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Funding agencies: This study was partially financed through ALF Grants, Region Ostergotland LIO-284291, LIO-284411, and LIO-448281, and LIU Cancer Projects Grants 2012.

Background: In 2007, the American Heart Association published updated evidence-based guidelines on the recommended use of antibiotic prophylaxis to prevent viridans group streptococcal (VGS) infective endocarditis (IE) in cardiac patients undergoing invasive procedures. The 2007 guidelines significantly scaled back the underlying conditions for which antibiotic prophylaxis was recommended, leaving only 4 categories thought to confer the highest risk of adverse outcome. The purpose of this update is to examine interval evidence of the acceptance and impact of the 2007 recommendations on VGS IE and, if needed, to make revisions based on this evidence. Methods and Results: A writing group was formed consisting of experts in prevention and treatment of infective endocarditis including members of the American Dental Association, the Infectious Diseases Society of America, and the American Academy of Pediatrics, in addition to the American Heart Association. MEDLINE database searches were done for English language articles on compliance with the recommendations in the 2007 guidelines and the frequency of and morbidity or mortality from VGS IE after publication of the 2007 guidelines. Overall, there was good general awareness of the 2007 guidelines but variable compliance with recommendations. There was no convincing evidence that VGS IE frequency, morbidity, or mortality has increased since 2007. Conclusions: On the basis of a review of the available evidence, there are no recommended changes to the 2007 VGS IE prevention guidelines. We continue to recommend VGS IE prophylaxis only for categories of patients at highest risk for adverse outcome while emphasizing the critical role of good oral health and regular access to dental care for all. Randomized controlled studies to determine whether antibiotic prophylaxis is effective against VGS IE are needed to further refine recommendations.

Background Costs can be a major barrier to medication adherence in low and middle-income countries and are an important target for policy-level interventions. The use of benzathine penicillin G (BPG) for secondary prevention of rheumatic heart disease (RHD) averts substantial morbidity and mortality, yet the total out-of-pocket costs for patients receiving this intervention are unknown. Objective To estimate the total out-of-pocket costs for obtaining BPG prophylaxis among RHD patients in India. Methods We prospectively collected self-reported drug-, transportation-, and provider-related costs for secondary prophylaxis among RHD patients presenting for follow-up to a tertiary care centre in New Delhi, India. Monthly costs were estimated by adjusting unit costs by frequency of drug administration. Results The cost data provided by 420 patients [mean age (±SD) 11.6 (±2.9) years] was analysed. Majority of the patients were male (65.2%), hailed from rural areas (87.1%), and belonged to lower socioeconomic strata (73.3%). The median monthly total out-of-pocket costs (IQR) for obtaining BPG injections was Indian rupee (INR) 62.5 (42.5–117.0). The median costs for procuring the drug (IQR) was INR 34.0(30.0–39.0). Whereas median costs (IQR) for health care provider and transportation was INR 16.0 [0–32.0]) and INR 11 [0–31.0] respectively. When expressed as mean (SD), the costs for transportation constituted 50% of the total costs, whereas the mean cost for drug procurement and drug administration constituted 30% and 22% of the total costs respectively. Conclusion RHD patients receiving BPG prophylaxis incur substantial out-of-pocket costs, with transportation costs constituting nearly half of the total expenditures. National investments in RHD control must be strategically directed at improving health care access and drug supply in order to lower the total costs of secondary prophylaxis and improve adherence rates.

Significant mitral valve regurgitation creates progressive adverse remodeling of the left ventricle (LV). Replacement of the failing valve with a prosthesis generally improves patient outcomes but leaves the patient with non-physiological intracardiac flow patterns that might contribute to their future risk of thrombus formation and embolism. It has been suggested that the angular orientation of the implanted valve might modify the postoperative distortion of the intraventricular flow field. In this study, we investigated the effect of prosthetic valve orientation on LV flow patterns by using heart geometry from a patient with LV dysfunction and a competent native mitral valve to calculate intracardiac flow fields with computational fluid dynamics (CFD). Results were validated using in vivo 4D Flow MRI. The computed flow fields were compared to calculations following virtual implantation of a mechanical heart valve oriented in four different angles to assess the effect of leaflet position. Flow patterns were visualized in longand short-axes and quantified with flow component analysis. In comparison to a native valve, valve implantation increased the proportion of the mitral inflow remaining in the basal region and further increased the residual volume in the apical area. Only slight changes due to valve orientation were observed. Using our numerical framework, we demonstrated quantitative changes in left ventricular blood flow due to prosthetic mitral replacement. This framework may be used to improve design of prosthetic heart valves and implantation procedures to minimize the potential for apical flow stasis, and potentially assist personalized treatment planning. (c) 2020 The Author(s). Published by Elsevier Ltd. This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/). Funding Agencies|Knut and Alice Wallenberg Foundation through the project Seeing Organ Function; Swedish Heart Lung FoundationSwedish Heart-Lung Foundation; VinnovaVinnova; Swedish Research CouncilSwedish Research CouncilEuropean Commission; County Council of Ostergotland

