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This chapter is devoted to the macroscopic and microscopic appearance of myocardial ischaemia and includes discussion of regional myocardial infarction and of papillary muscle rupture. Coronary atherosclerosis can occur, albeit rarely, in the child, and this is discussed particularly in relation to hypercholesterolaemia. Antiphospholipid syndrome and haemolytic-uraemic syndrome are also discussed.
Reef encrusting calcifiers (non-scleractinian species) constitute assemblages that participate in the carbon cycle at coral reefs. Despite their apparent secondary role in building the reef framework, they contribute to the reef consolidation binding sediments and inducing larval recruitment from other epilithic invertebrates. The contribution of encrusting calcifiers on reef accretion was examined by the assessment of their rate of carbonate deposition on four different simulated reef microhabitats using calcification accretion units (CAUs) during 12 months at Playa Las Gatas and Islote Zacatoso, two coral communities from the coast of the Mexican Pacific. Encrusting calcifiers from Playa Las Gatas, the most impacted site, showed a rate of carbonate deposition (mean ± SD) four times higher than at Islote Zacatoso (10.02 ± 3.22 g CaCO3 m−2 d−1vs 2.48 ± 1.01 g CaCO3 m−2 d−1). Overall, the rate of carbonate deposition on surfaces protected from sedimentation and light was up to 1.8 times higher than on exposed ones (11.40 ± 4.35 g CaCO3 m−2 d−1vs 6.18 ± 3.13 g CaCO3 m−2 d−1). Carbonate deposition by calcareous algae was higher on the well-lit exposed surfaces while filter-feeding invertebrates showed the major contribution on the shaded cryptic surfaces. Although rate of carbonate deposition by encrusting calcifiers seems to be lower than hermatypic corals, it seems to be relevant on coral reefs affected by anthropogenic impacts where coral calcification is low. Under global demise of coral reefs by environmental degradation and climate change, encrusting calcifiers may become relevant for the process of carbonate deposition.
Valvular heart diseases lead to over 300,000 heart valve replacements worldwide each year. Bioprosthetic heart valves (BHVs), derived from glutaraldehyde (GLUT) crosslinked porcine or bovine pericardium, are often used. However, valve failure can occur within 12–15 years due to progressive degradation and/or calcification. Being innovated by previous amino reagent studies used for GLUT detoxification and carbodiimide [1-ethyl-3-(3-dimethylaminopropyl)carbodiimide, EDC] chemistry, in this study, we developed a new fabrication method that utilizes exogenous amino donor arginine or lysine carbodiimide combined treatments to better stabilize the extracellular matrix of porcine pericardium. The carboxyl group density, amine content, differential scanning calorimetry, collagenase and elastase degradation, calcification by rat subdermal implantation, cytotoxicity, and platelet adhesion were characterized. We demonstrated that exogenous amino donor carbodiimide combined treatment for pericardiums had better resistance to elastase degradation (1.63 ± 0.11% and 1.44 ± 0.24% in arginine or lysine versus 3.68 ± 0.16% and 3.04 ± 0.11% in GLUT and GLUT/EDC control) and calcification (0.624 ± 0.193 and 0.637 ± 0.213 Ca µg/mg tissue in arginine or lysine versus 1.610 ± 0.124 and 1.512 ± 0.075 Ca µg/mg tissue in GLUT and GLUT/EDC control). This new strategy combined arginine or lysine and carbodiimide crosslinking would be a promising method to produce more robust BHVs with better structural stability and anticalcification property.
Echinoderms are vulnerable to ocean acidification because of their high magnesium calcite skeletons. Here, skeletal Mg/Ca ratios were examined within and between individuals of 20 Antarctic echinoderms representative of the asteroids, ophiuroids and echinoids. The highest mean Mg/Ca ratios occurred in the discs and arms (0.111 and 0.110, respectively) of brittle-stars and the lowest in the spines (0.010) of cidaroid sea urchins. Many taxa (11 of 14 species) from the collection sites showed no intraspecific differences in Mg/Ca ratios between given skeletal components. Exceptions were the spines of two regular sea urchins and the skeletal ossicles of the combined arms and disc of a brittle-star. The relationship between skeletal magnesium content and latitude was further evaluated and an inverse correlation was found between Antarctic echinoderm taxa skeletal magnesium content and latitude across 62° to 76°, indicating that the relationship occurs over relatively narrow latitudes. Upon examination of an even narrower range (70–76° latitude), a region where the mineralogy of echinoderm skeletons has not been investigated, the predicted inverse relationship between Mg/Ca ratio and latitude was still observed in sea-stars, but not in brittle-stars or sea urchins.
