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PubMed1997

Non-furosemide-related renal calcifications in premature infants with bronchopulmonary dysplasia.

Renal calcification is a known complication of long-term furosemide therapy in infants with bronchopulmonary dysplasia (BPD). In a prospective study the clinical course and long-term renal sequelae of renal calcifications of 19 consecutive premature neonates (birthweight < 1250 g) with bronchopulmonary dysplasia who did not receive furosemide were examined. Infants were divided into two different groups on the basis of ultrasound evidence of renal calcifications (RC group) or absence of renal calcifications (NRC group). Serial examinations, performed at the age of 1, 2, 3, 6, 9 and 12 months, showed that 12 infants at the mean age of 68.5 +/- 12.8 days of life had renal calcifications (63%), and 3 of them had nephrolithiasis; 8 had bilateral renal calcifications. Among the 9 survivors, 2 had chronic renal calcifications at the age of 9 months; however, all normalized at the age of 12 months. Twelve infants received hydrochlorothiazide and spironolactone (63%), 17 had prolonged courses of xanthines and dexamethasone (89.5%), while furosemide was not part of the routine pharmacological administration. Statistical analysis showed that birthweight, gestational age, Apgar score and length of parenteral nutrition were comparable in the RC and NRC group infants. Mean serum creatinine, creatinine clearance, fractional sodium excretion and urinary calcium excretion values during the 12-month study period were comparable in the RC and NRC groups. Mechanical ventilation and hospital stay length were instead associated with renal calcification occurrence. The strongest indicator of renal calcification risk for this high-risk population is the severity of the unresolved acute lung disease, where different facets of respiratory management, other than the addition of furosemide, represent sufficient stimuli and renal injury to potentiate stone formation.

Bronchopulmonary Dysplasia↗
PubMed1970

Pathological and clinical study of calcification of the mitral valve ring.

The pathology and clinical features of 258 cases of mitral ring calcification were reviewed. The overall incidence in patients over 50 years of age was 8.5%; it was more than twice as high in women (11.5%) as in men (4.5%) and rose sharply with age. Cardiac failure and systolic murmurs were each noted in over half the patients. Hypertension was slightly commoner than in age- and sex-matched groups without ring calcification, although the difference was not statistically significant. Small nodules of calcification were more frequent in men and heavy deposits in women. Distortion and atrial displacement of the posterior mitral cusp was present in 26% of the hearts with early ring calcification, in 56% of the hearts with moderate, and in almost all hearts with marked changes. Systolic murmurs had been heard in 73% of these cases. ;Caseation' of the calcified ring was seen in seven hearts and haemorrhagic valvulitis in three. Calcium had ulcerated through the cusp in 12 cases, with thrombotic and/or bacterial endocarditis in five. Aortic valve calcification was present in 36% of men and was quantitatively related to the severity of mitral ring calcification. In women the incidence was 30% and there was no corresponding quantitative relationship. Microscopy showed nonspecific chronic inflammatory changes adjacent to calcium in about half the cases in both sexes, with foreign body type giant cells in 6%. Similar inflammatory changes in the valve cusp were almost twice as common in women as in men. There was no evidence that previous endocarditis was responsible for mitral ring calcification, neither did parity influence its incidence. Severe coronary atherosclerosis was unrelated but severe aortic atherosclerosis was commoner in patients with calcified mitral rings. The difference, in women, was statistically significant. The higher incidence of severe degrees of ring calcification, complications, and valvular inflammation in women suggests a sex-determined difference in tissue response in the mitral area. Possible provoking factors apply to both sexes and both left side valves, and such a difference would account for the relative frequency and sex incidence of mitral ring calcification.

Age Factors↗
PubMed2001

Biopsy of amorphous breast calcifications: pathologic outcome and yield at stereotactic biopsy.