Introduction: The effects of heart rate, inotropy, and lusitropy on multidimensional flow patterns and energetics within the human heart remain undefined. Recently, reduced volume and end-diastolic kinetic energy (KE) of the portion of left ventricular (LV) inflow passing directly to outflow, Direct flow (DF), have been shown to reflect inefficient LV pumping and to be a marker of LV dysfunction in heart failure patients. In this study, we hypothesized that increasing heart rate, inotropy, and lusitropy would result in an increased efficiency of intraventricular blood flow transit. Therefore, we sought to investigate LV 4D blood flow patterns and energetics with dobutamine infusion.Methods: 4D flow and morphological cardiovascular magnetic resonance (CMR) data were acquired in twelve healthy subjects: at rest and with dobutamine infusion to achieve a target heart rate ~60% higher than the resting heart rate. A previously validated method was used for flow analysis: pathlines were emitted from the end-diastolic (ED) LV blood volume and traced forward and backward in time to separate four functional LV flow components. For each flow component, KE/mL blood volume at ED was calculated.Results: With dobutamine infusion there was an increase in heart rate (64%, p < 0.001), systolic blood pressure (p = 0.02) and stroke volume (p = 0.01). Of the 4D flow parameters, the most efficient flow component (DF), increased its proportion of EDV (p < 0.001). The EDV proportion of Residual volume, the blood residing in the ventricle over at least two cardiac cycles, decreased (p < 0.001). The KE/mL at ED for all flow components increased (p < 0.001). DF had the largest absolute and relative increase while Residual volume had the smallest absolute and relative increase.Conclusions: This study demonstrates that it is feasible to compare 4D flow patterns within the normal human heart at rest and with stress. At higher heart rate, inotropy and lusitropy, elicited by dobutamine infusion, the efficiency of intraventricular blood flow transit improves, as quantified by an increased relative volume and pre-systolic KE of the most efficient DF component of the LV volume. The change in these markers may allow a novel assessment of LV function and LV dysfunction over a range of stress.

The impact of left bundle branch block (LBBB) related mechanical dyssynchrony on left ventricular (LV) diastolic function remains unclear. 4D flow cardiovascular magnetic resonance (CMR) has provided reliable markers of LV dysfunction: reduced volume and kinetic energy (KE) of the portion of LV inflow which passes directly to outflow (Direct Flow) has been demonstrated in failing hearts compared to normal hearts. We sought to investigate the impact of mechanical dyssynchrony on diastolic function by comparing 4D flow in myopathic LVs with and without LBBB. CMR data were acquired at 3 T in 22 heart failure patients; 11 with LBBB and 11 without LBBB matched according to several demographic and clinical parameters. An established 4D flow analysis method was used to separate the LV end-diastolic (ED) volume into functional flow components based on the blood’s timing and route through the heart cavities. While the Direct Flow volume was not different between the groups, the KE possessed at ED was lower in LBBB patients (P = 0.018). Direct Flow entering the LV during early diastolic filling possessed less KE at ED in LBBB patients compared to non-LBBB patients, whereas no intergroup difference was observed during late filling. Pre-systolic KE of LV Direct Flow was reduced in patients with LBBB compared to matched patients with normal conduction. These intriguing findings propose that 4D flow specific measures can serve as markers of LV mechanical dyssynchrony in heart failure patients, and could possibly be investigated as predictors of response to cardiac resynchronization therapy. Electronic supplementary material The online version of this article (doi:10.1007/s10554-017-1261-5) contains supplementary material, which is available to authorized users.

This study aimed to develop a cardiorespiratory-resolved 3D magnetic resonance imaging (5D MRI: x-y-z-cardiac-respiratory) approach based on 3D motion tracking for investigating the influence of respiration on cardiac ventricular function. A highly-accelerated 2.5-minute sparse MR protocol was developed for a continuous acquisition of cardiac images through multiple cardiac and respiratory cycles. The heart displacement along respiration was extracted using a 3D image deformation algorithm, and this information was used to cluster the acquired data into multiple respiratory phases. The proposed approach was tested in 15 healthy volunteers (7 females). Cardiac function parameters, including the end-systolic volume (ESV), end-diastolic volume (EDV), stroke volume (SV), and ejection fraction (EF), were measured for the left and right ventricle in both end-expiration and end-inspiration. Although with the proposed 5D cardiac MRI, there were no significant differences (p > 0.05, t-test) between end-expiration and end-inspiration measurements of the cardiac function in volunteers, incremental respiratory motion parameters that were derived from 3D motion tracking, such as the depth, expiration and inspiration distribution, correlated (p

Myocardial infarction in the absence of obstructive coronary artery disease is found in ≈5% to 6% of all patients with acute infarction who are referred for coronary angiography. There are a variety of causes that can result in this clinical condition. As such, it is important that patients are appropriately diagnosed and an evaluation to uncover the correct cause is performed so that, when possible, specific therapies to treat the underlying cause can be prescribed. This statement provides a formal and updated definition for the broadly labelled term MINOCA (incorporating the definition of acute myocardial infarction from the newly released “Fourth Universal Definition of Myocardial Infarction”) and provides a clinically useful framework and algorithms for the diagnostic evaluation and management of patients with myocardial infarction in the absence of obstructive coronary artery disease.

