Presence Of Aortic Calcification Research Articles

Relevance of ultrasound detection and assessment of vascular calcifications in chronic kidney disease

Introduction: Chronic kidney disease (CKD) affects approximately 10% of the Spanish population and constitutes an independent cardiovascular risk factor. Vascular calcifications, especially in the abdominal aorta, are significantly associated with increased cardiovascular mortality in patients with CKD. This systematic review evaluates the evidence on the usefulness of ultrasound to detect and assess vascular calcifications in patients with CKD, and its relevance as a cardiovascular risk factor.Methods: A systematic search of multiple electronic databases was conducted until July 2024. Original studies published between 2000 and 2024 evaluating the use of ultrasound to detect vascular calcifications in adult patients with CKD at any stage were included. Reviews, letters, editorials, animal studies and those not published in English or Spanish were excluded. Methodological quality was assessed using the Newcastle-Ottawa scale for observational studies and the Cochrane tool for clinical trials.Results: Twenty-eight studies were included with a total of 50 to 3,000 participants per study. Most were observational studies, with 3 randomised clinical trials. Ultrasound showed good correlation with computed tomography (r=0.65-0.82) to quantify aortic and femoral calcifications. The presence of aortic calcifications was associated with increased risk of cardiovascular mortality (HR 1.8-3.2) in patients with advanced CKD and on haemodialysis. Iliac/femoral calcifications were associated with increased risk of cardiovascular events (RR 1.6-2.4) in patients with stage 3-5 CKD. Incorporation of ultrasound assessment of calcifications into CKD-specific risk algorithms significantly improved their predictive performance.Discussion: Ultrasonography emerges as a valuable tool for the detection of vascular calcifications due to its non-invasive nature, low cost and ability to perform repeated assessments. However, limitations such as heterogeneity in assessment methods, variable sample sizes and lack of long-term follow-up in some studies were identified. Further research is needed to standardise protocols and assess the long-term impact of interventions based on ultrasound detection of calcifications.Conclusions: Ultrasonography is an effective and accessible tool for detecting and assessing vascular calcifications in patients with CKD, providing relevant prognostic information for cardiovascular risk stratification. Its consideration as a first-line tool in nephrological practice is recommended. However, large-scale prospective studies are needed to definitively validate its prognostic value in different stages of CKD and to evaluate the efficacy of early interventions based on these findings.

Diagnosis and treatment of osteoporosis in patients with chronic kidney disease : Joint guidelines of the Austrian Society for Bone and Mineral Research (ÖGKM), the Austrian Society of Physical and Rehabilitation Medicine (ÖGPMR) and the Austrian Society of Nephrology (ÖGN)

Chronic kidney disease (CKD): abnormalities of kidney structure or function, present for over 3months. Staging of CKD is based on GFR and albuminuria (not graded). Osteoporosis: compromised bone strength (low bone mass, disturbance of microarchitecture) predisposing to fracture. By definition, osteoporosis is diagnosed if the bone mineral density T‑score is ≤ -2.5. Furthermore, osteoporosis is diagnosed if alow-trauma (inadequate trauma) fracture occurs, irrespective of the measured T‑score (not graded). The prevalence of osteoporosis, osteoporotic fractures and CKD is increasing worldwide (not graded). PATHOPHYSIOLOGY, DIAGNOSIS AND TREATMENT OF CHRONIC KIDNEY DISEASE-MINERAL AND BONE DISORDER (CKD-MBD): Definition of CKD-MBD: asystemic disorder of mineral and bone metabolism due to CKD manifested by either one or acombination of the following: abnormalities of calcium, phosphorus, PTH, or vitaminDmetabolism; renal osteodystrophy; vascular calcification (not graded). Increased, normal or decreased bone turnover can be found in renal osteodystrophy (not graded). Depending on CKD stage, routine monitoring of calcium, phosphorus, alkaline phosphatase, PTH and 25-OH-vitaminD is recommended (2C). Recommendations for treatment of CKD-MBD: Avoid hypercalcemia (1C). In cases of hyperphosphatemia, lower phosphorus towards normal range (2C). Keep PTH within or slightly above normal range (2D). VitaminDdeficiency should be avoided and treated when diagnosed (1C). Densitometry (using dual X‑ray absorptiometry, DXA): low T‑score correlates with increased fracture risk across all stages of CKD (not graded). Adecrease of the T‑score by 1unit approximately doubles the risk for osteoporotic fracture (not graded). AT-score ≥ -2.5 does not exclude osteoporosis (not graded). Bone mineral density of the lumbar spine measured by DXA can be increased and therefore should not be used for the diagnosis or monitoring of osteoporosis in the presence of aortic calcification, osteophytes or vertebral fracture (not graded). FRAX can be used to aid fracture risk estimation in all stages of CKD (1C). Bone turnover markers can be measured in individual cases to monitor treatment (2D). Bone biopsy may be considered in individual cases, especially in patients with CKD G5 (eGFR < 15 ml/min/1.73 m2) or CKD 5D (dialysis). Hypocalcemia should be treated and serum calcium normalized before initiating osteoporosis therapy (1C). CKD G1-G2 (eGFR ≥ 60 ml/min/1.73 m2): treat osteoporosis as recommended for the general population (1A). CKD G3-G5D (eGFR < 60 ml/min/1.73 m2 to dialysis): treat CKD-MBD first before initiating osteoporosis treatment (2C). CKD G3 (eGFR 30-59 ml/min/1.73 m2) with PTH within normal limits and osteoporotic fracture and/or high fracture risk according to FRAX: treat osteoporosis as recommended for the general population (2B). CKD G4-5 (eGFR < 30 ml/min/1.73 m2) with osteoporotic fracture (secondary prevention): Individualized treatment of osteoporosis is recommended (2C). CKD G4-5 (eGFR < 30 ml/min/1.73 m2) and high fracture risk (e.g. FRAX score > 20% for amajor osteoporotic fracture or > 5% for hip fracture) but without prevalent osteoporotic fracture (primary prevention): treatment of osteoporosis may be considered and initiated individually (2D). CKD G4-5D (eGFR < 30 ml/min/1.73 m2 to dialysis): Calcium should be measured 1-2weeks after initiation of antiresorptive therapy (1C). Resistance training prioritizing major muscle groups thrice weekly (1B). Aerobic exercise training for 40 min four times per week (1B). Coordination and balance exercises thrice weekly (1B). Flexibility exercise 3-7times per week (1B).

