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PubMed1987

Calcification of the driving diaphragm in a total artificial heart.

The implications of mineralization on the diaphragm of a TAH were highlighted. The problem was discussed from the point of view of time and site of calcifying deposit formation, and individual patterns of calcification as well as the question of the relationship between mineralization processes and thrombogenicity were considered. Attention was likewise given to actual calcification with regard to its mechanism, and to the risks that the calcification process in an artificial heart pose to the organism. Next, the options to prevent mineralization were reviewed. The issue as analysed especially on the basis of results obtained in the Centre of the State Research project called "Assistance and Replacement of the Heart", Regional Institute of National Health in Brno, Department of Pathological Physiology. It was pointed out that diaphragm calcification can compromise the life of an individual after many years of surviving with an artificial heart. Still, the risk is zero within the first two or three months following artificial heart implantation. The fact was underlined that the last model of a Czechoslovak-made artificial heart, called TNS Brno VII, re-designed in an effort to prevent the breaking away of calcified microemboli from the diaphragm, features optimal athrombogenity. Thus, the clinical version of this brand-new Czechoslovak TAH can be regarded as the best model of an artificial heart to be implanted as a life-saving measure tiding the patient over a period before a cardiac transplantation can be performed.

Animals↗
PubMed1977

Resolution of breast pain and calcification with renal transplantation.

Vascular calcification in chronic renal failure and dialysis patients is well-documented and generally considered to be a consequence of decreased phosphorus excretion, secondary hyperparathyroidism, and increased calcium-phosphorus product. Following renal transplantation or parathyroidectomy, gradual resolution of metastatic calcification in the affected areas occurs. The case presented documents the consequence of secondary hyperparathyroidism with calcification of mammary vessels leading to severe breast pain with resolution of the pain and vessel calcification after renal transplantation.

Breast↗
PubMedDate not supplied

[Echocardiographic diagnosis of pulmonary valve calcification].

Calcification of the pulmonary valve is a uncommon condition. Non invasive diagnostic methods such as M-mode and two dimensional echocardiography have facilitated the identification of vegetations and calcifications on the pulmonary valve. Very few cases of isolated calcification on the pulmonary valve have been reported; a previous lesion of the valve almost always exists. The purpose of this communication is to report two cases with calcification of pulmonary valves without underlying pathology and to highlight the great utility of echocardiography in diagnosis and follow-up of such cases.

Adolescent↗
PubMed1988

[Idiopathic laryngotracheobronchial calcifications in children. Apropos of 2 cases].

Calcifications of cartilage in the larynx, trachea and bronchi are rare in children. Two cases reported and listed with 5 similar cases of the literature. Such calcifications are generally discovered in young children and congenital stridor is commonly associated with. Calcifications of bronchi are not present in every case. The blood calcium is normal. Laryngoscopic examination shows in two cases a laryngeal stiffness. The prognosis is good. In two cases, one of the parents of under 40 years old, also had calcifications of the trachea and of the bronchi.

Adolescent↗
PubMed1988

Celiac disease associated with epilepsy and intracranial calcifications: report of two patients.

We describe two young adult patients with seizures and cerebral calcifications since childhood, diagnosed as Sturge Weber syndrome, who also had gluten enteropathy. Although the calcifications were located in regions similar to calcifications of Sturge Weber cases, many of the features of the syndrome were absent, and this diagnosis seems improbable. Whereas a coincidental involvement cannot be excluded, attention is drawn to this association between celiac disease and seizures with intracranial calcifications mimicking a Sturge Weber syndrome. After a gluten-free diet, antiepileptic therapy could be reduced in our patients.

Adolescent↗
PubMed1986

[A case of multilocular renal cyst with calcification].

A 55-year-old woman was incidentally found to have a calcified right renal mass on ultrasonography. A plain film of the abdomen revealed a 3.5 X 4.4 cm, curvilinear calcification in the midportion of the right kidney, and an excretory urogram showed no compression or distortion of the pelvocalyceal system. Computed tomography demonstrated a low density renal mass associated with both peripheral and central calcification. Renal arteriogram revealed a hypovascular mass. Right nephrectomy was performed and the multilocular renal cyst with calcification was confirmed histologically. In the Japanese literature, 53 cases of multilocular renal cyst have been reported, but calcification of the multilocular renal cyst seems to be the first as far as we know.

