Presence Of Aortic Valve Calcification Research Articles

The effect of the LPA gene on aortic valve calcification in a Portuguese population

Abstract Introduction Aortic valve calcium (AVC) deposition is one of the mechanisms behind aortic sclerosis and stenosis. There is a known association between LPA gene rs3798220 T>C polymorphism and the development of severe aortic stenosis. However, it is still unknown if it has been a driving factor since the early stages of the disease. Objective Investigate, in our population, the association between the LPA gene variant rs3798220 T>C and aortic valve calcification. Methods AVC was measured in 451 consecutive individuals from the prospective arm of the GENEMACOR study with a mean age of 63.4±9.7 years, 58.8% male. AVC score was performed by cardiac computed tomography and reported as Agatston units. Results were separated into two groups (Group A: AVC=0; Group B: AVC>0). Lp(a) levels were analyzed in the different groups. Each individual was genotyped for LPA rs3798220 T>C. This variant has a minor allele frequency (MAF)<2%; hence, the risk homozygous CC is a rare genotype, and we used the heterozygous CT in our analysis. The bivariate and multivariate logistic regression analysis evaluated the presence of AVC adjusting to traditional risk factors (TRFs) and the LPA heterozygous genotype (CT). Results LP(a) levels were higher in the CT allele versus the homozygous TT, but this difference did not reach a statistical significance. After multivariate analysis, the heterozygous LPA rs3798220 T>C polymorphism remained an independent risk factor for the presence of aortic valve calcification (OR=12.14, p=0.002) together with age (OR=1.13, p<0.0001), arterial hypertension (AHT) (OR=1.96, p=0.006) and alcohol consumption (OR=2.46, p=0.016). Conclusion The LPA gene variant rs3798220 T>C is associated with the presence of aortic valve calcification in a Portuguese population. In such an age-dependent disease as aortic stenosis, the inversion in the age pyramid will see a dramatic increase in the prevalence of aortic stenosis. The early identification of high-risk individuals might enable prompt traditional risk factors control and disease prevention. Larger population studies may help to determine if this difference is driven by Lp(a) levels.

#1624 The association between serum beclin 1 level and the presence of aortic valve calcification among individuals on hemodialysis

Abstract Background and Aims The autophagy pathway, a crucial regulator of cellular health and metabolism, plays a fundamental role in maintaining healthy blood vessel function. Studies have established its critical involvement in endothelial cell stability, vascular smooth muscle cell (VSMC) phenotype control, and VSMC calcium balance. Recent evidence, further, underlines autophagy's direct protective role against vascular calcification. It has been shown that autophagy can modulate different cardiovascular pathologies, including valvular calcification. We aimed to explore the potential link between the protein beclin 1 and heart valve calcification in dialysis patients. Method We compared two groups of 51 haemodialysis patients each, defined by the presence (Group 1) or absence of valve calcification (Group 2) on echocardiograms. Both groups underwent beclin 1 level measurements and other assessments (lipid profile). Cardiac valve calcification was diagnosed through echocardiography by identifying dense echoes exceeding 1 millimeter in thickness on one or more aortic valve cusps. The severity of calcification was then classified into three stages: Mild: Calcification thickness ranged from 1 to 3 millimeters and involved less than 50% of the valve leaflet. Moderate: Calcification thickness exceeded 3 millimeters but still affected less than half of the valve leaflet. Severe: Calcification thickness surpassed 3 millimeters and encompassed more than 50% of the valve leaflet. Results Our analysis demonstrated a statistically significant increase in beclin 1 levels in Group 2 compared to Group 1 (p<0.001), a striking relationship between lower beclin 1 levels and more severe valve calcification. Interestingly, a specific beclin 1 cutoff below 35.5 ng/ml offered the highest accuracy (98% sensitivity and 92% specificity) in predicting valve calcification. Notably, significant differences were found in lipid profiles (Analysis of the lipid profile revealed a striking trend in Group I, with significant elevations in cholesterol, triglycerides, and LDL. Conversely, HDL levels were significantly higher in Group II). and prevalence of heart disease between the groups. Analysis of IHD prevalence across the two groups yielded a striking result. Group 1 displayed a significantly higher proportion of individuals with IHD (17 cases) compared to group 2 (3 cases), with a statistically significant difference (p<0.001). Conclusion Based on these results, it appears promising to integrate serum Beclin 1 measurements into a risk assessment model for the development of heart valve calcification in dialysis patients.

