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PubMed2002

Immunohistochemical examination on intracranial calcification in neurodegenerative diseases.

Fahr-type calcification is a relatively common finding in the elderly, and in younger patients with Alzheimer's disease, calcification in the basal ganglia is not uncommon. However, as far as we know, an immunohistochemical study of intracranial calcification in neurodegenerative diseases has not been performed. In this study, we examined intracranial calcification of the basal ganglia and cerebellum with antibodies against noncollagenous bone matrix proteins. Nineteen brains were employed. The diagnoses were diffuse neurofibrillary tangles with calcification in five, Alzheimer's disease in five, Pick's disease in one, progressive supranuclear palsy in one, Parkinson's disease in one, and six controls. By conventional histology, three patterns of calcium (Ca) deposition were recognized: diffuse deposition within the tunica media of small and medium-sized vessels (type 1 deposition), free spherical or lobulated concretions (type 2 deposition) in the parenchyma, and rows of small calcospherites lying along capillaries (type 3 deposition). Type 3 deposition is relatively rare, and may be a hallmark of severe intracranial calcification. Immunohistochemistry demonstrated that osteopontin was present diffusely in all Ca deposition types. Osteocalcin was present chiefly in the peripheral region of type 2 and 3 depositions, as well as in only the rims of type 1 deposition. Bone sialoprotein and osteonectin were found only in the core portions of type 2 and 3 depositions. In brief, type 1 deposition shows a different staining pattern from type 2 and 3. Different Ca deposition patterns of noncollagenous bone matrix proteins may suggest their separate roles in the pathogenesis of intracranial calcification.

Aged↗
PubMed1998

Epithalamus calcifications in schizophrenia.

We evaluated the prevalence and the size of epithalamus calcifications (EC) and choroid plexus calcifications (CPC) on computed tomography (CT) scans in a group of 64 schizophrenic patients and in a group of 31 healthy controls. The associations between cerebral calcifications, demographic variables, and other brain morphological characteristics (particularly cerebral ventricular size and cortical atrophy) in both, patients and controls, were also considered. A significant increase in size of the epithalamic-region calcifications in schizophrenic patients was found, whereas there was no evidence of increase in both, dimension and prevalence, of choroid plexus calcification. Such dimensional increase was unrelated to the duration of illness and therefore did not seem to be iatrogenic or secondary to the disease. A correlation was found between epithalamus calcifications and cortical atrophy and third-ventricle enlargement, suggesting that calcifications of this cerebral region may be associated with lesions of third-periventricular areas and of circuitries hypothesized to be involved in the pathophysiology of schizophrenia.

Adolescent↗
PubMed2003

Cardiovascular calcifications in pediatric patients receiving maintenance dialysis.

Cardiovascular disease is a major cause of morbidity and mortality in adult patients with end-stage renal disease receiving maintenance dialysis. Coronary artery calcifications (CAC) contribute to the high prevalence of cardiac disease and are associated with hyperphosphatemia, an elevated calcium-phosphorus product (CaxP), and prolonged time on dialysis. Chronic inflammation and malnutrition are also associated with an increased risk for development of cardiac calcifications. Young adults receiving maintenance dialysis develop cardiac calcifications at a degree out of proportion to healthy adults of the same age and gender. Many of these young adults initiated dialysis as children or teenagers. Risk factors associated with the development of CAC are also seen in the pediatric dialysis population. To date, reports of cardiac calcifications in pediatric patients receiving maintenance dialysis are limited to post-mortem studies. We present two pediatric patients with ANCA-positive vasculitis diagnosed with cardiac calcifications while receiving maintenance dialysis. Hyperphosphatemia and an elevated CaxP product were seen in both patients and probably contributed to the development of extraskeletal calcifications. In addition, both patients had an underlying systemic inflammatory disease and significant weight loss/malnutrition that may have contributed to the early and rapid onset of cardiac calcifications.

Adolescent↗
PubMed1982

M mode and cross-sectional echocardiographic recognition of fibrosis and calcification of the mitral valve chordae and left ventricular papillary muscles.

