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An Expert Panel of the National Lipid Association reviewed the evidence related to the use of coronary artery calcium (CAC) scoring in clinical practice for adults seen for primary prevention of atherosclerotic cardiovascular disease. Recommendations for optimal use of this test in adults of various races/ethnicities, ages and multiple domains of primary prevention, including those with a 10-year ASCVD risk

Acquisition costs and cost-effectiveness have limited access and recommendations to use proprotein convertase subtilisin/kexin type 9 (PCSK9)-inhibiting monoclonal antibodies (mAbs). Recently, prices were reduced by 60% for alirocumab and evolocumab. This statement systematically reviewed subgroup analyses from statin and PCSK9 mAb trials to identify higher risk groups for which PCSK9 mAbs at the new price could be considered a reasonable (

BACKGROUND The effects of edge-to-edge percutaneous mitral valve repair on the shape and size of the mitral annulus and its relation to mitral regurgitation (MR) have not been well characterized. We evaluated acute changes in mitral annular shape and dimensions, and their effect on MR severity, in patients with functional and degenerative MR following MitraClip® . METHODS Patients that underwent MitraClip® between January 2013 and May 2016 at our institution were retrospectively reviewed. EXCLUSIONS inadequate images, prior mitral valve repair, and rapid atrial fibrillation. Intra-procedure TEE 3D images acquired prior to and after implantation of MitraClip® were analyzed using software to model the mitral valve apparatus. RESULTS Of seventy-eight patients that underwent MitraClip® procedure, 60 were eligible. Mean age was 78.3 ± 11 years. Severe MR (4+) was present in 37 patients, moderately/severe MR (3+) in 23. All patients achieved MR reduction to ≤2. 3D annular circumference, bicommissural diameter, and anteroposterior diameter had a significant size reduction after MitraClip® . None of the mitral annular measures had significantly different mean change between the large and small MR change groups at the 0.05 significance level. CONCLUSIONS In patients with functional or degenerative MR, the MitraClip® significantly affect mitral annular dimensions; however, these changes do not correlate with the immediate MR reduction.

We describe the role of three-dimensional echocardiography in the assessment of the aortic valve and the aorta. The manuscript is heavily illustrated with figures and movie clips.

Diagnosis, prognosis, treatment, and development of new therapies for diseases or syndromes depend on a reliable means of identifying phenotypes associated with distinct predictive probabilities for these various objectives. Left ventricular ejection fraction (LVEF) provides the current basis for combined functional and structural phenotyping in heart failure by classifying patients as those with heart failure with reduced ejection fraction (HFrEF) and those with heart failure with preserved ejection fraction (HFpEF). Recently the utility of LVEF as the major phenotypic determinant of heart failure has been challenged based on its load dependency and measurement variability. We review the history of the development and adoption of LVEF as a critical measurement of LV function and structure and demonstrate that, in chronic heart failure, load dependency is not an important practical issue, and we provide hemodynamic and molecular biomarker evidence that LVEF is superior or equal to more unwieldy methods of identifying phenotypes of ventricular remodeling. We conclude that, because it reliably measures both left ventricular function and structure, LVEF remains the best current method of assessing pathologic remodeling in heart failure in both individual clinical and multicenter group settings. Because of the present and future importance of left ventricular phenotyping in heart failure, LVEF should be measured by using the most accurate technology and methodologic refinements available, and improved characterization methods should continue to be sought.

Previous studies demonstrated that men were more likely to have plaque rupture and are at greater risk for myocardial infarction and stroke than women. We evaluated differences in carotid plaque characteristics by MRI between men and women with mild-moderate atherosclerosis and elevated ApoB levels. One hundred eighty-two subjects (104 men and 78 women) with CAD or carotid stenosis (≥ 15% by ultrasound), ApoB ≥ 120 mg/dL and carotid MRI scan were included. Percent wall volume (%WV) was calculated as (wall volume/total vessel volume) × 100%. Three major plaque compositions, fibrous tissue (FT), calcification (CA) and lipid rich necrotic core (LRNC), were identified and quantified using published MRI criteria. Adventitial and plaque neovascularization as fractional plasma volume (Vp) and permeability as transfer constant (Ktrans) were analyzed using kinetic modeling. These characteristics were compared between men and women. Men, compared to women, were younger (54 ± 8 vs. 58 ± 8 years, p = 0.01), had higher rate of previous MI (46 vs. 26%, p = 0.005) but lower proportions of metabolic syndrome (37 vs. 59%, p = 0.003). After adjusting for between-gender differences, men were significantly more likely to have LRNC (OR 2.22, 95% CI 1.04–4.89, p = 0.04) and showed significantly larger %LRNC than women (diff = 4.3%, 95% CI 1.6–6.9%, p = 0.002), while %WV, FT, and CA were similar between men and women. There were no statistically significant differences in adventitial and plaque Vp or Ktrans. Men were significantly more likely to have LRNC and had larger LRNC than women. However, men and women showed relatively similar levels of adventitial and plaque neovascularization and permeability. Trial registration: NCT00715273 at ClinicalTrials.gov. Registered 15 July 2008, retrospectively registered.