Background: Chagas disease, resulting from the protozoan Trypanosoma cruzi , is an important cause of heart failure, stroke, arrhythmia, and sudden death. Traditionally regarded as a tropical disease found only in Central America and South America, Chagas disease now affects at least 300 000 residents of the United States and is growing in prevalence in other traditionally nonendemic areas. Healthcare providers and health systems outside of Latin America need to be equipped to recognize, diagnose, and treat Chagas disease and to prevent further disease transmission. Methods and Results: The American Heart Association and the Inter-American Society of Cardiology commissioned this statement to increase global awareness among providers who may encounter patients with Chagas disease outside of traditionally endemic environments. In this document, we summarize the most updated information on diagnosis, screening, and treatment of T cruzi infection, focusing primarily on its cardiovascular aspects. This document also provides quick reference tables, highlighting salient considerations for a patient with suspected or confirmed Chagas disease. Conclusions: This statement provides a broad summary of current knowledge and practice in the diagnosis and management of Chagas cardiomyopathy. It is our intent that this document will serve to increase the recognition of Chagas cardiomyopathy in low-prevalence areas and to improve care for patients with Chagas heart disease around the world.

Background— Infective endocarditis is a potentially lethal disease that has undergone major changes in both host and pathogen. The epidemiology of infective endocarditis has become more complex with today’s myriad healthcare-associated factors that predispose to infection. Moreover, changes in pathogen prevalence, in particular a more common staphylococcal origin, have affected outcomes, which have not improved despite medical and surgical advances. Methods and Results— This statement updates the 2005 iteration, both of which were developed by the American Heart Association under the auspices of the Committee on Rheumatic Fever, Endocarditis, and Kawasaki Disease, Council on Cardiovascular Disease of the Young. It includes an evidence-based system for diagnostic and treatment recommendations used by the American College of Cardiology and the American Heart Association for treatment recommendations. Conclusions— Infective endocarditis is a complex disease, and patients with this disease generally require management by a team of physicians and allied health providers with a variety of areas of expertise. The recommendations provided in this document are intended to assist in the management of this uncommon but potentially deadly infection. The clinical variability and complexity in infective endocarditis, however, dictate that these recommendations be used to support and not supplant decisions in individual patient management.

Highly prevalent and commonly associated with complications, bicuspid aortic valve (BAV) disease presents a more significant burden than any other congenital heart disease [(1)][1]. Although the individual course is variable, many patients eventually require surgical intervention to address valve

Division of Cardiology, San Francisco General Hospital, San Francisco, CA, USA Department of Medicine, University of California San Francisco, San Francisco, CA, USA Department of Epidemiology & Biostatistics, University of California San Francisco, San Francisco, CA, USA Centre for Chronic Disease Control & Public Health Foundation of India, New Delhi, India *Author for correspondence: kazi@ucsf.edu January2015January 2015

In October 2007, the American Heart Association published guidelines that recommended against the use of prophylactic use of antibiotics before oral surgery among patients at moderate risk of adverse outcomes from infective endocarditis (IE) [(1)][1]. Analyzing the Nationwide Inpatient Sample

Patients who demonstrate worsening of cardiac wall motion (WM) during hemodialysis have higher 1-year mortality. We sought to identify risk factors for dialysis-induced WM abnormalities. Additionally, we examined the effects of hemodialysis on other parameters of cardiac function. Forty patients underwent echocardiography directly before dialysis and during the last hour of dialysis (79 dialysis sessions). Candidate predictors for intradialytic worsening of WM included age, a history of heart failure (HF) or coronary artery disease, changes in blood pressure or heart rate, high sensitivity cardiac troponin T and N-terminal brain natriuretic peptide. Among 40 patients, WM worsened segmentally in eight patients (20%), worsened globally in one patient (3%), and improved segmentally in four patients (10%). Diastolic function worsened in 44% of patients, and left ventricular ejection fraction was largely unchanged during dialysis. The case of globally worsened WM occurred in the setting of intradialytic hypertension in a patient without HF. Surprisingly, history of coronary artery disease, hemodynamics, and serologic factors were not associated with worsened segmental WM during dialysis. After adjustment for history of coronary artery disease and other cardiac risk factors, patients with a history of HF had a threefold higher risk of worsening segmental WM during dialysis (RR 3.1, 95% CI [1.1, 9], p = 0.04). In conclusion, patients with a history of clinical HF were at higher risk of intradialytic worsening of segmental WM. Further studies are needed to determine the mechanism of this association and whether cardioprotective medications could ameliorate this adverse cardiac effect of hemodialysis.