The echocardiographic appearance of fibrotic thickening and calcification of mitral valve chordae tendineae and left ventricular papillary muscles in 17 patients is described. Pathologic proof of excessive fibrosis or calcification was obtained in five patients. In a sixth patient, calcium was demonstrated on angiography to extend from the chordae into papillary muscle. The characteristic feature of chordal and papillary muscle fibrosis and calcification is the presence of highly echogenic densities best visualized within the left ventricle at a level below the mitral valve leaflets. The more inferior location of these densities, within the body of the left ventricle, enables them to be easily differentiated from densities indicating fibrosis and calcification of the mitral valve anulus. The pattern of chordal and papillary muscle fibrosis and calcification was frequently associated with mitral anular calcification, aortic valve fibrosis or calcification and left atrial enlargement. One patient had rheumatic mitral valve disease. Many patients had mitral regurgitation and most had a history, physical examination and radiologic findings compatible with congestive heart failure. Although the origin and importance of the chordal and papillary muscle changes reported are not known, their frequent association with mitral regurgitation and with congestive heart failure suggests possible interrelations.

Aged↗
PubMed1991

Cardiovascular implant calcification: a survey and update.

Calcification of cardiovascular prosthetic implants is a common and important problem. This review provides an update based upon the Conference on Cardiovascular Implant Calcification held as part of the 13th World Congress of the International Society for Heart Research, 1989. A variety of cardiovascular prostheses are affected clinically by calcification, including bioprosthetic heart valves, aortic homografts and trileaflet polymeric valve prostheses. In addition, experimental studies have demonstrated calcification of artificial heart devices in ventricular assist systems in long-term calf studies. The pathophysiology of this disease process is incompletely understood. A common element between the various types of cardiovascular implant calcification is the localization of calcific deposits to devitalized cells and membranous debris. Prevention of cardiovascular implant calcification by either biomaterial modifications or regional drug therapy (controlled release) is being investigated.

Animals↗
PubMed2005

Coronary artery calcifications in the long-term follow-up of Kawasaki disease.

BACKGROUND: To determine if detection of coronary artery calcifications in patients with Kawasaki disease may serve as a noninvasive predictor of future coronary artery events. METHODS: A prospective, cohort pilot study that included 18 patients with Kawasaki disease > 1 year from the acute disease was performed including 9 patients with coronary abnormalities during the acute illness (Group 1) and 9 without coronary abnormalities (Group 2). Patients were classified by echocardiography as having none, resolved, or residual coronary artery abnormalities. Electron beam computed tomography (EBCT) scans were completed using the Agatson coronary calcium scoring system. Intermediate follow-up was performed 2.5 years after EBCT to determine if clinically significant coronary artery events (myocardial infarction or sudden death) had occurred. RESULTS: Late echocardiographic abnormalities corresponded with the early echocardiographic abnormalities in 5 of 9 patients (P = .029) in Group 1. The late echocardiographic abnormalities significantly correlated with detection of calcifications by EBCT in 4 of 5 patients (95% CI 28%-99%). One patient with residual coronary abnormalities and coronary artery calcifications with the highest calcium score subsequently had a sudden death. Detection of coronary artery calcifications may be predictive of sudden death (P = .056). No residual echocardiographic abnormalities, coronary artery calcifications, or coronary artery events occurred in Group 2 patients. CONCLUSIONS: Patients with Kawasaki disease with residual coronary abnormalities show EBCT evidence of coronary artery calcifications. Detection of coronary artery calcifications may be useful for risk stratification in the long-term management of patients with Kawasaki disease.

Calcinosis↗
PubMed2004

Degree of carotid plaque calcification in relation to symptomatic outcome and plaque inflammation.

OBJECTIVE: We undertook this study to quantitate differences in the degree of calcification between symptomatic and asymptomatic plaques removed at carotid endarterectomy (CEA) and to determine associated extent of plaque macrophage infiltration, a histopathologic feature of plaque instability. METHODS: CEA plaques (n = 48) were imaged at 1.25-mm intervals with spiral computed tomography (CT; 10-15 images per plaque). Indications for CEA were transient ischemic attack (n = 16), stroke (n = 5), amaurosis (n = 4), and critical asymptomatic stenosis (n = 23). The percent area calcification for each plaque was determined in spiral CT serial sections and averaged for each plaque. In 31 of 48 plaques macrophage infiltration was quantitated in corresponding histologic sections with immunohistochemical techniques. RESULTS: The mean (+/- SD) age of patients with symptomatic and asymptomatic plaques was 66 +/- 7 years vs 71 +/- 7 years, respectively, and degree of stenosis was 76% versus 82%, respectively (P =.05). Atherosclerosis risk factors were similar between groups. Percent plaque area calcification was twofold greater in asymptomatic versus symptomatic plaques (48% +/- 19% vs 24% +/- 20%, respectively; P <.05). At receiver operating characteristic curve analysis, 80% of symptomatic plaques were below and 87% of asymptomatic plaques were above a cutoff point of 30% plaque area calcification. Macrophage burden was greater in the symptomatic plaques than in the asymptomatic plaques (52% vs 23%; P <.03). A strong inverse relationship between the degree of plaque calcification and macrophage infiltration was found in critical carotid stenoses (r = -0.87; P <.001). CONCLUSIONS: Symptomatic plaques are less calcified and more inflamed than asymptomatic plaques. Regardless of clinical outcome, a strong inverse correlation was found between the extent of carotid plaque calcification and the intensity of plaque fibrous cap inflammation as determined by the degree of macrophage infiltration. Carotid plaque calcification is associated with plaque stability, and is a potential spiral CT in vivo quantitative marker for cerebrovascular ischemic event risk.