PURPOSE: To assess the pathologic outcome of amorphous breast calcifications and the success of stereotactic biopsy for such lesions. MATERIALS AND METHODS: From July 1995 through February 2000, biopsy of all clustered amorphous calcifications not clearly stable for at least 5 years or in a diffuse scattered distribution was recommended. Logistic regression analysis was used to stratify the risk of malignancy by patient risk factors, calcification distribution, and stability. RESULTS: Calcifications were retrieved from 150 biopsies; 30 (20%) proved malignant and included 27 ductal carcinomas in situ and three low-grade invasive and intraductal carcinomas (2-5 mm). Another 30 (20%) yielded high-risk lesions, including 21 atypical ductal hyperplasia, eight atypical lobular hyperplasia, and one lobular carcinoma in situ. In 150 lesions, stereotactic biopsy was performed on 113 and aborted in 10. Calcifications were retrieved from all 113 stereotactic biopsies. Of those with calcification retrieval, there were three histologic underestimates (accuracy, 97%). Stereotactic biopsy spared a surgical procedure in 57 (46%) of 123 patients. Needle localization was required for 23 (15%) of 150 patients due to poor conspicuity. Five (45%) of 11 biopsies performed in women with ipsilateral breast cancer showed malignancy (P = .025). When multiple lesions of amorphous calcifications were present in one breast, sampling of one reliably predicted the outcome of others. CONCLUSION: We found a substantial rate of ductal carcinoma in situ and high-risk lesions associated with amorphous calcifications. Stereotactic biopsy can be successfully performed for the majority of subtle amorphous calcifications; however, only a minority were spared a surgical procedure.

Adult↗
PubMed2003

Calcification in cystic renal masses: is it important in diagnosis?

PURPOSE: To determine whether the presence of calcifications in cystic renal masses is important in diagnosis and to suggest an approach to the management of calcified cystic renal masses. MATERIALS AND METHODS: Eighty-one cystic renal masses containing calcification in a wall or septum were evaluated by means of review of computed tomographic (CT) images (n = 81), follow-up CT images (n = 28), and results of pathologic examination (n = 40) by the authors in consensus. Images were evaluated for lesion size, amount and morphology of calcification, and any association of calcification with soft-tissue structures. Lesions were categorized according to the Bosniak cyst classification system; the amount of calcification was determined with a subjective grading system. Progression of calcification was qualitatively determined with available follow-up CT scans. RESULTS: Twenty-one lesions were Bosniak category II (benign) and showed small amounts and thin strands of calcification. Nineteen lesions containing more extensive calcification but no enhancing tissue were category IIF. Follow-up CT results available for 16 of these lesions (average follow-up length, 5 years 8 months) showed no substantial change. The three remaining lesions were proved benign at surgery. Twenty-five lesions were category III; surgical intervention was performed in 21 of these (benign, n = 12; malignant, n = 9). Sixteen lesions that contained obvious areas of enhancing soft tissue were category IV and proved malignant at surgery. CONCLUSION: Calcification in a cystic renal mass is not as important in diagnosis as is the presence of associated enhancing soft-tissue elements. This information should enable a reasonable approach to the management of calcium-containing renal cystic lesions.

Calcinosis↗
PubMed1985

Breast arterial calcification in association with diabetes mellitus: too weak a correlation to have clinical utility.

A large-scale prospective study was designed to characterize the association between breast arterial calcification and diabetes mellitus. Arterial calcification was seen on the mammograms of 481 of 5,000 consecutive patients. The prevalence of arterial calcification was substantially higher among diabetics (45/106 = 42.5%) than among nondiabetics (436/4,894 = 8.9%). An even more significant association was found between arterial calcification and advancing age for both diabetics and nondiabetics. None of the 31 patients younger than 50 years with arterial calcification were diabetic, and none of the nine diabetics younger than 50 years had arterial calcification. Most important, less than 10% (45/481) of the patients who demonstrated arterial calcification were found to be diabetic. The presence of arterial calcification on mammograms is a more reliable indicator of advancing age than of diabetes, and the association of breast arterial calcification with diabetes is too weak to be clinically useful.

Adult↗
PubMed1995

Fetal liver calcifications: sonographic appearance and postnatal outcome.

PURPOSE: To determine the importance of intrahepatic calcifications seen sonographically in the fetus. MATERIALS AND METHODS: The authors retrospectively reviewed sonograms obtained in fetuses scanned between 16 and 40 gestational weeks in whom intrahepatic calcifications were seen. The number and character of these calcifications were determined. Follow-up scans obtained in utero and after birth were also reviewed. Outcome was determined after birth. RESULTS: Thirty-three fetuses had intrahepatic calcifications at 16-38 weeks gestation. Four of the 33 fetuses died, one of which had liver calcifications as the only sonographic finding. This fetus had cytomegalovirus and was the only fetus with increasing numbers of calcifications on follow-up scans. All fetuses with isolated liver calcifications had a normal postnatal outcome (96% survival rate for fetuses with isolated intrahepatic calcifications). Of eight fetuses with additional anomalies, five lived; only two were healthy newborns. CONCLUSION: The outcome in fetuses with isolated intrahepatic calcifications is usually excellent, although viral causes must be excluded if additional findings appear.

