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PubMed2003

Effects of adrenomedullin, C-type natriuretic peptide, and parathyroid hormone-related peptide on calcification in cultured rat vascular smooth muscle cells.

To clarify the regulating mechanism of vascular calcification, the investigators observed the effects of three vasoactive peptides, adrenomedullin (ADM), C-type natriuretic peptide (CNP), and parathyroid hormone-related peptide (PTHrP) on calcification in rat vascular smooth muscle cells (VSMCs). Beta-glycerophosphate stimulated growth and calcification in VSMCs. Adrenomedullin and CNP lowered beta-glycerophosphate-induced increase in VSMC growth. All three vasoactive peptides attenuated the increases of 45Ca accumulation, calcium content, and alkaline phosphatase activity in calcified VSMCs. As for comparing the inhibitory effects, the strongest was PTHrP. Both ADM and PTHrP increased cyclic adenosine monophosphate (cAMP) content in calcified VSMCs, but CNP upregulated cyclic guanosine monophosphate (cGMP) content. The PKA inhibitor PKAI completely reversed the inhibition of ADM on cell growth and all inhibitory effects of PTHrP on the parameters of calcification. The PKG inhibitor H8, however, strongly antagonized all the inhibitory effects of CNP on calcification. These data suggested that beta-glycerophosphate-induced calcification in VSMCs was inhibited by ADM, CNP, and PTHrP. Adrenomedullin and PTHrP inhibited VSMC calcification partially through the cAMP/PKA pathway, whereas CNP inhibited VSMC calcification through the cGMP/PKG pathway. This study could be of help in understanding the pathogenesis of vascular calcification, and providing new target for clinical treatment of cardiovascular diseases associated with vascular calcification.

Adrenomedullin↗
PubMed1997

Disc degeneration/back pain and calcification of the abdominal aorta. A 25-year follow-up study in Framingham.

STUDY DESIGN: A 25-year follow-up study of 606 members of the population-based Framingham cohort, who had received lateral lumbar radiographs in 1967-1968 and 1992-1993, and completed an interview on back symptoms at the second examination. OBJECTIVES: To evaluate whether calcific lesions in the posterior wall of the abdominal aorta, the source of the feeding arteries of the lumbar spine, are associated with disc degeneration or back pain, which would suggest that ischemia of the lumbar spine leads to disc degeneration. METHODS: The presence of radiographic aortic calcification was ascertained in front of each lumbar segment from L1 through L4, and disc degeneration at intervertebral spaces from L1-L2 through L4-L5. The associations between aortic calcification, disc degeneration, and back pain were tested using logistic regression with adjustment for age and sex. RESULTS: At the baseline examination, aortic calcification was significantly associated with general disc degeneration, that is, disc space narrowing or endplate sclerosis at any lumbar level (odds ratio 1.6; 95% confidence interval 1.0-2.5; P = 0.034). In longitudinal, level-specific analyses, comparing local aortic calcifications with disc degeneration at the matching level, aortic calcifications predicted disc deterioration, that is, a decrease in disc space or appearance of endplate sclerosis, between the examinations (odds ratio 1.5; 95% confidence interval 1.3-1.8; P < 0.001). Furthermore, subjects in whom aortic calcifications developed between the examinations had disc deterioration twice as frequently as those in whom aortic calcifications did not develop (odds ratio 2.0; 96% confidence interval 1.2-3.5; P = 0.013). Also, individuals with severe (Grade 3) posterior aortic calcification in front of any lumbar segment were more likely than others to report back pain during adult life (odds ratio 1.6; 95% confidence interval 1.1-2.2; P = 0.014). CONCLUSIONS: Advanced aortic atherosclerosis, presenting as calcific deposits in the posterior wall of the aorta, increases a person's risk for development of disc degeneration and is associated with the occurrence of back pain.

Aged↗
PubMed2005

Vascular calcification.