Computed tomographic (CT) coronary calcium scoring has been established by large prospective, population-based studies as the single best noninvasive predictor of atherosclerotic cardiovascular risk available today. The calcium score correlates highly with the total burden of coronary atherosclerosis demonstrated at autopsy. It adds significantly to traditional risk calculators such as the Framingham Risk Calculator or the Pooled Cohort Equations. The 2018 U.S. Cholesterol Guidelines endorse the use of CT coronary calcium scoring to refine risk estimates in the intermediate range of 7.5%–20% over 10 years. Most, but not all, adults with calcium scores of zero can reasonably elect to avoid or defer statin therapy, but repeating the calcium score should be considered in 5 to 10 years. Discussants at this roundtable urge that coronary calcium scoring be offered to many more adults than currently receiving this test, including those with borderline 10-year risk in the range of 5%–7.5%. CT coronary angiography is a procedure based on intravenous contrast injection, mostly used in low-risk patients with chest pain. In British guidelines, CT angiography is preferred over stress testing for initial assessment of suspected coronary symptoms. Carotid ultrasound evaluating both the carotid intima-media thickness and presence of plague is less predictive than coronary calcium scoring for overall atherosclerotic risk but more predictive for stroke risk.

Septic cardiomyopathy is commonly encountered in patients with severe sepsis and septic shock. This study explores whether novel global and segmental echocardiographic markers of myocardial deformation, using two-dimensional speckle tracking, are associated with adverse sepsis outcomes. We conducted a retrospective observational feasibility study, at a tertiary care centre, of patients admitted to the ICU with a diagnosis of sepsis who underwent an echocardiogram within the first week of sepsis diagnosis. Data were collected on chamber dimensions, systolic and diastolic function, demographics, haemodynamics, and laboratory parameters. Global and segmental left ventricular longitudinal strain (LVLS) and tissue mitral annular displacement (TMAD) were assessed on 12 left ventricular segments and six mitral annulus segments in apical views, respectively. We explored associations of abnormal LVLS and TMAD with duration of mechanical ventilation, hospital length of stay, and mortality. Fifty-four patients were included. Global LVLS was not associated with any of the primary study endpoints. However, reduced systolic LVLS of the basal anterior segment was associated with in-hospital mortality. There was a suggestion that patients with a reduced global TMAD were associated with an increased risk of mortality and a short length of hospital stay but these associations were not statistically significant. Reduced global LVLS was associated with lower ejection fraction. Reduced global TMAD was associated with reduced global and segmental LVLS, reduced left ventricular ejection fraction, and increased left ventricular end-systolic and end-diastolic volumes. Speckle-tracking echocardiography can be performed feasibly in patients in sepsis. Global and segmental left ventricular deformation indices are associated with ejection fraction. Further studies need to evaluate the ability of these new indices to predict sepsis outcomes.

The aim of this study was to describe the clinical characteristics and mortality of patients with conflicting diastolic function during follow-up. Up to 30% of patients have conflicting diastolic function by echo Doppler and therefore cannot be classified into a distinct diastolic dysfunction category of stage 1, 2 or 3. Using our established echocardiography data base, we studied a cohort of 250 subjects with conflicting diastolic function. Each individual was compared to two controls with normal diastolic and systolic function. The pre-specified goal of the analysis was a 6-year follow-up. Patients with conflicting diastolic function were more likely to have diabetes, hypertension, and established coronary artery disease. The Cox proportional hazards model determined that the risk of death was significantly higher for conflicting patients compared to patients with normal diastolic parameters (HR: 1.83; 95% CI: 1.32–2.53), P

We present two cases of cor triatriatum, a rare congenital anomaly that consists of a membrane that divides the left atrium into two chambers. The first case involves an older adult man admitted for evaluation of left-sided weakness attributed to stroke. The second is a case of a middle-aged woman with dyspnea. Both patients had transthoracic echocardiograms as a part of their initial evaluation, which revealed abnormal structures in the left atrium, and both subsequently underwent transesophageal echocardiography. During these exams, real-time 3D imaging was utilized to more completely define the pathology. (Echocardiography 2011;28:E125-E128)

Background It is well known that cardiovascular disease is the number one killer of men and women in the United States and in many parts of the developed world. However, early detection of atherosclerosis remains a challenging area of research and development. Stress echo and myocardial perfusion studies were not designed to be screening tests and the majority of literature using these tests is in populations with a high probability of disease. It must be emphasized that negative stress echo and stress MPI tests only imply a lack of flow limiting disease; they do not indicate lack of atherosclerotic disease. It is important to remember that when these tests are "negative," the implication is favorable short-term prognosis rather than any implication regarding lack of disease. In contrast, carotid intima-media thickness (CIMT) scanning protocols can detect atherosclerotic disease in early and asymptomatic stages. For a number of reasons reviewed in this article, CIMT may be a more optimal screening and risk-stratifying technology: CIMT directly visualizes vasculature unlike biomarkers such as LDL cholesterol, hsCRP, or PLA2. Methods We performed medline searches for original articles and reviews of carotid IMT from 1985 to the present. We particularly emphasized large multi-center epidemiologic studies of the natural history of patients with carotid IMT measurements. Conclusion There is substantial evidence that CIMT is a suitable surrogate for the coronary tree. CIMT is also (along with coronary calcium scoring) recognized by the American Heart Association as a surrogate marker for coronary artery disease. A recent commentary by Stein, et al reviewed the comparison of CIMT to coronary calcium scoring, with favorable findings for CIMT especially in the healthy young and middle-aged populations, as well as women and African American individuals where coronary calcification has more limited utility. Recent findings of the Multi-Ethnic Study of Atherosclerosis indicate further that increased CIMT predicted CVD events in individuals without coronary calcification.