Progression To Non-zero Coronary Artery Calcium Scores And Presence Of Aortic Calcifications: Insights From An Employer Health Benefits Screening Program

Introduction: Coronary artery calcium score (CACS) is a powerful tool to predict the risk of future cardiovascular events in asymptomatic individuals. Those with CACS of 0 have an extremely low annual event rate with a 10-year event rate of 1%. However, the warranty period and optimal interval for repeat CACS in this population is not well defined.

Predicting the risk of severe myocardial infarction in patientswith chronic 5D-stage kidneydisease and mineral-bone disorders

BACKGROUND. The increasing prevalence of chronic kidney disease is a global trend as well in general as in terminal kidney failure in particular. Of great interest is the analysis of the impact of mineral and bone disorders on the risk of cardiovascular complications and, first of all, acute myocardial infarction (AMI ). THE AIM: to assess the impact of bone mineral disorders on the risk of AMI in patients with stage 5D chronic kidney disease. PATIENTS AND METHODS. It was conducted a prospective (three-year) cohort study of 85 patients with CKD S5D treated with programmed hemodialysis. At the first stage, it were reg­istered the risk factors and clinical manifestations of CKD 5 St, as well as indicators that characterized bone mineral disorders (levels of blood inorganic phosphate, calcium, parathyroid hormone, 1,25(OH)D, fibroblast growth factor (FGF-23), a-Klotho). Signs of calcification of the heart valves and aortic wall were also determined. The second stage involved a re-examination of patients after 3.1±0.1 years, as well as registration of endpoints, which were identified as cases of fatal and non-fatal AMI. RESULTS. After 3 years of follow-up, the following endpoints were registered: nonfatal AMI - 6 cases, fatal AMI-4 cases. The risk of AMI increased in the presence of initial persistent hyperphosphatemia and 1,25(OH)D3 deficiency, as well as calcifica­tion of heart valves and high FGF-23 values, but only in combination with hyperphosphatemia and 1,25(OH)D3 deficiency. Hyperparathyroidism also increased the risk of AMI in conditions of a deficit of 1,25(OH)D3. The risk of nonfatal AMI cases was also increased by the presence of aortic calcification and its severity. The risk of AMI increases in the presence of initial persistent hyperphosphatemia and a deficit of 1.25 (OH)D3, as well as CCS, high FGF-23 values, but only in combination with hyperphosphatemia and a deficit of 1.25(OH)D3. Hyperparathyroidism also increases the risk of AMI in conditions of a deficit of 1.25(OH)D3. The risk of nonfatal cases of AMI also increases the presence of aortic calcification and its severity. CONCLU­SION. The risk of AMI increases in the presence of initial persistent hyperphosphatemia and a deficit of 1,25(OH)D3, as well as calcification of the heart valves, high FGF-23 values, but only in combination with hyperphosphatemia and a deficit of 1,25(OH) D3. Hyperparathyroidism also increases the risk of AMI in conditions of a deficit of 1.25(OH)D3. The risk of nonfatal cases of AMI also increases the presence of aortic calcification.

