Aggressive and diffuse coronary calcification in South Asian angina patients compared to Caucasians with similar risk factors

Background

Ethnic differences in prevalence and severity of coronary artery disease are well established and are usually attributed to risk factors variation. This study investigates the differences in coronary artery narrowing and coronary calcification between two age- and gender-matched cohorts of South Asian and Caucasian symptomatic angina patients.

Methods

We identified 101 symptomatic angina patients of South Asian origin who had undergone CT angiography and calcium scoring, and compared them with 101 age and gender matched Caucasian patients.

Results

South Asians had a greater mean number of arterial segments with both obstructive and non-obstructive plaque than Caucasians (p = 0.006 and p = 0.0003, respectively) and higher prevalence of triple-vessel disease (p = 0.0004). Similarly, South Asians had a higher mean CAC score (p < 0.0001) and the percentage of South Asians with CAC > 0 and in all categories of CAC score 100–1000 were also higher, as was the number of arterial segments with calcified and non-calcified plaque. These results were more marked in patients aged > 50 but in those ≤ 50, Caucasians showed a higher mean number of diseased segments (p = 0.019), with non-obstructive plaque (p = 0.02), possibly suggesting that Caucasians are likely to have more diffuse atherosclerosis at an earlier age. CAC prevalence and severity in this age-group were not significantly different between South Asians and Caucasians.

Conclusion

Despite similar conventional risk factors for CAD, symptomatic South Asians seem to have more aggressive and diffuse arterial calcification compared to Caucasians. These differences are more profound above the age of 50, suggesting potential genetic or other risk factors yet to be determined.     

Type 2 diabetes does not attenuate racial differences in coronary calcification

Aims

Coronary artery calcification (CAC) is a strong predictor of atherosclerotic cardiovascular disease (CVD). Whites appear to have a higher prevalence of CAC than African-Americans (AAs), but it is unknown if type 2 diabetes, a major cardiovascular risk factor, attenuates this difference. We investigated the relationship of race and CAC in a sample of patients with type 2 diabetes without clinical CVD.

Methods

Multivariable analyses of self-reported ethnicity and CAC scores, stratified by gender, in 861 subjects [32% AA, 66.9% male] with type 2 diabetes.

Results

AA race was associated with lower CAC scores in age-adjusted models in males [Tobit ratio for AAs vs. Whites 0.14 (95% CI 0.08-0.24, p < 0.001)] and females [Tobit ratio 0.26 (95% CI 0.09-0.77, p = 0.015)]. This persisted in men after adjustment for traditional, metabolic and inflammatory risk factors, but adjustment for plasma triglycerides [0.48 (95% CI 0.15-1.49, p = 0.201)] and HOMA-IR [0.28 (95% CI 0.08-1.03, p = 0.055)] partially attenuated the association in women.

Conclusions

Relative to African-Americans, White race is a strong predictor of CAC, even in the presence of type 2 diabetes. The relationship in women appears less robust possibly due to gender differences in metabolic risk factors.     

The relationship of insulin resistance and extracoronary calcification in the multi-ethnic study of atherosclerosis

Objective

We hypothesized that insulin resistance, measured by the homeostasis model assessment of insulin resistance (HOMA), is independently associated with prevalent and incident extra-coronary calcification (ECC).

Methods

We studied calcium scores of the aortic valve calcification (AVC), mitral valve calcification (MVC), thoracic aorta calcification (TAC) and aortic valve root calcification (AVR) in 6104 MESA participants not on diabetes medication who had baseline cardiac CT scans; 5312 had follow-up scans (mean 2.4 years). Relative-risk regression modeled prevalent and incident ECC adjusted for baseline demographics (model 1), and additionally for CVD risk factors (model 2).

Results

In model 1, prevalence and incidence risk-ratios for the highest versus lowest quartile of HOMA were 20–30% higher in all ECC locations (p-value for trend ≤0.05 for all but incident-AVC). In model 2, all associations were attenuated, primarily by adjustment for metabolic syndrome components.

Conclusions

HOMA has a positive and graded association with ECC, but not independently of cardiovascular risk factors—particularly metabolic syndrome components.     