Ambient air pollution has been associated with heart failure morbidity and mortality. The mechanisms responsible for these associations are unknown but may include the effects of traffic-related pollutants on vascular or autonomic function.We assessed the cross-sectional relation between long-term air pollution, traffic exposures, and important end-organ measures of alterations in cardiac function-left ventricular mass index (LVMI) and ejection fraction-in the Multi-Ethnic Study of Atherosclerosis, a multicenter study of adults without previous clinical cardiovascular disease.A total of 3,827 eligible participants (aged 45-84 yr) underwent cardiac magnetic resonance imaging between 2000 and 2002. We estimated air pollution exposures using residential proximity to major roadways and interpolated concentrations of fine particulate matter (less than 2.5 microns in diameter). We examined adjusted associations between these exposures and left ventricular mass and function.Relative to participants living more than 150 m from a major roadway, participants living within 50 m of a major roadway showed an adjusted 1.4 g/m(2) (95% CI, 0.3-2.5) higher LVMI, a difference in mass corresponding to a 5.6 mm Hg greater systolic blood pressure. Ejection fraction was not associated with proximity to major roadways. Limited variability in estimates of fine particulate matter was observed within cities, and no associations with particulate matter were found for either outcome after adjustment for center.Living in close proximity to major roadways is associated with higher LVMI, suggesting chronic vascular end-organ damage from a traffic-related environmental exposure. Air pollutants or another component of roadway proximity, such as noise, could be responsible.

The association between ambient fine particulate matter (PM) air pollution [particles with aerodynamic diameter ≤ 2.5 μm (PM2.5)] and increased cardiovascular morbidity and mortality in epidemiologic studies (Dominici et al. 2006; Miller et al. 2007; Pope et al. 2002) has led to investigation of underlying mechanisms, which remain cryptic (Bhatnagar 2006). Several studies link ambient (especially combustion-derived) PM with increased vascular tone (Brook et al. 2002; Campen et al. 2005; Proctor et al. 2006), and animal studies showed possible involvement of sympathetic nervous system activation (Proctor et al. 2006) and vasoconstriction pathways (Bouthillier et al. 1998; Li et al. 2005). Evidence suggests that the effect of PM on vascular reactivity may be greater in individuals at risk for coronary artery disease (O’Neill et al. 2005). Human studies to date have provided limited insight into the mechanism of the vascular effects of PM, although recent evidence has documented enhanced exercise-induced ischemia with controlled exposure to diesel exhaust (DE) (Mills et al. 2007). DE is a complex mixture of particulate and gaseous pollutants that comprise a substantial and biologically active fraction of urban ambient air pollution (Health Effects Institute 1995) and is a very appropriate experimental model exposure, especially with the current interest in traffic-related air pollution. Evidence suggests that inhalation of DE is associated with perturbation in endothelial function (Campen et al. 2005; Mills et al. 2005; Tornqvist et al. 2007). We exposed young adults, healthy or with metabolic syndrome, to DE under controlled settings. Young adults with metabolic syndrome have increased subclinical atherosclerosis (Tzou et al. 2005) and are at increased risk for cardiovascular morbidity and mortality (Isomaa et al. 2001). We focused on individuals with metabolic syndrome because they might be more susceptible to DE effects. We hypothesized that DE inhalation would result in vaso-constriction and decreased endothelium-dependent flow-mediated dilation (FMD) of the brachial artery within 30 min of exposure. We also hypothesized that vascular effects of DE might be related to activation of the sympathetic nervous system or increased release of the endothelium-dependent vasoconstrictor endothelin-1 (ET-1).

Three-dimensional echocardiography (3DE) has made a dramatic transition from predominantly a research tool to a technology useful in everyday clinical practice. This article outlines the history of 3DE from its beginnings to the most current technology.

Heart failure is exceedingly prevalent in the United States and in other developed countries. Treatment regimens are complex and now include electrical therapy. Methods for evaluating left ventricular dyssynchrony using echocardiography rather than QRS duration have been developed, with tissue Doppler velocity parameters being the most popular. Real-time three-dimensional echocardiography is another novel method for dyssynchrony evaluation that has potential advantages over existing techniques. The authors describe their experience with three-dimensional echocardiography dyssynchrony evaluation and offer insights into the direction that this technology must move to improve results.

A 53-year-old woman presented to the hospital with near syncope, reporting that she crawled on the floor for the past 3 days to prevent passing out. An ECG performed in the emergency department showed complete heart block. A temporary transvenous pacemaker was emergently positioned. A transthoracic echocardiogram was suboptimal, but demonstrated a mass in the left atrium. Transesophageal echocardiography revealed that the large mass (3.2×2.7 cm) was much more extensive, with infiltration of both the interatrial and interventricular septae, both atria, the left ventricular outflow tract, and the ventricular side of the mitral valve anterior leaflet (Figure 1A through 1D, Movie IA through ID in the online-only Data Supplement). Differential diagnosis included a primary cardiac tumor, metastatic disease, sarcoidosis or other granulomatous process, or an infectious process. A computed tomography scan of the chest, abdomen, and pelvis demonstrated the intracardiac mass and no other abnormalities (Figure 2). A permanent pacemaker was placed. The patient declined surgical management of the intracardiac mass. Figure 1. A , 2D TEE at midesophageal 4-chamber view at 0° shows a large cardiac mass (arrow) at interatrial septum and A-V node area that extends into both atria at end diastole. B , 2D TEE at lower midesophageal view at 117° shows large cardiac mass (arrow) at mid and basal interatrial septal area. C , 3D TEE at upper-esophageal short-axis view at 125° shows large mass (arrow) involving mid and basal interatrial septum and extending into midatrioventricular area. D , …