Background The use of synthetic material for reconstructive vascular surgery was first reported during the early 1950s. Infection involving vascular graft prostheses is an infrequent but devastating complication of reconstructive vascular graft surgery and is associated with a high morbidity and, in some situations, mortality. Improvements in surgical techniques and graft design, including the use of native venous or arterial tissue, have reduced the frequency of infection and severity of complications from vascular graft infection (VGI). However, these advances have also led to more frequent vascular graft procedures occurring in a patient population with multiple underlying comorbidities that would have previously disqualified them as candidates for vascular reconstructive surgery. Underlying comorbidities, such as diabetes mellitus or immune compromise, increase the risk of infection and serious infection-related complications. The major complications of VGI include sepsis, amputation, disruption of infected anastomotic suture line with rupture or pseudoaneurysm formation, embolization of infected thrombi, reinfection of reconstructed vascular grafts, enteric fistulae to the small or large bowel, bacteremic spread of infection to other sites, and death. VGIs can be categorized broadly into those that occur in an extracavitary location, primarily in the groin or lower extremities, or in an intracavitary location, primarily within the abdomen or less commonly within the thorax. ### Frequency The frequency of VGI depends on the anatomic location of the graft. The infection rate is 1.5% to 2% for most extracavitary grafts and as high as 6% with vascular grafts in the groin.1–9 For intracavitary grafts, the infection rate is ≈1% to 5%.1–6 Graft infection is most common after emergency procedures and after reoperation.1–4,10 Aortic graft erosion or fistulous communication into the duodenum or other areas of the bowel reportedly occurs in 1% to 2% of patients after aortic reconstruction.11, …

Aims: 4D flow magnetic resonance imaging (MRI) allows quantitative assessment of left ventricular (LV) function according to characteristics of the dynamic flow in the chamber. Marked abnormalities in flow components volume and kinetic energy (KE) have previously been demonstrated in moderately dilated and depressed LVs compared to healthy subjects. We hypothesized that these 4D flow-based measures would detect even subtle LV dysfunction and remodeling. Methods and Results: We acquired 4D flow and morphological MRI data from 26 patients with chronic ischemic heart disease with New York Heart Association (NYHA) class I and II and with no to mild LV systolic dysfunction and remodeling, and from 10 healthy controls. A previously validated method was used to separate the LV end-diastolic volume (LVEDV) into functional components: direct flow, which passes directly to ejection, and non-ejecting flow, which remains in the LV for at least 1 cycle. The direct flow and non-ejecting flow proportions of end-diastolic volume and KE were assessed. The proportions of direct flow volume and KE fell with increasing LVEDV-index (LVEDVI) and LVESV-index (LVESVI) (direct flow volume r = -0.64 and r = -0.74, both Pamp;lt;0.001; direct flow KE r = -0.48, P = 0.013, and r = -0.56, P = 0.003). The proportions of non-ejecting flow volume and KE rose with increasing LVEDVI and LVESVI (non-ejecting flow volume: r = 0.67 and r = 0.76, both Pamp;lt;0.001; non-ejecting flow KE: r = 0.53, P = 0.005 and r = 0.52, P = 0.006). The proportion of direct flow volume correlated moderately to LVEF (r = 0.68, P amp;lt; 0.001) and was higher in a sub-group of patients with LVEDVI amp;gt; 74 ml/m(2) compared to patients with LVEDVI amp;lt; 74 ml/m(2) and controls (both Pamp;lt;0.05). Conclusion: Direct flow volume and KE proportions diminish with increased LV volumes, while non-ejecting flow proportions increase. A decrease in direct flow volume and KE at end-diastole proposes that alterations in these novel 4D flow-specific markers may detect LV dysfunction even in subtle or subclinical LV remodeling. Funding Agencies|Swedish Heart Lung foundation [20140398]; Swedish Research Council [2014-6191]; European Union FP7 [223615]; Medical Research Council of Southeast Sweden [FORSS-35141, FORSS-88731, FORSS-157921]; County Council of Ostergotland/Heart and Medicine Center [20090120]

A link between oral health and cardiovascular disease has been proposed for more than a century. Recently, concern about possible links between periodontal disease (PD) and atherosclerotic vascular disease (ASVD) has intensified and is driving an active field of investigation into possible association and causality. The 2 disorders share several common risk factors, including cigarette smoking, age, and diabetes mellitus. Patients and providers are increasingly presented with claims that PD treatment strategies offer ASVD protection; these claims are often endorsed by professional and industrial stakeholders. The focus of this review is to assess whether available data support an independent association between ASVD and PD and whether PD treatment might modify ASVD risks or outcomes. It also presents mechanistic details of both PD and ASVD relevant to this topic. The correlation of PD with ASVD outcomes and surrogate markers is discussed, as well as the correlation of response to PD therapy with ASVD event rates. Methodological issues that complicate studies of this association are outlined, with an emphasis on the terms and metrics that would be applicable in future studies. Observational studies to date support an association between PD and ASVD independent of known confounders. They do not, however, support a causative relationship. Although periodontal interventions result in a reduction in systemic inflammation and endothelial dysfunction in short-term studies, there is no evidence that they prevent ASVD or modify its outcomes.

