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The objective of this study was to investigate whether patients with the metabolic syndrome (MetS) and an imbalance in cortisol metabolism express increased urinary albumin excretion compared to those patients with metabolic syndrome alone. Seventy-four patients with MetS were evaluated using a low-dose dexamethasone suppression test (LDDST) to identify disturbed cortisol balance (cortisol levels > 50 nmol/L after LDDST). The level of albumin in the urine was also evaluated. Disturbed cortisol balance was found in 8% of all evaluated patients with MetS. Microalbuminuria was present significantly more often (p A substantial percentage of patients with MetS had inappropriate cortisol homeostasis. Of importance, excretion of urinary albumin was increased in these patients. This observation may indicate that this subgroup within the MetS population has a higher cardiovascular risk and possible increased endothelial dysfunction, with a subsequent need for stricter control to prevent cardiovascular morbidity and mortality.

Echocardiography is used in cardiac resynchronisation therapy (CRT) to assess cardiac function, and in particular left ventricular (LV) volumetric status, and prediction of response. Despite its widespread applicability, LV volumes determined by echocardiography have inherent measurement errors, interobserver and intraobserver variability, and discrepancies with the gold standard magnetic resonance imaging. Echocardiographic predictors of CRT response are based on mechanical dyssynchrony. However, parameters are mainly tested in single-centre studies or lack feasibility. Speckle tracking echocardiography can guide LV lead placement, improving volumetric response and clinical outcome by guiding lead positioning towards the latest contracting segment. Results on optimisation of CRT device settings using echocardiographic indices have so far been rather disappointing, as results suffer from noise. Defining response by echocardiography seems valid, although re-assessment after 6 months is advisable, as patients can show both continuous improvement as well as deterioration after the initial response. Three-dimensional echocardiography is interesting for future implications, as it can determine volume, dyssynchrony and viability in a single recording, although image quality needs to be adequate. Deformation patterns from the septum and the derived parameters are promising, although validation in a multicentre trial is required. We conclude that echocardiography has a pivotal role in CRT, although clinicians should know its shortcomings.

Quantitative analysis of myocardial exercise scintigraphy has been previously reported to be superior to visual image interpretation for detection of the presence and extent of coronary artery disease. Computer analysis of perfusion defects and washout rate of thallium 201 was performed on scintigrams from a group of 131 consecutive patients (prospective group), using criteria defined from a previous group of 72 patients (initial group), and compared with visual interpretation of scintigrams for detection and evaluation of coronary artery disease. The sensitivity of the quantitative technique with regard to overall detection of coronary artery disease was not significantly different from the visual method (69% and 74%, respectively), whereas the specificity was higher (86% and 68%). Quantitative analysis did not increase the sensitivity of thallium imaging over the visual method in the left anterior descending artery (46% vs 65%) and the right coronary artery (51% vs 72%) but did increase sensitivity in the left circumflex artery (75% vs 47%). Whereas in the initial group quantitative analysis resulted in a better identification of multivessel disease (sensitivity 81% vs 57%), in the prospective group sensitivity decreased (54% vs 67%) without significant loss of specificity. The initial group had a 40% incidence of three-vessel disease and the prospective group, 22% (P less than 0.05). One-vessel disease was higher in the prospective group (32% vs 11%, P less than 0.05). Thus, assessing the quantitative technique in a larger prospective patient population, there was no improvement of detection of the presence and extent of coronary artery disease when compared with visual interpretation.

In this study the role of visual assessment and quantitative analysis of thallium-201 myocardial stress perfusion scintigraphy (MPS) was evaluated in patients with a normal electrocardiogram (ECG) (group I) and in patients with an abnormal baseline repolarization on the ECG (group II). One-hundred-and-thirty-five patients were studied. Group I consisted of 93 patients, 65 of whom had coronary artery disease (CAD), i.e. a luminal stenosis of greater than or equal to 50%; group II consisted of 42 patients, 32 of whom had CAD. In group II the exercise ECG was considered uninterpretable and thus only visual and quantitative analysis of MPS was investigated. Sensitivity and specificity of exercise electrocardiography, visual assessment and quantitative analysis of MPS were not significantly different in group I: sensitivities of the three methods were 66, 62 and 55% respectively, and specificities 86, 79 and 96% respectively. In group II there were no significant differences in the sensitivities and specificities of visual assessment or quantitative analysis of MPS: sensitivities of the two methods being both 88% and specificities both 80%. Visual assessment of redistribution (P less than 0.05) and quantitative analysis of washout (P less than 0.005) was significantly superior in group II than in group I; probably because of a higher incidence of three-vessel disease in the second group.(ABSTRACT TRUNCATED AT 250 WORDS)