The leadership of the National Lipid Association convened an Expert Panel to develop a consensus set of recommendations for patient-centered management of dyslipidemia in clinical medicine. An Executive Summary of those recommendations was previously published. This document provides support for the recommendations outlined in the Executive Summary. The major conclusions include (1) an elevated level of cholesterol carried by circulating apolipoprotein B-containing lipoproteins (non-high-density lipoprotein cholesterol and low-density lipoprotein cholesterol [LDL-C], termed atherogenic cholesterol) is a root cause of atherosclerosis, the key underlying process contributing to most clinical atherosclerotic cardiovascular disease (ASCVD) events; (2) reducing elevated levels of atherogenic cholesterol will lower ASCVD risk in proportion to the extent that atherogenic cholesterol is reduced. This benefit is presumed to result from atherogenic cholesterol lowering through multiple modalities, including lifestyle and drug therapies; (3) the intensity of risk-reduction therapy should generally be adjusted to the patient's absolute risk for an ASCVD event; (4) atherosclerosis is a process that often begins early in life and progresses for decades before resulting a clinical ASCVD event. Therefore, both intermediate-term and long-term or lifetime risk should be considered when assessing the potential benefits and hazards of risk-reduction therapies; (5) for patients in whom lipid-lowering drug therapy is indicated, statin treatment is the primary modality for reducing ASCVD risk; (6) nonlipid ASCVD risk factors should also be managed appropriately, particularly high blood pressure, cigarette smoking, and diabetes mellitus; and (7) the measurement and monitoring of atherogenic cholesterol levels remain an important part of a comprehensive ASCVD prevention strategy.

Migraine headaches have a high prevalence rate in the general population and account for significant morbidity, lost productivity, health care visits, and dollars spent. Increasingly, emerging data show a link between migraine headache, especially migraine headaches with aura, and patent foramen ovale (PFO). Closure of PFO as a cure for migraine headache is a tantalizing idea; this article examines the data supporting that possibility including studies showing improvement in migraine headache after PFO closure and case reports in which migraine headaches worsened after closure of an atrial septal defect.

The platypnea-orthodeoxia syndrome is a rare but important condition caused by a variety of clinical entities. Several mechanisms have been postulated to cause platypnea and orthodeoxia. These mechanisms mainly involve intracardiac shunting, pulmonary vascular shunting, and ventilation-perfusion mismatching. Patent foramen ovale is an important type of intracardiac shunt that can produce platypnea-orthodeoxia in select patients. Concomitant pulmonary hypertension must be ruled out, but symptoms can occur without pulmonary hypertension in cases with altered intrathoracic anatomy and physiology. Diagnosis usually entails transthoracic or trans-esophageal echocardiogram, ideally with postural provocation by the tilt-table test. Treatment with surgical or percutaneous closure may result in symptomatic relief. The decision to intervene is based mainly on the severity of symptoms and potential morbidities associated with the defect.

Endothelial dilator function is impaired in people with type 2 diabetes mellitus (T2DM). Prior research indicates that this can be improved with intravenous administration of ascorbate or L-arginine, but whether these agents have this effect when administered by the clinically practical oral route is unknown. To investigate this question, 10 premenopausal women with T2DM and 10 healthy, premenopausal, non-diabetic women received, in random sequence, a 1-week administration of oral L-arginine (9 g daily) or vitamins E (1800 mg) and C (1000 mg) with an intervening 1-week washout period. Flow-mediated brachial artery dilation (FMD) was measured by ultrasonography and forearm blood flow was measured by plethysmography before and following blood pressure cuff-induced forearm ischemia before and after each week of treatment. At baseline, the women with T2DM had lesser FMD responses (0.028 ± 0.006 cm vs 0.056 ± 0.008 cm, p, 0.05). Post-ischemic forearm hyperemia was reduced at baseline in T2DM compared with controls (16.4 ± 1.8 vs 26.0 ± 1.4 ml 100 ml-1min-1, p

Background —Valve regurgitation has been associated with dexfenfluramine, but its prevalence and severity are uncertain. Additional factors that may contribute to valve regurgitation in patients exposed to this drug are poorly understood. Methods and Results —Echocardiography was performed on subjects recruited from 26 prescribing sites in 15 states. The total sample of 412 subjects included 172 dexfenfluramine patients and 172 unexposed controls matched for age, sex, and body mass index and 68 unmatched subjects meeting the same entry criteria (51 dexfenfluramine patients and 17 controls). Mean treatment duration was 6.9 months; mean interval from treatment discontinuation to echocardiogram was 8.5 months. Each echocardiogram was interpreted independently by 3 echocardiographers. FDA-grade regurgitation (at least mild aortic regurgitation or at least moderate mitral regurgitation) was significantly more frequent in dexfenfluramine patients (7.6% versus 2.1% for controls; P =0.01; odds ratio, 3.82). This difference was primarily due to more frequent mild aortic regurgitation in dexfenfluramine patients (6.3% versus 1.6% in controls; P Conclusions —Dexfenfluramine use is associated with an increase in the prevalence of abnormal valve regurgitation. Age and blood pressure may also affect the prevalence of regurgitation. Dexfenfluramine-related valve regurgitation may regress after drug discontinuation.