PURPOSE OF REVIEW: Accumulating evidence suggests that the high cardiovascular mortality observed in patients with end-stage renal disease is due in part to the deleterious effects of vascular calcification that develops over time on dialysis. This review focuses on recent cell biological and animal studies that have shed light on the mechanisms and regulators of vascular smooth muscle cell calcification in end-stage renal disease. RECENT FINDINGS: Clinical studies demonstrate that high circulating levels of phosphate or calcium predict vascular calcification. Recent cell biological studies have provided novel insights into how vascular smooth muscle cells regulate calcification in response to such insults. Vascular smooth muscle cell damage and subsequent vesicle release from viable and dying cells create an environment permissive for the nucleation of basic calcium phosphate mineral. This, combined with osteogenic conversion of vascular smooth muscle cells and consequent loss of their normal inhibitory processes/pathways, results in calcification. Circulating factors such as fetuin-A, with the potential to impact on vessel wall calcification, have also been identified. Animal studies suggest that the 'uremic milieu' potentiates calcification and have clearly established a link between vascular calcification and bone metabolism. However, our understanding of the factors that contribute to vascular smooth muscle cell calcification in end-stage renal disease remains incomplete. SUMMARY: Systematic studies are required that integrate epidemiological studies to identify risk factors with in-vitro experiments to investigate mechanisms leading to vascular smooth muscle cell calcification in response to these factors. Animal and clinical studies can subsequently be used to assess how modifying risk factors under the complex physiological conditions of end-stage renal disease impacts on vessel wall health.

Animals↗
PubMed2005

Early calcification of renal allografts detected by protocol biopsies: causes and clinical implications.

Interstitial calcification has been described in renal allografts, however, the etiology and significance of this finding for the graft are unclear. The aim of this study was to examine calcification in serial protocol biopsies, to test the hypothesis that calcification is related to parameters of calcium homeostasis in these patients and to analyze a possible relation between calcification and graft function at 1 year. We studied 213 patients with 586 protocol biopsies obtained 6 weeks, 3 and 6 months after transplantation. Calcifications increased over time, from 6.1% at 6 weeks to 17.8% at 6 months. Out of the 213 patients, 56 had calcification in one or more biopsies. Patients age and gender, underlying renal disease, dialysis mode and duration, previous transplantations, donor type, age and gender, HLA matches and ischemia time had no influence on calcification. Calcification was not related to rejection episodes, acute tubular lesions, calcineurin inhibitor toxicity or tubulointerstitial fibrosis and tubular atrophy. Patients with calcification had significantly higher serum parathormone and calcium levels. In patients with calcification, high PTH levels correlated with an inferior outcome of graft function at 1 year after transplantation (p<0.05). Therefore, treatment of hyperparathyroidism should be considered earlier and more often in these patients.

Adult↗
PubMed1992

Localised pulmonary metastatic calcification associated with pulmonary artery obstruction.

BACKGROUND: Metastatic pulmonary calcification, a complication of uraemia and disordered calcium metabolism, may be diffuse or localised. The factors that determine calcium precipitation are complex, but tissue alkalosis is thought to be important. As obstruction of the pulmonary artery theoretically causes local alkalosis a retrospective necropsy study was carried out to examine the relation between metastatic pulmonary calcification and vascular obstruction. METHODS: Five patients with focal and two with diffuse metastatic calcification in the lungs were identified over eight years. Lungs were studied macroscopically and by light microscopy, haematoxylin and eosin and histochemical stains being used for calcium. RESULTS: Underlying risk factors for calcification in these patients included renal failure in six and disseminated malignancy in five. In the five patients with localised calcification obstruction of the pulmonary artery by thrombus or tumour was found proximal or adjacent to areas of calcium deposition. In two patients metastatic calcification was confined to a lung with unilateral pulmonary artery thromboembolic occlusion. Calcification was not specifically associated with infarction, pneumonia, or diffuse alveolar damage. Lesions of the pulmonary artery were not seen in the two patients with diffuse bilateral metastatic calcification. CONCLUSION: In this small series there was a spatial association between pulmonary artery obstruction and localised metastatic calcification. It is proposed that pulmonary artery obstruction alters the microchemical environment of the lung, favouring tissue alkalosis and thereby enhancing parenchymal calcification in patients predisposed to this condition.

Adult↗
PubMed1986

Morphology, progression, and regression of arterial and periarterial calcifications in patients with end-stage renal disease.

