Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “CALCIFICATION”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 649 records · Page 36Linked to original sources

Extracoronary atherosclerotic plaque at multiple sites and total coronary calcification deposit in asymptomatic men. Association with coronary risk profile.

BACKGROUND: Recent studies have suggested that knowledge of the extent of subclinical atherosclerosis may improve prognostic information in subjects at risk of cardiovascular disease. Therefore, we tested the value of extracoronary plaque detected with echography at multiple sites and that of total coronary calcification deposit evaluated with ultrafast computed tomography for predicting the risk of coronary events estimated on the basis of traditional risk factors. METHODS AND RESULTS: We analyzed in 618 asymptomatic at-risk men the extent of extracoronary atherosclerosis, as assessed with ultrasound imaging of carotid, aortic, and femoral sites and coded as number of disease sites (none, one, two, or three) on the basis of the presence of plaque at each site, and the amount of total coronary calcification deposit, as evaluated with ultrafast computed tomography and coded as grade 0, 1, 2, or 3 on the basis of the determination of a total coronary calcium score. Concomitantly, age, systolic pressure, total and HDL cholesterol levels, current smoking, presence of diabetes, and presence of ECG left ventricular hypertrophy (ECG-LVH) were evaluated with the goal of estimating coronary risk with the use of the Framingham Study risk algorithm. The prevalence rates of at least one extracoronary disease site and coronary calcification (any grade) were high (72% and 63%). There was a strong association between the number of extracoronary disease sites and the grade of coronary calcification (P < .001). As the number of extracoronary disease sites increased, age, systolic pressure, smoking frequency, and number of risk factors increased (P < .001). As the grade of coronary calcification increased, age and systolic pressure increased (P < .001), as did the number of risk factors (P < .01). The estimated coronary risk increased with the number of extracoronary disease sites and the grade of coronary calcification (P < .001). The odds ratio of coronary risk between three and no extracoronary disease site was 2.37 (95% confidence interval [CI], 1.08 to 5.21), whereas that between grade 3 and grade 0 of coronary calcification was 1.79 (95% CI, 0.94 to 3.40). CONCLUSIONS: In an apparently healthy population, the extracoronary atherosclerotic burden as measured with multiple-site echography appears to be more powerful than the ultrafast computed tomography-detected coronary calcium burden in reflecting the multifactorial coronary risk profile. However, only men were included in the present study, and the present findings cannot be extrapolated to women.

Adult↗

High-density lipoprotein regulates calcification of vascular cells.

Accumulating evidence has suggested the protective role of HDL in cardiovascular disease processes. Calcification is a common feature of atherosclerotic lesions and contributes to cardiovascular complications due to the loss of aortic resilience and function. Recent studies have suggested that vascular calcification shares several features with skeletal bone formation at the cellular and molecular levels. These include the presence of osteoblast-like calcifying vascular cells in the artery wall that undergo osteoblastic differentiation and calcification in vitro. We hypothesized that HDL may also protect against vascular calcification by regulating the osteogenic activity of these calcifying vascular cells. When treated with HDL, alkaline phosphatase activity, a marker of osteogenic differentiation of osteoblastic cells, was significantly reduced in those cells. Prolonged treatment with HDL also inhibited calcification of these cells, further supporting the antiosteogenic differentiation property of HDL when applied to vascular cells. Furthermore, HDL inhibited the osteogenic activity that was induced by inflammatory cytokines interleukin (IL)-1beta and IL-6 as well as by minimally oxidized LDL. HDL also partially inhibited the IL-6-induced activation of signal transducer and activator of transcription 3 in calcifying vascular cells, suggesting that HDL may inhibit cytokine-induced signal transduction pathways. The inhibitory effects of HDL were mimicked by lipids extracted from HDL but not by HDL-associated apolipoproteins or reconstituted HDL. Furthermore, oxidation of HDL rendered it pro-osteogenic. Taken together, these results suggest that HDL regulates the osteoblastic differentiation and calcification of vascular cells and that vascular calcification may be another target of HDL action in the artery wall.

Alkaline Phosphatase↗

Coronary calcification improves cardiovascular risk prediction in the elderly.