Objectives. This study evaluated whether left ventricular mass increases during cellular or vascular (humoral) cardiac allograft rejection. Background. An increase in left ventricular mass during cellular cardiac allograft rejection has been described by other investigators, although controversy has existed over the validity of these findings. Left ventricular mass changes have not been evaluated in the setting of vascular (humoral) cardiac allograft rejection. Methods. To determine the effect of allograft rejection on left ventricular mass, we retrospectively reviewed endomyocardial biopsy results and corresponding echocardiograms in 41 cardiac transplant recipients undergoing treatment for allograft rejection. Left ventricular mass was assessed by two-dimensional echocardiography using the method of Schiller. Maintenance immunosuppression included cyclosporine in all patients. Results. Although significant changes in left ventricular wall thickness, mass and dimensions were not observed in patients experiencing moderate or severe cellular allograft rejection (International Society for Heart and Lung Transplantation grades III and IV, n = 27), marked changes were noted in patients with vascular (humoral) rejection (n = 14). Patients with vascular rejection demonstrated an echocardiographic mean (±SEM) increase in left ventricular wall mass (from 109 ± 17 to 151 ± 17g), and left ventricular wall thickness (from 1.3 ± 0.1 to 1.6 ± 0.1cm) during the rejection episode. Additionally, vascular rejection was associated with a trend toward an increase in left ventricular systolic dimension (from 2.6 ± 0.1 to 3.0 ± 0.2 cm) and a decrease in left ventricular fractional shortening and increased incidence of hemodynamic compromise with rejection (50% for vascular vs. 11% for cellular rejection). Conclusions. Left ventricular mass increases during episodes of vascular (humoral) rejection, but there is no significant change in left ventricular mass during cellular cardiac allograft rejection.

Survivors of sudden cardiac arrest may be exposed to iodinated contrast from invasive coronary angiography or contrast-enhanced computed tomography, although the effects on incident acute kidney injury are unknown. The study objective was to determine whether contrast administration within the first 24 hours was associated with acute kidney injury in survivors of sudden cardiac arrest.This cohort study, derived from a prospective clinical trial, included patients with sudden cardiac arrest who survived for 48 hours, had no history of end-stage renal disease, and had at least 2 serum creatinine measurements during hospitalization. The contrast group included patients with exposure to iodinated contrast within 24 hours of sudden cardiac arrest. Incident acute kidney injury and first-time dialysis were compared between contrast and no contrast groups and then controlled for known acute kidney injury risk factors.Of the 199 survivors of sudden cardiac arrest, 94 received iodinated contrast. Mean baseline serum creatinine level was 1.3 mg/dL (95% confidence interval [CI] 1.4 to 1.5 mg/dL) for the contrast group and 1.6 mg/dL (95% CI 1.4 to 1.7 mg/dL) for the no contrast group. Incident acute kidney injury was lower in the contrast group (12.8%) than the no contrast group (17.1%; difference 4.4%; 95% CI -9.2% to 17.5%). Contrast administration was not associated with significant increases in incident acute kidney injury within quartiles of baseline serum creatinine level or after controlling for age, sex, race, congestive heart failure, diabetes, and admission serum creatinine level by regression analysis. Older age was independently associated with acute kidney injury.Despite elevated baseline serum creatinine level in most survivors of sudden cardiac arrest, iodinated contrast administration was not associated with incident acute kidney injury even when other acute kidney injury risk factors were controlled for. Thus, although acute kidney injury is not uncommon among survivors of sudden cardiac arrest, early (24 hours) contrast administration from imaging procedures did not confer an increased risk for acute kidney injury.

Coronary atherosclerosis is a leading cause of death in the United States and worldwide, accounting for close to 1 million deaths annually in the United States alone. The evaluation of coronary disease by CT-derived calcium scores is a rapidly evolving field of medical imaging. Furthermore, until recently, whether or not regression or progression of coronary disease could accurately be assessed by coronary calcium scores had been a question of considerable debate among experts in this field. If the medical treatment of coronary artery disease by statin pharmacotherapy could be accurately assessed by coronary calcium scoring, this would take much of the current guess work out of statin pharmacotherapy. Initial retrospective studies and observational data suggested that statin treatment resulted in reduction of coronary calcium. More recently, five randomized controlled trials have demonstrated that not only does statin treatment not reduce coronary calcium, but in fact, the progression of coronary calcium by CT scanning is indistinguishable from placebo treatment.

Background Elevated left ventricular mass (LVM) is a strong predictor of negative cardiovascular outcomes, including heart failure, stroke, and sudden cardiac death. A relationship between close (< 50 m compared with > 150 m) residential proximity to major roadways and higher LVM has previously been described, but the mechanistic pathways that are involved in this relationship are not known. Understanding genetic factors that influence susceptibility to these effects may provide insight into relevant mechanistic pathways. Objective We set out to determine whether genetic polymorphisms in genes affecting vascular and autonomic function, blood pressure, or inflammation influence the relationship between traffic proximity and LVM. Methods This was a cross-sectional study of 1,376 genotyped participants in the Multi-Ethnic Study of Atherosclerosis, with cardiac magnetic resonance imaging performed between 2000 and 2002. The impact of tagged single-nucleotide polymorphisms (tagSNPs) and inferred haplotypes in 12 candidate genes (ACE, ADRB2, AGT, AGTR1, ALOX15, EDN1, GRK4, PTGS1, PTGS2, TLR4, VEGFA, and VEGFB) on the relationship between residential proximity to major roadways and LVM was analyzed using multiple linear regression, adjusting for multiple potential confounders. Results After accounting for multiple testing and comparing homozygotes, tagSNPs in the type 1 angiotensin II receptor (AGTR1, rs6801836) and arachidonate 15-lipoxygenase (ALOX15, rs2664593) genes were each significantly (q < 0.2) associated with a 9–10% difference in the association between residential proximity to major roadways and LVM. Participants with suboptimal blood pressure control demonstrated stronger interactions between AGTR1 and traffic proximity. Conclusions Common polymorphisms in genes responsible for vascular function, inflammation, and oxidative stress appear to modify associations between proximity to major roadways and LVM. Further understanding of how genes modify effects of air pollution on CVD may help guide research efforts into specific mechanistic pathways.