The appearance of arterial calcifications over time was studied radiographically in 143 patients with end-stage renal disease. Of these, 85 patients had only slight calcifications; 58 had the well-known, linear, pipe stem-like arterial calcifications. In 44 of the 58, small nodular calcifications were noted, often external to the linear calcifications. Nine patients had larger periarterial calcifications, which have not been previously described to our knowledge. Arterial calcifications progressed in 82 of 143 patients (57%) and regressed in 19 (13%). During progression, thickening of the linear calcifications was often observed, and in ten patients this caused definite luminal narrowing. From 1976 to 1984, five of 71 patients (7%) required amputations; all five had marked arterial calcifications. Better controlled clinical studies are indicated to detect factors that may prevent the progression and promote the regression of arterial calcifications.

Adult↗
PubMed1999

Calcification of vascular smooth muscle cell cultures: inhibition by osteopontin.

Calcification of vascular tissue is a common complication in aging, atherosclerosis, diabetes, renal failure, aortic stenosis, and prosthetic valve replacement. Osteopontin is a noncollagenous adhesive protein routinely found at sites of dystrophic calcification and synthesized at high levels by macrophages in calcified aortic valves and atherosclerotic plaques. In the present study, we have characterized the calcification of bovine aortic smooth muscle cell (BASMC) cultures in vitro and have studied the effects of exogenous osteopontin on mineral deposition. Induction of calcification in BASMC cultures was alkaline phosphatase-dependent and was characterized by a multilayer cell morphology. Mineral deposition occurred in the basal matrix of multilayered areas as indicated by von Kossa staining, and transmission electron microscopy and electron diffraction identified the mineral as apatite. Ultrastructural analysis of the cultures showed the presence of extracellular matrix vesicles, calcifying collagen fibrils, and nodular-type calcifications similar to those found in calcified heart valves and atherosclerotic plaques. Purified osteopontin (0.05 to 5 microgram/mL) dose dependently inhibited calcification of BASMC cultures, whereas vitronectin and fibronectin had no effect. In contrast to the inhibitory mechanism of levamisole on mineral deposition, osteopontin did not inhibit alkaline phosphatase activity or reduce phosphorus levels in the culture medium. Addition of calcium to the cultures overcame the inhibitory effect of osteopontin on BASMC culture calcification and resulted in decreased levels of calcium in the culture medium and increased levels in the cell layer. Moreover, using high-resolution, colloidal-gold immunocytochemistry, osteopontin was found intimately associated with growing apatite crystals. These data indicate that the effect of osteopontin, although calcium-dependent, was not mediated by simple calcium chelation but most likely by direct interaction of osteopontin with crystal surfaces. These studies suggest that BASMCs can be used to model vascular calcification in vitro and that soluble osteopontin released near sites of vascular calcification may represent an adaptive mechanism aimed at preventing vascular calcification.

Adaptation, Physiological↗
PubMed1993

The relevance of detecting carotid artery calcification on plain radiograph.

BACKGROUND AND PURPOSE: The aim of this study was to determine the potential value of carotid artery calcification observed on plain radiographs in patients referred for carotid angiogram in the diagnosis of carotid artery stenosis. METHODS: One hundred sixty consecutive patients with suspected carotid artery stenosis underwent both plain radiographs of the carotid arteries and digital subtraction angiography of the same vessels. In addition, 108 of these patients also had duplex ultrasound of the same vascular area. The clinical usefulness of the carotid artery calcification was assessed by calculating the likelihood ratios for different test results against results of angiography and duplex ultrasound. RESULTS: There is a statistically significant association between the degrees of calcification and carotid disease as demonstrated by angiography (P = .0001), although positive correlations of the degrees of stenosis and calcification was only fair (Spearman correlation coefficient r = .4). The sensitivity of carotid calcification in detecting clinically significant stenosis assuming any calcification is abnormal was 89% with a specificity of 46%. The likelihood ratios for 50% stenosis by angiography varied from 0.24 (no calcification) to 3.41 (level III) and for 50% stenosis by duplex ultrasound varied from 0.21 (no calcification) to more than 5.87 (level III). Assessments of the degree of calcification based on plain radiographs had excellent reproducibility (all intraclass correlation coefficients were greater than .9). CONCLUSIONS: In this population with a high prevalence of carotid artery disease, there is an association between the presence of carotid calcification and atheromatous disease. If subsequent studies were to show this to apply in the general population, this could be of value in identifying asymptomatic patients at increased risk.

Aged↗
PubMed2004

Aortic calcification and the risk of osteoporosis and fractures.