Valvular and thoracic aortic calcium as a marker of the extent and severity of angiographic coronary artery disease

Background

The presence of calcified extracoronary structures as a useful indicator of underlying coronary artery disease (CAD) has not yet been established. The purpose of this study was to evaluate whether valvular and thoracic aortic calcification is associated with obstructive CAD.

Methods

We evaluated 99 patients who underwent both coronary angiography and electron beam tomography (EBT) coronary scanning. We identified the presence, absence, and amount of calcification in the aortic valve (AVC), mitral annulus (MAC), descending aorta (DAC), and ascending aorta (AAC). The extent of CAD was graded according to the number of vessels diseased (VD).

Results

Patients with multivessel disease (MVD) had a higher proportion of DAC. The presence of DAC significantly increased the specificity of EBT to detect CAD (58% with a calcium score >0 to 88% for calcium score>0 and DAC >0, P < .001). Both AAC and DAC were associated with a significantly higher rate of MVD in women (DAC, 63% in MVD vs 19% without, P < .01.; AAC, 65% vs 22%, P < .05). MAC had no relationship to either stenosis severity or the presence of obstructive CAD. AVC was the strongest predictor of the severity of CAD and predicted the presence of 3-vessel disease.

Conclusion

AVC and thoracic aortic calcification as detected with EBT are associated with the angiographic extent and severity of CAD and add incremental diagnostic value to the coronary artery calcium score. MAC does not add incremental value. (Am Heart J 2003;145:xxx-xxx.)     

Serum phosphate is associated with aortic valve calcification in the Multi-ethnic Study of Atherosclerosis (MESA)

Objectives

This study sought to investigate associations of phosphate metabolism biomarkers with aortic valve calcification (AVC).

Background

Calcific aortic valve disease (CAVD) is a common progressive condition that involves inflammatory and calcification mediators. Currently there are no effective medical treatments, but mineral metabolism pathways may be important in the development and progression of disease.

Methods

We examined associations of phosphate metabolism biomarkers, including serum phosphate, urine phosphate, parathyroid hormone (PTH) and serum fibroblast growth factor (FGF)-23, with CT-assessed AVC at study baseline and in short-term follow-up in 6814 participants of the Multi-Ethnic Study of Atherosclerosis (MESA).

Results

At baseline, AVC prevalence was 13.2%. Higher serum phosphate levels were associated with significantly greater AVC prevalence (relative risk 1.3 per 1 mg/dL increment, 95% confidence incidence: 1.1 to 1.5, p < 0.001). Serum FGF-23, serum PTH, and urine phosphate were not associated with prevalent AVC. Average follow-up CT evaluation was 2.4 years (range 0.9–4.9 years) with an AVC incidence of 4.1%. Overall, phosphate metabolism biomarkers were not associated with incident AVC except in the top FGF-23 quartile.

Conclusions

Serum phosphate levels are significantly associated with AVC prevalence. Further study of phosphate metabolism as a modifiable risk factor for AVC is warranted.     

Incremental prognostic value of cardiac computed tomography angiography in asymptomatic aortic stenosis: Significance of aortic valve calcium score

Background

Cardiac computed tomography angiography (CCTA) provides the simultaneous evaluation of the aortic valve, myocardium, and coronary arteries. In particular, aortic valve calcium score (AVCS) can be accurately measured on the same scanning sequence used to measure coronary artery calcification, with no additional cost or radiation exposure. We sought to evaluate the prognostic value of CCTA measures, including AVCS, in asymptomatic aortic stenosis (AS).

Methods and results

Sixty-four initially asymptomatic patients with AS with a normal ejection fraction were prospectively enrolled and followed for median 29 (IQR = 18–50) months. During follow-up, 27 (42%) patients experienced cardiac events, including five cardiac deaths, eleven aortic valve replacements. Multivariate Cox proportional hazards analysis identified three CCTA measures as significant predictors of cardiac events: aortic valve area (per 0.1 cm² decrease; hazard ratio [HR]: 1.19, 95% confidence interval [CI]: 1.05–1.34); multi-vessel obstructive coronary artery disease (HR: 2.84, 95% CI: 1.10–7.32); and AVCS (per 100; HR: 1.09, 95% CI: 1.04–1.15). Kaplan–Meier analysis showed that patients with AVCS greater than or equal to the median value of 723 had significantly worse outcomes than those with AVCS less than 723 (p < 0.0001). The C-statistic value for cardiac events substantially increased when these CCTA measures were added to clinical characteristics plus echocardiographic peak transaortic velocity (0.913 vs. 0.702, p < 0.001).