The report by Messika-Zeitoun et al. ([1][1]) evaluating the association of commissural opening (CO) after percutaneous mitral commissurotomy (PMC) with improved long-term clinical outcomes shows the utility of combining CO with other echocardiography parameters in the post-procedure assessment of

To establish a classification of bicuspid aortic valve (BAV) that includes both leaflet morphology and aortic shape.Two academic medical centres of the University of Washington, Seattle.191 adult patients with BAV.Review of clinical data and transthoracic echocardiograms.Assessment of leaflet morphology; valve function; aortic shape and dimensions.We identified three morphologies: type 1, fusion of right and left coronary cusp (n = 152); type 2, right and non-coronary fusion (n = 39); and type 3, left and non-coronary fusion (n = 1). Comparing type 1 and 2 BAV, there were no significant differences in age, height, weight, blood pressure or aortic valve function. Type 1 was more common in men (69 vs 45%). The aortic sinuses were larger in type 1, while type 2 had larger arch dimensions. Myxomatous mitral valves were more common in type 2 BAV (13% vs 2.6%, p0.05). Three aortic shapes were defined: normal (N), sinus effacement (E), and ascending dilatation (A). Comparing type 1 to type 2 BAV, shape N was more common in type 1 (60% vs 32%), and type A was more common in type 2 (35% vs 54%,); type E was rare (p0.01 across all groups).A comprehensive BAV phenotype includes aortic shape. Type 1 BAV is associated with male gender and normal aortic shape but a larger sinus diameter. Type 2 leaflet morphology is associated with ascending aorta dilatation , larger arch dimensions and higher prevalence of myxomatous mitral valve disease.

To date, mitral stenosis has been evaluated by both hemodynamic data derived from catheterization as well as 2D and Doppler echocardiography. However, the advent of real-time 3D echocardiography has allowed more precise measurement of the mitral valve orifice by planimetry. In addition, evaluation of the mitral commissures prior to and after percutaneous mitral valvuloplasty is greatly aided by 3D echocardiography. Here we discuss these subjects as well as provide specific clinical trials that support the use of real-time 3D echocardiography for the evaulation and treatment of mitral stenosis.

This article presents an approach to real-time three-dimensional imaging of the tricuspid valve from three different views. This is followed by some representative cases that illustrate these views and some unique tricuspid valve abnormalities, including one case of corrected transposition.

A system is proposed for measuring the three dimensional flow pattern of the left ventricle during filling, with sufficient spatial and temporal resolution to characterize vortex behavior. At least one vortex is known to form during diastolic filling and is thought to play a role in cardiac function. Variations in the vorticity field are hypothesized to be sensitive indicators of heart abnormalities. To test this hypothesis, new techniques were developed for high-resolution reconstruction of phase contrast (velocity encoded) MRI data, computation of vorticity from sampled velocities, and 3D display of vorticity information. In preliminary evaluations, these techniques showed an absence of the vortex in patients with congestive heart failure related to diastolic dysfunction.

PFO is diagnosed by echocardiography using the combination of transthoracic two-dimensional imaging of the interatrial septum, followed by color and spectral Doppler (and if necessary saline contrast) imaging. Transesophageal imaging is an important adjunct when transthoracic imaging is not conclusive or yields suboptimal images.Three-dimensional echocardiography is useful for defining fenestrations within a PFO.

We report two cases of patients presenting to the emergency department with chest pain who had low risk electrocardiographic findings. Myocardial perfusion imaging (MPI) revealed a significant area of decreased uptake suggestive of acute transmural infarction. In both cases, biochemical markers later confirmed the diagnosis of myocardial infarction. Cardiac catheterization revealed a large area at risk which was then treated with percutaneous intervention. As MPI is increasingly utilized in the acute evaluation of chest pain, it may serve as a useful adjunct in selecting patients who may benefit from emergent cathertization and revascularization.

Carvedilol has been shown to improve survival and morbidity in patients with heart failure. It has been demonstrated that carvedilol use is associated with dose-dependent reduction in QT dispersion (QTd) independent of the cause of heart failure, suggesting that reduction in QTd may be a mechanism by which carvedilol improves outcomes in heart failure.