Thoracic aortic calcification across the clinical dysglycemic continuum in a large Asian population free of cardiovascular symptoms.

Thoracic aortic calcification (TAC) is tightly linked to pathological atherosclerosis and associated with certain cardiovascular diseases. While diabetes mellitus (DM) is known as a coronary heart disease equivalent, we examined the presence of TAC across the dysglycemic spectrum of diabetes mellitus (DM). We consecutively studied 3003 asymptomatic ethnic Asians underwent annual cardiovacular health survey, and further categorized them into: 1) 1760 normo-glycemic, 2) 968 pre-diabetic, and 3) 274 overt DM based on dysglycemic indices and medical histories. Several TAC parameters were assessed using non-contrast multi-detector computed tomography (MDCT), and related to dysglycemic indices or diabetes mellitus status. A remarkably graded increases of adjusted total TAC calcium burden, volume and density were seen across Non-diabetes, Pre-diabetes, and diabetes mellitus categories and positively correlated with all dysglycemic profiles (all p<0.001). Multi-variate logistic and linear regression models demonstrated independent associations between greater TAC density and all dysglycemic indices (Coef: 2.5, 1.4, 6.8 for fasting, postprandial sugar and HbA1c) and diabetes mellitus status (all p<0.05). Furthermore, Receiver-operating characteristic curves (ROC) showed fasting sugar and postprandial sugar set at 103mg/dL and 111mg/dL, separately, with HbA1c set at 5.8% all predict the presence of aortic calcification. Dysglycemic status, even without overt diabetes mellitus, were tighly linked to subclinical, pathological thoracic aortic calcification.

Longitudinal changes in bone mineral density, bone mineral content and bone area at the lumbar spine and hip in postmenopausal women, and the influence of abdominal aortic calcification

Longitudinal studies often report that spine bone mineral density (BMD), measured by DXA, is stable in older adults, which has been attributed to osteophyte development and the presence of aortic calcification. A decline in projected spine area as a result of loss of intervertebral disc height might also contribute to higher BMD. We utilised data from 297 postmenopausal women (mean 73 years) who had DXA measurements of the lumbar spine, total hip and femoral neck 5 years apart, and abdominal aortic calcification scoring from vertebral morphometry. BMD declined by −4.4% at the total hip and −3.9% at the femoral neck (p < 0.001), but did not change at the spine (−0.5%, p = 0.12). In contrast, bone mineral content (BMC) declined by −4.0% at the total hip, −2.5% at the femoral neck and −1.7% at the spine (all p < 0.001). Bone area increased by 0.5% at the hip and 1.6% at the femoral neck but declined by −1.2% at the spine (all p < 0.001). 43% of the cohort had abdominal aortic calcification (AAC) present at baseline. The presence of AAC at baseline was not related to changes in BMD or BMC at the total hip or femoral neck, nor to BMD at the spine. However, women with AAC present had a smaller loss of BMC at the spine than those without (−0.8% versus −2.4%, p = 0.03). AAC score increased more over 5 years among those with AAC at baseline than those without (0.28 versus 0.16, p = 0.036). Thus, the stability of spine BMD is the result of both a loss of projected bone area (as a result of intervertebral disc changes and/or a decrease in projected area of the vertebral bodies) and the effects of aortic calcification. Future clinical trials should consider assessing changes in spine BMC as a more informative index of spine mineral status.

Abdominal aortic calcification can predict all-cause mortality and CV events in dialysis patients: A systematic review and meta-analysis.

BackgroundAbdominal aortic calcification (AAC) has a pretty high incidence in dialysis patients and may be associated with their prognosis. AAC can be assessed by abdominal CT or X-ray. We determined to investigate whether the occurrence of AAC is associated with all-cause mortality and cardiovascular (CV) events in dialysis patients through this meta-analysis and systematic review.MethodsA comprehensive literature search was conducted using the PubMed, Cochrane library, Embase, Medline databases to collect cohort studies investigating whether AAC is associated with all-cause mortality and CV events of patients, and we also searched gray articles and conferences abstracts. Meta-analysis was performed by STATA software. Pooled results were expressed as hazard ratio (HR) with corresponding 95% confidence intervals (CI). Fixed-effect models were used to pool the HR of each trial.Results10 studies (2,724 dialysis patients) were identified. The presence of AAC was associated with increased risk for all-cause mortality among dialysis patients (HR, 2.84; 95% CI, 2.03–3.98; I2 = 9.8%; P = 0.354). Meanwhile, there was an association between AAC and increased risk for all CV events (fatal and non-fatal) in patients (HR, 2.04; 95% CI, 1.51–2.76, I2 = 44.6%; P = 0.125). 3 studies presented their endpoint as CV mortality, and the pooled HR was 2.46 (95%CI 1.38–4.40; I2 = 0.0%; P = 0.952).There were also 2 studies that reported their primary endpoint as all-cause mortality and CV events, and the pooled HR was 5.72 (95% CI 3.24–10.10; I2 = 0.0%; P = 0.453).ConclusionsAmong patients treated with dialysis, AAC is associated with adverse outcomes, including all-cause mortality and CV events (fatal and non-fatal). The abdominal X-ray or CT scan can be used as a useful added method to evaluate the patient’s calcification. This may provide reasonable data for estimating the risk of adverse events in dialysis patients, which is helpful in guiding clinical treatment and improving the prognosis of dialysis patients.

