprost, and an antimicrobial cationic amphiphilic drug, 1,5-bis-(4-tetradecyl-1,4-diazoniabicyclo [2.2.2]octan-1-yl) pentane tetrabromide, to the luminal surface of electrospun poly(ε-caprolactone) (PCL) TEVGs for preventing thrombosis and infection, additionally enveloped such TEVGs into the PCL sheath to preclude aneurysms, and implanted PCLIlo/CAD TEVGs into the ovine carotid artery (n = 12) for 6 months. The primary patency was 50% (6/12 animals). TEVGs were completely replaced with the vascular tissue, free from aneurysms, calcification, atherosclerosis and infection, completely endothelialised, and had clearly distinguishable medial and adventitial layers. Comparative proteomic profiling of TEVGs and contralateral carotid arteries found that TEVGs lacked contractile vascular smooth muscle cell markers, basement membrane components, and proteins mediating antioxidant defense, concurrently showing the protein signatures of upregulated protein synthesis, folding and assembly, enhanced energy metabolism, and macrophage-driven inflammation. Collectively, these results suggested a synchronised replacement of PCL with a newly formed vascular tissue but insufficient compliance of PCLIlo/CAD TEVGs, demanding their testing in the muscular artery position or stimulation of vascular smooth muscle cell specification after the implantation.

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Paulson, William D. "Does Vascular Elasticity Affect Arteriovenous Fistula Maturation?" Open Urology & Nephrology Journal 7, no. 1 (May 30, 2014): 26–32. http://dx.doi.org/10.2174/1874303x01407010026.

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The vasculopathy of ESRD affects both arteries and veins. The arteries develop arteriosclerosis, which is largely a disease of the media characterized by increased collagen content, calcification, and both hypertrophy and hyperplasia of vascular smooth muscle cells. Veins may exhibit increased width of the intimal and medial layers, and may develop neointimal hyperplasia and calcification. Successful fistula maturation depends upon dilatation and remodeling of the artery and vein, but the stiff and thickened vessels of ESRD patients may respond poorly to signals that promote these adaptations. There is intense interest in accurately predicting fistula maturation outcome and preventing maturation failure. However, definitive criteria for preoperative testing of vessel elasticity have not yet been established. Tests that are adopted for widespread clinical use will need to be easy to apply - a standard that many of these tests may not meet. Finally, effective treatments are needed that prevent or reduce the stiffness of vessels. In conclusion, although there are many promising developments in this emerging field, effective methods of predicting fistula maturation outcome and preventing maturation failure remain to be established.

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Van Berkel, Brecht, Chantal Van Ongeval, Amaryllis H. Van Craenenbroeck, Hans Pottel, Katrien De Vusser, and Pieter Evenepoel. "Prevalence, progression and implications of breast artery calcification in patients with chronic kidney disease." Clinical Kidney Journal 15, no. 2 (October 5, 2021): 295–302. http://dx.doi.org/10.1093/ckj/sfab178.

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ABSTRACT Breast arterial calcification (BAC) is increasingly recognized as a specific marker of medial calcification. The present retrospective observational cohort study aimed to define the prevalence, progression rate, risk factors and clinical implications of BAC in chronic kidney disease (CKD) patients across stages of disease. The presence and extent of BAC were determined on mammograms in 310 females (58.7 ± 10.8 years, Caucasian) with CKD across various stages of disease [CKD G2–5D n = 132; transplant (Tx) recipients n = 178]. In a subset of 88 patients, repeat mammography was performed, allowing us to calculate the annualized BAC rate. Overall, BAC was observed in 34.7% of the patients. BAC prevalence (P = 0.02) and BAC score (P = 0.05) increased along the progression of CKD. In the overall cohort, patients with BAC were characterized by older age, more cardiovascular disease, more inflammation, higher pulse pressure and borderline higher prevalence of diabetes and were more often treated with a vitamin K antagonist (VKA). The BAC progression rate was significantly lower in Tx patients as compared with CKD G5D. Progressors were characterized by more inflammation, worse kidney function, higher BAC score and higher serum phosphate level (Tx only) at baseline and were more often treated with a VKA. Major adverse cardiovascular event-free survival was significantly worse in Tx patients with BAC. In conclusion, BAC is common among CKD patients, progresses at a slower pace in Tx patients as compared with CKD 5D and associates with dismal cardiovascular outcomes. BAC score, kidney function, serum phosphate at baseline and VKA usage seem to be important determinants of progression.

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Krzanowski, Marcin, Katarzyna Krzanowska, Mariusz Gajda, Paulina Dumnicka, Danuta Fedak, Przemysław Miarka, Ireneusz Kaczmarczyk, Jan A. Litwin, and Władysław Sułowicz. "FP642OSTEOPROTEGERIN AS A VASCULAR RISK FACTOR: FOR RADIAL MEDIAL ARTERY CALCIFICATION AND DEVELOPMENT OF ATHEROSLEROSIS IN CKD PATIENTS." Nephrology Dialysis Transplantation 30, suppl_3 (May 2015): iii288. http://dx.doi.org/10.1093/ndt/gfv181.35.

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Journal articles on the topic 'Medial artery calcification'

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