Quantitative thallium-201 myocardial exercise scintigraphy was tested in two patient populations representing alternative standards for cardiac normality: group I comprised 18 male uncatheterized patients with a low likelihood of coronary artery disease (CAD); group II contained 41 patients with normal coronary arteriograms. Group I patients were younger, they achieved a higher rate-pressure product than group II patients; all had normal findings by physical examination and electrocardiography at rest and exercise. Group II patients comprised 21 females, 11 patients showed abnormal electrocardiography at rest, and five patients showed ischemic ST depression during exercise. Twelve patients had signs of minimal CAD. Twelve patients revealed abnormal visual and quantitative thallium findings, three of these patients had minimal CAD. Profiles of uptake and washout of thallium-201 were derived from both patient groups, and compared with normal limits developed by Maddahi et al. Furthermore, low likelihood and angiographically normal patients may differ substantially, and both sets of normal patients should be considered when establishing criteria for abnormality in exercise thallium imaging. When commercial software containing normal limits for quantitative analysis of exercise thallium-201 imaging is used in clinical practice, it is mandatory to compare these with normal limits of uptake and washout of thallium-201, derived from the less heterogeneous group of low-likelihood subjects, which should be used in selecting a normal population to define normality.

Objective We sought to compare the feasibility and results of Doppler tissue imaging–derived and 2-dimensional strain echocardiography–derived deformation assessment of the right ventricular (RV) free wall. Methods Absolute values and timing of strain and strain rate (SR) obtained by both techniques in the basal, mid, and apical segments of the RV free wall were prospectively analyzed and compared in individuals with varying RV function and geometry: patients with an impaired RV function (n = 23), endurance athletes (n = 22), and control subjects (n = 22). Results Both techniques yielded a 93% technical feasibility and had a similar interobserver and intraobserver variability. The overall correlation for onset strain values was 0.59, with better correlation in the pathologic RV ( r = 0.77). The overall correlation of peak strain was moderately good for strain values ( r = 0.73) and timing ( r = 0.56). Over the entire range of systolic and diastolic values, SR correlated closely ( r = 0.90). Systolic SR correlated moderately ( r = 0.59), but its timing poorly ( r = 0.35). There was a small bias toward higher values of strain and SR when using Doppler tissue imaging, except in the basal segment. Conclusion Overall, in the assessment of RV deformation, Doppler tissue imaging and 2-dimensional strain echocardiography correlate moderately well and display a comparable feasibility.

Background— Cyclooxygenase (COX)-2 expression in the heart increases after myocardial infarction (MI). In murine models of MI, COX-2 inhibition preserves left ventricular dimensions and function. We studied the effect of selective COX-2 inhibition on left ventricular remodeling and function after MI in a pig model. Methods and Results— Twenty-two pigs were assigned to COX-2 inhibition with a COX-2 inhibitor (COX-2i; celecoxib 400 mg twice daily; n=14) or a control group (n=8). MI was induced by left circumflex coronary artery ligation, and the animals were euthanized 6 weeks later. Cardiac dimensions and function were assessed with echocardiography and conductance catheters. Infarct size and collagen density were analyzed with triphenyltetrazolium chloride staining and picrosirius red staining, respectively. COX-2 inhibition increased mortality compared with controls (50% versus 0%, P =0.022), whereas infarct size was similar (13.1±0.7% versus 14.1±0.1%, P =0.536). The decrease in thickness of the infarcted myocardial wall was more pronounced in the COX-2i group (60.6±9.6% versus 36.2±5.7%, P =0.001). End-diastolic volume was higher in the COX-2i group (133.9±33.5 versus 91.1±24.0 mL; P =0.021), as was the end-systolic volume at 100 mm Hg (81.7±27.8 versus 56.3±21.1 mL; P =0.037), which indicates that systolic function was more severely impaired. Infarct collagen density was lower after COX-2i treatment (25.3±3.9 versus 56.1±23.8 gray value/mm 2 ; P =0.005). Conclusions— In pigs, COX-2 inhibition after MI is associated with increased mortality, enhanced left ventricular remodeling, and impaired systolic function, probably due to decreased infarct collagen fiber density.

Despite the benefit of cardiac resynchronization therapy (CRT) in patients with heart failure and conduction delay, a considerable number of patients do not respond substantially. Left ventricular lead position is an important factor in response, restricted by the patient’s specific anatomy and local pathophysiology. Quadripolar leads could enhance response to CRT, offering 4 pacing locations along the distal end of the lead. Several quadripolar leads are available, all with different shapes and electrode spacing. Electrodes can be positioned in an ideal pacing location, determined by delayed mechanical or electrical activation, and away from phrenic nerve stimulation, high pacing thresholds, and fibrosis. Implantation is safe, with comparable or even lower complication rates compared with standard bipolar leads. Studies on biventricular pacing with quadripolar leads show apparent variations in acute hemodynamic response between pacing configurations, implying a patient-specific response. Pacing with an optimal pacing vector of a quadripolar lead benefits acute hemodynamic response. Multipoint pacing, pacing the left ventricle with 2 of 4 electrodes, could further enhance response. However, larger trials are needed to confirm these results, and results on long-term outcome of CRT with quadripolar leads and the benefit of multipoint pacing are warranted. We conclude that quadripolar leads are an important improvement in the treatment of heart failure patients with CRT.