Right ventricular (RV) function is a powerful prognostic indicator in many forms of heart disease, but its assessment remains challenging and inexact. RV dysfunction may alter the normal patterns of RV blood flow, but those patterns have been incompletely characterized. We hypothesized that, based on anatomic differences, the proportions and energetics of RV flow components would differ from those identified in the left ventricle (LV) and that the portion of the RV inflow passing directly to outflow ( Direct Flow) would be prepared for effective systolic ejection as a result of preserved kinetic energy (KE) compared with other RV flow components. Three-dimensional, time-resolved phase-contrast velocity, and balanced steady-state free-precession morphological data were acquired in 10 healthy subjects using MRI. A previously validated method was used to separate the RV and LV end-diastolic volumes into four flow components and measure their volume and KE over the cardiac cycle. The RV Direct Flow: 1) followed a smoothly curving route that did not extend into the apical region of the ventricle; 2) had a larger volume and possessed a larger presystolic KE (0.4 ± 0.3 mJ) than the other flow components ( P < 0.001 and P < 0.01, respectively); and 3) represented a larger part of the end-diastolic blood volume compared with the LV Direct Flow ( P < 0.01). These findings suggest that diastolic flow patterns distinct to the normal RV create favorable conditions for ensuing systolic ejection of the Direct Flow component. These flow-specific aspects of RV diastolic-systolic coupling provide novel perspectives on RV physiology and may add to the understanding of RV pathophysiology.

Background The purpose of this statement is to update the recommendations by the American Heart Association (AHA) for cardiovascular implantable electronic device (CIED) infections and their management, which were last published in 2003. Methods and Results The AHA commissioned this scientific statement to educate clinicians about CIED infections, provide explicit recommendations for the care of patients with suspected or established CIED infections and highlight areas of needed research. The recommendations in this statement reflect analyses of relevant literature, to include recent advances in our understanding of the epidemiology, risk factors, microbiology, management and prevention of CIED infections. Conclusion There are no scientific data to support the use of antimicrobial prophylaxis for dental or other invasive procedures. Clinical Implications The concerns about life-threatening drug reactions, the development of resistant strains of bacterial pathogens, medicolegal issues and cost to the health care system are, thus, avoided.

Heart failure is diverse in its manifestations and pathophysiology with changes in chamber size and volume, wall motion, valvular competence, intracardiac pressures, and electrical events. These are routinely measured with well-established methods. However, it is common to observe different degrees of compensation despite echocardiographically similar degrees of cardiac dysfunction. How can we explain this phenomenon? One persistent gap in our understanding of the failing heart is the global behavior of the intracardiac blood flow and its potential impact on pump efficiency and disease progression. The concepts that ventricular filling and ejection are separate events distinct in timing and location and that acceleration and ejection of the stroke volume are only events due to systolic myocardial contraction are familiar but likely oversimplified. It seems reasonable that rather than coming to a halt at end diastole, flowing blood would keep moving as filling transitions to ejection and that it would be efficient for blood in the end-diastolic left ventricle (LV) to already be moving toward the aortic valve for ejection. Until recently, there was a lack of measurement tools able to accurately resolve the complex in vivo 3D flow fields to investigate these and other flow-based questions. New tools that can measure 3D flow throughout the cardiac cycle noninvasively are becoming increasingly mature, and a more detailed perspective is emerging on the organization of intracardiac blood flow. It is now possible to investigate the routes, behaviors, and interactions of the blood transiting the ventricles in normal and failing hearts1–3 and to consider the possible impact of flow characteristics on the efficiency of ventricular function. A focus on the flow aspects of cardiac function allows us to address a new and complementary set of questions. How does the efficiency of flow through the heart change with chamber dimensions, shape, and wall properties, …

Despite improvements in cardiovascular implantable electronic device (CIED) design, application of timely infection control practices, and administration of antibiotic prophylaxis at the time of device placement, CIED infections continue to occur and can be life-threatening. This has prompted the study of all aspects of CIED infections. Recognizing the recent advances in our understanding of the epidemiology, risk factors, microbiology, management, and prevention of CIED infections, the American Heart Association commissioned this scientific statement to educate clinicians about CIED infections, provide explicit recommendations for the care of patients with suspected or established CIED infections, and highlight areas of needed research.