Abnormalities, Multiple↗
PubMed2003

Vascular calcification in chronic renal failure.

The prevalence and extent of vascular calcification (VC) increases rapidly with time on dialysis. There is increasing evidence that medial calcification of conduit arteries, without intimal disease, is associated with important abnormalities of vascular compliance and increased risk of cardiovascular death. Coronary artery calcification is also common in end-stage renal disease, but further research is required to determine how much of this calcification is in the form of calcified intimal atherosclerotic plaque and how much in the tunica media. Calcific uraemic arteriolopathy causes a syndrome of ischaemic necrosis of the skin and subcutaneous tissue and appears to be increasing in incidence. At all sites, arterial calcification is a biologically controlled process, with expression in vascular smooth muscle cells of genes usually expressed in osteoblasts and the formation of hydroxyapatite. High extracellular phosphate concentration induces these phenotypic changes in vitro, and much of the clinical evidence supports hyperphosphataemia as the major driver of VC. Whether warfarin treatment plays a role, by inhibiting production of vitamin-K-dependent inhibitors of calcification in humans, remains uncertain but possible. High doses of prescribed calcium-based phosphate binders are associated with VC, whereas use of sevelamer to achieve the same serum phosphate level greatly retards progression of coronary and aortic calcification. The biological mechanism by which positive calcium balance and/or episodes of hypercalcaemia promotes VC remains unclear. Treatment of established calcific uraemic arteriolopathy consists of aggressive reduction of serum calcium x phosphate product; the roles of hyperbaric oxygen, steroid therapy, and non-warfarin anticoagulation remain uncertain.

Arteries↗
PubMed2005

Quantification of calcification in atherosclerotic lesions.

Calcification can be deposited throughout the vasculature in several forms of calcium phosphate, including calcium hydroxyapatite (CHA). Calcium accumulation in arteries by mineralization and calcium loss from bone by osteoporosis often coexist, and vascular calcification may share common mechanisms with bone remodeling. Deposition of calcification in valves and arteries diminishes the valvular or arterial wall elasticity, a major cause of aneurysm and stenosis. Obstruction of arteries by calcification and other components can lead to heart attack and stroke. Mineralization in the femoral arteries can cause intermittent claudication in the legs, causing decreased mobility. Accurate measurement of calcification is essential for identifying other factors associated with this process and ultimately for elucidating the mechanism(s) of calcification. A wide range of methods for visualizing and measuring calcification for diagnosis and treatment in vivo and for studying the calcification process ex vivo are available. This review provides a critical comparison of older established methods and newer evolving technologies for quantifying calcification.

Animals↗
PubMed2002

Acetylated low-density lipoprotein stimulates human vascular smooth muscle cell calcification by promoting osteoblastic differentiation and inhibiting phagocytosis.

BACKGROUND: Vascular smooth muscle cells (VSMCs) in atherosclerotic lesions display an osteogenic phenotype, and calcification commonly occurs in association with lipid. We therefore tested the hypothesis that lipid components in atherosclerotic lesions influenced VSMC phenotype and calcification using an in vitro model of calcification. METHODS AND RESULTS: In situ hybridization of human atherosclerotic plaques (n=10) collected from patients undergoing carotid endarterectomy demonstrated that subsets of lipid-filled VSMCs adjacent to sites of calcification expressed alkaline phosphatase, bone Gla protein, and bone sialoprotein, suggesting an osteogenic phenotype. Treatment of VSMCs in culture with acetylated low-density lipoprotein (acLDL) or lipoprotein-deficient serum altered the time course of bone-associated protein gene expression and calcification. AcLDL increased nodule calcification 3-fold, whereas lipoprotein-deficient serum significantly inhibited it. Reverse transcriptase-polymerase chain reaction and Western analysis demonstrated the presence of the acLDL receptor, SRA1, exclusively in calcifying nodular VSMCs, and blockade of SRA with polyinosinic acid inhibited acLDL-induced calcification. Because apoptotic bodies can serve as nucleation sites for calcification, we investigated whether acLDL could stimulate apoptosis in nodules. Apoptosis of nodular VSMCs was unaltered, but the number of apoptotic bodies per nodule increased approximately 3-fold, implying a defect in phagocytosis. Consistent with these observations, binding of apoptotic bodies to VSMCs was decreased in the presence of acLDL. CONCLUSIONS: These studies suggest that modified lipoproteins stimulate calcification by enhancing osteogenic differentiation of VSMCs and by a novel mechanism whereby acLDL interacts with SRA on VSMCs and blocks phagocytic removal of apoptotic bodies.