Over the past few decades, remarkable progress has been achieved in terms of understanding the molecular and cellular mechanisms of atherosclerotic vascular calcification and the important role of matrix vesicles in initiating and propagating pathologic tissue mineralization has been widely recognized. Despite these recent advances, however, no definitive data are currently available regarding the texture and composition of the minerals that grow in the vessel wall during the course of the disease. Using different electron microscopy imaging and analysis, we demonstrate that vascular cells can produce and secrete more than one type of matrix vesicles which act as sites for initial mineral deposition independently of their structural features. Our results reveal that apatite formation in the atherosclerotic lesions of the human aorta occur through the deposition of amorphous calcium phosphate that matures over time, transforms into crystalline hydroxyapatite, and radiates towards the lumen of the vesicles, finally forming the calcified spherules. Elemental and mineralogical analyses also demonstrate that the presence of mature and stable amorphous calcium phosphate deposits in the affected tissues is linked to the incorporation of magnesium, which probably delay the conversion to the crystalline phase. Though more rarely, the presence of calcium oxalate crystals has been also documented.
Fetal hepatic calcifications can be caused by infections, chromosomal disorders, thrombotic events, ischemic hepatic necrosis and subcapsular hematomas among others events. Its features and clinical significance are still not well known. We performed an observational study to describe fetal hepatic calcifications and its association with main clinical and histopathological findings from the fetal autopsy database, between 2007 and 2014. Raw odds ratio analysis was performed. We reviewed 591 fetal autopsies: 14 cases with hepatic calcifications, 102 fetuses with chromosomal disorders; 13 with diagnosis of TORSCH (toxoplasma, rubella, syphilis, cytomegalovirus, herpes virus 1 and 2, and others) and 207 with any abnormality in the umbilical cord (UC). The relation between hepatic calcifications and chromosomal disorders in our series had significance. It is known that hepatic calcifications are common in chromosomal disorders, transplacental infections and UC abnormalities, those conditions are risk factor for hepatic calcifications formation; we suggest hepatic calcifications should alert the pathologists in order to consider these etiologies in first instance.
Equol, a metabolite of the dietary isoflavone daidzein, is produced by the action of gut bacteria in some individuals who are termed as equol-producers. It is proposed to have stronger atheroprotective properties than dietary isoflavones. We examined a cross-sectional association of dietary isoflavones and equol-producer status with coronary artery calcification (CAC), a biomarker of coronary atherosclerosis, among men in Japan. A population-based sample of 272 Japanese men aged 40–49 years recruited from 2004 to 2007 was examined for serum isoflavones, serum equol, CAC and other factors. Equol-producers were classified as individuals having a serum level of equol >83 nm. The presence of CAC was defined as a coronary Ca score ≥10 Agatston units. The associations of dietary isoflavones and equol-producers with CAC were analysed using multiple logistic regression. The median of dietary isoflavones, equol and CAC were 512·7 (interquartile range (IQR) 194·1, 1170·0), 9·1 (IQR 0·10, 33·1) and 0·0 (IQR 0·0, 1·0) nm, respectively. Prevalence of CAC and equol-producers was 9·6 and 16·0 %, respectively. Dietary isoflavones were not significantly associated with CAC. After multivariable adjustment, the OR for the presence of CAC in equol-producers compared with equol non-producers was 0·10 (95 % CI 0·01, 0·90, P<0·04). Equol-producers had significantly lower CAC than equol non-producers, but there was no significant association between dietary isoflavones and CAC, suggesting that equol may be a key factor for atheroprotective properties of isoflavones in Japanese men. This finding must be confirmed in larger studies or clinical trials of equol that is now available as a dietary supplement.
Vitamin K is considered to be involved in the pathological mechanisms of coronary artery calcification (CAC). Correlation between CAC and plasma vitamin K levels was studied. A total of 103 patients, with at least one coronary risk factor, were studied. CAC was measured using 64-slice multislice computed tomography (MSCT) and divided into three groups: none (CAC score = 0; n 25), mild to moderate (0 < CAC score < 400; n 52) and severe (CAC score > 400; n 26). Phylloquinone (PK) and menaquinone (MK)-4 and MK-7 were measured by HPLC-tandem MS. Mean age of patients was 64 (sd 13) years, of which 57 % were male. Median CAC score was 57·2. Median levels of PK, MK-4 and MK-7 were 1·33, 0 and 6·99 ng/ml, showing that MK-7 was the dominant vitamin K in this population. MK-7 showed a significant inverse correlation with uncarboxylated osteocalcin (ucOC, P = 0·014), protein induced by vitamin K absence of antagonist-2 (PIVKA-2, P = 0·013), intact parathyroid hormone (P = 0·007) and bone-specific alkaline phosphatase (P = 0·018). CAC showed an inverse correlation with total circulating uncarboxylated matrix Gla protein (t-ucMGP, P = 0·018) and Hb (P = 0·05), and a positive correlation with age (P < 0·001), creatinine, collagen type 1 cross-linked N-terminal telopeptide (NTX, P = 0·03), pulse wave velocity (P < 0·001) and osteoprotegerin (P < 0·001). However, CAC did not have a significant correlation with plasma levels of PK, MK-4 or MK-7. In conclusion, plasma MK-7, MK-4 or PK level did not show significant correlation with CAC despite the association between plasma vitamin K levels and vitamin K-dependent proteins such as ucOC or PIVKA-2.