Background— Patients with HIV have increased risk for cardiovascular disease, but the underlying mechanisms remain unknown. The purpose of this study was to determine the prevalence of echocardiographic abnormalities among asymptomatic HIV-infected individuals compared with HIV-uninfected individuals. Methods/Results— We performed echocardiography in 196 HIV-infected adults and 52 controls. Left ventricular ejection fraction, left ventricular mass indexed to the body surface area, and diastolic function were assessed according to American Society of Echocardiography standards. Left ventricular mass index was higher in HIV-infected patients (77.2 g/m 2 in patients with HIV versus 66.5 g/m 2 in controls, P P =0.008). After adjustment for hypertension and race, HIV-infected participants had a mean 8 g/m 2 larger left ventricular mass index compared with controls ( P =0.001). Higher left ventricular mass index was independently associated with lower nadir CD4 T-cell count, suggesting that immunodeficiency may play a role in this process. After adjustment for age and traditional risk factors, patients with HIV had a 2.4 greater odds of having diastolic dysfunction as compared with controls ( P =0.019). Conclusions— HIV-infected patients had a higher prevalence of diastolic dysfunction and higher left ventricular mass index compared with controls. These differences were not readily explained by differences in traditional risk factors and were independently associated with HIV infection. These results suggest that contemporary asymptomatic patients with HIV manifest mild functional and morphological cardiac abnormalities, which are independently associated with HIV infection.

The diaphoretic patient with tearing chest or back pain is a dreaded clinical scenario which demands the very best of our diagnostic acumen and tools. Acute aortic syndromes1 comprise a spectrum of abnormalities, all of which have the potential for acute mortality and rapid progression. This group of disorders includes: These may all present with severe pain and be clinically indistinguishable, one from the other, before imaging. Any of them can be mistaken for acute coronary syndrome, an error which can lead to inappropriate anticoagulation and disastrous complications.2 With the advent of more detailed and frequent imaging of the aorta in the evaluation of patients presenting with chest pain, understanding the variable pathology, prognosis and treatment of aortic syndromes has become critical. The extent to which these diseases share aetiology, prognosis and response to surgical, medical or endovascular therapy is still being defined, just as the options for treatment continue to improve. Of the acute aortic syndromes, intramural haematoma (IMH) stands out as a lesion that can be very challenging to clearly separate from the other acute aortic syndromes, particularly aortic dissection or penetrating ulcer. The presence of an intramural collection of blood without identifiable intimal flap, tear or ulceration is the pathognomonic finding of this condition.3 Over the first 30 days after diagnosis, IMH can evolve into classic dissection, contained rupture or aneurysm, or reabsorb without further sequelae.4 Indeed, IMH may represent a phase in the evolution of these other highly morbid conditions; IMH is found in 10–15% of patients with suspected dissection.5 Reliable methods for defining the individual’s risk for complications and best therapy is a critical need, and continues to be the subject of intensive investigation. #### Acute aortic syndromes

Background The purpose of this statement is to update the recommendations by the American Heart Association (AHA) for the prevention of infective endocarditis, which were last published in 1997. Methods and Results A writing group appointed by the AHA for their expertise in prevention and treatment of infective endocarditis (IE) with liaison members representing the American Dental Association, the Infectious Diseases Society of America and the American Academy of Pediatrics. The writing group reviewed input from national and international experts on IE. The recommendations in this document reflect analyses of relevant literature regarding procedure-related bacteremia and IE; in vitro susceptibility data of the most common microorganisms, which cause IE; results of prophylactic studies in animal models of experimental endocarditis; and retrospective and prospective studies of prevention of IE. MEDLINE database searches from 1950 through 2006 were done for English language articles using the following search terms: endocarditis, infective endocarditis, prophylaxis, prevention, antibiotic, antimicrobial, pathogens, organisms, dental, gastrointestinal, genitourinary, streptococcus, enterococcus, staphylococcus, respiratory, dental surgery, pathogenesis, vaccine, immunization and bacteremia. The reference lists of the identified articles were also searched. The writing group also searched the AHA online library. The American College of Cardiology/AHA classification of recommendations and levels of evidence for practice guidelines were used. The article subsequently was reviewed by outside experts not affiliated with the writing group and by the AHA Science Advisory and Coordinating Committee. Conclusions The major changes in the updated recommendations include the following. (1) The committee concluded that only an extremely small number of cases of IE might be prevented by antibiotic prophylaxis for dental procedures even if such prophylactic therapy were 100 percent effective. (2) IE prophylaxis for dental procedures should be recommended only for patients with underlying cardiac conditions associated with the highest risk of adverse outcome from IE. (3) For patients with these underlying cardiac conditions, prophylaxis is recommended for all dental procedures that involve manipulation of gingival tissue or the periapical region of teeth or perforation of the oral mucosa. (4) Prophylaxis is not recommended based solely on an increased lifetime risk of acquisition of IE. (5) Administration of antibiotics solely to prevent endocarditis is not recommended for patients who undergo a genitourinary or gastrointestinal tract procedure. These changes are intended to define more clearly when IE prophylaxis is or is not recommended and to provide more uniform and consistent global recommendations.