Adolescent↗
PubMed1998

1,25-Dihydroxyvitamin D3 increases in vitro vascular calcification by modulating secretion of endogenous parathyroid hormone-related peptide.

BACKGROUND: A significant association between vascular calcification and osteoporosis has been noted, suggesting that calcium homeostasis is important in vascular calcification as well as in osteoporosis. Moreover, results of our previous studies suggest that calcium-regulating hormones such as parathyroid hormone-related peptide (PTHrP) may modulate vascular calcification. Therefore, we hypothesized that 1alpha,25-dihydroxyvitamin D3 [1,25(OH)2D3] may have a direct impact on the calcium-regulating system of vascular smooth muscle cells, resulting in deposition of calcium in vascular wall. METHODS AND RESULTS: We investigated the effect of 1,25(OH)2D3 on in vitro calcification by bovine vascular smooth muscle cells (BVSMCs). 1,25(OH)2D3 dose dependently increased BVSMC calcification and alkaline phosphatase activity. 1,25(OH)2D3 also decreased secretion of PTHrP by BVSMCs in a dose-dependent manner and depressed its gene expression. Furthermore, exogenous PTHrP (fragment 1-34) antagonized the stimulatory effect of 1,25(OH)2D3 on BVSMCs. Finally, 1,25(OH)2D3 dose dependently increased the expression of the osteopontin gene, one of the bone matrix proteins in BVSMCs, contributing to its stimulatory action on BVSMC calcification. CONCLUSIONS: These data suggest that 1,25(OH)2D3 exerts a stimulatory effect on vascular calcification through direct inhibition of the expression of PTHrP in BVSMCs as an endogenous inhibitor of vascular calcification. Moreover, the stimulatory effects of 1,25(OH)2D3 on alkaline phosphatase activity and osteopontin expression may contribute to its promoting action in vascular calcification.

Alkaline Phosphatase↗
PubMed2005

Bone morphogenetic proteins in vascular calcification.

Vascular calcification is a common problem among the elderly and those with chronic kidney disease (CKD) and diabetes. The process of tunica media vascular calcification in CKD appears to involve a phenotypic change in the vascular smooth muscle cell (VSMC) resulting in cell-mediated mineralization of the extracellular matrix. The bone morphogenetic proteins (BMPs) are important regulators in orthotopic bone formation, and their localization at sites of vascular calcification raises the question of their role. In this review, we will discuss the actions of the BMPs in vascular calcification. Although the role of BMP-2 in vascular calcification is not proven, it has been the most studied member of the BMP family in this disease process. The role of BMP-2 may be through inducing osteoblastic differentiation of VSMCs through induction of MSX-2, or by inducing apoptosis of VSMCs, a process thought critical in the initiation of vascular calcification. Additionally, BMP-2 may be related to loss of regulation of the matrix Gla protein. A second BMP, BMP-7, less studied than BMP-2 may have opposing actions in vascular calcification. In postnatal life, BMP-7 is expressed primarily in the kidney, and expression is diminished by renal injury. BMP-7 is an important regulator of skeletal remodeling and the VSMC phenotype. BMP-7 restores skeletal anabolic balance in animal models of CKD with disordered skeletal modeling, also reducing serum phosphate in the process. BMP-7 also reverses vascular calcification in CKD, and reduction in vascular calcification is due, in part, to reduced serum phosphate, an important inducer of VSMC-mediated vascular mineralization and in part to direct actions on the VSMC.

Animals↗
PubMed2005

Acculturation and socioeconomic position as predictors of coronary calcification in a multiethnic sample.