Can severe aortic stenosis be identified by emergency physicians when interpreting a simplified two-view echocardiogram obtained by trained echocardiographers?

BackgroundAortic stenosis (AS) is a common valve problem that causes significant morbidity and mortality. The goal of this study was to determine whether an emergency physician (EP) could determine severe AS by reviewing only two B-mode echocardiographic views (parasternal long axis (PSLA) and parasternal short axis (PSSA)) obtained by trained echocardiographers.MethodsA convenience sample of 60 patients with no AS, mild/moderate AS or severe AS was selected for health record and echocardiogram review. The echocardiograms were performed in an accredited echocardiography laboratory. An EP blinded to the cardiologist’s final report reviewed the PSLA and PSSA views after the cases were randomly sorted. Severe AS was defined as no cusp movement seen by the EP reviewers. A second EP independently reviewed 25% of randomly selected patients for inter-rater reliability. Collected data included patient demographics, EP interpretation and details of each echo view (quality, the number of cusps visualized, presence of calcification) and compared to final cardiology reports. Analyses included descriptive statistics, test characteristics for severe AS and kappa for agreement.ResultsThe mean age was 75.3 years (range 18 to 90) with 36.7% females. The cardiologist’s diagnosis was as follows: 38.3% severe AS, 28.3% mild/moderate AS and 33.3% no AS. The PSSA view was poorer in quality compared with the PSLA (33.3% vs. 13.3%, p = 0.02), but the PSSA view was better than PSLA to visualize all three cusps (83.3% vs. 0%, p = 0.001). There was no difference in the presence of calcification between the mild/moderate and severe AS groups (94.1% vs. 100.0%, p = 0.46). The sensitivity and specificity for EP diagnosis of severe AS was 75.0% (95% CI 56.7% to 85.4%) and 92.5% (83.3% to 97.7%). The kappa for severe AS was 0.69 (0.41 to 0.85), and there was no significant difference between observers in the quality of the view, presence of aortic calcification and the number of cusps visible.ConclusionsPSLA and PSSA views obtained by trained echocardiographers can be interpreted by an EP with appropriate training to identify severe AS with good specificity. Further larger prospective studies are required before widespread use by EPs.Electronic supplementary materialThe online version of this article (doi:10.1186/s13089-015-0022-8) contains supplementary material, which is available to authorized users.

Porcelain Aorta

Calcification of the thoracic aorta is often associated with valvular and coronary calcification, reflecting an underlying atherosclerotic process.1,2 It has been found to be associated with an increased rate of mortality and cardiovascular disease.1 Porcelain aorta (PA) is extensive calcification of the ascending aorta or aortic arch that can be completely or near completely circumferential.3–5 This entity is rare in the general population, but it has an increasing incidence in older patients and in patients with coronary artery disease (CAD) or aortic stenosis (AS).6,7 The clinical relevance is based on the fact that it can complicate surgical aortic valve replacement (SAVR) for the treatment of severe AS by preventing safe access via the ascending aorta. PA is associated with increased morbidity and mortality, especially as a result of increased perioperative stroke risk.8,9 Recently, transcatheter aortic valve replacement (TAVR) has emerged as a less invasive and feasible treatment option in patients at high risk for conventional SAVR.10 In some series, ≈20% (5%–33%) of patients undergoing TAVR were diagnosed with PA.11 Inconsistencies in the definition and the use of different diagnostic modalities contribute to this wide range of PA prevalence. We reviewed the available published data to seek a consistent, clinically relevant definition based on contemporary imaging, a firm understanding of the pathogenesis and associations, and the clinical implications of this disease entity. PA has been used to address extensive circumferential or nearly circumferential calcification of the thoracic aorta such that it precludes safe cross-clamping or entry to the ascending aorta. However, there is no clear description or definition used; thus, cardiac surgeons and cardiologists use this term inconsistently. In the 1980s, Coselli and Crawford12 initially described 2 …

Clinical and Radiological Characteristics of Concomitant Peripheral Arterial Obstructive Disease in Patients with Lumbar Spinal Stenosis