Aged↗
PubMed2003

Homocysteine potentiates calcification of cultured rat aortic smooth muscle cells.

Aortic calcification was demonstrated in experimental animal models of hyperhomocysteinemia. Mild hyperhomocysteinemia was associated with aortic calcification, suggesting a relationship between homocysteine (HCY) and the pathogenesis of aortic calcification. In the present study, the effect of HCY on vascular calcification was examined in calcifying and non-calcifying vascular smooth muscle cells (VSMCs). Cell calcification was induced by incubation of VSMCs with beta-glycerophosphate. Proliferation of VSMCs was studied by cell counting, 3H-thymidine (3H-TdR) and 3H-leucine (3H-Leu) incorporation. 45Ca accumulation, cell calcium content, and alkaline phosphatase (ALP) activity were measured as indices of calcification. The results showed that the proliferation of calcifying VSMCs, which was indicated by cell counting, 3H-TdR and 3H-Leu incorporation in calcifying VSMCs, was enhanced as compared with that of non-calcifying VSMCs. HCY promoted increases in cell number, 3H-TdR and 3H-Leu incorporation in both calcifying and non-calcifying VSMCs, but with more prominent effect in calcifying VSMCs. The stimulating effects of HCY on the three parameters in calcifying VSMCs were antagonized by PD98059, a specific inhibitor of mitogen activated protein kinase kinase (MAPKK). The ALP activity, 45Ca uptake, and calcium deposition in the calcifying VSMCs were greater than those in non-calcifying VSMCs. PD98059 had no effect on ALP activity, 45Ca uptake, and calcium deposition in calcifying VSMCs. HCY caused marked increases in 45Ca uptake and calcium deposition both in calcifying and non-calcifying VSMCs. HCY, however, enhanced ALP activity in the calcified VSMCs but not in the non-calcifying VSMCs. The non-calcifying VSMCs treated with HCY showed the same low ALP activity, as did the control VSMCs. In calcifying VSMCs, the HCY-induced increases in 45Ca uptake, calcium deposition, and ALP activity were also attenuated by PD98059. The results demonstrated that HCY potentiated VSMC calcification probably through the mechanisms by which HCY promotes atherosclerosis.

Alkaline Phosphatase↗
PubMed2006

Prevention of diabetic vascular calcification by nifedipine, a dihydropyridine-based calcium channel blocker.

Vascular calcification is a common feature in advanced atherosclerosis and also a predictor of future cardiovascular events such as unstable angina and myocardial infarction, especially in diabetes. There is a growing body of evidence that advanced glycation end products (AGEs), senescent macroprotein derivatives formed at an accelerated rate in diabetes, exist within atherosclerotic lesions, thereby being implicated in the pathogenesis of accelerated atherosclerosis in diabetes. Indeed, we have previously shown that AGE - their receptor (RAGE) interaction could induce angiogenesis through autocrine production of vascular endothelial growth factor, suggesting its role for plaque formation and enlargement in diabetes. Furthermore, we have found that AGEs have the ability to induce the osteoblatic differentiation of pericytes, thus contributing to the development of vascular calcification as well. These observations suggest that the inhibition of AGE formation or blockade of the downstream signaling of RAGE may be a novel therapeutic target for the inhibition of vascular calcification in diabetic atherosclerosis. Since we, along with others, have shown that nifedipine inhibits glycation of low-density lipoprotein in vitro and blocks the AGE-induced RAGE expression in endothelial cells through its anti-oxidative properties, nifedipine could inhibit vascular calcification by blocking the AGE formation or the downstream signaling in diabetes. In this paper, we would like to propose the possible ways of testing our hypothesis. Does nifedipine treatment slow down the progression of coronary calcification in diabetic patients? If the answer is yes, is this beneficial effect of nifedipine superior to that of other DHPs with equihypotensive properties? Does nifedipine treatment decrease expression levels of AGEs and RAGE in diabetic atherosclerosis? Is the unique effect of nifedipine on vascular calcification correlated with its AGE or RAGE-suppressing properties? These prospective studies will provide further valuable information whether nifedipine could prevent vascular calcification in diabetic atherosclerosis by blockade the AGE-RAGE signaling in vascular wall cells.