OBJECTIVE Our aim is to compare the effect of type 2 diabetes on recurrent major cardiovascular events (MCVE) for patients with symptomatic vascular disease at different locations. RESEARCH DESIGN AND METHODS A total of 6,841 patients from the single-center, prospective Second Manifestations of ARTerial disease (SMART) cohort study from Utrecht, the Netherlands, with clinically manifest vascular disease with (n = 1,155) and without (n = 5,686) type 2 diabetes were monitored between 1996 and 2013. The effect of type 2 diabetes on recurrent MCVE was analyzed with Cox proportional hazards models, stratified for disease location (cerebrovascular disease, peripheral artery disease, abdominal aortic aneurysm, coronary artery disease, or polyvascular disease, defined as ≥2 vascular locations). RESULTS Five-year risks for recurrent MCVE were 9% in cerebrovascular disease, 9% in peripheral artery disease, 20% in those with an abdominal aortic aneurysm, 7% in coronary artery disease, and 21% in polyvascular disease. Type 2 diabetes increased the risk of recurrent MCVE in coronary artery disease (hazard ratio [HR] 1.67; 95% CI 1.25–2.21) and seemed to increase the risk in cerebrovascular disease (HR 1.36; 95% CI 0.90–2.07), while being no risk factor in polyvascular disease (HR 1.12; 95% CI 0.83–1.50). Results for patients with peripheral artery disease (HR 1.42; 95% CI 0.79–2.56) or an abdominal aortic aneurysm (HR 0.93; 95% CI 0.23–3.68) were inconclusive. CONCLUSIONS Type 2 diabetes increased the risk of recurrent MCVE in patients with coronary artery disease, but there is no convincing evidence that it is a major risk factor for subsequent MCVE in all patients with symptomatic vascular disease.

Arrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVD/C) is an inherited progressive cardiomyopathy, clinically characterized by ventricular arrhythmias and increased risk of sudden cardiac death. Echocardiography has a role in the diagnosis and prognosis of ARVD/C. However, in the current era of magnetic resonance imaging (MRI), the role of echocardiography in ARVD/C patients and family member screening is subject to debate. Relatively novel echocardiographic techniques, such as three-dimensional right ventricular (3D-RV) imaging and tissue deformation imaging, may improve the diagnostic and prognostic performance of echocardiography in these patients. 3D-RV imaging provides more insights on RV anatomy and global function compared to conventional echocardiography. Subtle RV regional wall motion abnormalities, and mechanical dyssynchrony, are accurately measured by tissue deformation imaging. Several studies suggest an incremental value of novel echocardiographic parameters in addition to conventional measurements. Moreover, new parameters indicating subtle RV dysfunction, and mechanical dyssynchrony, are of predictive value and could help in risk stratification of ARVD/C patients. New robust parameters, derived from 3D-RV echocardiography and RV tissue deformation imaging, in combination with established conventional parameters, suggest that there is a current and future role for echocardiography in ARVD/C supplementing MRI.

Despite an improvement in the therapeutic strategies available for an acute ischemic event, cardiac disease is still the principal cause of morbidity and mortality in Western societies. A shift from acute towards more chronic heart disease due to atherosclerotic disease has been recognized. Modification of adaptive capacities of the cardiac muscle after damage remains a key component in the prevention of chronic cardiac disease, such as overt heart failure. It has recently been demonstrated that local insulin-like growth factor (IGF)-1 homeostasis in the cardiac tissue is closely involved in postischemic adaptation, such as the process of remodeling. Both experimental and clinical data support the theory that IGF-1 plays a key role in the adaptive response of the myocardium during both acute myocardial ischemia and chronic myocardial failure, regulating left ventricular remodeling and thereby restoring left ventricular architecture. This eventually leads to improvement in the function of the failing heart. While most experimental data support the beneficial role of IGF-1 in restoring architecture and function of the failing heart, clinical trials investigating the role of IGF-1 treatment of patients in cardiac failure show conflicting results. In this bench-to-bedside review, the authors aim to highlight recent advances in knowledge of the role of paracrine and autocrine IGF balances during postischemic cardiac adaptation, in order to present possible new initiatives concerning therapeutic strategies in maladaptive cardiac performance, such as the syndrome of heart failure.