BACKGROUND: Coronary calcification detected by electron beam tomography may improve cardiovascular risk prediction. The technique is particularly promising in the elderly because the predictive power of cardiovascular risk factors weakens with age. We investigated the prognostic value of coronary calcification for cardiovascular events and mortality in a general, asymptomatic population of elderly subjects. METHODS AND RESULTS: From 1997 to 2000, electron beam tomography scanning to assess coronary calcification was performed in subjects of the population-based Rotterdam Study. Risk factors were measured by standardized procedures. Coronary calcium scores were available for 1795 asymptomatic participants (mean age, 71 years; range, 62 to 85 years). During a mean follow-up of 3.3 years, 88 cardiovascular events, including 50 coronary events, occurred. The risk of coronary heart disease increased with increasing calcium score. The multivariate-adjusted relative risk of coronary events was 3.1 (95% CI, 1.2 to 7.9) for calcium scores of 101 to 400, 4.6 (95% CI, 1.8 to 11.8) for calcium scores of 401 to 1000, and 8.3 (95% CI, 3.3 to 21.1) for calcium scores >1000 compared with calcium scores of 0 to 100. The predictive value in subjects >70 years of age was similar. Risk prediction based on the cardiovascular risk factors improved when coronary calcification was added. CONCLUSIONS: Coronary calcification is a strong and independent predictor of coronary heart disease, also in the elderly. Coronary calcification improves prediction of coronary events based on cardiovascular risk factors. Risk stratification by assessment of coronary calcification may have an important role in the primary prevention of coronary heart disease events in the elderly.

Aged↗

Mitral and aortic annular calcification are highly associated with systemic calcified atherosclerosis.

BACKGROUND: Atherosclerosis has been implicated as a cause of valvular calcification. The aim of this study was to determine whether atherosclerotic calcification in multiple vascular areas is significantly associated with aortic or mitral annular calcification independent of traditional risk factors. METHODS AND RESULTS: A total of 1242 consecutive asymptomatic patients free of clinical coronary heart disease were studied by electron-beam computed tomography for the extent of calcium due to atherosclerosis in 5 distinct vascular beds and calcium in the aortic and mitral annuli. Nearly 24% had calcium in the aortic annulus, whereas 8% were found to have mitral annular calcification. Age and a history of hypertension were the only traditional cardiovascular risk factors that were independently associated with prevalent calcification in the aortic and mitral annuli. After adjustment for age, gender, and cardiovascular disease risk factors, subjects with calcium in the thoracic aorta had the highest odds for the presence of aortic annular calcium (OR=3.9, P<0.01), whereas those with calcium in the abdominal aorta had the highest odds for mitral annular calcification (OR=5.1, P=0.01). Standardized increases in calcium in the abdominal aorta (OR=2.0, P<0.01) and iliacs (OR=1.8, P=0.01) were significantly associated with calcium in the aortic annulus after adjustment for the extent of calcium in the other vascular beds, whereas the thoracic aorta was significantly associated (OR=1.4, P=0.02) with calcium in the mitral annulus. CONCLUSIONS: This study supports the hypothesis that calcification of the mitral and aortic annuli is related to atherosclerosis in other vascular beds.

Adult↗

Arterial calcifications, arterial stiffness, and cardiovascular risk in end-stage renal disease.

To test the predictive values of and independent contributions to cardiovascular and all-cause mortality of various arterial parameters exploring characteristics of the arterial wall at different sites, we studied prospectively 110 stable end-stage renal disease patients on hemodialysis. These parameters involved carotid diameter, carotid intima-media thickness, carotid compliance, carotid distensibility, carotid incremental elastic modulus, aortic diameter, aortic pulse wave velocity, and the presence of arterial calcifications measured at the sites of the carotid artery, abdominal aorta, iliofemoral axis, and legs. The presence of calcifications was analyzed semiquantitatively as a score (0 to 4) according to the number of arterial sites with calcifications. During a follow-up of 53+/-21 months (mean+/-SD), 25 cardiovascular and 14 noncardiovascular deaths occurred. In univariate analysis, the carotid incremental elastic modulus was the most closely related to prognosis. Risk of death increased with the number of vascular sites involved by calcifications. Moreover, information (in terms of prediction) given by carotid elastic incremental modulus was additive to the presence and extent of vascular calcification-related prediction value. Adjusted hazard ratios of all-cause and cardiovascular mortality for an increase of 1 unit in calcification score were 1.9 (95% confidence interval [CI], 1.4 to 2.6) and 2.6 (95% CI, 1.5 to 4.4), respectively (P<0.001 for both). Adjusted hazard ratios of all-cause and cardiovascular mortality for a 1-SD increase in carotid incremental elastic modulus were 1.6 (95% CI, 1.2 to 2.2) and 1.7 (95% CI, 1.2 to 2.4), respectively (P<0.01 for both). The results of this study showed that the presence and extent of vascular calcifications were strong predictors of cardiovascular and all-cause mortality. Carotid incremental elastic modulus gave additional predictive value.