BACKGROUND: Coronary calcium has recently emerged as a marker of subclinical coronary heart disease. Although there has been much interest in race differences in calcification, heterogeneity within race or ethnic groups has not been investigated. METHODS AND RESULTS: Data from the Multi-Ethnic Study of Atherosclerosis (MESA), a population-based study of coronary calcification, were used to investigate acculturation and socioeconomic position as predictors of coronary calcification within 2553 non-Hispanic whites, 1734 non-Hispanic blacks, 1457 Hispanics, and 797 Chinese residing in the United States. Coronary calcium was assessed by chest CT. Relative risk regression and linear regression were used to estimate adjusted associations of sociodemographic variables with the presence and amount of calcium. Not being born in the United States was associated with a lower prevalence of calcification in blacks (relative prevalence [RP], 0.75; 95% confidence limit [CL], 0.61 to 0.94) and Hispanics (RP, 0.89; 95% CL, 0.81 to 0.98) after adjustment for age, sex, income, and education. Years in the United States was positively associated with prevalence of calcification in non-US-born Chinese (adjusted RP per 10 years in United States, 1.06; 95% CL, 1.01 to 1.11) and non-US-born blacks (RP, 1.59; 95% CL, 1.22 to 2.06). Low education was associated with a higher prevalence of calcification in whites (adjusted RP for no high school versus complete college, 1.17; 95% CL, 1.05 to 1.32) but with lower prevalence of calcification in Hispanics (RP, 0.91; 95% CL, 0.77 to 1.09) (P for interaction=0.02). US birth and time in the United States were also positively associated with the extent of calcification in persons with detectable calcium. These differences did not appear to be accounted for by smoking, body mass index, LDL and HDL cholesterol, hypertension, and diabetes. CONCLUSIONS: Acculturation and socioeconomic factors are associated with differences in the prevalence and amount of coronary calcification within whites, Chinese, blacks, and Hispanics. The presence of this heterogeneity needs to be acknowledged in the quantification and investigation of race/ethnic differences.

Acculturation↗
PubMed2006

Aortic valve calcification in systemic lupus erythematosus.

Aortic valve calcification is associated with atherosclerosis in the general population. We investigated the prevalence of and associates of aortic valve calcification in systemic lupus erythematosus (SLE). One-hundred and ninety-nine SLE patients enrolled in a clinical trial had aortic valve calcification assessed by helical CT. The patients had a mean age of 44.3 +/- 11.4 years and were 92% female, 61% Caucasian, 34% African-American, 2% Asian and 2% Hispanic. Aortic valve calcification was present in 1.5%, whereas coronary calcium was found in 43% and carotid plaque in 17%. Among cardiovascular risk factors, hs-CRP (P = 0.0592), fibrinogen (P = 0.0507), and lipoprotein(a) (P = 0.0250), were associated with aortic valve calcification. Prednisone use (P = 0.049) and use of methotrexate (P = 0.0174) were also associated with aortic valve calcification. Aortic valve calcification was associated with antiphospholipid antibody positivity (0.0287) (lupus anticoagulant, by dilute Russell viper venom time). It was not associated with coronary calcium or carotid plaque. Aortic valve calcification, although rare in SLE, was associated with some novel cardiovascular risk factors and with a marker of hypercoagulability (lupus anticoagulant). In contrast to the general population, aortic valve calcification in SLE is not associated with subclinical measures of atherosclerosis, such as coronary calcium or carotid plaque.

Adult↗
PubMed1999

Prevalence of soft tissue calcifications in patients with SLE and effects of alfacarcidol.

OBJECTIVE: To clarify the prevalence and etiology of ectopic calcification in patients with systemic lupus erythematosus (SLE), especially under the active vitamin D3 administrations and to reveal the risk factors of ectopic calcification. METHODS: Sixty patients with SLE, excluding the patients on dialysis were studied. We examined radiographs of hands, forearms, upper and lower extremities, and pelvises of all patients to evaluate ectopic calcification. RESULTS: The prevalence of ectopic calcification in SLE was 40% (24 out of 60 patients), found in 6.7% (4 patients) in peripheral arteries, 33.3% (20 patients) in periarticular area and 16.7% (10 patients) in other soft tissues. The incidence of lupus nephritis and nephrotic syndrome were significantly higher (respectively: P=0. 0144 and P=0.0348) in the calcification-positive than negative group. Total protein levels (7.04+/-0.6 g/dl) of patients in the calcification-positive group were decreased significantly (P=0.0056) compared with 7.48+/-0.55 g/dl in the negative group. However, other biochemical parameters were not significantly different between the two groups. Sixty-three percent of the SLE patients with ectopic calcification received alfacarcidol, which is significantly (P=0. 0007) higher than the 19% in patients without calcification. CONCLUSION: It is suggested that the alfacarcidol therapy and lupus nephritis could increase the risk of ectopic calcification in SLE patients.

Adult↗
PubMed2004

Frequency and effects of intratendinous and peritendinous calcifications after open Achilles tendon repair.