High JAK2V617F variant allele frequency is associated with coronary artery but not aortic valve calcifications in patients with Philadelphia-negative myeloproliferative neoplasms.

Patients with Philadelphia-negative myeloproliferative neoplasms (MPNs) have a higher burden of cardiac calcifications compared to the general population. It is not known whether the JAK2V617F mutation is associated with increased cardiac calcification. To investigate if a higher JAK2V617F variant allele frequency (VAF) is associated with severe coronary atherosclerosis and the presence of aortic valve calcification (AVC). Patients with MPNs were examined by cardiac computer tomography to establish coronary artery calcium score (CACS) and AVC score. The first VAF after diagnosis was registered. Severe coronary atherosclerosis was defined as a CACS >400 and AVC was defined as an AVC score >0. Among 161 patients, 137 were JAK2V617F mutation-positive, with a median VAF of 26% (interquartile range 12%-52%). A VAF in the upper quartile range was associated with a CACS >400 [odds ratio (OR) 15.96, 95% confidence interval [CI] 2.13-119.53, p = .0070], after adjustment for cardiovascular risk factors and MPN subtype. An association was not found for the presence of AVC (OR 2.30, 95% CI 0.47-11.33, p = 0.31). In patients with MPNs, there is a significant association between having a VAF in the upper quartile (>52%), and severe coronary atherosclerosis, defined as a CACS >400. The presence of AVC is not associated with VAF.

Assessment of Magnesium level Among Hemodialysis Patients and Its Relation to Vascular Stiffness

Abstract Background The pathogenesis of vascular calcification in Chronic kidney disease (CKD) patients is multifactorial and complicated. It has been proposed that Magnesium (Mg) may be implicated in the process of vascular calcification on various levels. Aim This study aims to assess the level of magnesium in hemodialysis patients and its relation to the vascular stiffness. Patients and methods 100 prevalent hemodialysis patients were included in the study and they were clinically stable with absence of cardiovascular complications, all patients underwent the following laboratory investigation including complete blood picture, median of magnesium level over 3 months, electrolytes, ipth, lipid profile and radiological investigations including transthoracic echocardiography and carotid duplex. Results The studied population was divided into two groups, group I included 68 patients with normal mg level and group II included 32 patients with low mg level. There was statistically significant difference between the two groups as regard hemoglobin level (pvalue=0.033), otherwise there was no statistically significant difference as regard other laboratory and radiological investigations. Then they were divided into another two groups according to the presence of mitral valve calcification (MVC), group III involved 85 patients without MVC and group IV involved 15 patients with MVC. There was statistically significant difference between 2 groups as regard aortic wave pulse velocity (aPWV) with (pvalue=0.002), presence of plaques with (pvalue <0.001) and intimal media thickness with (pvalue<0.001). Another group was divided according to presence of aortic valve calcification (AVC) into two groups, first group V included 39 patients without AVC and second group VI included 61 patients with AVC. There was statistically significant difference between two groups as regard age with (pvalue<0.001), ipth with (pvalue=0.033), presence of plaques with (pvalue=0.048) and intimal media thickness with (pvalue<0.001). Conclusion There was high prevalence of vascular calcification among hemodialysis patients which may be related to age and hyperparathyroidism but without statistically significant correlation to Mg level.

Lipoprotein Particle Profiles Compared With Standard Lipids in the Association With Subclinical Aortic Valve Calcification in Apparently Healthy Japanese Men.