Conclusions

In patients with asymptomatic AS, CCTA measures of valve area, coronary stenosis, and calcification severity provide independent and incremental prognostic value after accounting for the echocardiographic severity of stenosis.     

Intracardiac calcification is a marker of generalized atherosclerosis

Aortic valve calcification (AVC) and carotid artery calcification (CAC) are considered to be markers of generalized atherosclerosis. However, the role of intracardiac calcification (ICC) (valvular and perivalvular calcification) is unclear. The objective of this retrospective study was to analyze the relationship between ICC and CAC, risk factors, and clinical atherosclerotic disease. Risk factors included age, sex, diabetes mellitus, hypercholesterolemia, and hypertension; clinical atherosclerosis comprised stroke, coronary artery disease, and peripheral artery disease. Between January 1, 2001, and January 1, 2004, all consecutive patients were enrolled into the study who underwent both carotid ultrasonography and transthoracic echocardiography examinations within 2 months. Patients with renal failure, substantial aortic stenosis, and carotid artery occlusion were excluded. There were 320 patients (104 men; mean +/- SEM age, 66.6 +/- 0.76 years). Positive results on carotid ultrasonography are defined as any CAC. Patients were categorized as having mild, moderate, or severe CAC. Positive results on transthoracic echocardiography were defined as any ICC; AVC was defined as mitral anulus calcification (MAC) or both. Intracardiac calcification was found in 181 patients, AVC in 51 patients, MAC in 48 patients, and calcification of both structures in 82 patients. Using multiple logistic regression analysis, ICC (odds ratio, 1.9), age (10-year periods) (odds ratio, 2.0), and the presence of peripheral artery disease (odds ratio, 1.7) were independent predictors of CAC. Carotid ultrasonography results were positive in 227 patients. For CAC, the sensitivities of AVC, MAC, both, and any ICC were 52.4%, 52.0%, 33.5%, and 71.2%, respectively, and the specificities were 84.9%, 87.1%, 92.5%, and 78.5%, respectively. The extension of ICC as 0, 1 location (AVC or MAC) , or 2 locations (AVC and MAC) was associated with the severity of CAC (P < .001, tau = 0.42). There was no difference between patients with AVC vs patients with MAC in the presence of different stages of CAC (P = .62). Intracardiac calcification (MAC or AVC) is an independent predictor of CAC as a marker of atherosclerosis, although the lack of ICC does not rule out atherosclerosis. Intracardiac calcification is related to CAC, with high specificity. The extension of ICC is related to the severity of atherosclerosis. Based on our results, antiatherothrombotic therapy should be considered in patients with ICC even before obtaining a positive carotid ultrasonography result.     

Significance of commissural calcification on outcome of mitral balloon valvotomy

OBJECTIVE—To evaluate the significance of commissural calcification, identified by transthoracic echocardiography, on the haemodynamic and symptomatic outcome of mitral balloon valvotomy.
METHODS—Commissural calcification was graded from 0-4 using parasternal short axis transthoracic views. The morphology of the mitral valve was also assessed using the Massachusetts General Hospital echo score.
SETTING—A tertiary cardiac centre in Scotland.
PATIENTS—300 patients were studied, 85 retrospectively and 215 prospectively. Mean (SD) age was 59.8 (12.7) years, range 13 to 87; 30% had been judged unsuitable for surgery. Median echo score was 6.8 (3.0), range 2-16.
MAIN OUTCOME MEASURES—Immediate increase in mitral valve area and in New York Heart Association functional class 1-3 months after balloon valvotomy.
RESULTS—On univariate and multivariate analysis, commissural calcification grade was a significant predictor of achieving a mitral valve area of > 1.50 cm² without severe mitral reflux. Its influence was greatest in patients with an echo score ⩽ 8: those with commissural calcification grade 0/1 had significantly greater improvement in valve area and symptom status than those with grade 2/3; the proportions of patients achieving a final valve area of > 1.50 cm² were 67% and 46%, respectively (p < 0.05). In patients with an echo score of > 8, the influence of commissural calcification was smaller and not significant.
CONCLUSIONS—Commissural calcification as assessed by transthoracic echocardiography is a useful predictor of outcome in patients with otherwise "good" valves (echo score ⩽ 8). Calcification of one commissure or more predicts a less than 50% probability of achieving a valve area above 1.50 cm² and is an indication for valve replacement in those who are suitable for surgery.