Background: Intermittent claudication is a typical symptom of lumbar spinal stenosis (LSS) and peripheral arterial obstructive disease (PAD). Because both LSS and PAD are predominantly associated with degenerative conditions, concomitant conditions are not uncommon. However, few reports of the demographic, clinical, and radiological characteristics of concomitant LSS and PAD (LSSPAD) have been published. Objective: To identify the demographic, clinical, and radiological risk factors for concomitant PAD in LSS. Study Design: A retrospective matched-control study. Methods: This study involved a retrospective cohort of 43 consecutive patients with LSSPAD and a control cohort of 45 age- and gender-matched patients diagnosed with LSS without PAD. Each patient in both groups underwent plain lumbar radiographs, magnetic resonance imaging of the lumbar spine, and ankle-brachial index (ABI) measurement. Demographic and clinical parameters were obtained. The abdominal aorta calcification score (AACS) was evaluated on the lateral lumbar radiographs. Computed tomographic angiography (CTA) of the lower limb was performed to confirm PAD. Results: The mean age of the LSSPAD group was 67.7 ± 10.7 years (52 – 88 years). The prevalence of diabetes mellitus (DM) was significantly higher in the LSSPAD group than in the LSS group (P = 0.022). The mean ABI was 0.71 ± 0.22 (0.32 – 0.91) for the LSSPAD group and 0.96 ± 0.18 (0.83 – 1.10) for LSS group (P &lt; 0.001). The prevalence of aortic calcification was significantly higher in the LSSPAD group than in the LSS group (P &lt; 0.001). The mean AACS was 10.2 ± 3.2 (2 – 18) for the LSSPAD group and 3.4 ± 4.1 (0 – 14) for the LSS group (P &lt; 0.001). Limitations: Retrospective design. Conclusion: We found that concomitant PAD in patients with LSS is associated with old age, DM, the presence of aortic calcification, and ABI &lt; 0.9. When these risk factors exist, further work up is needed to exclude the concomitant PAD. Key words: Claudication, lumbar spinal stenosis, peripheral arterial obstructive disease, aortic calcification, ankle-brachial index

Effect of a magnesium-based phosphate binder on medial calcification in a rat model of uremia

Calcium-based phosphate binders are used to control hyperphosphatemia; however, they promote hypercalcemia and may accelerate aortic calcification. Here we compared the effect of a phosphate binder containing calcium acetate and magnesium carbonate (CaMg) to that of sevelamer carbonate on the development of medial calcification in rats with chronic renal failure induced by an adenine diet for 4 weeks. After 1 week, rats with chronic renal failure were treated with vehicle, 375 or 750 mg/kg CaMg, or 750 mg/kg sevelamer by daily gavage for 5 weeks. Renal function was significantly impaired in all groups. Vehicle-treated rats with chronic renal failure developed severe hyperphosphatemia, but this was controlled in treated groups, particularly by CaMg. Neither CaMg nor sevelamer increased serum calcium ion levels. Induction of chronic renal failure significantly increased serum PTH, dose-dependently prevented by CaMg but not sevelamer. The aortic calcium content was significantly reduced by CaMg but not by sevelamer. The percent calcified area of the aorta was significantly lower than vehicle-treated animals for all three groups. The presence of aortic calcification was associated with increased sox9, bmp-2, and matrix gla protein expression, but this did not differ in the treatment groups. Calcium content in the carotid artery was lower with sevelamer than with CaMg but that in the femoral artery did not differ between groups. Thus, treatment with either CaMg or sevelamer effectively controlled serum phosphate levels in CRF rats and reduced aortic calcification.

Quantitative Analysis of Abdominal Aortic Calcification in CKD Patients Without Dialysis Therapy by Use of the Agatston Score

Background/Aim: The aim of the present study was to quantitatively examine factors associated with aortic calcification in non-dialysis CKD patients. Methods: We quantitatively investigated aortic calcification from the renal artery to the bifurcation in 149 non-dialysis CKD patients (58±16 years; 96 males and 53 females, 48 diabetics; eGFR 40.3±29.3 ml/min), and measured Agatston scores using multi-slice computed tomography. Result: Of 149 patients, aortic calcification was present in 117. In patients with aortic calcification, age (p<0.001), C-reactive protein (p<0.001), and intact-PTH (p < 0.001) were significantly higher, estimated glomerular filtration rate (eGFR) was significantly lower (p<0.001), and diabetes was observed more often (p<0.05). In regards to the degree of aortic calcification, the Agatston scores correlated significantly and positively with age (ρ=0.438, p<0.001) and serum phosphate (ρ=0.208, p=0.024), and correlated significantly but negatively with e-GFR (ρ=-0.353, p<0.001). In multiple regression analysis, eGFR was associated significantly and independently with the log [Agatston score] (β=-0.346, p<0.01), after adjustment for several confounders including serum phosphate and the presence of diabetes. Conclusions: Hyperphospatemia, chronic inflammation, diabetes, and decreased GFR are associated significantly with the presence of aortic calcification in non-dialysis CKD patients. Decreased eGFR was associated significantly and independently with the quantitative degree of aortic calcification.