To the Editor: With much interest we have read the article by Sarnak et al1 on the risk of kidney disease for the development of cardiovascular disease. Considering the rising prevalence of chronic kidney disease and heart failure, we propose to perceive the reciprocal relationship of heart and kidney failure as a separate disease entity. This severe cardiorenal syndrome (SCRS) can be defined as the accelerated and extensive cardiovascular disease exclusively related to the coexistence of renal failure and heart disease. In agreement with Sarnak et al, we feel that many questions remain unanswered. However, we …

A left atrial myxoma was surgically removed in a 58-year-old man following several embolic events. Five months later, a new myxoma was found in the right ventricular outflow tract and surgically removed. In this patient, we visualized two more recurrences 14 years later, one in the left atrium and the other in the left ventricle. A short review of the literature concerning recurrent cardiac myxomas is given.

Background: Survivors of major vascular surgery are at increased risk of late cardiac complications. Objective: To examine the cardioprotective effect of β-blockers. Methods: A follow-up study was conducted in 1286 patients who survived surgery for at least 30 days. Patients were screened for cardiac risk factors and dobutamine stress echocardiography (DSE) results; 1034 patients (80%) underwent preoperative DSE, and 370 (29%) received β-blockers. The main outcome measure was late cardiac death or myocardial infarction. Results: Seventy-four patients (5.8%) had late cardiac events. Cardiac event rates in patients with 0, 1 to 2, and 3 or more risk factors were 1.6%, 4.7%, and 19.2%, respectively. In patients without risk factors, β-blockers were associated with improved event-free survival (2.8% vs 0%), and DSE had no additional prognostic value. In patients with 1 to 2 risk factors, the presence of ischemia during DSE increased cardiac events from 3.9% to 9.8%. However, if patients with ischemia were treated with β-blockers, the risk decreased to 7.2%. In patients with 3 or more risk factors, DSE and β-blockers stratified patients into intermediate- and high-risk groups. In patients without ischemia, β-blockers reduced the cardiac event rate from 15.1% to 9.5%, whereas the cardioprotective effect was limited in patients with 3 or more risk factors and positive DSE findings. Conclusions: Long-term β-blocker use is associated with a reduction in the cardiac event rate, except for patients with 3 or more risk factors and positive findings on DSE.

Background Conventional Doppler echocardiography offers an indirect assessment of left ventricular (LV) diastolic function, hampered by preload dependency. Tissue Doppler imaging (TDI) is a tool to study diastolic function in a more direct and less preload-dependent manner. Methods The Medline database has been searched for literature on TDI for the analysis of diastolic function. A secondary search reviewed the relevant references related to TDI or diastolic function in general. Results TDI measures myocardial velocities with a high temporal and velocity resolution but lacks spatial information. In particular, the velocity of early diastolic wall motion (E m ) and its timing are promising indices of local myocardial relaxation. E m at the mitral annulus offers fair estimates of ventricular relaxation, relatively independent of preload and systolic function. Combined with early transmitral flow velocity (E), detection of pseudo-normalized filling patterns and estimation of filling pressures are enhanced by E/E m . Conclusion TDI has an emerging role in the study and assessment of diastolic function. However, TDI-derived information needs to be integrated with other echocardiographic data because single diagnostic accuracy remains unsatisfactory.

Many changes occur during reperfusion of the myocardium after ischemic damage. Necrosis and apoptosis appear to be ongoing during ischemia, while apoptosis is boosted by the reperfusion event. In the past 10 years, distinct intracellular pathways important for hypertrophy, apoptosis, cardiac failure, ischemic preconditioning and reperfusion damage have been recognized. The eventual response of the cardiomyocyte will depend on energy and time available as well as changes in pH and ion handling and the delicate balance of activation of signaling molecules and transcription factors. There is agreement on the central role of mitochondria and nitric oxide (NO) in programmed cell death. However, although many groups analyzed the contribution of NO to cell death, still the circumstances and levels required for cardioprotection or death are unclear. Growth factors, cytokines, and downstream signaling molecules have been shown to influence programmed cell death through mechanisms reminiscent of preconditioning. Here, the role of apoptosis in ischemia reperfusion-related cell death is reviewed. Important data have been obtained in isolated cells, intact hearts and intact animals. Both pharmacological as well as genetic interventions are discussed. Proof for apoptosis in man post-myocardial infarction (MI) treated through primary Percutaneous Trans-luminal Coronary Angioplasty or other reperfusion therapy is reviewed. Finally, the currently available quantification methods for apoptosis post-MI are mentioned.