     

Relationship of change in traditional cardiometabolic risk factors to change in coronary artery calcification among individuals with detectable subclinical atherosclerosis: The multi-ethnic study of atherosclerosis

Background/Objectives

Data describing relationships between change in risk factors and coronary artery calcification (CAC) are lacking and could inform optimal cardiovascular disease prevention and treatment strategies. This study aimed to examine how change in traditional cardiometabolic risk factors related to change in CAC among individuals with detectable subclinical atherosclerosis.

Methods

Latent growth modeling was used to examine change in cardiometabolic risk factors (waist circumference, body mass index, systolic and diastolic blood pressure, high- and low-density lipoprotein cholesterol, triglycerides, and glucose) related to change in CAC up to an average 4.9-year follow-up in a multi-ethnic cohort of 3398 asymptomatic individuals (57.8% men) who had detectable CAC (score > 0) at baseline, adjusting for baseline risk factor levels and CAC values, age, gender, race/ethnicity, smoking, family history of CVD, income, and use of antihypertensive, lipid-lowering, and glucose-lowering medications.

Results

Greater declines in blood pressure (systolic and diastolic) and low-density lipoprotein cholesterol at follow-up were each associated with greater CAC progression. The observed inverse associations were attributable to greater CAC progression in participants taking antihypertensive and lipid-lowering drugs who, as expected, had declines in blood pressure and lipid levels, respectively. These inverse associations did not emerge in participants not taking these medications.

Conclusions

Among individuals with subclinical atherosclerosis, the unexpected inverse associations observed between change in blood pressure and lipid levels with CAC progression emphasize the importance of considering medication use, and, when feasible, the severity and duration of disease, in exploring associations between risk factors and CAC change.     

Impact of Aortic Valve Calcification,as Measured by MDCT,on Survival in Patients With Aortic Stenosis : Results of an International Registry Study

Background

Aortic valve calcification (AVC) load measures lesion severity in aortic stenosis (AS) and is useful for diagnostic purposes. Whether AVC predicts survival after diagnosis, independent of clinical and Doppler echocardiographic AS characteristics, has not been studied.

Objectives

This study evaluated the impact of AVC load, absolute and relative to aortic annulus size (AVC_density), on overall mortality in patients with AS under conservative treatment and without regard to treatment.

Methods

In 3 academic centers, we enrolled 794 patients (mean age, 73 ± 12 years; 274 women) diagnosed with AS by Doppler echocardiography who underwent multidetector computed tomography (MDCT) within the same episode of care. Absolute AVC load and AVC_density (ratio of absolute AVC to cross-sectional area of aortic annulus) were measured, and severe AVC was separately defined in men and women.

Results

During follow-up, there were 440 aortic valve implantations (AVIs) and 194 deaths (115 under medical treatment). Univariate analysis showed strong association of absolute AVC and AVC_density with survival (both, p < 0.0001) with a spline curve analysis pattern of threshold and plateau of risk. After adjustment for age, sex, coronary artery disease, diabetes, symptoms, AS severity on hemodynamic assessment, and LV ejection fraction, severe absolute AVC (adjusted hazard ratio [HR]: 1.75; 95% confidence interval [CI]: 1.04 to 2.92; p = 0.03) or severe AVC_density (adjusted HR: 2.44; 95% CI: 1.37 to 4.37; p = 0.002) independently predicted mortality under medical treatment, with additive model predictive value (all, p ≤ 0.04) and a net reclassification index of 12.5% (p = 0.04). Severe absolute AVC (adjusted HR: 1.71; 95% CI: 1.12 to 2.62; p = 0.01) and severe AVC_density (adjusted HR: 2.22; 95% CI: 1.40 to 3.52; p = 0.001) also independently predicted overall mortality, even with adjustment for time-dependent AVI.