Adult↗

Diffuse calcification in human coronary arteries. Association of osteopontin with atherosclerosis.

Coronary atherosclerosis is frequently associated with calcification of arterial plaque. To understand the mechanisms responsible for the formation of atherosclerotic calcification, we examined human coronary arteries for the presence and extent of mineral. In sections stained specifically for mineral, staining was diffuse and present in all atherosclerotic plaques. Hydroxyapatite was not detected in normal coronary artery sections. Distribution of hydroxyapatite coincided with a similar distribution of calcium detected by a radiodense pattern using contact microradiography of the same sections before cytochemical staining. By energy-dispersive x-ray microanalysis, the chemical composition of calcified sites was identical to hydroxyapatite (Ca10[PO4]6[OH]2), the major inorganic component of bone. Osteopontin is a phosphorylated glycoprotein with known involvement in the formation and calcification of bone and is regulated by local cytokines. Human coronary artery segments (14 normal and 34 atherosclerotic) obtained at autopsy were evaluated immunohistochemically using polyclonal antibodies generated against human osteopontin. Immunohistochemistry for osteopontin indicated intense, highly specific staining in the outer margins of all diseased segments at each calcification front; staining was evident throughout the entire plaque. Conversely, arterial segments free of atheroma and calcification and sections treated with nonimmune serum had no evidence of positive staining. Osteopontin, a protein involved in mineralization is specifically associated with calcific coronary atheroma and may play an important role in the onset and progression of this disease in human coronary arteries. The deposition of noncollagenous proteins such as osteopontin may regulate the presence or absence of calcification and ultimately alter vessel compliance.

Adult↗

Arterial calcifications in beta-thalassemia.

The purpose of this study was to define the incidence of arterial calcifications in patients with beta-thalassemia. Beta-thalassemia patients have been shown to present a high prevalence of angioid streaks and skin lesions characteristic of pseudoxanthoma elasticum (PXE). Given the fact that vascular involvement in the form of arterial calcifications is also a common manifestation of PXE, the authors investigated radiographically the presence of arterial calcifications in beta-thalassemia patients. They studied 40 patients with beta-thalassemia over 30 years of age. Forty healthy, age- and sex-matched subjects were chosen as a control group. Radiographs of the tibias were performed in order to disclose arterial calcifications. The occurrence of PXE skin lesions and of angioid streaks (AS) was also investigated. Arterial calcifications were detected in the posterior tibial artery in 22 (55%) beta-thalassemia patients and in six (15%) controls (P < 0.01 for the comparison). PXE skin lesions and AS were found in eight (20%) and 21 (52%) patients respectively. A total of 34 patients (85%) had at least one of the three lesions, namely, arterial calcifications, angioid streaks, and/or PXE-like skin lesions. Stepwise logistic regression analysis did not reveal prognostic value in independent variables such as transfusions, chelation therapy, pseudoxanthoma elasticum skin lesions and/or angioid streaks, diabetes, hemoglobin, serum ferritin, and uric acid. It was concluded that arterial calcifications are common in older beta-thalassemia patients. This finding could be a manifestation of an acquired PXE syndrome associated with beta-thalassemia, and consequently, vascular events complicating PXE should be expected in these patients.

Adult↗

Lymph node calcification in malignant lymphoma. Presentation of nine cases and a review of the literature.

Lymph node calcification in malignant lymphoma is an uncommon radiologic finding. Eight cases are added to the 61 cases of lymph node calcification following radiation therapy for Hodgkin's disease, assembled from the literature. The typical radiographic appearance of punctate calcifications, usually found in the upper mediastinum, at times together with egg-shell type calcification, is confirmed. The mean time before appearance of calcification was 3 years after initial treatment. The calcification seems to be associated with a good prognosis and long-term survival. In addition, the radiologic and clinical findings in a patient with non-Hodgkin's lymphoma who developed calcifications in the involved area after treatment are presented.