Risk factors for atherosclerotic disease including dyslipidemia have been shown to be associated with aortic valve calcification (AVC). Nuclear magnetic resonance (NMR)-measured lipoprotein particles, low-density and high-density lipoprotein particles (LDL-p, HDL-p) in particular, have emerged as novel markers of atherosclerotic disease; however, whether NMR-measured particles are associated with AVC remains to be determined. This study aimed to examine the association between NMR-based lipoprotein particle measurements and standard lipids with AVC. The primary variables of interest were LDL-p (nmol/L), HDL-p (μmol/L), LDL-cholesterol, and HDL-cholesterol (both in mg/dL). A community-based random sample of Japanese men aged 40-79 years examined in 2006-2008, in Shiga, Japan was studied. Presence of AVC was defined as an Agatston score >0. Lipoprotein particles were measured using NMR spectroscopy. In the main analysis, multivariable-adjusted odds ratios (ORs) and 95% confidence intervals (95% CIs) for the prevalence of AVC across the higher quartiles of lipids in reference to the lowest ones were obtained. Of 874 participants analyzed, 153 men had AVC. Multivariable-adjusted ORs of prevalent AVC for the highest vs. the lowest quartile were significantly elevated for LDL-p (OR, 2.20; 95% CI: 1.23-3.93) and LDL-cholesterol (OR, 2.16; 95% CI: 1.23-3.78). In contrast, neither HDL-p nor HDL-cholesterol was associated with AVC. The association of prevalent AVC with NMR-based LDL-p was comparable to that with LDL-cholesterol.

A study on the prevalence, distribution and related factors of heart valve calcification using coronary CT angiography.

The concept of active atherosclerotic disease has been accepted for heart valve calcification (HVC). We investigated prevalence, distribution and related factors of HVC in patients who had undergone coronary CT angiography (CCTA). Subjects were consecutive 200 patients who underwent CCTA. The prevalence and the distribution of HVC using ECG gated non-contrast CT were investigated. Logistic regression analysis and simple regression analysis for factors associated with presence of the calcification and quantitative calcification in the aortic and mitral valve were conducted. HVC was detected in 48.0%. Aortic valve calcification (AVC) was found in 92 cases, the most, followed by mitral valve calcification (MVC) in 25 cases, pulmonary valve in 3 cases, and tricuspid valve in 1 case. Although the left coronary cusp showed the most in 65.2%, no statistic significant difference for Agatston score was detected among each cusp in AVC. Multiple logistic regression analysis showed that age (OR:1.211, 95%C.I.:1.0716-1.1728, p<0.0001) and coronary artery calcium score (CACS) grade (grade2 OR:7.3393, 95%C.I.:1.7699-30.4349, p=0.0060, grade3 OR:7.2214, 95%C.I.:1.4376-36.2762, p=0.0164) were significant factors associated with presence of AVC. The significant factors associated with quantitative AVC were age (p=0.0043), dyslipidemia (p=0.0117), and statin use (p=0.0221). Only age (OR:1.1589, 95%C.I.:1.0726-1.2520, p=0.0002) was significant factor related to presence of MVC. No significant related factor was found in quantitative MVC. There was an association between presence of AVC and CACS, but not a significant association with presence of MVC. Neither quantitative AVC nor MVC had a significant association with CACS or coronary artery disease.

The rs10455872-G allele of the LPA gene is associated with high lipoprotein(a) levels and increased aortic valve calcium in a Mexican adult population.