Postoperative new-onset atrial fibrillation (PNAF) is very common after cardiac surgery. The inflammatory response due to surgery and cardiopulmonary bypass (CPB) may contribute to PNAF by inducing atrial dysfunction [1]. Corticosteroids reduce the inflammatory response and may thus reduce atrial dysfunction and PNAF [2]. The aim of this study was to determine whether dexamethasone protects from left atrial dysfunction and PNAF in cardiac surgical patients.

583 Added value of a statistical atlas-based quantification of motion abnormalities for the prediction of CRT response {#article-title-2} Purpose: The presence of septal flash (SF), a specific inward/outward motion pattern of the septum during the isovolumic contraction period, recently shown up as good predictor of cardiac resynchronization therapy (CRT) outcome. The ability of accurately identifying a SF fully conditions the predictive value of this mechanism. Current SF detection from US images is based on visual inspection only and suffers low reproducibility. Thus, we created an atlas-based statistical method for the automatic quantification of motion abnormalities that we apply to SF detection, and evaluated its predicting capability. Method: We built an atlas of normal motion from 21 healthy volunteers (age 30±5y, 14 male), to which we compared 75 CRT candidates (age 68±9y, 56 male) with left ventricle dyssynchrony. Abnormal motion is quantified locally in apical 4-chamber 2DUS sequences, from a p-value based on a statistical distance to normality. SF is identified using automatic recognition of the inward/outward events on spatiotemporal abnormality maps, as shown in Fig1. CRT response was defined at 6 months follow-up, as increase ≥10% in the 6' walking test or NYHA functional class reduction ≥1pt. Results: Comparison of atlas-based and visual assessment of SF leads to a Cohen's Kappa of 0.54 and an observed agreement of 0.81 (48 SF and 13 without SF). We reached a positive predictive value of CRT outcome of 85%, the visual assessment one being of 83%. Conclusion: We have demonstrated the potential of an atlas-based automatic quantification of motion abnormalities for the understanding of CRT outcome. In particular, we have demonstrated its performance for the prediction of clinical response when the methodology is applied to the identification of SF[⇓][1]. # 584 How reliably can myocardial blood flow be tracked? – a validation of commercial tracking software using computer-generated datasets {#article-title-3} Background: Recent advances in myocardial tracking technology have stimulated attempts to also track contrast enhanced intracavitary blood flow. Little is known, however, how basic imaging parameters (line density, frame rate, contrast bubble density) affect the quality of such tracking results. Our study aimed at investigating this by using simulated echo data sets. Methods: A 3D blood flow field of the entire left ventricle (LV) was calculated for a cardiac cycle based on mitral inflow and LV volume data using Fluent 12.1 (ANSYS Inc., USA). Then, the 3D motion of contrast microbubbles was simulated and 2D B-mode image loops were obtained (f = 4.5MHz; 50° sector angle). After conversion to DICOM, image loops were analyzed using flow tracking software (Qflow, Siemens, Mountainview, USA). Vorticity and amplitude of the resulting in-plane velocity vector field was calculated at different frame rates (227, 113 and 76 fps) and bubble densities (BD) (60, 35 and 18 B/ml) and compared to the ground truth known from the CFD model. Results: Quality of tracking was clearly related to BD and frame rate. Velocities, estimated by tracking, correlated best with the ground truth at 60 B/ml and 227fps (r = 0.61, p < 0.01) and deteriorated with lower settings (e.g. r = 0.25 at 60 B/ml and 76 fps). Estimated averaged vorticity also correlated best with the ground truth at 60 B/ml and 227fps. Interestingly, at low frame rates (76fps), tracking results improved with decreasing BD (r = 0.57 at 60 B/ml vs. r = 0.67 at 18 B/ml). Conclusions: Flow tracking by contrast enhanced echocardiography is feasible. Good tracking requires high frame rates and an optimized bubble density. Currently available tracking software shows acceptable quality of velocity estimates, facilitating the recognition of basic flow patterns, such as vortices[⇓][2]. # 585 Early detection of functional abnormalities in asymptomatic arrhythmogenic right ventricular cardiomyopathy gene carriers using echocardiographic deformation imaging {#article-title-4} Purpose: The first presentation of arrhythmogenic right ventricular cardiomyopathy (ARVC) is often potentially lethal ventricular arrhythmias originating from the right ventricle (RV), typically at a young age. This emphasizes the importance of an early recognition of this disease, for instance in ARVC- family members. The aim of this study is to evaluate the value of tissue deformation imaging to detect subclinical RV functional abnormalities in asymptomatic genotyped carriers of ARVC. Methods: A total of 43 asymptomatic first degree family members of ARVC probands (not fulfilling the diagnosis of ARVC according to the task-force criteria (TF-c)) were prospectively enrolled for echocardiographic examination. In a total of 14 (38.0±13.2 years), a genetic mutation (PKP2) could be identified (others had no mutation or genetic screening). All individuals were age-matched with 4 controls (n = 56, 38.2±12.7 years) undergoing the same echocardiographic evaluation (dimensions, global systolic parameters, visual assessment, and deformation imaging of the RV free wall). Echocardiographic evaluation was performed blinded. Deformation analysis was analyzed blinded to group and findings from the conventional echocardiogram. A peak systolic strain >−18% and/or post-systolic shortening (post-systolic index >15%) in any segment was considered abnormal. Results: No significant differences in baseline characteristics were seen between the groups. RV dimensions in the family group were similar to the controls (RVOT 15.4±2.9 vs. 14.4±1.9 mm/m2, RVIT 18.6±2.6 vs. 19.1±2.6 mm/m2, p=NS). Global systolic parameters were moderately reduced in the family group (TVI-syst 9.1±1.6 vs. 11.1±1.7 cm/s, TAPSE 20.0±3.2 vs. 23.9±2.8 mm, p −18% was seen in 6 family members (43%) and post systolic strain in 10 (71%). Either abnormality was observed in 11 (79%), almost exclusively in the basal segment, and in non of the controls. 2D-strain showed abnormal segments in 8 (57%) of family members and 5 (9%) controls. Conclusion: Echocardiographic deformation imaging detects functional abnormalities in the basal RV segment in almost 80% of asymptomatic ARVC gene carriers. Furthermore, false positive findings in visual assessment (28%) could be prevented since all showed normal deformation values and patterns. [1]: #F1 [2]: #F2