Conclusions

This large-scale, multicenter outcomes study of quantitative Doppler echocardiographic and MDCT assessment of AS shows that measuring AVC load provides incremental prognostic value for survival beyond clinical and Doppler echocardiographic assessment. Severe AVC independently predicts excess mortality after AS diagnosis, which is greatly alleviated by AVI. Thus, measurement of AVC by MDCT should be considered for not only diagnostic but also risk-stratification purposes in patients with AS.     

Cardiac valve calcification: characteristics of patients with calcification of the mitral annulus or aortic valve

Aims—To determine whether mitral annular calcification and aortic valve calcification, with or without stenosis, are expressions of atherosclerotic disease.Methods—The incidence of atherosclerotic risk factors was analysed in patients with mitral annular calcification and aortic valve calcification and in control patients from a prospective echocardiographic database of 8160 consecutive patients; 657 patients (8%) were identified with mitral annular calcification and 815 (9%) with a calcified aortic valve, of whom 515 (6.3%) had stenosis with a minimal aortic valve gradient of 16 mm Hg. In these patients, cardiac and vascular risk factors were compared with 568 control patients using multiple logistic regression analysis.Results—Age (odds ratio (OR) varying from 5.78 to 104, depending on age class), female sex (OR 1.75), hypertension (OR 2.38), diabetes mellitus (OR 2.85), and hypercholesterolaemia (OR 2.95) were strongly and significantly associated with aortic valve calcification without stenosis, as were age (OR varying from 8.82 to 67, depending on age class), female sex (OR 2.22), hypertension (OR 2.72), diabetes mellitus (OR 2.49), and hypercholesterolaemia (OR 2.86) with mitral annular calcification. Age (OR varying from 1.11 to 7.7), hypertension (OR 1.91), and hypercholesterolaemia (OR 2.55) were strongly and significantly associated with stenotic aortic valve calcification.Conclusions—Mitral annular calcification and stenotic or non-stenotic aortic valve calcification have a high incidence of atherosclerotic risk factors, suggesting they should be considered as manifestations of generalised atherosclerosis.     

FBN1 gene mutation characteristics and clinical features for the prediction of mitral valve disease progression

Background

Until today, FBN1 gene mutation characteristics were not compared with clinical features for the prediction of mitral valve disease progression.

Methods

Therefore, we conducted a study of 116 patients (53 men, 63 women aged 33 ± 15 years) with a causative FBN1 gene mutation and ≤ moderate mitral valve regurgitation at baseline.

Results

During 7.4 ± 6.8 years 30 patients developed progression of mitral valve regurgitation ≥ 1 grade (primary endpoint), and 26 patients required mitral valve surgery (secondary endpoint). Cox regression analysis identified an association of atrial fibrillation (hazard ratio (HR) = 2.703; 95% confidence interval (CI) 1.013–7.211; P = .047), left ventricular ejection fraction (HR = .970; 95%CI .944–.997; P = .032), indexed end-diastolic left ventricular diameter (HR = 15.165; 95%CI 4.498–51.128; P < .001), indexed left atrial diameter (HR = 1.107; 95%CI 1.045–1.173; P = .001), tricuspid valve prolapse (HR = 2.599; 95%CI 1.243–5.437; P = .011), posterior leaflet prolapse (HR = 1.075; 95%CI 1.023–1.130; P = .009), and posterior leaflet thickening (HR = 3.368; 95%CI 1.265–8.968; P = .015) with progression of mitral valve disease, whereas none of the FBN1 gene mutation characteristics were associated with progression of mitral valve disease. However, Cox regression analysis identified a marginal relationship of FBN1 gene mutations located both in a transforming-growth-factor beta-binding protein-like (TGFb-BP) domain (HR = 3.453; 95%CI .982–12.143; P = .053), and in the calcium-binding epidermal growth factor-like (cbEGF) domain (HR = 2.909; 95%CI .957–8.848; P = .060) with mitral valve surgery, a finding that was corroborated by Kaplan–Meier analysis (P = .014; and P = .041, respectively).