We investigated the relation between computed tomography measures of aortic calcification and values for bone density and the number of fragility fractures in 2348 healthy, postmenopausal women. To determine whether increases in vascular calcification and bone loss progress in parallel, baseline values were compared with measurements obtained 9 months to 8 yr later in a subgroup of 228 women. Of the 2348 subjects studied, 70% had osteoporosis, 30% had at least one vertebral fracture, and 9% had at least one hip fracture. Aortic calcifications were inversely related to bone density and directly related to fractures. After adjusting for age and potential confounders, measures for aortic calcification predicted 26.1% of the variance in bone density (P < 0.001). Compared with women without calcification, the odds ratios for vertebral and hip fractures in those with calcification were estimated to be 4.8 (95% confidence interval, 3.6-6.5) and 2.9 (95% confidence interval, 1.8-4.8), respectively. The subgroup analysis of 228 women longitudinally studied showed that the percentage of yearly increase in aortic calcification accounted for 47% of the variance in the percentage rate of bone loss (P < 0.001). Moreover, a strong graded association was observed between the progression of vascular calcification and bone loss for each quartile. Women in the highest quartile for gains in aortic calcification had four times greater yearly bone loss (5.3 vs.1.3% yearly; P < 0.001) than women of similar age in the lowest quartile. Smaller, but highly significant differences were also found between all other quartiles. We conclude that aortic calcifications are a strong predictor for low bone density and fragility fractures.

Aged↗
PubMed2005

Myocardial stiffness, cardiac remodeling, and diastolic dysfunction in calcification-prone fetuin-A-deficient mice.

Accelerated atherosclerosis in dialysis patients is characterized by severe vascular calcification, and the magnitude of vascular calcification is associated with increased cardiovascular mortality. Calcification-dependent arterial stiffness is considered to be a major determinant of cardiac failure in uremia. Fetuin-A/alpha(2)-Heremans-Schmid glycoprotein is an abundant serum protein with powerful calcification inhibitory properties. Fetuin-A deficiency was recently linked to cardiovascular mortality in dialysis patients. Fetuin-A knockout (fetuin-KO) mice spontaneously develop widespread soft tissue calcification, including significant myocardial calcification, whereas larger arteries are spared. Therefore, this investigation offers the unique opportunity to study the functional role of isolated myocardial calcification independent of arterial stiffness by assessing the hemodynamics of fetuin-KO mice. Cardiac output in fetuin-KO mice was lower than in wild-type mice (fetuin-KO 1.81 +/- 0.18 versus WT 2.45 +/- 0.29 ml/min per g; P < 0.005), and fetuin-KO mice were refractory to dobutamine stimulation. Left ventricular relaxation was significantly impaired in fetuin-KO hearts with the relaxation index reduced by 23% (P < 0.005). After ischemia, fetuin-KO hearts displayed a continuous decline in left ventricular developed pressure after the initial phase of reperfusion, resulting in 77 +/- 15% of preischemic left ventricular developed pressure (P < 0.05 versus wild-type). In fetuin-KO mice, dystrophic cardiac calcification, with myocardial calcium contents increased 60-fold, was associated with profound induction of profibrotic TGF-beta and downstream collagen and fibronectin mRNA synthesis. In conclusion, independent of arterial stiffness, calcification-associated "myocardial stiffness" characterized by cardiac fibrosis, diastolic dysfunction, impaired tolerance to ischemia, and catecholamine resistance thus may constitute an underestimated cardiovascular risk factor that contributes to cardiac failure in calcification-prone states.

Animals↗
PubMed1992

Calcified renal stones and cyst calcifications in autosomal dominant polycystic kidney disease: clinical and CT study in 84 patients.