BACKGROUND: Although calcification of the Achilles tendon has been described by several authors, a detailed evaluation of its frequency and effects on clinical outcome has not been reported. The purposes of this work were to determine the frequency of calcifications in the Achilles tendon after open repair and their effects on clinical outcomes and to identify possible risk factors for postoperative calcification. METHODS: Thirty-six patients with open Achilles tendon repair were evaluated at an average followup of 19 months. Evaluation included a self-assessment questionnaire concerning treatment outcomes, clinical examination, and radiographic and ultrasonographic examinations. RESULTS: No patient had calcifications in the Achilles tendon area before surgery. Postoperatively, intratendinous or peritendinous calcifications, ranging in size from 3 mm to 37 mm, were found in 10 (28%) of the 36 patients. The development of calcifications was associated with chronic swelling, decreased range of motion of the ankle joint, and increase pain, especially with calcifications larger than 10 mm. No association was found between the development of calcifications and the surgical technique, suture materials, time from injury to surgery, or postoperative management, and no risk factors could be identified. CONCLUSIONS: Calcifications of the Achilles tendon appear to be frequent after open tendon repair and to have a negative effect on clinical outcome.

Achilles Tendon↗
PubMed2004

Calcification in carotid atheromatous plaque: delineation by 3D-CT angiography, compared with pathological findings.

The authors investigated calcification in the carotid plaque of patients with carotid stenosis, using three-dimensional CT angiography (3D-CTA) and comparing the images with findings from pathological inspection. Calcification was clearly visualized using volume rendering (VR) images constructed with a refined workstation as well as maximum intensity projection and multiplanar reconstruction images. Calcification in VR images was classified into bean- and island-like shaped groups, while calcification in microscopic examination was classified into granular, lump and laminar types. Granular type of calcification tended to be found at the intimal side of the plaque, while lump/laminar calcification was preferentially located at the side of the internal elastic fiber. Though carotid endarterectomy successfully removed calcification at both sides, the presence of a granular calcification assembly when massive calcification is observed with 3D-CTA might alert us to the importance of predicting the hardness of plaque in carotid angioplasty and stenting.

Aged↗
PubMed2004

Molecular, endocrine, and genetic mechanisms of arterial calcification.

Pathologists have recognized arterial calcification for over a century. Recent years have witnessed a strong resurgence of interest in atherosclerotic plaque calcification because it: 1) can be easily detected noninvasively; 2) closely correlates with the amount of atherosclerotic plaque; 3) serves as a surrogate measure for atherosclerosis, allowing preclinical detection of the disease; and 4) is associated with heightened risk of adverse cardiovascular events. There are two major types of calcification in arteries: calcification of the media tunica layer (sometimes called Mönckeberg's sclerosis), and calcification within subdomains of atherosclerotic plaque within the intimal layer of the artery. There are important similarities and differences between these two entities. Of particular interest are increasing parallels between cellular and molecular features of arterial calcification and bone biology, and this has led to accelerating interest in understanding how and why bone-like mineral deposits may form in arteries. Here, we review the two major pathological types of arterial calcification, the proposed models of calcification, and endocrine and genetic determinants that affect arterial calcification. In addition, we highlight areas requiring further investigation.

Animals↗
PubMed2003

Influence of commissural calcification on the immediate outcomes of percutaneous balloon mitral valvuloplasty.

OBJECTIVES: To evaluate the impact of mild to moderate commissural calcification on the immediate outcomes of percutaneous balloon mitral valvuloplasty (PBMV). METHODS AND RESULTS: We analysed the results of 223 consecutive patients (mean age 37.6 +/- 8.7 years) who underwent PBMV for rheumatic mitral stenosis. Commissural calcification was identified with a two-dimensional echocardiography (echo) in 65 (29.1%) patients with the severity of calcification being graded from 0-3. The anatomy and function of the mitral valve were assessed byWilkins echo score. In patients with no commissural calcification the increase in mitral valve area after PBMV was 0.90 +/- 0.42 cm2, which was greater than the increase in those with calcification grade 1 (0.83 +/- 0.42 cm2, p < 0.05), grade 2 (0.72 +/- 0.38 cm2, p < 0.05) and grade 3 (0.63 +/- 0.13 cm2, p < 0.05). In patients with an echo score of < or = 8, the presence of commissural calcification was associated with a smaller increase in mitral valve area (p < 0.05) and a smaller reduction in New York Heart Association (NYHA) function class after PBMV (p < 0.05). In patients with an echo score of more than 8, commissural calcification had no significant effect on the valve area increase and NYHA function class reduction (p > 0.05). CONCLUSIONS: Commissural calcification has an adverse effect on the clinical results of PBMV. Detailed pre-procedural assessment of commissural calcification with echocardiography must be performed to provide background information on the immediate outcomes of PBMV.

Adolescent↗