Polymorphisms in the LPA gene have been associated with aortic valve calcification (AVC). There are wide differences in the allelic frequencies, Lp(a) levels, and the association with AVC among ethnic groups. The aim of this study was to determine the association of the LPA gene polymorphisms with Lp(a) levels and risk of developing AVC, in Mexican-Mestizos population. Six LPA polymorphisms (rs10455872, rs7765803, rs6907156, rs1321195, rs12212807 and rs6919346) were genotyped by TaqMan assays in 1,265 individuals without premature coronary artery disease. The presence of AVC was determined by computed tomography. The association of the LPA polymorphisms with AVC, Lp(a), and other cardiovascular risk factors (CVRF) was evaluated using logistic regression analysis. Compared to AA genotype, subjects with AG+GG genotypes had high prevalence of Lp(a) ≥ 30 mg/dL (7.1% vs. 23.7%, p<0.001) and AVC (19.0% vs. 29.4%, p=0.007). In a model adjusted for several CVRF, the LPA rs10455872-G allele was associated with high Lp(a) levels and AVC. Carriers of G allele had a high risk of Lp(a) ≥ 30 mg/dL (OR= 3.86, CI 95%: 2.2 - 6.7, p=0.001) and AVC (OR= 2.54, CI 95%: 1.56 - 4.14, p=0.001), independently of other CVRF. In this population, carriers of rs10455872-G allele had 3.86 and 2.54 higher risk of Lp(a) ≥ 30 mg/dL or presence of AVC, respectively.

Lipoproteins in Cardiovascular Calcification: Potential Targets and Challenges.

Previously considered a degenerative process, cardiovascular calcification is now established as an active process that is regulated in several ways by lipids, phospholipids, and lipoproteins. These compounds serve many of the same functions in vascular and valvular calcification as they do in skeletal bone calcification. Hyperlipidemia leads to accumulation of lipoproteins in the subendothelial space of cardiovascular tissues, which leads to formation of mildly oxidized phospholipids, which are known bioactive factors in vascular cell calcification. One lipoprotein of particular interest is Lp(a), which showed genome-wide significance for the presence of aortic valve calcification and stenosis. It carries an important enzyme, autotaxin, which produces lysophosphatidic acid (LPA), and thus has a key role in inflammation among other functions. Matrix vesicles, extruded from the plasma membrane of cells, are the sites of initiation of mineral formation. Phosphatidylserine, a phospholipid in the membranes of matrix vesicles, is believed to complex with calcium and phosphate ions, creating a nidus for hydroxyapatite crystal formation in cardiovascular as well as in skeletal bone mineralization. This review focuses on the contributions of lipids, phospholipids, lipoproteins, and autotaxin in cardiovascular calcification, and discusses possible therapeutic targets.

Aortic Valve Calcification and the Risk of dementia: A Population-Based Study.

The association of aortic valve calcification (AVC) with dementia remains unknown. In 2,428 non-demented participants from the population-based Rotterdam Study, we investigated the association of CT-assessed AVC with risk of dementia and cognitive decline. AVC was present in 33.1% of the population. During a median follow-up of 9.3 years, 160 participants developed dementia. We found no association between presence of AVC and risk of all-cause dementia [hazard ratio (HR): 0.89 (95% confidence interval (CI):0.63;1.26)]. Presence of AVC was not associated with cognitive decline on any of the cognitive tests, nor with a measure of global cognition.

Aortic Valve Calcification and Risk of Stroke: The Rotterdam Study.

It remains uncertain whether aortic valve calcification (AVC) is a risk factor for stroke. From the population-based Rotterdam Study, 2471 participants (mean age: 69.6 years; 51.8% women) underwent computed tomography to quantify AVC. We assessed prevalent stroke and continuously monitored the remaining participants for the incidence of stroke. Logistic and Cox regression models were used to investigate associations of AVC with prevalent stroke and risk of incident stroke. AVC was present in 33.1% of people. At baseline, 97 participants had ever suffered a stroke. During 18 665 person-years of follow-up (mean: 7.9 years), 135 people experienced a first-ever stroke. The presence of AVC was not associated with prevalent stroke (fully adjusted odds ratio: 0.97 (95% confidence interval, 0.61-1.53]) or with an increased risk of stroke (fully adjusted hazard ratio: 0.99 (95% confidence interval, 0.69-1.44]). Although AVC is a common finding in middle-aged and elderly community-dwelling people, our results suggest that AVC is not associated with an increased risk of stroke.