Adult↗

Pathophysiology of coronary calcification.

Calcification is a prominent feature of atherosclerosis, frequently associated with myocardial infarction and other adverse cardiovascular outcomes. Currently, calcification is widely viewed as an end-stage, degenerative process which is inevitable in advanced atherosclerosis. Pathologists, however, have long noted that calcification may occur early in atherosclerosis and, at times, may appear histologically identical to organized bone, including areas resembling bone marrow. These observations suggest that rather than being a passive process, atherosclerotic calcification may instead be an active, regulated process similar to that of osteogenesis. Using an in-vitro model of arterial calcification a subpopulation of artery wall cells, capable of producing hydroxyapatite mineral in vitro was discovered. This article discusses some of the cellular and molecular mechanisms of arterial calcification identified utilizing this in-vitro model of vascular calcification.

Animals↗

Effects of dietary calcium on atherosclerosis, aortic calcification, and icterus in rabbits fed a supplemental cholesterol diet.

BACKGROUND: Vascular calcification is implicated in myocardial infarction, instability and rigidity of the aortic wall, and bioprosthetic failures. Although an increase in the calcium (Ca) content in atherogenic diets has been shown to decrease atherosclerosis in rabbits, whether Ca supplementation and deficiency can affect atherosclerosis-related aortic calcification remains unknown. RESULTS: New Zealand White male rabbit littermates were fed an atherogenic diet containing 0.5% cholesterol and 2% peanut oil. The Ca content of the diet, which normally contains 1%, was adjusted to 0.5 or 3%. Segments of thoracic aortas were dissected from rabbits for histological evaluations and Ca and Pi determinations. Rabbits with calcium supplementation were maintained for 4 months, whereas those with calcium deficiency were maintained for 2 1/2 months due to severe icterus beyond this stage. The ratios of intimal to medial areas and calcified to intimal areas were used to semi-quantify lesion accumulation and calcification, respectively. Icterus was estimated from the extent of yellowing of the skin, sclera, and mucous membranes along with gross evidence of hepatic lipidosis and/or biliary obstructions. Statistical analysis of 16 matched littermates shows that Ca supplementation significantly decreased the lesions by 41% (p < 0.05) and markedly inhibited calcification by 62% (p < 0.05). Statistical analysis of 11 matched littermates shows that Ca deficiency significantly increased the lesions by 2.7-fold (p < 0.05) and that the diet caused a small but significant calcification not seen in the sibling groups with normal dietary Ca. Ca supplementation caused a significant 30% decrease in serum cholesterol (p < 0.05). Calcium deficiency increased serum cholesterol by 57% (p < 0.001). Serum cholesterol and LDL-cholesterol levels in Ca deficient rabbits were 2-fold higher than those with high Ca diets. Ca supplementation decreased soluble Ca and Pi content in aortas, suggesting that this effect may underlie the effects of Ca supplementation on calcification. Calcium deficiency increased icterus by 33% (p < 0.05), which may affect hepatic clearance of cholesterol, while calcium supplementation decreased it by 43% (p < 0.001). CONCLUSION: Ca supplementation to an atherogenic diet inhibits atherosclerosis, aortic calcification, and icterus, whereas a Ca deficient-diet promotes them.

Animals↗

Osteogenic regulation of vascular calcification.