Objectives To develop prediction models that better estimate the pretest probability of coronary artery disease in low prevalence populations. Design Retrospective pooled analysis of individual patient data. Setting 18 hospitals in Europe and the United States. Participants Patients with stable chest pain without evidence for previous coronary artery disease, if they were referred for computed tomography (CT) based coronary angiography or catheter based coronary angiography (indicated as low and high prevalence settings, respectively). Main outcome measures Obstructive coronary artery disease (≥50% diameter stenosis in at least one vessel found on catheter based coronary angiography). Multiple imputation accounted for missing predictors and outcomes, exploiting strong correlation between the two angiography procedures. Predictive models included a basic model (age, sex, symptoms, and setting), clinical model (basic model factors and diabetes, hypertension, dyslipidaemia, and smoking), and extended model (clinical model factors and use of the CT based coronary calcium score). We assessed discrimination (c statistic), calibration, and continuous net reclassification improvement by cross validation for the four largest low prevalence datasets separately and the smaller remaining low prevalence datasets combined. Results We included 5677 patients (3283 men, 2394 women), of whom 1634 had obstructive coronary artery disease found on catheter based coronary angiography. All potential predictors were significantly associated with the presence of disease in univariable and multivariable analyses. The clinical model improved the prediction, compared with the basic model (cross validated c statistic improvement from 0.77 to 0.79, net reclassification improvement 35%); the coronary calcium score in the extended model was a major predictor (0.79 to 0.88, 102%). Calibration for low prevalence datasets was satisfactory. Conclusions Updated prediction models including age, sex, symptoms, and cardiovascular risk factors allow for accurate estimation of the pretest probability of coronary artery disease in low prevalence populations. Addition of coronary calcium scores to the prediction models improves the estimates.

Study objective – The aim was to evaluate discriminant analysis, performed in patients without prior myocardial infarction, in enhancing the diagnostic value of quantitative exercise 201thallium scintigraphy. Design – All clinical, electrocardiographic, and scintigraphic variables were first subjected to a univariate analysis. Afterwards a discriminant analysis was done. Patients – 135 patients (104 male) were studied. Age was 24-70 years, mean 55 years. Measurements and main results – Two discriminant analyses were done. In the first analysis, the ability to detect the presence of coronary artery disease was tested. Significant variables were: (1) history of angina, (2) sex, (3) quantitative analysis of 201thallium scintigraphy, (4) age, (5) ischaemic ST response, (6) angina during the test, and (7) the pressure-rate product. The sensitivity, specificity, and accuracy of classification using the discriminant function were 91%, 87%, and 90%, respectively. The sensitivity was higher than when using only visual interpretation (sensitivity 70%; p