Angiography↗
PubMed1987

[Arterial calcifications of the hand: normal aging and the course in chronic dialysis patients].

Normally, arterial calcifications in the hand progress from proximal to distal and do not reach the fingers by the 8th decade. In patients on maintenance dialysis arterial calcifications begin earlier and do not progress with age. The most severe arterial calcifications occur in patients with renal failure caused by diabetic nephropathy. Prognostically arterial calcifications in the finger-metacarpal region are an unfavourable sign.

Adult↗
PubMed1987

Hepatic calcification in the course of hemodialysis.

Hepatocellular calcification is extremely rare and only one case has been recorded in the literature. The patient, a 74-yr-old Japanese woman, received hemodialysis for 5 months because of uremia due to chronic glomerulonephritis. Four months before death, she was once in a state of shock which lasted for 4 h due to massive hemorrhage from the shunt vein for hemodialysis. She died of disseminated intravascular coagulopathy and respiratory failure due to uremia. Postmortem liver biopsy showed centri- and midzonal necrosis associated with septal fibrosis where intracellular and extracellular calcification were noted. The calcifications were round or rod shaped and single or multiple in distribution. The calcification was thought to occur as the result of shock, which caused hepatocellular damage, due to consumption of a high calcium-phosphorus product.

Aged↗
PubMed1986

[Conduction disorders and sites of calcification of the mitral ring: 2-dimensional echocardiographic study].

The association between a calcified mitral annulus and impairment of cardiac impulse transmission is well known. However informations on the relations between the site of mitral calcification and conduction disturbance are still scanty. Twenty-nine patients (22 women and 7 men, mean age 64.4 +/- 13.1 years) with M-mode and two-dimensional echocardiographic evidence of mitral annulus calcifications were studied. The "annulus" was subdivided in 4 segments: antero-medial, antero-lateral, postero-medial and postero-lateral. Conduction disturbances were present in 15 patients (51.7%). Atrio-ventricular or intra-ventricular conduction defects were found in 12 out of 15 patients with calcifications of the antero-medial segment and only in 3 of 14 subjects without antero-medial calcifications (P less than .01). The presence of conduction defects therefore seems to be significantly increased when calcium deposition is located near the conduction system.

Adult↗
PubMed1985

Idiopathic arterial calcification of infancy in newborn siblings with unusual light and electron microscopic manifestations.

We report two cases of idiopathic arterial calcification of infancy (IACI) occurring in newborn siblings. Unusual gross and light microscopic findings included calcification of multiple nonarterial tissues, renal infarction, and macroscopic aortic involvement. One case manifested an extensive acute panarteritis suggesting that IACI may be the result of an inflammatory or infectious process. Ultrastructural examination confirmed that the mineral deposits were hydroxyapatite and also indicated that they contained iron. Calcified tissue components included smooth-muscle cells, fibroblasts, and collagen fibers, as well as elastic fibers. No matrix vesicles or mitochondrial calcifications that may serve as nucleation sites for crystalline calcium phosphate were identified. Thus, the mechanism of calcification in IACI may be unique, and may relate to altered iron metabolism.

Adipose Tissue↗
PubMed1985

[Mitral valvular disease secondary to mitral ring calcification: a clinicopathologic study].