Conclusion

Clinical features were better predictors of mitral valve disease progression than FBN1 gene mutation characteristics.     

Catheter based inhibition of arterial calcification by bisphosphonates in an experimental atherosclerotic rabbit animal model

Background

Vascular calcification is an active process, sharing common molecular mechanisms with bone formation. Bisphosphonates are components, which inhibit calcification. The aim of the present study was to evaluate the safety and effectiveness of local delivery of the bisphosphonate zoledronate on inhibition of calcium formation in the arterial wall in an experimental animal model.

Methods

Sixteen New Zealand rabbits were placed on vitamin D enriched atherogenic diet for 3 weeks. Subsequently, all animals underwent angiography of abdominal aorta and common iliac arteries. A mixture containing 500 μg/l zoledronate was delivered on the vascular wall of the target iliac artery, using a dedicated balloon catheter. A placebo mixture was administered on the contralateral iliac artery of each animal, which was used as control. At 28 days all animals were sacrificed. Histologic sections of each common iliac artery were stained with hematoxylin–eosin and von Kossa. Computer-assisted histomorphometry was performed for the calcium content quantification of each section from the target and the control iliac artery.

Results

In all animals the local delivery of zoledronate and placebo mixtures was successful and uncomplicated. The mean percentage of the calcium content of the media was higher in the control artery segments compared to the target (2.66 ± 0.73 versus 1.08 ± 0.62 % of the area of the media, p < 0.01).

Conclusions

Inhibition of vascular calcification by local catheter-based delivery of bisphosphonate zolendronic acid is effective without evident short-term complications. These finding and its potential clinical implication remain to be confirmed in human studies.     

Statins moderate coronary stenoses but not coronary calcification: Results from meta-analyses

Introduction

Coronary artery stenoses have been shown in various trials to be moderated by treatment with statins. A similar effect on coronary artery calcification has not been demonstrated. We therefore undertook meta-analyses of trials examining the effect of statin treatment on coronary artery stenoses and coronary artery calcification.

Methods

Literature searches identified five controlled trials suitable for inclusion in the analysis of the effect of statins (high dose versus either low dose or placebo) on coronary artery calcification and six trials suitable for inclusion in the analysis of the effect of statins on coronary artery stenoses.

Results

All trials reported substantial and significant reductions in LDL-C with statin treatment which results in net reductions of LDL-C in the CAC and coronary stenoses trials of 1.0 mmol/L and 0.9 mmol/L, respectively. Analysis of the CAC trials did not demonstrate any effect of statins on the progression of calcification. In contrast, in the coronary stenoses trials there was a consistent moderation of stenosis severity progression with statins (p < 0.0001).

Conclusions

Meta-analyses of the available trials have demonstrated a significant moderation of coronary stenoses associated with the statin-induced reduction in LDL-C. In contrast, there was no effect on coronary calcification despite a similar reduction in LDL-C levels. This suggests that the pathogenesis of the two conditions may be different, if not in aetiology, then certainly in their development. It further suggests that statin use to moderate arterial calcification is not effective.     

Soluble urokinase plasminogen activator receptor is in contrast to high-sensitive C-reactive-protein associated with coronary artery calcifications in healthy middle-aged subjects

Objective

The main objective of this study was to investigate the association between two markers of low-grade inflammation; soluble urokinase plasminogen activator receptor (suPAR) and high-sensitive C-reactive protein (hs-CRP); and coronary artery calcification (CAC) score detected by cardiac computed tomography (CT) scan.

Design

A cross sectional study of 1126 randomly sampled middle-aged men and women.