Pulmonary artery, and rarely aortic, calcifications have been reported in sporadic case reports in the recipient twin of twin-to-twin transfusion syndrome. This presentation is more likely to be secondary to the haemodynamic alterations in the recipient twin, but must be differentiated from idiopathic infantile arterial calcification as the clinical implications, treatment, and prognosis may be drastically different.
Calcification in cardiovascular aortic atherosclerotic plaque contains Ca-phosphate minerals. However, most research on cardiovascular calcification has focused on its physiological properties rather than its mineralogical features. In this present study, cardiovascular calcification was characterized by collecting samples from patients’ tissues and applying mineralogical techniques. Synchrotron radiation-based micro-X-ray diffraction showed the calcification had a similar structure to hydroxylapatite (HAp). Transmission electron microscopy showed some structurally HAp-like spherical particles with a diameter of ∼200 nm and acicular crystals ∼100 nm × ∼20 nm in size. Selected-area electron diffraction indicated that these mineral particles belonged to the hexagonal crystal system. Fourier-transform infrared (FTIR) spectroscopy showed three typical peaks at 1469 cm−1, 1455 cm−1 and 1413 cm−1, indicating that the carbonate group in the calcification plaque substituted for a hydroxyl group to form B-type CHAp (Ca10(PO4,CO3)x(OH)y). The FTIR mapping results illustrated the intergrowth of calcification and organic tissues and the inhomogeneous substitution of phosphate by carbonate in the calcification area. X-ray absorption near-edge structure analysis affirmed that the chemical environments of Ca in the calcification were close to those in HAp. Based on these mineralogical characteristics, the calcification in plaque is identified as a mixture phase of HAp and B-type carbonate HAp, which is similar to the composition of bones.
A laboratory-scale X-ray diffractometer for obtaining high X-ray intensity data was developed. The apparatus, equipped with 600 W CuKα radiation with a Ni filter, incorporates technology that dramatically improves the quality of X-ray diffraction. The system comprises of a low-noise one-dimensional silicon strip detector, a variable slit, and a goniometer with a radius as small as 150 mm. A variable knife edge was used as a countermeasure for unwanted scattering, particularly in the low angle range. With this system, cement may be analyzed within 5 min. NIST 2686 standard reference material was analyzed using the newly developed diffractometer, and the quantitative analysis results for the major phases are in agreement with the certified values of the reference material.
Information about acute coronary syndrome caused by Kawasaki disease-related coronary artery lesions in adults is sketchy. We reviewed the clinical features of 50 adult patients who had an acute coronary syndrome caused by coronary artery lesions due to Kawasaki disease or probable Kawasaki disease from 1980 to 2008. Of the 50 patients, 43 (90%) were male and seven were female (10%). Their ages at the onset of acute coronary syndrome ranged from 18 to 69 years, with a median of 28 years. The culprit lesion in 43 patients was thrombotic occlusion of an aneurysm, and 40 patients had giant aneurysms. In the three patients in whom no aneurysms were seen in coronary angiograms performed at the time of acute myocardial infarction, either giant aneurysms or aneurysms had been visualised in childhood. The initial treatment of acute coronary syndrome was as follows: intracoronary thrombolysis, 11; primary percutaneous coronary intervention, 9; emergency coronary artery bypass grafting, 3; and medication, 26. Elective coronary artery bypass grafting was performed in 15 patients. Three patients (6%) died. Of the 27 patients with additional coronary risk factors, 20 were smokers. Giant aneurysms due to Kawasaki disease continued to cause acute coronary syndrome in adult life with onset at a younger age than typifies that due to atherosclerosis in the general population, especially in male population rather than female population. Even when giant aneurysms regressed after the acute phase, a few patients still developed acute coronary syndrome in adult life. Smoking appears to be the most prominent additional risk factor.