Objective: Decreased insulin-like growth factor-I (IGF-I) levels in adults have been associated with an increased risk of ischemic heart disease and heart failure. It is currently unknown whether patients with low circulating IGF-I levels due to a homozygous acid-labile subunit (IGFALS) gene mutation also have increased risk of cardiovascular disease. Therefore, we evaluated atherosclerotic burden in a 27 year old male patient who was diagnosed with a homozygous IGFALS mutation and consequently had extremely low circulating IGF-I levels. Methods: Ten year's cardiovascular risk was calculated using the Framingham risk score. Presence of (subclinical) atherosclerosis was assessed using a 64-slice CT scan of the coronary arteries. Cardiac performance was measured by conventional echocardiographic measurements, three dimensional (3D)-echocardiography, and tissue deformation imaging. Results: Despite his extremely low circulating IGF-I levels due to Acid-Labile Subunit (ALS) deficiency, our patient had a low Framingham risk score and no signs of coronary atherosclerosis. Adjusted for physical height, cardiac performance was not impaired compared with healthy subjects. Conclusion: The present case report does not lend support to routine cardiovascular screening in patients with extremely low circulating IGF-I levels due to a homozygous IGFALS mutation, when cardiovascular risk is low. (C) 2011 Elsevier Ltd. All rights reserved.

Background: Left ventricular hypertrophy (LVH) is often observed in athletes, which should be differentiated from hypertrophic cardiomyopathy. The aim of the study was to explore the functional changes measured using tissue Doppler imaging (TDI) deformation analysis in athletes fulfilling LVH criteria participating in different endurance sports. Methods: Healthy controls (n = 62, 58% men) and endurance athletes (n = 120, 62% men) aged 18-40 years were prospectively enrolled and underwent both standard echocardiography as well as TDI. Longitudinal TDI-derived strain and strain rate (SR) were calculated in the septal and posterior wall in three segments. LVH was defined as a left ventricular mass (LVM) over 132 g/m2 in men and over 109 g/m 2 in women. Results: Echocardiographic LVH was observed in 33 athletes (67% men). LVM was significantly increased in both athlete groups (102.6 g/m2 (SD 16.0) and 135.7 g/m2 (SD 15.9) vs 88.0 g/m2 (SD 16.5) in controls, p< 0.001). Diastolic parameters were not significantly different between groups. Athletes with LVH showed no significant difference in strain and SR values in any segment of the septal or posterior wall compared with controls or those without LVH. A weak but significant correlation (also after multivariate analysis) was found for septal wall thickness and LVM in peak systolic strain (r = 0.26, p

Background Uncertainty remains about possible cardiac adaptation to resistance training. Androgenic anabolic steroids (AAS) use plays a potential role and may have adverse cardiovascular effects. Objective To elucidate the effect of resistance training and of AAS-use on cardiac dimensions and function. Participants Cardiac magnetic resonance (CMR) were performed in 156 male subjects aged 18–40years: 52 non-athletes (maximum of 3exercise hours/week), 52 strength–endurance (high dynamic–high static, HD–HS) athletes and 52 strength (low dynamic–high static, LD–HS) trained athletes (athletes ≥6exercise hours/week). 28 LD–HS athletes denied and 24 admitted to AAS use for an average duration of 5years (range 3months–20years). Results No significant differences were found between non-athletes and non-AAS-using LD–HS athletes. AAS-using LD–HS athletes had significantly larger LV and RV volumes and LV wall mass than non-AAS-using LD–HS athletes, but lower than HD–HS athletes. In comparison to all other groups AAS-using LD–HS athletes showed lower ejection fractions of both ventricles (LV/RV EF 51/48% versus 55–57/51–52%) and lower E/A ratios (LV/RV 1.5/1.2 versus 1.9–2.0/1.4–1.5) as an indirect measure of diastolic function. Linear regression models demonstrated a significant effect of AAS-use on LV EDV, LV EDM, systolic function and mitral valve E/A ratio (all ANOVA-tests p Conclusions Strength athletes who use AAS show significantly different cardiac dimensions and biventricular systolic dysfunction and impaired ventricular inflow as compared to non-athletes and non-AAS-using strength athletes. Increased ventricular volume and mass did not exceed that of strength–endurance athletes. These findings may help raise awareness of the consequences of AAS use.

Background Although cardiovascular magnetic resonance imaging (CMR) is well established, its diagnostic accuracy in identifying chronic heart failure (CHF) in patients with chronic obstructive pulmonary disease (COPD) has not yet been quantified. Methods Participants were recruited from a cohort of 405 patients aged ≥65 years, with mild to moderate and stable COPD. In this population, 83 (20.5%) patients had a new diagnosis of CHF, all left-sided, established by an expert panel using all available diagnostic information, including echocardiography. In a nested case-control study design, 37 consecutive COPD patients with newly detected CHF (cases) and a random sample of 41 of the remaining COPD patients (controls) received additional CMR measurements. The value of CMR in diagnosing heart failure was quantified using univariable and multivariable logistic modeling in combination with area under the receiver operating characteristic curves (ROC-area). Results Combination of CMR measurements of left ventricular ejection fraction, indexed left and right atrial volume, and left ventricular end-systolic dimensions provided high added diagnostic value beyond clinical items (ROC-area 0.91) for identifying CHF. Left-sided measurements of CMR and echocardiography correlated well, including ejection fraction. Right ventricular mass divided by right ventricular end-diastolic volume was higher in COPD patients with CHF than in those without concomitant CHF. Conclusions Easily assessable morphologic and volume-based CMR measurements have excellent capacities to identify previously unknown left-sided chronic heart failure in mild to moderate COPD patients. There seems to be an adaptive tendency to concentric right ventricular hypertrophy in COPD patients with left-sided CHF.