Vascular calcification increasingly afflicts our aging and dysmetabolic population, predisposing patients to cardiovascular mortality and lower extremity amputation. Active osteogenic processes are evident in most histoanatomic variants, including elaboration of BMP2-Msx2 signals required for craniofacial bone formation. We developed an animal model of diet-induced diabetes, dyslipidemia, and vascular calcification. High-fat diets promote vascular calcification in male low-density lipoprotein receptor (LDLR)-deficient mice, with concomitant upregulation of aortic BMP2 and Msx2 gene expression. We wished to test if Msx2 exerts pro-calcific actions during vascular calcification, as it does in craniofacial bone. We studied CMV-Msx2Tg+;LDLR+ transgenic mice (C57Bl/6), a model previously demonstrated to recapitulate features of Msx2 signaling during craniosynostosis. After 16 weeks of fatty diets, vascular calcification was studied in CMV-Msx2Tg+ versus nontransgenic sibs. Only CMV-Msx2Tg+ mice fed high-fat diets exhibited vascular calcium accumulation by alizarin red staining, noted in the tunica media of coronary arteries and the aorta. Gene expression studies revealed that while Msx2 was expressed primarily in adventitial cells, alkaline phosphatase (ALP) expression and calcification occurred primarily in the tunica media. Msx2 promotes the elaboration of a pro-osteogenic milieu by upregulating expression of Wingless type (Wnt) ligands while downregulating the canonical antagonist, Dickkopf (Dkk1). Msx2 upregulates aortic Wnt signaling in vivo, revealed by the analysis of TOPGAL+ (Wnt reporter) versus CMV-Msx2Tg+; TOPGAL+ mice. Aortic Msx2 exerts pro-osteogenic signaling in vivo and in vitro, mediated in part via the enhancement of paracrine Wnt signaling. Strategies that selectively inhibit aortic Msx2-Wnt cascades may help diminish the initiation and progression of diabetic vascular disease.

Animals↗

Basal ganglia calcifications on CT: relation to hypoparathyroidism.

Eleven of 12 patients with primary hypoparathyroidism had CT evidence of bilateral intracerebral calcifications, mostly within the basal ganglia, but also in other sites. None of the 12 patients with secondary hypoparathyroidism had intracerebral calcifications. Among 20 patients with calcifications discovered incidentally, idiopathic hypoparathyroidism was diagnosed in 2 patients. Four patients had calcifications associated with antiepileptic treatment, parkinsonism, or Kearns-Sayre syndrome. The cause of the calcifications was unknown in 14 patients. No specific neurologic sign was related to the localization of the intracerebral calcifications. Incidentally discovered basal ganglia calcifications should lead to endocrinologic evaluation of parathyroid function. CT examination of the skull may be used to ascertain the diagnosis of idiopathic hypoparathyroidism.

Basal Ganglia Diseases↗

Aortic calcification detected in a mass chest screening program using a mobile helical computed tomography unit. Relationship to risk factors and coronary artery disease.

BACKGROUND: There is a significant relationship between calcification of the aortic arch (Arch) detected by chest X-ray examination and coronary artery disease (CAD), but the relationship between risk factors, CAD and aortic calcification detected during a mass screening program using a mobile helical computed tomography (CT) unit remains unknown. METHODS AND RESULTS: In total 2,623 subjects (1,347 men, and 1,276 women; mean age, 52.9+/-13.8) underwent an examination for lung cancer and tuberculosis using a mobile helical CT unit. The frequency of calcification was 19.6% in the Arch, 2.7% in the ascending aorta, and 10.1% in the descending aorta, values that were positively associated with age in both genders. Hypertension and smoking were significantly related to calcification of the thoracic aorta. There was a significant relationship between CAD and aortic calcification. The odds ratio of aortic calcification for patients with CAD increased as the number of calcified segments increased. CONCLUSIONS: These results suggest that detection of calcification in the thoracic aorta during a mass chest screening using a mobile helical CT unit can be used to evaluate the risk of CAD.

Adolescent↗

Clinical significance of aortic knob width and calcification in unstable angina.

BACKGROUND: Chest radiography is a routine examination evaluating those patients with chest pain. There are few data about the correlation between aortic knob width, calcification and coronary atherosclerosis. METHODS AND RESULTS: The aortic knob width was measured and the presence of aortic knob calcification was assessed via a chest posteroanterior view in 178 consecutive patients. The aortic knob width and calcification were compared to the risk factor and the extent of coronary artery disease. Patient's age (69.5+/-7.95 vs 61.1+/-10.29 years, p=0.010), the prevalence of hypertension (65.9 vs 46.3%, p=0.024) and diabetes (43.2 vs 26.1%, p=0.033), the level of total cholesterol (196.8+/-63.21 vs 188.6+/-44.45 mg/dl, p=0.049) and the incidence of multi-vessel disease (65.9 vs 38.1%, p<0.001) were higher in patients with aortic knob calcification than in patients without calcification. The aortic knob width and the prevalence of aortic knob calcification were significantly correlated with the severity of coronary artery disease. Multivariate analysis demonstrated that aortic knob calcification and diabetes were independent factors for multi-vessel disease (p=0.018 and p=0.012). CONCLUSIONS: The observation of aortic knob on a chest radiograph can provide important predictive information of coronary atherosclerosis.