Role of arterial stiffness in cardiovascular disease

Propagation of the pressure wave along the arterial tree (pulse wave velocity [PWV]) is related to the intrinsic elasticity of the arterial wall. PWV is increased in stiffer arteries and, when measured over the aorta, is an independent predictor of cardiovascular morbidity and mortality. Given the predictive power of PWV, identifying strategies that prevent or reduce stiffening may be important in prevention of cardiovascular events. One view is that aortic stiffness occurs as a result of atherosclerosis along the aorta. However, there is little or no association between PWV and classical risk factors for atherosclerosis, other than age and blood pressure. Furthermore, PWV does not increase during early stages of atherosclerosis, as measured by intima-media thickness and non-calcified atheroma, but it does increase in the presence of aortic calcification that occurs within advanced atherosclerotic plaque. Age-related widening of pulse pressure is the major cause of age-related increase in prevalence of hypertension and has been attributed to arterial stiffening. This review summarizes the methods of measuring aortic stiffness in humans, the pathophysiological mechanisms leading to aortic stiffness, including its association with atherosclerosis, and the haemodynamic consequences of increased aortic stiffness.

Assessment of the relationship between aortic pulse wave velocity and aortic arch calcification

We aimed to assess arterial stiffness parameters and to investigate the relationship between these parameters and aortic calcification in patients with aortic arch calcification and without symptomatic atherosclerotic disease. The population of this study consisted of 41 patients with aortic arch calcification verified by chest X-ray (group I, 17 males, mean age 70±5 years) and individuals without aortic arch calcification (group II, 17 males, mean age 68±6 years). Subjects with symptomatic or known vascular disease were excluded from the study. The arterial stiffness parameters of all subjects were measured non-invasively with a SphygmoCor device. Aortic pulse wave velocity (PWV), augmentation pressure (AP), augmentation index (AIx) and heart rate normalized augmentation index (AIx@75) were used as parameters of arterial stiffness. The two groups were compared according to demographic characteristics, medications currently being taken, and levels of serum lipids. There was no significant difference between the groups. AP in group I was significantly higher than that of group II (p=0.002). AIx and AIx@75 were similar in both groups. Aortic PWV of group I was significantly higher than that of group II (p<0.0001). According to the results of this study, the presence of aortic calcification, verified by chest radiography, was associated with increased aortic PWV.

Tricky mitral insufficiency during heart beating surgery

Hemodynamic management during beating heart surgery can be challenging. Blood pressure variations can be caused by many different phenomena more or less common. This report describes a patient in whom hemodynamic became extremely unstable because of the sudden and massive aggravation of a pre-existing moderate mitral regurgitation. On the other hand, strong heart displacement appeared to temporally treat this pre-existing leak and to improve cardiac function. These uncommon events could be attached to trivial anatomic specificities. A 78-year-old man with a history of worsening angina was scheduled for coronary artery bypass graft surgery. Coronary angiography revealed critical stenosis in the origin of the left main coronary artery. Other active medical problems included obesity, type 2 Diabetes mellitus, atherosclerosis and obstructive sleep apnoea syndrome. He was deemed unsuitable for endovascular revascularization and was referred for surgery. Because of the presence of aortic calcifications, off-pump surgery was preferred. The preoperative echocardiogram showed a preserved left ventricular ejection fraction (LVEF 55%) and a moderate mitral regurgitation (MR) (grade II/IV). The mechanism of MR was typically ischemic with a slightly enlarged annulus (anterior leaflet/annulus ≥1.3) combined with an increased tethering of the posterior leaflet. The jet was central and its proximal width was 0.35 cm. It reached the middle of the left atrium and its surface area was 37 mm (Fig. 1). The patient was induced with a target-controlled infusion of remifentanil in association with midazolam, propofol and cis-

Effect modification of obesity on associations between endogenous steroid sex hormones and arterial calcification in women at midlife