Predominance of Abdominal Visceral Adipose Tissue Reflects the Presence of Aortic Valve Calcification

Background. Aortic valve calcification (AVC) is a common feature of aging and is related to coronary artery disease. Although abdominal visceral adipose tissue (VAT) plays fundamental roles in coronary artery disease, the relationship between abdominal VAT and AVC is not fully understood. Methods. We investigated 259 patients who underwent cardiac and abdominal computed tomography (CT). AVC was defined as calcified lesion on the aortic valve by CT. %abdominal VAT was calculated as abdominal VAT area/total adipose tissue area. Results. AVC was detected in 75 patients, and these patients showed higher %abdominal VAT (44% versus 38%, p < 0.05) compared to those without AVC. When the cutoff value of %abdominal VAT was set at 40.9%, the area under the curve to diagnose AVC was 0.626. Multivariable logistic regression analysis showed that age (OR 1.120, 95% CI 1.078–1.168, p < 0.01), diabetes (OR 2.587, 95% CI 1.323–5.130, p < 0.01), and %abdominal VAT (OR 1.032, 95% CI 1.003–1.065, p < 0.05) were independent risk factors for AVC. The net reclassification improvement value for detecting AVC was increased when %abdominal VAT was added to the model: 0.5093 (95% CI 0.2489–0.7697, p < 0.01). Conclusion. We determined that predominance of VAT is associated with AVC.

Abstract 13360: Impact of Aortic Valve Calcification on the Incidence of Periprocedual Myocardial Injury in Patients Undergoing Coronary Stent Implantation

Object: Previous studies have shown an association between aortic valve calcification (AVC) and cardiovascular events and mortality. On the other hand, periprocedual myocardial injury (PMI) is known as a predictor of subsequent mortality and other poor clinical outcomes. Hypohtesis: We assessed the hypothesis that presence of AVC could predict PMI in elective percutaneous coronary intervention (PCI). Methods: This study included a total of 372 patients treated with PCI for stable angina pectoris. Aortic valve calcification was defined as bright echoes &gt;1mm on one or more cusps of aortic valve by ultrasound cardiography. PMI was defined as an increase in high-sensitivity troponin T &gt;5 times (0.070 ng/ml) the upper normal limit at 24hours after PCI. Results: AVC was detected in 46.0% (n = 171). The incidence of PMI was significantly higher in patients with AVC than in those without AVC (43.9% vs 10.9%, respectively, p &lt; 0.001). The presence of AVC independently predicted PMI after adjusting for other significant variables (OR 2.18, 95% CI 1.30 to 3.66, p = 0.003). Other predictors were estimated glomerular filtration rate (OR 0.975, 95% CI 0.962 to 0.989, p &lt; 0.001), left anterior descending artery lesion (OR 0.496, 95% CI 0.293 to 0.840, p = 0.01) and total stent length (odds ratio 1.02, 95% confidence interval 1.00 to 1.05, p = 0.03). Conclusion: In conclusion, presence of AVC could predict incidence of PMI. Because detection of AVC by ultrasound cardiography is very simple, it is useful for risk stratifications in elective PCI with stent implantation.

Abstract 16680: Lipoprotein(a) and Progression Rate of Aortic Valve Stenosis - A Pooled-Analysis of Two Prospective Studies