Methods

CAC score was measured by a non-contrast cardiac CT scan and total 10-year cardiovascular mortality risk was estimated using the Systematic Coronary Risk Evaluation (SCORE). Plasma samples were analysed for suPAR and hs-CRP. The association of suPAR and hs-CRP to CAC was evaluated by logistic regression analyses adjusting for categorised SCORE. The additive effect of suPAR to SCORE was evaluated by comparing area under curve (AUC) and net reclassification improvement (NRI).

Results

The odds of being in a higher CAC category, i.e. having more severe CAC, increased 16% (odds ratio (OR) 1.16, p = 0.02) when plasma suPAR concentration increased 1 ng/ml, and this was more pronounced in women (OR 1.30, p = 0.01) than in men (OR 1.15, p = 0.05). In comparison, hs-CRP was not associated with CAC category (OR 1.00, p = 0.90). When adding suPAR to categorised SCORE, AUC increased from 0.66 to 0.70 (p = 0.04) in women and from 0.65 to 0.68 (p = 0.03) in men. NRI was significant in men (NRI 19.3%, 95% CI 6.1–32.6, p = 0.004) as well as in women (NRI 20.8%, 95%CI 1.0–40.7, p = 0.04), without significant gender difference.

Conclusions

suPAR, but not hs-CRP, appeared to be associated with CAC score independently of SCORE. The association was strongest in women.     

Mitral annular calcification and aortic valve calcification may help in predicting significant coronary artery disease

Mitral annular calcification (MAC) and aortic valve calcification (AVC) are manifestations of atherosclerosis. To determine whether mitral annular calcification and aortic valve calcification detected by transthoracic echocardiography (TTE) might help in predicting significant coronary artery disease (CAD), 123 patients with significant CAD and 93 patients without CAD detected by coronary angiography were investigated. MAC and AVC identified CAD with a sensitivity and specificity of 60.2%, 55.9% and 74.8%, 52.7%, respectively, and with a negative and a positive predictive values of 51.5%, 64.3% and 61.3% and 67.6%, respectively. The positive predictive value of MAC was greater than gender, hypertension, and hypercholesterolemia. AVC showed a positive predictive value greater than gender, hypertension, family history, and hypercholesterolemia. The negative predictive values of MAC and AVC for CAD were greater than those of all risk factors except diabetes mellitus. In conclusion, presence of MAC and AVC on TTE may help in predicting CAD and should be added to conventional risk factors. Absence of MVC and AVC is a stronger predictor for absence of CAD than all conventional risk factors, except diabetes mellitus. Patients with MAC and AVC should be taken into consideration for the presence of significant CAD and thereby for diagnostic and therapeutic interventions in order to improve the prognosis.     

Heart involvement in Rheumatoid Arthritis: Systematic review and meta-analysis

Objective

The aim of our study was to conduct a systematic review with meta-analysis of the current case–control studies about the valvular and pericardial involvement in patients with Rheumatoid Arthritis (RA), asymptomatic for cardiovascular diseases.

Methods

Case–control studies were identified by searching PubMed (1975–2010) and the Cochrane Central Register of Controlled Trials (CENTRAL) (1975–2010). Participants were adult patients with RA asymptomatic for cardiovascular diseases, and the outcome measure was the presence of cardiac involvement.

Results

Quantitative synthesis included 10 relevant studies out of 2326 bibliographic citations that had been found. RA resulted significantly associated to pericardial effusion (OR 10.7; 95% CI 5.0–23.0), valvular nodules (OR 12.5; 95% CI 2.8–55.4), tricuspidal valve insufficiency (OR 5.3; 95% CI 2.4–11.6), aortic valve stenosis (OR 5.2; 95% CI 1.1–24.1), mitral valve insufficiency (OR 3.4; 95% CI 1.7–6.7), aortic valve insufficiency (OR 1.7; 95% CI 1.0–2.7), combined valvular alterations (OR 4.3; 95% CI 2.3–8.0), mitral valve thickening and/or calcification (OR 5.0; 95% CI 2.0–12.7), aortic valve thickening and/or calcification (OR 4.4; 95% CI 1.1–17.4), valvular thickening and/or calcification (OR 4.8; 95% CI 2.2–10.5), and mitral valve prolapse (OR 2.2; 95% CI 1.2–4.0).