Calcinosis↗
PubMed2004

Calcifications of the heart.

Cardiac calcification usually represents the result of a pathologic process. Some forms of calcification represent chronic change in an ageing population, and must be differentiated from pathologic calcification. Still other forms of calcification are associated with ageing and chronic degeneration, but also reflect ongoing pathologic processes. Recognition of cardiac calcification may be an early sign or only sign of a pathologic process. Characterization of the calcification in terms of its distribution and appearance is a helpful means for determining which structures are calcified, differentiating pathologic from nonpathologic processes. This article provides an overview of the types of calcifications of the heart, pathogenesis, and utility of the various imaging modalities for their detection.

Calcinosis↗
PubMed2006

Management of vascular calcification in CKD patients.

Vascular calcification is common in patients with chronic kidney disease (CKD) and it may affect almost every artery. It is associated with a significant increase in morbidity and mortality. Therefore, the detection, prevention and treatment of vascular calcification in CKD patients are critical for the overall approach for the management of these patients. Hyperphosphatemia, especially when the blood levels of serum phosphorus are above 5.5 mg/dl, plays a major role in the development of vascular calcification. Hyperphosphatemia induces vascular calcification by both passive and active processes. By increasing calcium-phosphate product, hyperphosphatemia results in direct deposition of calcium salts in the arteries and in cardiac valves. The active process involves the uptake of phosphate by the smooth muscle cells of the arteries by a Na-P co-transporter. This increase in cell phosphate then induces phenotypic changes of these cells, rendering them into osteoblasts which in turn, begin laying calcium salts in the arterial walls. Therefore, it is critical that the blood levels of serum phosphorus be maintained below 5.5 mg/dl in CKD patients. Inflammation and the production of C-reactive protein (CRP) and interleukin 6 are also risk factors for vascular injury and vascular calcification. In a study of 254 dialysis patients with elevated blood levels of CRP (>1.0 mg/l) and 258 patients with CRP levels equal to or less than 1.0 mg/l, it was found that higher levels of CRP are significantly associated with the presence of both atheromatous and medial calcification of the aorta and hand arteries. Also, it was reported that a significant association between CRP levels and cardiac valves calcification in patients undergoing continuous ambulatory peritoneal dialysis. The reasons for the elevation in CRP in dialysis patients are not clear, but certainly, is more evident in those with obvious inflammatory processes. Therefore, any inflammation that is detected should be treated appropriately.

Calcinosis↗
PubMed2005

Detection of muscle calcifications by thigh CT scan in neurocysticercosis patients.

Twenty-five patients with calcified neurocysticercosis (two to four intraparenchymal brain calcifications) were asked to have a non-contrasted computed tomography (CT) scan of the thighs to determine the frequency of muscle calcifications detected by this technique. Thirteen (52%) showed one or more muscle calcifications. The numbers of calcifications in the thighs and the brain were not correlated. Patients with a positive CT scan for muscle calcifications were also examined by X-rays to compare both methods. Only 6 of 13 had visible calcifications on X-ray. Thigh CT scans can demonstrate muscle calcifications in a significant proportion of patients with calcified neurocysticercosis.

Adolescent↗
PubMed2002

Osteopontin inhibits mineral deposition and promotes regression of ectopic calcification.

Ectopic calcification, the abnormal calcification of soft tissues, can have severe clinical consequences especially when localized to vital organs such as heart valves, arteries, and kidneys. Recent observations suggest that ectopic calcification, like bone biomineralization, is an actively regulated process. These observations have led a search for molecular determinants of ectopic calcification. A candidate molecule is osteopontin (OPN), a secreted phosphoprotein invariantly associated with both normal and pathological mineral deposits. In the present study, OPN was found to be a natural inhibitor of ectopic calcification in vivo. Glutaraldehyde-fixed aortic valve leaflets showed accelerated and fourfold to fivefold greater calcification after subcutaneous implantation into OPN-null mice compared to wild-type mice. In vitro and in vivo studies suggest that OPN not only inhibits mineral deposition but also actively promotes its dissolution by physically blocking hydroxyapatite crystal growth and inducing expression of carbonic anhydrase II in monocytic cells and promoting acidification of the extracellular milieu. These findings suggest a novel mechanism of OPN action and potential therapeutic approach to the treatment of ectopic calcification.