BACKGROUND: Recent studies have reported a single nucleotide polymorphism (i.e. rs10455872) at the LPA gene locus, encoding the lipoprotein(a) [Lp(a)], is associated with the presence of aortic valve calcification and clinical aortic stenosis (AS). The objectives of this study were to examine the association of Lp(a) plasma levels and rs 10455872 with the progression rate of AS. METHODS: Lp(a) plasma levels were measured in 203 patients with AS included in the ASTRONOMER (NCT00800800) trial and 246 patients in the PROGRESSA study (NCT01679431). The polymorphism rs10455872 was genotyped in the PROGRESSA cohort. Hemodynamic progression rate of AS severity was assessed by measuring the annualized increase in peak aortic jet velocity (Vpeak) by Doppler-echocardiography. RESULTS: Twenty-seven (13%) patients of the ASTRONOMER trial and 47 (19%) of the PROGRESSA study had high Lp(a) plasma levels (i.e. &gt;50mg/dL). Baseline AS severity was similar in patients with high vs. low Lp(a) levels (p&gt;0.10). In the pooled-analysis of both cohorts (a total of 449 patients with mean follow-up: 3.0 ±1.4 yrs), AS progression rate was similar in patients with Lp(a)&gt;50 mg/dL compared to those with Lp(a)≤50 mg/dL (annualized change in Vpeak: +0.17±0.21 vs. +0.17±0.21 m/s/yr; p=0.97). Stratified analyses by cohort provided consistent results (ASTRONOMER: +0.20±0.21 vs. +0.25±0.19 m/s/yr; p=0.20; and PROGRESSA: +0.12±0.21 vs. +0.14±0.20 m/s/yr; p=0.46). In the PROGRESSA study, 38 (16%) patients carried at least one rs10455872 risk allele. Carriers of the risk allele had higher Lp(a) levels (58±24 vs. 20±38 mg/dL; p&lt;0.0001). Baseline AS severity was similar in carriers and non-carriers whereas there was a borderline significant association for lower AS progression rate in carriers compared to non-carriers (+0.07±0.17 vs. +0.15±0.21 m/s/yr; p=0.05). Similar results were obtained for baseline and annualized progression rate assessed by aortic valve area. CONCLUSION: This prospective study shows that neither LPA gene variant nor Lp(a) plasma levels are associated with faster AS progression rate. Our findings do not support the notion that Lp(a) levels are related to AS progression rate in patients with AS.

LIPOPROTEIN(A) AND PROGRESSION RATE OF AORTIC VALVE STENOSIS - THE PROGRESSA STUDY

Recent studies have reported a single nucleotide polymorphism (i.e. rs10455872) at the LPA gene locus, encoding the lipoprotein(a) [Lp(a)], associated with the presence of aortic valve calcification and the incidence of clinical aortic stenosis (AS). The objectives of this study was to examine the association of rs10455872 and Lp(a) plasma levels with the progression rate of AS. 246 consecutive patients with AS were prospectively recruited in the PROGRESSA study and underwent a comprehensive Doppler-echocardiography annually. Blood-DNA and plasma samples were collected to genotype the rs10455872 polymorphism and to measure Lp(a) plasma levels. Hemodynamic progression rate of AS severity was assessed by measuring the annualized increase in peak aortic jet velocity (Vpeak). Among the 246 patients included in the study, 38 (16%) patients carried at least one rs10455872 risk allele and 47 (19%) had high Lp(a) plasma level (i.e. >50mg/dL). Carriers of the risk allele had higher Lp(a) levels (58±24 vs. 20±38 mg/dL; p<0.0001). Baseline AS severity was similar in carriers and non-carriers (Vpeak: 2.8±0.4 vs. 2.9±0.7 m/s; p=0.33), as well as in patients with high vs. low Lp(a) levels (2.9±0.5 vs. 2.9±0.6 m/s; p=0.97). There was a borderline significant association for lower AS progression rate in carriers compared to non-carriers (annualized change in Vpeak: +0.07±0.17 vs. +0.15±0.21 m/s/yr; p=0.05), whereas patients with high Lp(a) levels had similar stenosis progression rate (+0.12±0.21 vs. +0.14±0.20 m/s/yr; p=0.46). Similar results were obtained with the analysis of baseline and annualized change in aortic valve area. This prospective study shows that neither LPA gene variant nor Lp(a) plasma levels are associated with faster AS progression rate. These findings suggest that Lp(a) lowering therapy may not be efficient to delay or stop stenosis progression in patients with AS.