The aim of this study was to examine whether obesity modifies the effects of endogenous steroid sex hormones on arterial calcification in women at midlife. Associations between estradiol, testosterone, sex hormone-binding globulin, and free androgen index and the presence and extent of coronary and aortic calcification were evaluated in 187 obese (body mass index, ≥30 kg/m) and 281 nonobese (body mass index, <30 kg/m) women from the Study of Women's Health Across the Nation. Logistic and linear regressions were used as appropriate. Prevalence rates of coronary and aortic calcification were significantly higher among obese compared with nonobese women (P < 0.001, for both). In multivariable analyses, steroid sex hormones were not associated with the presence of coronary calcification. However, for the extent of coronary calcification, significant interactions were found between obesity and both sex hormone-binding globulin (P < 0.0001) and free androgen index (P = 0.008). In nonobese women, higher sex hormone-binding globulin (P = 0.0006) and lower free androgen index (P = 0.01) were associated with a greater extent of coronary calcification, whereas lower sex hormone-binding globulin was associated with greater extent of coronary calcification in obese women (P = 0.05). For aortic calcification outcomes, higher sex hormone-binding globulin was associated with the presence of aortic calcification among nonobese women (odds ratio, 1.64; 95% CI, 1.16-2.32, for each 1-SD greater sex hormone-binding globulin). Associations between endogenous steroid sex hormones and arterial calcification vary by obesity status among perimenopausal women. Further research is needed to better understand the possible mechanisms of these associations.

New insights into the risk factors for coronary calcifications

The arterial calcification process was recognized as soon as 1812 to be a common feature of atherosclerosis [1]. The common belief is that calcification results from the passive deposit of calcium in vascular tissues. This view is not correct. By contrast, many lines of evidence demonstrate that calcification is an active and regulated process involving a change of phenotype of vascular smooth muscle cells into osteoblast-like cell, leading to focal ossification points. This phenomenon may be associated with atherosclerotic plaques and has a focal intimal expression, or it may be a systemic, generalized process, interesting the media, corresponding to the classical Monckeberg disease. It remains to be discussed whether the intimal and medial calcifications share the same pathophysiology [2]. The presence of calcification has been used as a screening tool for early detection of atherosclerosis. Non-invasive (albeit implying exposure to radiation) techniques are available for detection of large artery calcifications. Standard X-rays of the abdomen may detect aortic calcifications in a specific, but not sensitive way. Despite that, the presence of aortic calcifications is associated with excess mortality in the general population [3], and in patients with end-stage renal disease [4]. London [4] has also clearly shown that, in addition to being a prognostic marker of all-cause and cardiovascular mortality in haemodialysis patients, independently of classical atherogenic factors, the principal effect of arterial medial calcifications on arterial function is increased arterial stiffness. More quantitative techniques have been developed to assess calcification. Coronary calcifications may be detected by electron beam computed tomography. This technique has been widely tested in epidemiological studies, and was proven to have an independent prognostic value for cardiovascular disease [5]. This screening tool has proven to be useful, especially when the cardiovascular risk is medium to high. Calcifications are often detected during coronary angiography. In the current issue of the Journal, Mayer et al.[6] took advantage of a cohort of patients with coronary heart disease, in whom coronary angiography was clinically indicated, to assess the risk factors for coronary calcifications. They show that age, systolic blood pressure and family history are positively correlated with coronary calcifications. On the other hand, coronary calcifications are positively correlated with the extent and severity of coronary artery disease. The demonstration that systolic blood pressure is a risk factor or an expression of coronary calcifications was not totally unexpected. Indeed, arterial calcification was shown to be associated with large artery stiffness [7], the major determinant of systolic hypertension and pulse pressure. Unfortunately, because of the multicentric character of their study, Mayer et al.[6] could not record the central pressures measured during coronary angiography. It is likely that central pressure would have been even more closely correlated with coronary calcification than brachial pressure. The study by Mayer et al.[6] also raises questions about the role of drugs in the development and/or prevention of calcification. Indeed, several of the identified risk factors for coronary calcifications, such as age and family history, are not modifiable. However, the fact that systolic blood pressure has been found to be a potent risk factor for coronary calcification is important. We know that systolic blood pressure is under-controlled, and targeting treatment on either systolic blood pressure or preferably central systolic blood pressure may better prevent calcification of the coronary arteries over the long term. Recently, London et al. showed that nutritional vitamin D deficiency in patients with end-stage renal disease had a profound effect on large artery stiffness and endothelial function [8]. Among the drugs involved in vascular calcification, vitamin K antagonists play a central role. Warfarin inhibits the synthesis of GLA residues, which in turn have an inhibitory effect on two key enzymes for calcification of the extracellular matrix, the matrix GLA protein and osteocalcin. Murine models treated with warfarin [8] or invalidated for matrix GLA protein [9] or GLA [10] show extensive vascular calcifications. Unfortunately, the study by Mayer et al.[6] does not provide information about warfarin therapy or vitamin D status in their patients. The study by Mayer et al.[6] raises the important issue of risk markers among patients with coronary stenosis. The number, extent and degree of stenosis, together with left ventricular dysfunction, are essential risk factors for secondary cardiovascular mortality, but they represent only one part of the story. Indeed, patients with diffuse coronary heart disease are at an even higher risk than patients with focal stenosis. In this context, the presence of calcification may represent a useful marker of risk, either related to the procedure (stenting complications, restenosis), or consisting of the recurrence of coronary heart disease or other cardiovascular disease. This excellently-phenotyped cohort may represent a unique opportunity to address this important question. This would allow application to an ‘orphan’ screening test.