Fifteen cases with mitral valvular disease caused by mitral ring calcification (MRC) were observed among 2,800 consecutive autopsy patients more than 60 years of age. They consisted of one man and 14 women whose average age was 86.4 years. All had been diagnosed as having mitral valvular disease during life. For this clinicopathologic study, the cases were categorized as nine cases with mitral regurgitation (MR Group) and six with mitral stenosis (MS Group). Among the 15 cases, phonocardiograms were obtained in 14 and echocardiograms in 6. In addition, 122 cases with MRC, the length of which was 5 mm or more, were selected from 900 recent consecutive autopsies of senile patients, to evaluate the site of calcification and to analyze the ratio of calcification length to mitral valve ring circumference. The following conclusions were obtained: The prevalence of mitral valvular disease due to MRC in the aged was 15/2,800 (0.5%). MR was observed in nine cases and MS in six. Phonocardiograms of the MR Group revealed a holosystolic murmur in seven cases, a late systolic murmur in one, a third heart sound in four and a fourth heart sound in five. In the MS Group, a holosystolic murmur was found in four, a presystolic murmur in four, a diastolic rumble in one, but no opening snap in any case. A diamond-shaped systolic murmur was found in nine cases with MS or MR, suggesting an ejection systolic murmur caused by an associated calcified aortic valve. Echocardiograms showed markedly decreased DDR in five cases and increased echo intensity of the aortic valve in four. Pathologic findings revealed that the mean length of MRC was 36.6 mm in the MR Group and 58.0 mm in the MS Group. The calcification ring ratio (CRR = MRC/MVR X 100) was 50.3% in the MR Group and 69.8% in the MS Group. In the MR Group, MRC involved the anterolateral commissure in three, posteromedial commissure in five, and both in one. In five of six cases with MS, both commissures were involved by MRC. The study of 122 cases with MRC length greater than or equal to 5 mm suggested that MRC occurred first in the middle scallop of the posterior mitral leaflet, and extended to the posterior scallop, subsequently extending up to the anterior scallop, and finally involved the anterior mitral leaflet beyond the commissures.(ABSTRACT TRUNCATED AT 400 WORDS)

Aged↗
PubMed1985

In vitro computerized evaluation of biological cardiac prosthesis calcification.

The late valvular bioprostheses failure is mainly related to leaflet calcification. This study reports a new approach to testing the biological prostheses calcification applying a computerized technique to x-ray picture. A bovine glutaraldehyde-fixed bioprostheses (BB) was implanted in two sheep in mitral position. The experimental procedure was performed on valves explanted six months after surgery. The BB x-ray pictures were tested by means of a video display computer (VDC) that can process radiographic, photographic or microscopic images and also evaluate the optical density of image quantifiable. The calcification zone assumes different values according to the calcification degree. The VDC can colour the BB x-ray images and display them on monitors (one black and white, one colour) with the colours strictly related to the grey levels of the image.

Animals↗
PubMed1985

Does vitamin K excess induce ectopic calcifications in hemodialysis patients?

Vitamin K promotes the formation of gamma-carboxylated glutamic acid (Gla) residues within different protein classes such as vitamin K-dependent clotting factors, bone Gla-protein (BGP or osteocalcin), and atherocalcin. Gla-containing proteins have a high affinity for the Ca2+ ion. In addition to bone and atheromatous plaques they are also regularly found in ectopic calcifications, but not in uncalcified soft tissue. In the present study we investigate the possibility that vitamin K and BGP, in addition to previously recognized factors, may play a role in soft tissue calcification of chronic hemodialysis patients. Patients without radiovisible ectopic calcifications (group A) are compared to patients with such Ca deposits (group B). Both patient groups have comparable values of predialysis plasma Ca, P, alkaline phosphatases, parathyroid hormone (PTH) and 25 hydroxyvitamin D. The CaxP product is slightly higher in group B than in group A patients. Plasma vitamin K1 levels of group B patients are increased to more than twice the values observed in group A patients. Plasma BGP, even though not significantly different, shows a trend towards decreased levels in group B patients. A positive correlation exists between plasma vitamin K1 and BGP for patient group A alone, but not for group B alone. A correlation is also observed between plasma PTH and BGP (all patients) and between serum alkaline phosphatases and plasma BGP (all patients). Taken together, these results favor the hypothesis that in addition to an increased CaxP product a vitamin K excess may induce soft tissue calcification in hemodialysis patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1985

[Calcification in the heart. I. Spontaneous coronary embolism due to calcified material].

Thirty-one hearts with advanced calcification of one or both left heart valves were investigated for the presence of spontaneous "calcific" emboli. X-ray (mammography) showed coronary emboli in 14 cases, that is in 45% of the whole series. A total of 265 "calcific" emboli (205 intracoronary and 60 in the left ventricular cavity) was demonstrated. The embolisation occurred most frequently and most extensively in association with postrheumatic mitral valve disease. Coronary "calcific" embolisation must be considered in the differential diagnosis of symptoms of ischemic heart disease in patients suffering from valvular heart lesions.

Adult↗
PubMed1979

CO2-induced kidney calcification.