Association Between Aortic Valve Calcification and Myocardial Ischemia, Especially in Asymptomatic Patients

Aortic valve calcification (AVC) is recognized as a manifestation of systemic arteriosclerosis. However, it is unclear whether AVC is associated with myocardial ischemia. Stress myocardial perfusion SPECT (MPS) is widely used for the diagnosis of myocardial ischemia. However, routine MPS is not recommended, particularly in asymptomatic patients. Accordingly, we investigated the hypothesis that the presence of AVC is strongly associated with inducible myocardial ischemia, even among asymptomatic patients. We investigated 669 consecutive patients who underwent both adenosine stress (201)Tl MPS and echocardiography. We evaluated the extent and severity of myocardial ischemia by the summed difference score (SDS). We defined the presence of myocardial ischemia as SDS ≥ 3 and moderate to severe ischemia as SDS ≥ 8. We classified the severity of AVC according to the number of affected aortic leaflets. We also compared the mean SDS and the prevalence of SDS ≥ 3 and SDS ≥ 8 among patients stratified by the severity of AVC. The presence of AVC was significantly associated with myocardial ischemia (odds ratio [OR], 1.56; 95% confidence interval [CI], 1.10-2.23; P = 0.013) and moderate to severe ischemia (OR, 2.16; 95% CI, 1.26-3.80; P = 0.0061). In 311 asymptomatic patients, AVC was strongly associated with moderate to severe ischemia (OR, 4.31; 95% CI, 1.67-12.8; P = 0.0043). However, the SDS value and the prevalence of SDS ≥ 3 and SDS ≥ 8 did not increase with increasing number of affected aortic leaflets. The presence of AVC may be associated with the presence of myocardial ischemia, particularly in asymptomatic patients. However, we found no association between the extent of AVC and inducible myocardial ischemia. The presence of AVC may be a useful anatomic marker to help identify patients at high risk of myocardial ischemia, particularly asymptomatic patients.

Wapniejące uszkodzenie zastawki aortalnej jako czynnik ryzyka zdarzeń sercowo-naczyniowych

Aortic valve calcification (AVC) is a common disease of the elderly. It is a progressive disease ranging from mild valve thickening to severe calcification with aortic valve stenosis. Risk factors for AVC are similar to those for atherosclerosis: age, gender, hypercholesterolemia, diabetes, hypertension, smoking and renal failure. AVC shares many similarities to atherosclerosis, including inflammatory cells and calcium deposits, and correlates with coronary plaque burden. Presence of AVC is associated with increased risk of adverse cardiovascular events. The objective for this review is to discuss the clinical features, natural history and prognostic significance of aortic valve calcifications, including mechanical and hemodynamic factors of flow distribution.

120 Relationship between biomarkers and intracardiac calcification in patients with mild to moderate aortic stenosis

120 Relationship between biomarkers and intracardiac calcification in patients with mild to moderate aortic stenosis

Imaging of the Aortic Valve Using Fluorodeoxyglucose Positron Emission Tomography: Increased Valvular Fluorodeoxyglucose Uptake in Aortic Stenosis

Because fluorodeoxyglucose positron emission tomography (FDG-PET) imaging provides a noninvasive index of inflammation, we sought to assess whether FDG uptake in the aortic valve (AV) is increased in aortic stenosis (AS). AS is associated with valvular inflammation. FDG-PET/computed tomography data were retrospectively evaluated in 84 patients (age 73 ± 9 years, 45% female), 42 patients with AS, and 42 age-matched controls. FDG uptake was determined within the AV while blinded to AS severity. Target-to-background ratio (TBR) was calculated as valvular/blood activity. Stenosis severity was established on echocardiography, and presence of AV calcification was independently assessed on computed tomography. The aortic valve PET signal (TBR) was increased in AS compared with controls (median 1.53 [interquartile range (IQR): 1.42 to 1.76] vs. 1.34 [IQR: 1.20 to 1.55]; p < 0.001). Further, compared with controls, TBR was increased in mild (median 1.50 [IQR: 1.36 to 1.75]; p = 0.01) and moderate (median 1.70 [IQR: 1.52 to 1.94]; p < 0.001), but not in severe AS (median 1.49 [IQR: 1.40 to 1.54]; p = 0.08). When subjects were categorized according to AV calcification, valvular FDG uptake was increased in mildly (median 1.50 [IQR: 1.36 to 1.79]; p < 0.01) and moderately (median 1.67 [IQR: 1.50 to 1.85]; p < 0.001), but not severely calcified valves (median 1.51 [IQR: 1.38 to 1.54]; p = 0.15), compared with noncalcified valves (median 1.35 [IQR: 1.20 to 1.52]). This study supports the hypothesis that AS is an inflammatory condition and suggests that inflammation may be reduced in late-stage disease. This may have important implications in the design of studies assessing the effect of therapeutic agents in modifying progression of AS.