Animals↗
PubMed2004

Role of oral bacterial flora in calcific aortic stenosis: an animal model.

BACKGROUND: Calcific aortic stenosis is a major public health problem in the United States. The mechanism of calcification remains unclear. The hypothesis that low grade chronic or recurrent bacterial endocarditis with specific calcifiable bacteria is a cause of calcification of the aortic valves was investigated using an animal model. Such bacteria are typically present as part of the normal human oral flora. METHODS: Forty New Zealand white rabbits were divided into four groups: group 1, control (1 ml of normal saline); group 2, Corynebacterium matruchotti 100,000 colonies; group 3, Streptococcus sanguis II 10 colonies; and group 4, C matruchotti 100,000 colonies plus S sanguis II 10 colonies. Animals were inoculated with bacteria through a flexible catheter placed through the aortic valve through a right carotid cut down. Inoculations were repeated every 3 days the first 2 weeks and then twice a week thereafter. At postmortem examination the aortic valves were harvested, embedded in paraffin, and stained with von Kossa stain. They were also examined by scanning and transmission electron micrography. RESULTS: Group 4 had 93.3% large calcifications (confluent calcium densities that are easily recognized with minimal magnification) and 6.6% small microcalcifications (dustlike microscopic particles requiring a compound microscope to appreciate) of the aortic valves. Group 3 exhibited large calcification in 20% and small in 40% of the aortic valves. Group 1 and group 2 had no evidence of calcification. CONCLUSIONS: These results suggest that recurrent low-grade endocarditis from calcifying oral bacteria, particularly when occurring with synergistic strains, may be one cause of calcific aortic stenosis.

Animals↗
PubMed1983

Porcine bioprosthetic valve calcification in bovine left ventricle-aorta shunts: studies of the deposition of vitamin K-dependent proteins.

Calcification of glutaraldehyde-preserved bioprosthetic cardiac valves represents a serious clinical problem. Previous work from this laboratory has established the presence in clinical bioprosthetic valve calcifications of vitamin K-dependent calcium-binding proteins, which contain the calcium-binding amino acid gamma-carboxyglutamic acid; no proteins containing gamma-carboxyglutamic acid are present in nonmineralized valves. The purpose of the present study was to examine a series of bovine circulatory bioprosthetic valve explants for calcification and proteins containing gamma-carboxyglutamic acid. Biochemical analyses of explanted bioprosthetic valves from calves demonstrated proteins with gamma-carboxyglutamic acid accumulating in calcified valves during both the onset and progression of valve calcification; calcium levels in the explanted calf bioprostheses were in the same range as those noted in clinical material. Accumulation of calcium and protein with gamma-carboxyglutamic acid occurred simultaneously and progressively, beginning 2 months after implantation. Small amounts of osteocalcin, the bone-derived protein containing gamma-carboxyglutamic acid, were present in both human and bovine bioprosthetic valve calcifications at comparable levels. No osteocalcin was detectable in non-mineralized valve tissue. Warfarin anticoagulant therapy did not prevent calcification or accumulation of protein with gamma-carboxyglutamic acid. It is concluded that proteins containing gamma-carboxyglutamic acid are involved in both the onset and progression of bioprosthetic valve calcification, and that conventional means of vitamin K antagonism do not alter this association or the course of bioprosthetic valve mineralization.

1-Carboxyglutamic Acid↗
PubMed1995

Association of Chlamydia trachomatis immunoglobulin gamma titers with dystrophic peritoneal calcification, psammoma bodies, adhesions, and hydrosalpinges.