Aged↗

The detection and significance of calcifications in the breast: a radiological and pathological study.

The radiological detection of calcification is compared using xeroradiography, non-screen film and a film-screen combination. The "threshold" values of the smallest detectable size of calcification, under simulated clinical conditions, are found to be approximately 100 mum for xeroradiography and 400 mum for both the film techniques in this study. The incidence of calcification seen on the preoperative mammograms of patients with carcinoma of the breast is 48-5 per cent. Further calcification revealed by histological examination raises the overall incidence of calcification in mammary carcinomas to 63 per cent. The incidence on preoperative mammograms in benign breast disease is 20 per cent. The radiological features of calcification occurring in malignant and benign breast lesions are recorded, and no definitive distinguishing features are established. The histological appearance of calcification in malignant and benign breast disease is discussed.

Breast Diseases↗

Visceral and testicular calcifications as part of the phenotype in pseudoxanthoma elasticum: ultrasound findings in Belgian patients and healthy carriers.

Occasionally calcifications in abdominal organs, breasts and testicles have been reported in pseudoxanthoma elasticum (PXE) patients. In the present study, an ultrasound evaluation was performed of the abdomen and--in male patients--of the testicles in 17 PXE patients and 17 heterozygous carriers. Blood samples were taken to evaluate calcium load, liver and kidney function. Calcifications in liver, kidneys and spleen were detected in 59% of the patients and in 23.5% of healthy carriers. Parameters of kidney and liver function were normal in both groups, suggesting that the calcifications have no direct effect on organ function. Testicular ultrasound revealed parenchymous calcifications in all males investigated. Widespread, small hyperechogenic foci resembling testicular microlithiasis were seen. In some carriers, focal calcifications were identified. The current data suggest that visceral and testicular calcifications are part of the phenotype of PXE patients. Their presence in some of the healthy carriers are suggestive of subclinical manifestations in these relatives. The natural history and long-term effects of the parenchymal calcifications remain to be elucidated. As testicular microlithiasis may be associated with a higher risk for malignancy, regular clinical and ultrasound follow-up seems indicated in these patients.

Adolescent↗

Spontaneous coronary artery embolus associated with calcific aortic stenosis.

Calcific embolization from aortic stenosis may be more frequent than commonly appreciated. Most calcific emboli are clinically silent, although transient ischemic attacks, cerebral infarcts, blindness (from central retinal artery occlusions), and myocardial infarctions have been reported. We describe a patient with calcific bicuspid aortic stenosis who presented with transient ischemic attacks and angina secondary to a calcific embolus to the second circumflex marginal coronary artery. The calcific embolus was retrieved during aortic valve replacement surgery. A review of the literature suggests that calcific embolization from calcific aortic stenosis may occur more commonly in patients with bicuspid valves.

Aortic Valve Stenosis↗

Cross-sectional echocardiographic observations on the mechanism of preservation of the opening snap in calcific mitral stenosis.

Cross-sectional echocardiography (CSE) was performed on 19 patients with mitral stenosis (MS). Nine patients (group 1) had little or no mitral valve (MV) calcification; ten patients (group 2) had heavy MV calcification. An opening snap was present in each of the patients in group 1. Of the group 2 patients, five (group 2A) had an opening snap and five (group 2B) did not. CSE in the long axis revealed in group 1 patients a mobile MV with sharp anterior arching of the anterior leaflet in early diastole; in group 2A, dense echoes suggestive of calcification were noted near the tip of the MV, while the body of the leaflet was relatively thin and it arched anteriorly sharply in early diastole; and in group 2B, dense echoes were noted at the tip and body of the MV with reduction in mobility of the valve, and the sharp anterior arching of the anterior leaflet in early diastole was absent. Preservation of the OS in calcific MS depends on the distribution of calcification. Heavy calcification confined to the tip of the MV allows the anterior leaflet to arch anteriorly in early diastole, allowing preservation of the OS, whereas heavy calcification of the tip and body of the MV reduces the pliability of the valve with consequent disappearance of the OS.

Adult↗