Prevalence and severity of coronary artery disease in diabetic patients with aortic valve calcifi cation

Objective Aortic valve calcifi cation (AVC) is common in the elderly and associated with increased cardiovascular mortality, while diabetes is one of the confi rmed risk factors for coronary artery disease (CAD). In this study, we aimed to evaluate the prevalence and severity of CAD in type-2 diabetic patients with AVC.Methods From June to December in 2007, a total of 325 consecutive patients with chest pain or chest distress were admitted for coronary angiography. The severity of CAD was evaluated by the Gensini score and the number of stenosed vessels. All patients underwent transthoracic echocardiography for detecting AVC.Results Compared with the patients without diabetes (n = 221), the type-2 diabetic patients (n = 104) had a similar prevalence of CAD (66.5% vs. 72.1%, P= 0.312). Further classifi ed by the presence of AVC, patients with AVC had a higher prevalence of CAD, average Gensini score and the number of stenosed vessels, both in the group with and without diabetes. It was also demonstrated that the odds ratio (OR) of AVC for CAD in the diabetic patientswas higher than in the non-diabetic ones (3.405 vs 2.515) after chi-square analysis (single-variable). However, at multivariable logistic regression analysis for CAD, the OR of AVC was 3.757 (P= 0.03) in diabetic group, while it did not achieve statistical signifi cance in the non-diabetic group (OR = 2.130, P= 0.074).Conclusions Type-2 diabetic patients with AVC had a higher prevalence of and more severe CAD.

Combined presence of aortic valve calcification and mitral annular calcification as a marker of the extent and vulnerable characteristics of coronary artery plaque assessed by 64-multidetector computed tomography

Objective We examined the association of aortic valve calcification (AVC) and mitral annular calcification (MAC) to coronary atherosclerosis using 64-multidetector computed tomography (MDCT). Background Valvular calcification is considered a manifestation of atherosclerosis. The impact of multiple heart valve calcium deposits on the distribution and characteristics of coronary plaque is unknown. Methods We evaluated 322 patients referred for 64-MDCT, and assessed valvular calcification and the extent of calcified (CAP), mixed (MCAP), and noncalcified coronary atherosclerotic plaque (NCAP) in accordance with the 17-coronary segments model. We assessed the vulnerable characteristics of coronary plaque with positive remodeling, low-density plaque (CT density ≤38 Hounsfield units), and the presence of adjacent spotty calcification. Results In 49 patients with both AVC and MAC, the segment numbers of CAP and MCAP were larger than in those with a lack of valvular calcification and an isolated AVC ( p < 0.001 for both). Multivariate analyses revealed that a combined presence of AVC and MAC was independently associated with the presence (odds ratio [OR] 9.36, 95% confidence interval [95%CI] 1.55–56.53, p = 0.015) and extent ( β-estimate 1.86, p < 0.001) of overall coronary plaque. When stratified by plaque composition, it was associated with the extent of CAP ( β-estimate 1.77, p < 0.001) and MCAP ( β-estimate 1.04, p < 0.001), but not with NCAP. Moreover, it was also related to the presence of coronary plaque with all three vulnerable characteristics (OR 4.87, 95%CI 1.85–12.83, p = 0.001). Conclusion The combined presence of AVC and MAC is highly associated with the presence, extent, and vulnerable characteristics of coronary plaque identified by 64-MDCT.