The Churg-Strauss syndrome (CSS) is an unusual disease that presents as a systemic vasculitis and peripheral eosinophilia in a patient with chronic atopic disease. Although often not prominent on initial presentation, cardiac involvement is a major cause of morbidity and mortality in patients with CSS. We report a case of a young woman with CSS who had a myocardial infarction. Coronary arteriography was performed for recurrent chest pain and demonstrated diffuse vasculopathy consistent with vasculitis in CSS. We have also included a review of the literature on cardiac involvement in CSS.

s 279 placebo for 2 years. Total cholesterol (TC), LDL-C, nonHDL-cholesterol, HDL-cholesterol, VLDL-cholesterol, triglycerides, apolipoprotein A, apolipoprotein B, high-sensitivity C-reactive protein (hs-CRP), and SAAwere measured at 1 and 2 years. Student’s t-tests comparing O3FA versus placebo were used to analyze the change in each lipid parameter at each time point. Results: There were no significant differences in any baseline characteristic between groups (supplement vs. placebo), indicating appropriate randomization. The mean age of subjects was 55 6 10 years, and 53% were women. The mean waist circumference was 110 6 14 cm, median TGs were 157 mg/dL, mean HDL-C was 45 6 13 mg/dL, mean glucose was 103 6 8mg/dL, mean systolic BP was 132 6 13 mmHg, and mean diastolic BP was 83 6 9 mmHg. There were no significant differences (supplement vs. placebo) in TC, LDL-C, non-HDL-C, or HDL-C at year 1 or 2 from baseline. Change in TGs at year 1 from baseline was 37.3 mg/dL lower in the intervention group (P 5 .015) and 30.4 mg/dL lower at year 2 from baseline in the intervention group (P 5 .09). Change in VLDL-C from baseline was 7.41 mg/dL lower at year 1 (P 5 .016) and 6.11 mg/dL lower at year 2 in the intervention group (P 5 .08). There were no significant differences in apoA1 at year 1, but at year 2 the change in apoA1 from baseline was 9.7 mg/dL lower in the intervention group (0.013). Change in apoB at year 1 from baseline was 7.83 mg/dL lower in the intervention group (P 5 .034) and 8.16 mg/dL lower (P 5 .037) at 2 years. There were no significant differences in change in hs-CRP or SAA at year 1 or 2 comparing intervention with placebo. Conclusions: O3FA supplementation in the form of EPA and DHA improves the atherogenic dyslipidemia of MetS by decreasing TGs, VLDL-C and apolipoprotein B in subjects with MetS. Supplementation does not, however, improve inflammatory markers.

The objective of this study was to report the frequency of disulfiram-related elevations of four commonly used hepatic screening chemistries using a retrospective record review design. An inpatient alcoholism program was selected for the setting. Patients who had initial laboratory values within the normal range started daily supervised doses of disulfiram, then underwent follow-up testing after 2 and 4 weeks on the drug. The study population consisted of 108 patients receiving disulfiram and 27 patients who did not receive disulfiram (controls). The four screening serum chemistries performed were aspartate aminotransferase (SGOT), alanine aminotransferase (SGPT), alkaline phosphatase, and gamma-glutamyl transferase. Twenty-seven (25%) of the 108 patients who were taking 250 mg of disulfiram a day for 2 to 4 weeks had disulfiram-related elevations in alanine aminotransferase above the upper limit of normal, as opposed to one elevation in 27 patients (4%) for whom disulfiram was not prescribed. In the 108 patients (with initially normal serum chemistries) who were prescribed disulfiram, 32 were discontinued from the drug at 2 weeks and an additional 11 were discontinued from the drug at 4 weeks because of one or more abnormal serum chemistries. Alanine aminotransferase was the most specific and sensitive indicator of the four screening chemistries performed.

Echocardiography is recommended for the detection of valvular regurgitation in asymptomatic users of anorexigens with a heart murmur. To determine the prevalence and diagnostic value of heart murmurs for valvular regurgitation, 223 patients receiving dexfenfluramine therapy for 6.9 months and 189 matched controls underwent history and cardiac auscultation by experienced noncardiologists unaware of echocardiography. Color Doppler echocardiograms were interpreted by 3 observers unaware of patients' clinical data. The frequency of at least mild regurgitation of any valve and abnormal regurgitation (moderate mitral or tricuspid or mild aortic regurgitation) were determined. Heart murmurs heard in 31 dexfenfluramine users (14%) and in 20 controls (11%) were all systolic and of grade I to II/VI intensity. Mild or worse regurgitation of any valve showed a trend in patients (18% vs 11.6% in controls, odds ratio [OR] 1.66, confidence interval [CI] 0.95 to 2.9, p = 0.08), but abnormal regurgitation (includes Food and Drug Administration grade regurgitation) was more common in patients (9% vs 3% in controls, OR 3.0, CI 1.18 to 7.65, p = 0.02). In dexfenfluramine users, heart murmurs were associated with at least mild or abnormal regurgitation (OR 3.1 and 3.05, 95% CI 1.34 to 7.13 and 1.1 to 8.67; p = 0.008 and 0.036, respectively), had a specificity of 89% and 88%, negative predictive value of 85% and 93%, but sensitivity of 37% and 30%, and positive predictive value of 35% and 19%, respectively. Most valves missed by cardiac auscultation had normal morphology and mild regurgitation. Finally, heart murmurs had better diagnostic value for either type of valvular regurgitation than heart murmurs and clinical variables or clinical variables alone. In summary, in dexfenfluramine users the prevalence of heart murmurs was low and their absence predicted absence of mild or worse regurgitation of any valve or abnormal valvular regurgitation. Therefore, cardiac auscultation should be the screening method of choice for detecting valvular regurgitation in users of anorexigens.