Background. The purpose of this statement is to update the recommendations by the American Heart Association (AHA) for the prevention of infective endocarditis, which were last published in 1997. Methods and Results. A writing group appointed by the AHA for their expertise in prevention and treatment of infective endocarditis (IE) with liaison members representing the American Dental Association, the Infectious Diseases Society of America and the American Academy of Pediatrics. The writing group reviewed input from national and international experts on IE. The recommendations in this document reflect analyses of relevant literature regarding procedure-related bacteremia and IE; in vitro susceptibility data of the most common microorganisms, which cause IE; results of prophylactic studies in animal models of experimental endocarditis; and retrospective and prospective studies of prevention of IE. MEDLINE database searches from 1950 through 2006 were done for English language articles using the following search terms: endocarditis, infective endocarditis, prophylaxis, prevention, antibiotic, antimicrobial, pathogens, organisms, dental, gastrointestinal, genitourinary, streptococcus, enterococcus, staphylococcus, respiratory, dental surgery, pathogenesis, vaccine, immunization and bacteremia. The reference lists of the identified articles were also searched. The writing group also searched the AHA online library. The American College of Cardiology/AHA classification of recommendations and levels of evidence for practice guidelines were used. The article subsequently was reviewed by outside experts not affiliated with the writing group and by the AHA Science Advisory and Coordinating Committee. Conclusions. The major changes in the updated recommendations include the following. (1) The committee concluded that only an extremely small number of cases of IE might be prevented by antibiotic prophylaxis for dental procedures even if such prophylactic therapy were 100 percent effective. (2) IE prophylaxis for dental procedures should be recommended only for patients with underlying cardiac conditions associated with the highest risk of adverse outcome from IE. (3) For patients with these underlying cardiac conditions, prophylaxis is recommended for all dental procedures that involve manipulation of gingival tissue or the periapical region of teeth or perforation of the oral mucosa. (4) Prophylaxis is not recommended based solely on an increased lifetime risk of acquisition of IE. (5) Administration of antibiotics solely to prevent endocarditis is not recommended for patients who undergo a genitourinary or gastrointestinal tract procedure. These changes are intended to define more clearly when IE prophylaxis is or is not recommended and to provide more uniform and consistent global recommendations.

Pulsatile blood flow through the cavities of the heart and great vessels is time-varying and multidirectional. Access to all regions, phases and directions of cardiovascular flows has formerly been limited. Four-dimensional (4D) flow cardiovascular magnetic resonance (CMR) has enabled more comprehensive access to such flows, with typical spatial resolution of 1.5x1.5x1.5 - 3x3x3 mm(3), typical temporal resolution of 30-40 ms, and acquisition times in the order of 5 to 25 min. This consensus paper is the work of physicists, physicians and biomedical engineers, active in the development and implementation of 4D Flow CMR, who have repeatedly met to share experience and ideas. The paper aims to assist understanding of acquisition and analysis methods, and their potential clinical applications with a focus on the heart and greater vessels. We describe that 4D Flow CMR can be clinically advantageous because placement of a single acquisition volume is straightforward and enables flow through any plane across it to be calculated retrospectively and with good accuracy. We also specify research and development goals that have yet to be satisfactorily achieved. Derived flow parameters, generally needing further development or validation for clinical use, include measurements of wall shear stress, pressure difference, turbulent kinetic energy, and intracardiac flow components. The dependence of measurement accuracy on acquisition parameters is considered, as are the uses of different visualization strategies for appropriate representation of time-varying multidirectional flow fields. Finally, we offer suggestions for more consistent, user-friendly implementation of 4D Flow CMR acquisition and data handling with a view to multicenter studies and more widespread adoption of the approach in routine clinical investigations. Funding Agencies|Swedish Research Council; Medical Research Council of Southeast Sweden; Linkoping University; British Heart Foundation Centre of Research Excellence; Oxford NIHR Biomedical Research Centre; NIH [K25HL119608]; Swedish Heart and Lung Foundation; European Research Council [HEART4FLOW, 310612]; Radiological Society of North America (RSNA); NIHR Cardiovascular Biomedical Research Unit at the Royal Brompton and Harefield NHS Foundation Trust; Imperial College London; National Institutes of Health (NIH) National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) [R01 R01DK096169]; National Institute of Health (NIH) National Heart, Lung, and Blood Institute (NHLBI) [R01HL115828]

Background Adverse cardiac remodeling is a key component of the failing heart. Increased diastolic wall stress plays a pivotal role in the development and progression of adverse cardiac remodeling. The forces generated by the left ventricular (LV) myocardium initiate blood flow, while the moving blood itself also exerts a force on the ventricular wall and heart valves. Abnormal hemodynamic forces may contribute to increased diastolic wall stress. We calculated LV hemodynamic forces from the moving blood, and hypothesized that these forces are mostly directed along the “mitral valve (MV) to apex axis” in the healthy LV, while the distribution is altered in myopathic LVs.