Conclusions

Our systematic review pointed out the strength and the grade of both pericardial and cardiac valvular involvement in RA patients. Our findings underscore the importance of an echocardiographic assessment at least in clinical research when RA patients are involved. Moreover, further research is needed to understand the possible relationship of our findings and the increased cardiovascular mortality.     

The increasing detection of asymptomatic left ventricular dysfunction in patients with type 2 diabetes mellitus without overt cardiac disease: Data from the SHORTWAVE study

Aims

Type 2 diabetes mellitus (DM) is associated with higher risk of heart failure. Over the last three decades several studies demonstrated the presence of asymptomatic systolic and/or diastolic left ventricular (LV) dysfunction (asymLVD) in patients with normal LV ejection fraction (LVEF). Purpose of our study was to assess the prevalence and factors associated with asymLVD in DM patients by echocardiographic indexes more sensitive than LVEF and transmitral flow detected by pulsed Doppler.

Methods

386 DM patients without overt cardiac disease were enrolled from January to October 2011. Stress-corrected midwall shortening (sc-MS) and mitral annular peak systolic velocity (S′) were considered as indexes of systolic function of circumferential and longitudinal myocardial fibers, respectively. Early diastolic velocity of transmitral flow was divided by early diastolic Tissue Doppler velocity of mitral annulus for identifying diastolic LVD.

Results

asymLVD was detected in 262 patients (68%). 106 (27%) had isolated systolic asymLVD, 61 (16%) isolated diastolic asymLVD; in 95 (25%) systolic and diastolic asymLVD coexisted. Patients with asymLVD were older, had lower glomerular filtration rate, higher levels of glycated hemoglobin, C reactive protein, LV mass, relative wall thickness and prevalence of valve calcifications. Older age (HR 1.1 [1.02–1.18], p = 0.01), aortic valve calcifications (HR 6.3 [1.31–30.31], p = 0.02), LV concentric geometry defined as relative wall thickness ≥0.43 (HR 15.44 [2.96–80.44], p = 0.001) were independent predictors of asymLVD at multivariate analysis.

Conclusions

Using suitable echocardiographic indexes, asymLVD is detectable in two/third of DM patients without overt cardiac disease and is predicted by older age, cardiac valve calcifications and LV concentric remodeling.     

Perivascular adipose tissue of the descending thoracic aorta is associated with systemic lupus erythematosus and vascular calcification in women

Objective

Women with systemic lupus erythematosus (SLE) have an increased risk of cardiovascular disease (CVD). Traditional CVD and SLE-disease related risk factors do not fully account for this increased risk. Perivascular adipose tissue (PVAT) is a visceral adipose depot in close proximity to blood vessels possibly influencing CVD. We hypothesized that women with SLE have an increased volume of descending thoracic aortic PVAT (aPVAT) associated with increased vascular calcification.

Methods

Using electron beam computed tomography, we quantified the aPVAT in clinically CVD-free SLE women (n = 135) and age-/race-matched healthy controls (HC, n = 152). Coronary artery calcification (CAC) and aortic calcification (AC) were quantified using Agatston scores and the aPVAT was quantified using standard Hounsfield Units (HU) for adipose tissue.

Results

Women with SLE had greater median aPVAT (32.2 cm³ vs HC aPVAT 28.6 cm³, p = 0.0071) and greater median AC (26.0 vs HC AC 6.0, p = 0.0013) than the healthy control women. Total aPVAT (per 25 cm³) remained significantly associated with SLE after adjusting for CVD risk factors (Odds Ratio 1.74 [95% Confidence Interval: 1.04–2.9], p = 0.034), but was attenuated when adjusting for circulating inflammatory markers (p = 0.34). In a logistic regression analysis, SLE aPVAT (per 25 cm³) was associated with AC (6.78 [2.0–23], p = 0.0019), which remained significant after adjusting for circulating inflammatory markers (p = 0.0074), and CAC (2.66 [1.4–5.0], p = 0.0028).

Conclusions

Total aPVAT is greater in clinically CVD-free SLE women than in age-/race-matched controls and is associated with calcification in different vascular beds.