Although renal calculi and cyst calcifications occur commonly in patients with autosomal dominant polycystic kidney disease (ADPKD), their true frequency is unknown because it is difficult to distinguish between the two with excretory urography and sonography. A detailed analysis of renal calcifications in ADPKD based on CT findings has not been performed. Accordingly, we retrospectively evaluated clinical and CT findings in 84 patients with ADPKD to determine the frequency of calculi and cyst calcifications, the relationship of these abnormalities to symptoms, and possible factors in their pathogenesis. Of the 84 patients, 53 had both IV contrast-enhanced and unenhanced CT scans and 31 had unenhanced scans only. We examined unenhanced CT scans of all 84 patients for renal calcifications. However, we classified renal calcifications into stones and cyst calcifications in only the 53 patients, because it is often difficult to distinguish between the two when only unenhanced scans are available. Of 84 patients, 18 (21%) had passed renal calculi or had stones treated surgically and 42 (50%) had renal calcifications on CT. Of the 53 patients who had both enhanced and unenhanced CT scans, 19 (36%) had renal calculi on CT. Patients with stones had significantly higher frequencies of previous flank pain (68% vs 35%) and of urinary tract infections (63% vs 18%) than did those without calculi. Cyst calcifications occurred in 13 (25%) of 53 patients and were probably a consequence of cyst hemorrhage. Cyst calcifications were found significantly more often in older patients with larger kidneys and worse renal function. We conclude that renal stones have a high rate of occurrence among patients with ADPKD and are a significant cause of morbidity in this disorder. Cyst calcification is also common in patients with ADPKD, particularly those with more advanced cystic disease.

Adolescent↗
PubMed1994

Metastatic pulmonary calcification in patients with hypercalcemia: findings on chest radiographs and CT scans.

OBJECTIVE: The objective of this study was to characterize the findings on chest radiographs and CT scans in patients with metastatic pulmonary calcification due to hypercalcemia. MATERIALS AND METHODS: The chest radiographs and CT scans of seven patients with biopsy-proved metastatic pulmonary calcification were reviewed by two observers. Metastatic calcification was due to chronic renal failure (n = 4), T-cell leukemia (n = 1), multiple endocrine neoplasia type I syndrome (n = 1), and idiopathic hypercalcemia (n = 1). RESULTS: Numerous nodular opacities measuring 3-10 mm in diameter were seen on the chest radiographs in five cases, and patchy areas of parenchymal opacification were seen in two cases. Calcification of the nodules was evident in two cases. On CT scans, pulmonary nodules were present in all seven cases. These nodules were predominant in the upper lung zone in three cases, were diffuse in three cases, and were predominant in the lower lung zone in one case. Calcification of the nodules was evident on the CT scans in four of the seven cases, and calcification of vessels in the chest wall was evident in six of seven cases. Other findings on CT scans included diffuse areas of ground-glass attenuation (n = 3) and patchy consolidation (n = 2). CONCLUSION: Numerous small nodules are the most common finding on the chest radiographs of patients with metastatic pulmonary calcification. The calcific nature of the nodules is seldom obvious, however. Pulmonary nodules are also the most common finding on CT scans, where the calcific nature of the nodules is more readily apparent. Additionally, calcification is often seen in the vessels of the chest wall on CT scans. The combination of calcified nodules and calcified vessels in the chest wall on CT scans may be characteristic.

Adult↗
PubMed1995

Calcification and fibrosis in mesenteric carcinoid tumor: CT findings and pathologic correlation.

OBJECTIVE: The purposes of this study were to determine the frequency and characteristics of calcification and fibrosis in mesenteric carcinoid tumor as seen on CT scans and to evaluate their possible role in diagnosis. MATERIALS AND METHODS: The CT findings in 29 cases of proved mesenteric carcinoid tumor were analyzed retrospectively. Tumors were assessed for size, margin, density, radiating strands, calcification, and associated thickening of the small-bowel wall. Matching histologic sections were available for 21 of the cases. They were reviewed independently for histologic pattern, degree of fibrosis, degree of infiltration along neurovascular bundles, necrosis, lymph node architecture, and calcification or ossification within the mass. CT and pathologic findings were then assessed for possible relationships. RESULTS: Calcification was detected by CT in 70% (21 of 30) of mesenteric masses. Three patterns of calcification were noted: small, stippled calcification (n = 11); coarse, dense calcification (n = 7); and diffuse calcification (n = 3). All calcification was localized within areas of poorly cellular mature fibrous tissue. The degree of radiating strands detected by CT tended to increase with the degree of fibrosis seen histopathologically (p = .06). CONCLUSION: Calcification in mesenteric carcinoid tumors was observed by CT in most cases of this series. The triad of a calcified mesenteric mass, radiating strands, and adjacent bowel-wall thickening should be considered highly suggestive of carcinoid tumor.

Aged↗
PubMed2000

Comparison of rate of development and rate of change for benign and malignant breast calcifications at the lumpectomy bed.