PURPOSE: With the increased use of genetic testing for arrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVD/C), this disease is being increasingly recognised among elderly patients. However, elderly ARVD/C patients were underrepresented in prior cohorts. We aimed to describe the phenotypical characteristics and outcomes among ARVD/C patients surviving ≥50 years. METHODS: We assessed detailed phenotypical data of 29 patients who (1) presented at ≥50 years of age; and (2) fulfilled 2010 Task Force Criteria (TFC) for ARVD/C by last follow-up. Primary outcome was the occurrence of a major ventricular arrhythmia (sudden cardiac death, resuscitated sudden cardiac arrest or sustained ventricular tachycardia). RESULTS: The majority (55 %) of elderly ARVD/C subjects were male, with a mean age of 59.0 ± 5.8 years at presentation. Study participants fulfilled a median of six (IQR 5-8) TFC criteria by last follow-up, of which arrhythmia criteria were most frequent (97 %), followed by structural criteria (83 %), depolarisation criteria (72 %) and repolarisation criteria (69 %). By last follow-up, 15 (52 %) patients had experienced major ventricular arrhythmias. Most patients (n = 12) presented with this arrhythmia, while three experienced the event during 5.4 ± 3.2 years of follow-up. Compared with patients without an arrhythmic event, patients with major arrhythmias were more likely to be proband (p < 0.001) and male (p = 0.042). Likewise, survival free from sustained ventricular arrhythmia was lower among probands and males. CONCLUSION: Phenotypic characteristics of elderly ARVD/C patients are characterised by depolarisation abnormalities and structural cardiac changes. Ventricular arrhythmias in this elderly cohort are associated with male gender and proband status.

Myocardial strain imaging could potentially improve patient selection for cardiac resynchronization therapy (CRT). Available techniques are CMR tagging (CMR-TAG), feature tracking (CMR-FT) and speckle tracking echocardiography (STE). Despite promising results per modality, a direct comparison is

Background Peripheral arterial disease (PAD) is a common disease associated with a considerably increased risk of future cardiovascular events and most of these patients will die from coronary artery disease (CAD). Screening for silent CAD has become an option with recent non-invasive developments in CT (computed tomography)-angiography and MR (magnetic resonance) stress testing. Screening in combination with more aggressive treatment may improve prognosis. Therefore we propose to study whether a cardiac imaging algorithm, using non-invasive imaging techniques followed by treatment will reduce the risk of cardiovascular disease in PAD patients free from cardiac symptoms. Design The GROUND study is designed as a prospective, multi-center, randomized clinical trial. Patients with peripheral arterial disease, but without symptomatic cardiac disease will be asked to participate. All patients receive a proper risk factor management before randomization. Half of the recruited patients will enter the 'control group' and only undergo CT calcium scoring. The other half of the recruited patients (index group) will undergo the non invasive cardiac imaging algorithm followed by evidence-based treatment. First, patients are submitted to CT calcium scoring and CT angiography. Patients with a left main (or equivalent) coronary artery stenosis of > 50% on CT will be referred to a cardiologist without further imaging. All other patients in this group will undergo dobutamine stress magnetic resonance (DSMR) testing. Patients with a DSMR positive for ischemia will also be referred to a cardiologist. These patients are candidates for conventional coronary angiography and cardiac interventions (coronary artery bypass grafting (CABG) or percutaneous cardiac interventions (PCI)), if indicated. All participants of the trial will enter a 5 year follow up period for the occurrence of cardiovascular events. Sequential interim analysis will take place. Based on sample size calculations about 1200 patients are needed to detect a 24% reduction in primary outcome. Implications The GROUND study will provide insight into the question whether non-invasive cardiac imaging reduces the risk of cardiovascular events in patients with peripheral arterial disease, but without symptoms of coronary artery disease. Trial registration Clinicaltrials.gov NCT00189111

In a recent issue of the Journal, Duckett et al. ([1][1]) published a study indicating that the acute hemodynamic response ([AHR], assessed by LVdP/dtmax, the maximum rate of rise of left ventricular pressure) predicts reverse remodeling ([RR], which is the decrease in left ventricular end-systolic