Light microscopic examination of kidney tissue of guinea pigs exposed to 1.5% CO2, 21% O2, and balance N2 for periods as long as 42 days and of rats exposed to the same CO2 concentrations for up to 91 days showed that the incidence of focal kidney calcification increased with length of exposure. Calcification occurred primarily in the tubules of the renal cortex. Another group of guinea pigs were exposed to 1% CO2, 21% O2, and the balance N2 for periods up to six weeks and were later killed at regular intervals, together with control animals of the same litter. In the exposed animals, arterial PCO2 was elevated by 3-4 mmHg and hydrogen ions by about 4 nmol/liter. The standard bicarbonate level was lowered by 1-1.5 mmol, indicating a lack of renal reabsorption of bicarbonate (HCO3), which in turn placed greater stress on the bone buffer system and apparently caused bone calcium and phosphorus mobilization. Bone calcium and phosphorus levels exhibited a cyclic decrease, which resulted in cyclic hypercalcemia and hyperphosphatemia, after one week and six weeks of exposure to 1% CO2. Kidney calcium content increased significantly after two weeks of exposure (27%) and remained at this elevated level during subsequent exposures between the third and sixth weeks. These findings indicate that once the kidney calcification process has started, kidney mineralization is independent of fluctuations in the blood calcium level. A rise in plasma phosphate level that occurred after one day of exposure could have been a precipitating factor in the calcification process. The small but consistent increases in ionized calcium during a 4-week exposure to 1% CO2 may have stimulated the parathyroid, causing an increased blood calcium level that was independent of the two calcium tides in the blood associated with marked bone calcium loss.

Acid-Base Equilibrium↗
PubMed1979

Vascular calcification in dermatopathology.

Calcification in cutaneous blood vessels is an uncommon finding in biopsies submitted for dermatopathological examination. Of 14 biopsy specimens showing the phenomenon that was studied by us, the greater number was from women who had a combination of severe diabetes, hypertension, and atherosclerosis. Unusual clinical syndromes as the bases for the vascular calcification were hyperthyroidism in three patients and arteritis in two patients. Three patients died as a consequence of massive cutaneous infarction and sepsis, probably stemming from cutaneous vascular calcification. Vascular calcification in biopsy of skin may result from metabolic, inflammatory, or degenerative diseases of blood vessels.

Aged↗
PubMed1978

Detection and pathogenesis of visceral calcification in dialysis patients and patients with malignant disease.

Scintiscanning to detect the uptake of bone-seeking radioactive isotopes by soft tissue is a promising technique for the in vivo study of visceral calcification. Visceral uptake of such radioisotopes was studied in 40 patients: 22 undergoing long-term dialysis, 9 with malignant disease and hypercalcemia and 9 with primary hyperparathyroidism and hypercalcemia.Fifteen patients, 11 undergoing dialysis and 4 with malignant disease, had radioisotope uptake in the lungs, and 5, 3 undergoing dialysis and 2 with malignant disease, had uptake in the stomach. None of the patients with primary hyperparathyroidism had visceral uptake, nor did the patients with uptake have radiologic evidence of pulmonary or gastric calcification. The dialysis patients with visceral uptake had a mean calcium x phosphate product of 84.3 +/- 23.7 (standard deviation), which was significantly greater (P < 0.001) than that of patients without such uptake (59.2 +/- 14.0). Similarly, in patients with malignant disease and visceral uptake the Ca x P product was 72.2 +/- 6.4 - significantly greater (P < 0.005) than that of patients without such uptake (49.3 +/- 6.7).These findings indicate that scintiscanning for the visceral uptake of a bone-seeking radioisotope is a simple and effective technique for the in vivo study of visceral calcification. An elevation in the Ca x P product seems to be the single most important factor in the production of visceral calcification.

Adult↗
PubMedDate not supplied

Calcification of the vertebral artery.

A series of 3,648 computed tomographic (CT) scans was reviewed to determine the incidence of intracranial vertebral artery calcification. Calcification was identified in one or both vertebral arteries in 3.4% and was more frequent in the higher age groups. Skull radiographs demonstrated vertebral artery calcification in only one of 48 patients in whom CT studies showed it. A high correlation was observed between vertebral artery calcification on CT and vertebral artery stenosis on cerebral angiography.

Adult↗