OBJECTIVE: The study purpose was to evaluate the rate of development and the rate of change for benign and malignant breast calcifications at the lumpectomy bed. MATERIALS AND METHODS: Retrospective review identified 53 new calcifications at the lumpectomy bed in patients with available mammograms and medical records. Breast Imaging Reporting and Data System (BI-RADS) categories were retrospectively assigned on the basis of initial prospective recommendation for yearly follow-up (category 2), 6-month follow-up (category 3), or biopsy (category 4 or 5). Outcomes were defined as benign for no recurrence at the lumpectomy bed on biopsy or follow-up and malignant if biopsy-proven at the lumpectomy bed. RESULTS: The median rate of development after lumpectomy was 23 months (range, 2-174 months) for benign and 39 months (range, 15-112 months) for malignant calcifications. Fifteen (28%) of 53 calcifications were classified as BI-RADS category 3. Twelve (80%) of 15 were downgraded to BI-RADS category 2 at a median follow-up of 6.5 months (range, 6-16 months); none represented recurrent disease. Three (20%) of 15 were upgraded to BI-RADS category 4 at the 6-month follow-up, one despite stability (benign) and two for increasing pleomorphism (malignant). Nine (17%) of 53 calcifications were classified as BI-RADS category 4 or 5; six (67%) of the nine were malignant and three (33%) were benign at biopsy. Twenty-nine (55%) of 53 calcifications were classified as BI-RADS category 2, none representing recurrent disease. CONCLUSION: Benign calcifications at the lumpectomy bed usually develop earlier than malignant calcifications, but the rate of development overlaps. Most calcifications initially placed in the probably benign category evolve quickly to more benign or more malignant morphology. Most calcifications heralding recurrence appear suspicious on first presentation.

Adult↗
PubMed2000

Heterotopic calcification and tears of the ulnar collateral ligament: radiographic and MR imaging findings.

OBJECTIVE: The purpose of this paper is to describe the radiographic and MR imaging appearance of heterotopic calcification in the ulnar collateral ligament. MATERIALS AND METHODS: Retrospective radiographic review of 710 patients examined for elbow pain yielded 42 individuals (age range, 16-38 years) with heterotopic calcification in the ulnar collateral ligament. Radiographic and MR imaging findings were compared with surgical findings. RESULTS: Fifty-one heterotopic calcifications were identified in 42 patients; nine patients had two sites of heterotopic calcification. Average initial calcification size in the craniocaudal dimension was 4 mm (range, 1-12 mm) and in the transverse dimension was 1 mm (range, 1-4 mm). Five of 42 patients had enlargement of the calcification on follow-up radiography. The largest heterotopic calcification that was not visualized on MR imaging measured 5 x 4 mm in craniocaudal and transverse dimensions. Of 34 patients with heterotopic calcification who underwent surgery, 26 patients (76%) had either partial or complete tears of the ulnar collateral ligament. CONCLUSION: Heterotopic calcification in the ulnar collateral ligament may be associated with partial or complete tears. The MR imaging detection of heterotopic calcification is less sensitive than that of radiography of the elbow.

Adolescent↗
PubMed2004

Aortic valve calcification as a marker for aortic stenosis severity: assessment on 16-MDCT.

OBJECTIVE: The degree of valvular calcification in patients with aortic stenosis was determined with retrospectively ECG-gated 16-MDCT and correlated with the severity of stenosis assessed at cardiac catheterization. SUBJECTS AND METHODS: We conducted a prospective study of 72 patients (38 men and 34 women; mean age +/- SD, 69.5 +/- 8.8 years) with aortic stenosis who underwent 16-MDCT and cardiac catheterization. Aortic valve calcification was assessed using the aortic Agatston score, aortic mass score, and aortic volume score. Severity of aortic stenosis was classified at cardiac catheterization. Aortic valve area and peak-to-peak and mean transvalvular gradients were correlated with the degree of calcification determined on MDCT. RESULTS: All measured aortic valve calcification scores were significantly higher in patients with severe aortic stenosis (n = 46) than in patients with moderate (n = 15) or mild (n = 11, p < 0.001) aortic stenosis. Aortic valve calcification scores were inversely related to aortic valve area (r = -0.67, p < 0.001 for aortic mass score) and correlated significantly with peak-to-peak (r = 0.70, p < 0.001) and mean transvalvular (r = 0.72, p < 0.001) gradients. No correlation between the aortic valve calcification and the total coronary calcium scores was observed. CONCLUSION: Aortic valve calcification assessed on 16-MDCT is associated with severity of aortic stenosis. Thus, aortic valve calcification scores should be calculated routinely in all patients undergoing MDCT for assessment of coronary calcification. High aortic valve calcification scores indicate possibly severe aortic stenosis and should prompt a further functional evaluation.