This chapter deals with mitral valve (MV) disease. Mitral stenosis is obstruction of left ventricular inflow at the level of the MV, as a result of structural abnormalities of the MV apparatus that limit proper opening during diastole. Mitral annular calcification is a degenerative process, and is a common incidental finding in the elderly. Rheumatic carditis is the commonest cause of mitral stenosis in both developed and developing countries. Mitral regurgitation (MR) is the most commonly encountered valvular lesion in modern clinical practice. Primary MV prolapse syndrome (MVPS) refers to a disease spectrum with frank myxomatous degeneration at one extreme. The transesophageal echocardiography (TEE) variables used in the assessment of MR severity can be classified as semi-quantitative or quantitative. The vena contracta (VC) refers to the narrowest portion or neck of the regurgitant jet, which occurs at or just beyond the regurgitant orifice.
Scleroderma (progressive systemic sclerosis) is a multisystem connective tissue disorder characterized by inflammation, fibrosis, and vasculopathy of affected tissues. CNS vasculitis, segmental vasospasm, and cerebrovascular calcifications may all play a role in causing strokes in patients with scleroderma. CNS vasculitis has been diagnosed in several patients with scleroderma and has been posited to cause strokes. Cerebral infarction in scleroderma patients in the absence of other plausible, causative factors should prompt an aggressive workup for vasculitis including angiography. Results of cerebral angiography in several patients thought to have vasculitis are consistent with the diagnosis of vasoconstriction. Arteriography revealed segmental, often smoothly contoured, narrowing of arteries of multiple sizes (small, medium, and large) in both the anterior and posterior circulations. Whether vascular calcium deposits were responsible for the patients' cerebrovascular symptoms is speculative. Scleroderma patients with cerebrovascular disease must take into consideration the potential causes of stroke.
Cogan's syndrome is characterized by nonsyphilitic interstitial keratitis, vestibulo-auditory Menière-like symptoms, and, occasionally, systemic manifestations of vasculitis. Although neurologic manifestations are rare, several patients with stroke in the setting of Cogan's syndrome have been reported. The most common and classic ocular manifestation of Cogan's syndrome is bilateral interstitial keratitis. The diagnosis is classically suggested by the association of interstitial keratitis with acute-onset sensorineuronal hearing loss in a patient who has a negative laboratory evaluation for syphilis. Computed tomography (CT) scans may occasionally show intralabyrinthine calcifications, whereas magnetic resonance imaging (MRIs) often show soft tissue obliteration of the membranous labyrinth and may also show multiple lesions of the white matter consistent with cerebral vasculitis. The treatment of Cogan's syndrome varies based on the severity of the clinical manifestations. Due to the presumed autoimmune mechanism with vasculitis, most treatments have included steroids and immunosuppressants.
This chapter introduces the state-of-the-art noninvasive magnetic resonance imaging (MRI) techniques that are used to monitor atherosclerosis of the carotid artery. High-resolution MRI is an ideal plaque imaging technique because it is noninvasive and able to create excellent soft tissue contrast and distinguish flowing blood from surrounding stationary tissues. Multicontrast weighted imaging protocol provides an oblique view of the carotid artery to better visualize the location of the carotid bifurcation and to demonstrate plaque distribution. The objective of the American Heart Association (AHA) histological classification of atherosclerosis, first published in 1995, was to provide a clinically relevant categorization of human atherosclerotic lesions based on their histological composition and structure. Major plaque components include fibrous connective tissue, the lipid-rich necrotic core, intraplaque hemorrhage, and calcification. MRI is capable of identifying many of the key vulnerable plaque features defined by the expert panel with a high level of accuracy and reproducibility.
This chapter focuses on the role of depression in the development of coronary atherosclerosis and in the aetiology of coronary heart disease (CHD). It evaluates the strength and consistency of the association between depression and future CHD and describes the biological processes that are probably involved. The chapter reviews the existing evidence from longitudinal observational studies that depression and depressive symptoms are associated prospectively with CHD in initially healthy adults. Three studies have used computed tomography (CT) to assess coronary artery calcification, a more direct measure than carotid thickness of the intima-medial layer (IMT) of coronary disease. The chapter outlines the different pathways that may translate depressive emotional experience into CHD. A number of behavioural factors contribute to CHD, including cigarette smoking, certain patterns of alcohol consumption, eating behaviour and physical activity. It is known that psychological stress provokes acute haemostatic responses in healthy individuals and in patients with CHD.
A 54-year-old man complained of severe throat pain and showed subglottic oedema on fibre-optic endoscopy with a distinctly narrowed subglottic space on anteroposterior radiography of the neck and dense linear opacity at the level of the cricoid cartilage on lateral plain radiography. These findings suggested a foreign body just posterior to the cricopharyngeus, but a computed tomography (CT) scan demonstrated a dense calcified ridge on the posterior lamina of the cricoid cartilage but no foreign body.
The patient improved symptomatically with systemic antibiotics and topical steroids, and gastrointestinal endoscopy did not detect any foreign body. This is a rare case of vertical ossification of the cricoid lamina masquerading as a foreign body.