Hypertension occurs commonly and early in the natural history of autosomal dominant polycystic kidney disease (ADPKD), affecting both renal and patient outcome. Activation of the renin angiotensin aldosterone system due to cyst expansion and local renal ischaemia plays an important role in the development of ADPKD related hypertension and left ventricular hypertrophy (LVH), a known important risk factor for cardiovascular morbidity and mortality. The aim of this study was to investigate the effects of an angiotensin converting enzyme (ACE) inhibitor, enalapril, on renal function, blood pressure and LVH in hypertensive ADPKD patients.Fourteen hypertensive ADPKD patients (11 men, 3 women; mean age: 40 years) were included in the study. All patients had LVH and creatinine clearance (Cer) greater than 50 ml/min/1.73 m2. The patients were followed for 7 years on enalapril therapy. The effects of enalapril on renal function, blood pressure and LVH were investigated.Baseline measurements of mean arterial pressure (MAP), Ccr and left ventricular mass index (LVMI) were 110 +/- 2 mmHg, 84 +/- 6 ml/min/1.73 m2 and 146 +/- 4 g/m2, respectively. After one year of enalapril therapy there was a significant decrease in MAP (94 +/- 3 mmHg, P0.005) which remained stable until the end of the study at 7 years (94 +/- 1 mmHg, P0.005 vs baseline). There was also a significant decrease in LVMI (131 +/- 6 g/m2, P0.05) after year 1 which continued to decrease until the end of the study reaching 98 +/- 6 g/m2 (P0.01 vs year 1 and baseline). Although Ccr remained stable after year 1, a significant decrease was observed after 7 years of follow-up (59 +/- 6 ml/min, P0.001 vs year 1 and baseline).ACE inhibition in hypertensive ADPKD patients provided long-term reversal of LVH in association with a mean 3.6 ml/min/year decline of Ccr. These preliminary results have potential important implications for cardiovascular and renal protection in ADPKD.

We and others have previously shown that carvedilol improves left ventricular (LV) function and symptoms in chronic heart failure. This improvement in LV function has also been shown to be associated with an improvement in survival. This study evaluates the effect of carvedilol on LV mass, geometry, and degree of mitral regurgitation (MR). In 59 patients with symptomatic heart failure and LV ejection fraction

Noninvasive cardiac imaging techniques now make it possible to determine the morphologic and hemodynamic status of patients with aortic stenosis, even in early asymptomatic stages of the disease. This is particularly important since the prognosis is generally poor once symptoms are apparent and since replacement of the aortic valve is usually the only recourse when stenosis is severe.

Background Polymorphonuclear leukocytes, particularly neutrophils, are important mediators of ischemia/reperfusion–induced myocardial and coronary vascular injury. The selectin family of glycoprotein receptors mediates neutrophil “rolling,” a loose, transient adhesion to the coronary endothelium that precedes the firmer adhesion associated with cardiovascular injury. The oligosaccharide sialyl-Lewis x (SLe x ) is the probable neutrophil counterligand for endothelial E- and P-selectin. Administration of analogues of SLe x could potentially prevent neutrophil rolling by competing for the selectin-adhesion sites. We investigated the effects of treatment with an analogue of SLe x in a chronic canine model of ischemia/reperfusion. Methods and Results Anesthetized mongrel dogs were subjected to 90 minutes of ischemia through occlusion of the left anterior descending coronary artery and 48 hours of reperfusion. Five minutes before the onset of reperfusion, dogs received either the SLe x analogue CY-1503 at a dose of 20 mg/kg or normal saline. Myocardial infarct size was measured through triphenyltetrazolium chloride staining, and polymorphonuclear leukocyte accumulation was evaluated through measurement of cardiac myeloperoxidase activity. After adjustment for blood flow, the mean infarct size of control dogs (44.7±4.2%) was not different from that of treated dogs (33.4±4.0%, P =.06), although there was a trend toward a slightly lower value in the treated dogs. Myeloperoxidase activity was not different in the infarcted myocardium of the treated group compared with that of the control group (2.7±0.71 treated versus 1.08±0.41 units/mg protein control, P =.06). Conclusions We conclude that CY-1503 does not substantially or consistently reduce myocardial infarct size or neutrophil accumulation in dogs subjected to ischemia followed by a prolonged period (48 hours) of reperfusion.

Background In order to establish a consistent method for brachial artery reactivity assessment, we analyzed commonly used approaches to the test and their effects on the magnitude and time-course of flow mediated dilation (FMD), and on test variability and repeatability. As a popular and noninvasive assessment of endothelial function, several different approaches have been employed to measure brachial artery reactivity with B-mode ultrasound. Despite some efforts, there remains a lack of defined normal values and large variability in measurement technique. Methods Twenty-six healthy volunteers underwent repeated brachial artery diameter measurements by B-mode ultrasound. Following baseline diameter recordings we assessed endothelium-dependent flow mediated dilation by inflating a blood pressure cuff either on the upper arm (proximal) or on the forearm (distal). Results Thirty-seven measures were performed using proximal occlusion and 25 with distal occlusion. Following proximal occlusion relative to distal occlusion, FMD was larger (16.2 ± 1.2% vs. 7.3 ± 0.9%, p < 0.0001) and elongated (107.2 s vs. 67.8 s, p = 0.0001). Measurement of the test repeatability showed that differences between the repeated measures were greater on average when the measurements were done using the proximal method as compared to the distal method (2.4%; 95% CI 0.5–4.3; p = 0.013). Conclusion These findings suggest that forearm compression holds statistical advantages over upper arm compression. Added to documented physiological and practical reasons, we propose that future studies should use forearm compression in the assessment of endothelial function.

In 1925, Dr. Carl J. Wiggers demonstrated that pacing from the canine left ventricle (LV) improved acute hemodynamics [(1)][1]. The advent of pacing catheters delivered by the coronary sinus allowed practical use and exploration of LV or biventricular (BiV) pacing for improving heart failure (HF)