Aged↗
PubMed2002

Evaluation of calcific tendonitis of the rotator cuff: role of color Doppler ultrasonography.

OBJECTIVE: To use color Doppler ultrasonography to evaluate the morphology and vascularity of calcific tendonitis and to predict the formative and resorptive phases of the calcification. METHODS: Ninety-four patients with shoulder calcification on plain radiographs were enrolled in this study. Ultrasonography of the shoulder was focused on the rotator cuff. Color Doppler ultrasonography was applied in the calcific region. Patient symptoms were graded as painless, mild, moderate, and severe. The calcific plaques were classified as arc-shaped, fragmented or punctate, nodular, and cystic types. Color Doppler ultrasonographic signals were graded 0 to 3. The formative and resorptive phases of calcification were categorized by patient symptoms; acute onset of moderate or severe pain indicated the resorptive phase. RESULTS: The calcific plaques appeared arc shaped in 59 patients (20 painless, 19 mild, and 20 moderate), fragmented or punctate in 27 (2 painless, 3 mild, 20 moderate, and 2 severe), nodular in 6 (1 moderate and 5 severe), and cystic in 2 (severe). There was a significant difference between the morphology of the calcific plaques and clinical symptoms (P < .01). On color Doppler ultrasonography, grade 0 signals were found in 28 patients (22 painless and 6 with mild pain); grade 1 in 18 (16 mild and 2 severe); grade 2 in 41 (all moderate); and grade 3 in 7 (all severe). The correspondence between color Doppler ultrasonographic findings and clinical symptoms was excellent (P < .01). CONCLUSIONS: High-resolution ultrasonography with color Doppler imaging could differentiate the formative and resorptive phases of the calcification and could be used as a follow-up modality in calcific tendonitis of the shoulder.

Calcinosis↗
PubMed2000

[Calcification in culprit lesions of coronary artery disease].

Coronary calcification, a type of coronary atherosclerosis, has recently been closely examined in clinical cardiology because its presence may influence the selection of interventional therapy. In addition, plaque instability is one of the most important factors in the mechanism of acute coronary syndrome, and calcium deposit is frequently detected in advanced lesions. However, little is known about the clinical significance of coronary calcification. The incidence of calcium deposits was investigated in the culprit lesions (culprit coronary calcification) of patients with serious coronary artery disease to discover any cardioprotective effect. Initial coronary angiography was performed in 179 consecutive patients with acute myocardial infarction with Q wave on electrocardiography (AMI group; male 139, female 40, mean age 60.2 +/- 10 yr) and in 119 consecutive patients with stable effort angina pectoris (SAP group; male 78, female 41, mean age 63.8 +/- 8 yr) for which balloon plasty or bypass surgery was necessary from 1990 to 1997. Culprit coronary calcification was defined positive if the calcification deposit was present cinefluoroscopically within 5 mm from the culprit point. The culprit point was defined as the narrowest point after successful intracoronary thrombolytic therapy or the latest point to be dilated during a balloon inflation in direct or rescue percutaneous transluminal coronary angioplasty in the AMI group, and the narrowest point of the culprit lesion in the SAP group. There was no statistical difference in clinical background between the 2 groups other than male dominance in the AMI group and high incidence of family history of ischemic heart disease in the SAP group (p < 0.05). Culprit coronary calcification in patients over 50 years old was less frequently positive in the AMI group than the SAP group (26% vs 66%, p < 0.005, respectively). In younger patients under 50 years old, the incidence of culprit coronary calcification was low (14-15%) in both groups. Culprit coronary calcification was frequently positive in the right or the left anterior descending coronary artery in the SAP group (p < 0.005). There was no incidental sex difference of culprit coronary calcification. This comparison suggests that if a plaque contains cinefluoroscopically visible calcification, it may be regarded as less vulnerable or having a history of chronic process of atherosclerosis which results in protecting plaque rupture.

Adult↗