OBJECTIVE: To correlate Chlamydia trachomatis immunoglobulin gamma (IgG) titers with psammoma bodies, dystrophic peritoneal calcification, degree of calcification, adhesions, and hydrosalpinges. DESIGN: This is a prospective single-blinded histologic analysis of tissue and retrospective analysis of historical laboratory and clinical variables. SETTING: Tertiary hospital and private practice patient charts. PATIENTS: Sixty consecutive patients with C. trachomatis IgG titers reported on the coding sheets of a previous study for endometriosis. MAIN OUTCOME MEASURES: The histologic slides were reviewed in a blinded fashion for calcification. Previously used data sheets were reviewed for C. trachomatis IgG titers. Historical data, adhesion scores, hystrosalpingogram findings, and laparoscopic findings were obtained from charts. RESULTS: Dystrophic calcification, psammoma bodies, moderate-to-severe dystrophic calcification and hydrosalpinges were associated with positive C. trachomatis IgG titers. CONCLUSION: This study suggests relationship of C. trachomatis with dystrophic calcification, psammoma bodies, adhesions, and hydrosalpinges. This relationship suggests that C. trachomatis IgG titers can be used as a marker to help determine those infertility patients who might best benefit from hysterosalpingogram or laparoscopy and in clinical studies of endometriosis, infertility, pain, or ovarian cancer. However, there is no current data to suggest a need for therapy on the basis of a positive C. trachomatis IgG titer or of dystrophic peritoneal calcification.

Body Fluids↗
PubMed1992

Kidney function in very low birth weight infants with furosemide-related renal calcifications at ages 1 to 2 years.

To determine whether long-term renal sequelae follow the use of furosemide in preterm infants, we evaluated renal function in 27 former very low birth weight infants (less than 1500 gm) at 1 to 2 years of age. Patients were classified into three groups on the basis of status at the time of discharge from the hospital: group 1 (n = 7) had no furosemide treatment or renal calcifications, group 2 (n = 10) had furosemide therapy but no calcifications, and group 3 (n = 10) had furosemide therapy with renal calcifications. Renal ultrasonography at the time of the study demonstrated resolution of the calcifications in six patients in group 3. No differences in renal function were observed between groups 1 and 2. Creatinine clearance (mean +/- SEM) in group 3 (83.6 +/- 7.8 ml/min per 1.73 m2) was significantly lower than clearance in groups 1 and 2 (103.2 +/- 6.5 and 109.1 +/- 5.1, respectively; p less than 0.05). Children in group 3 had significantly higher urinary calcium/creatinine ratios and fractional excretion of sodium and lower tubular reabsorption of phosphate than children in the two other groups had. Urine-blood difference in carbon dioxide tension after oral acetazolamide load, which indicates the ability of the distal tubule to secrete hydrogen ions, was 8.4 +/- 3.4 mm Hg in group 3, significantly lower than values in groups 1 and 2 (22.6 +/- 3.1 and 28.0 +/- 4.3 mm Hg, respectively, p less than 0.05). Within group 3 the four children with persistent renal calcifications had significantly lower urine-blood carbon dioxide tension differences than did those with resolution of calcifications (p = 0.02). We conclude that furosemide-related renal calcifications in very low birth weight infants may lead to glomerular and tubular dysfunction; further long-term follow-up of this population is recommended.

Absorption↗
PubMed2003

Hypercholesterolemia is a risk factor for bioprosthetic valve calcification and explantation.

OBJECTIVE: There are pathophysiologic similarities between calcification and atherosclerosis. We wished to determine whether risk factors for atherosclerosis were linked to bioprosthetic valve calcification and dysfunction. METHODS: We performed a retrospective cohort study on 144 patients at a single institution who had bioprosthetic aortic or mitral valves removed, serum cholesterol levels recorded, and valve calcification assessed on the basis of hematoxylin and eosin staining and radiography of the valve. We also performed case-control analysis of a group of 66 patients whose tissue valves were explanted and compared them with an age- and position-matched group of 66 patients with similar duration of implantation. We also compared mean serum cholesterol levels. RESULTS: In the retrospective cohort study cholesterol (P =.035), younger age at implantation (P =.014), and coronary artery disease (P =.017) were linked to calcification of the valve by means of univariate analysis. In stepwise multiple regression analysis only the mean serum cholesterol level was linked to calcification (P =.02). Sex, hypertension, smoking, diabetes, and implant position were not linked to calcification. In the case-control analysis the mean serum cholesterol level of the explanted valve group was significantly higher (189 vs 163 mg/dL, P <.0001) than that of the group whose valves did not require explantation. For those whose serum cholesterol levels were greater than 200 mg/dL, the odds ratio was 3.9 (95% confidence interval, 1.7-8.9) for valve explantation. CONCLUSIONS: Increased serum cholesterol level may be a risk factor for bioprosthetic valve calcification requiring explantation.

Adult↗