Association of pulse wave velocity with vascular and valvular calcification in hemodialysis patients

The recent Kidney Disease: Improving Quality Outcomes (KDIGO) recommendations called for an investigation of the relationship between various radiological methods to assess cardiovascular calcification and measures of arterial stiffness. Accordingly, in 131 adult maintenance hemodialysis patients, we investigated the association of aortic pulse wave velocity (PWV) with calcification of cardiac valves on echocardiography, coronary artery, and thoracic aorta calcium on computed tomography and a calcification score of the abdominal aorta obtained on a plain abdominal X-ray. All tests were performed within a week. Mean PWV increased as the severity of coronary artery, thoracic, and abdominal aorta calcium scores increased (each P<0.05). No trend was present for number of valves with calcification. After multivariable adjustment, abdominal aorta X-ray calcium scores remained associated with PWV (P=0.004), whereas the association of PWV with thoracic aorta and coronary artery calcium scores became marginal (P=0.308 and P=0.083, respectively). No association was found between number of calcified valves and PWV. This study demonstrates a strong association between abdominal aorta calcification on plain X-ray and PWV and a borderline association with thoracic aorta and coronary artery calcification. Sudden death and congestive heart failure, two frequent causes of death in hemodialysis, are likely caused by increased arterial stiffness that can be closely predicted by the presence of aortic calcification on plain X-rays.

Does Atherosclerotic Aortic Plaque Detected by Telecardiography Indicate an Increased Risk of Coronary Artery Disease?

The purpose of this study was to determine the cause of aortic arch calcification and to evaluate its prognostic value as an indicator of cardiovascular disease and its severity. The study was conducted prospectively among 1027 patients who underwent a coronary angiography in our hospital between April 2002 and September 2002 for suspected coronary artery disease. All chest x-rays were reviewed by a radiologist, who categorized aortic arch calcifications by their presence or absence. The patients were stratified according to age (< or =50, 51-64, and > or =65 years) to eliminate the influence of age on aortic arch calcification. Coronary lesions were considered either single-vessel or multivessel disease. Univariate analysis revealed significant correlation with age (r = 0.37; P < .001), presence of hypertension (r = 0.14; P < .001), smoking (r = -0.10; P = .001), presence of coronary artery disease (r = 0.10; P = .001), and the existence of multi-vessel disease (r = 0.09; P = .006). Multivariate analysis disclosed significant association with age and hypertension and no association with smoking, coronary artery disease, and other risk factors. The aortic arch calcifications observed on plain chest x-rays are usually age related, and both aortic arch calcifications and coronary artery disease are strongly associated with age. The presence of aortic calcification on chest x-rays was not an indicator of the presence and extent of coronary artery disease.

Osteoprotegerin (OPG) inhibits vascular calcification in vivo

Vascular calcification shares many features with bone mineralization. Recent evidence suggests that it may be governed by two factors now known to critically regulate bone metabolism: RANKL, a TNF-alpha superfamily member and its soluble decoy receptor, OPG. Both OPG and RANKL are expressed in human arteries, RANKL is increased in plaque, and OPG deficient mice develop aortic calcification. To test whether OPG inhibits vascular calcification, we treated hyperlipidemic ldlr(−/−) mice on a high fat diet with Fc-OPG or vehicle control. After 2 and 5 months, we assessed atherosclerotic lesion size and number, presence of aortic calcification, and osteogenic markers in aortic tissue. At 2 months, atherosclerotic lesion number was significantly reduced with Fc-OPG treatment compared to control (0.03±0.02 vs. 0.07±0.05 lesions/mm media; p < 0.05), but lesion size and area were not different, suggesting that OPG may inhibit initiation, but not growth, of lesions. At 5 months, aortic calcification incidence, detected by von Kossa histochemical staining, was significantly decreased in mice treated with Fc-OPG vs. vehicle control (4 of 14 vs. 11 of 17). Based on ELISA, osteocalcin, an osteogenic marker, was reduced by 72% in the aortas of OPG-treated mice (8.3±10.3 vs. 29.3±25 ng/ml/mg total protein; p < 0.05). Expression of the other markers, msx2, runx2, and osterix mRNA, was not significantly different. These findings suggest that OPG may decrease osteogenic differentiation and mineralization in the artery wall. Supported in part by NIH grant HL/AR69261.