Author(s): Lange, David C; Glidden, David; Secemsky, Eric A; Ordovas, Karen; Deeks, Steven G; Martin, Jeffrey N; Bolger, Ann F; Hsue, Priscilla Y | Abstract: BackgroundHIV infection increases cardiovascular risk. Coronary artery calcification (CAC) and mitral annular calcification (MAC) identify patients at risk for cardiovascular disease (CVD). The purpose of this study was to examine the association between MAC, CAC and mortality in HIV-infected individuals.Methods and resultsWe studied 152 asymptomatic HIV-infected individuals with transthoracic echocardiography (TTE) and computed tomography (CT). MAC was identified on TTE using standardized criteria. Presence of CAC, CAC score and CAC percentiles were determined using the modified Agatston criteria. Mortality data was obtained from the Social Security and National Death Indices (SSDI/NDI). The median age was 49 years; 87% were male. The median duration of HIV was 16 years; 84% took antiretroviral therapy; 64% had an undetectable viral load. CVD risk factors included hypertension (35%), smoking (62%) and dyslipidemia (35%). Twenty-five percent of individuals had MAC, and 42% had CAC. Over a median follow-up of 8 years, 11 subjects died. Subjects with CAC had significantly higher mortality compared to those with MAC only or no MAC. The Harrell's C-statistic of CAC was 0.66 and increased to 0.75 when MAC was added (p = 0.05). MAC, prior CVD, age and HIV viral load were independently associated with higher age- and gender-adjusted CAC percentiles in an adjusted model (p l 0.05 for all).ConclusionIn HIV patients, the presence of MAC, traditional risk factors and HIV viral load were independently associated with CAC. Presence of CAC and MAC may be useful in identifying HIV-infected individuals at higher risk for death.

Purpose: To assess the spatial heterogeneity of the four-dimensional (4D) relative pressure fields in the healthy human left ventricle (LV) and provide reference data for normal LV relative pressure. Methods: Twelve healthy subjects underwent a cardiac MRI examination where 4D flow and morphological data were acquired. The latter data were segmented and used to define the borders of the LV for computation of relative pressure fields using the pressure Poisson equation. The LV lumen was divided into 17 pie-shaped segments. Results: In the normal left ventricle, the relative pressure in the apical segments was significantly higher relative to the basal segments (P < 0.0005) along both the anteroseptal and inferolateral sides after the peaks of early (E-wave) and late (A-wave) diastolic filling. The basal anteroseptal segment showed significantly lower median pressure than the opposite basal inferolateral segment during both E-wave (P < 0.0005) and A-wave (P = 0.0024). Conclusion: Relative pressure in the left ventricle is heterogeneous. During diastole, the main pressure differences in the LV occur along the basal-apical axis. However, pressure differences were also found in the short axis direction and may reflect important aspects of atrioventricular coupling. Additionally, this study provides reference data on LV pressure dynamics for a group of healthy subjects. (C) 2014 Wiley Periodicals, Inc. Funding Agencies|Swedish Research Council [621-2011-5204]; Swedish Heart and Lung foundation [hlf 2010/273-31]; Emil and Vera Cornell Foundation; European Research Council [HEART4FLOW, 310612]

Infective endocarditis (IE) is a rare disease. Although its incidence and bacteriology have remained relatively stable in outpatient populations without injection drug use, health care-associated infections, particularly with staphylococcus, are becoming more common. Large-scale prospective clinical trials are unavailable to guide strategies for preventing IE, timing surgical intervention, and avoiding complications. We continue to rely on new data from smaller series and large observational databases to track these changes and improve care of patients. At the present time, there are several controversies regarding best practices in IE. In this review, we address the following questions: What is the future of recommendations for antibiotic prophylaxis against IE? How should we best use echocardiography in diagnosis, management and follow up of IE patients? What are the most appropriate antibiotic regimens for different patients in the face of shifting microbiology and demographics? Lastly, how should patients be selected for early surgery to avoid the complications of these infections?

Background— Despite advances in medical, surgical, and critical care interventions, infective endocarditis remains a disease that is associated with considerable morbidity and mortality. The continuing evolution of antimicrobial resistance among common pathogens that cause infective endocarditis creates additional therapeutic issues for physicians to manage in this potentially life-threatening illness. Methods and Results— This work represents the third iteration of an infective endocarditis “treatment” document developed by the American Heart Association under the auspices of the Committee on Rheumatic Fever, Endocarditis, and Kawasaki Disease, Council on Cardiovascular Disease of the Young. It updates recommendations for diagnosis, treatment, and management of complications of infective endocarditis. A multidisciplinary committee of experts drafted this document to assist physicians in the evolving care of patients with infective endocarditis in the new millennium. This extensive document is accompanied by an executive summary that covers the key points of the diagnosis, antimicrobial therapy, and management of infective endocarditis. For the first time, an evidence-based scoring system that is used by the American College of Cardiology and the American Heart Association was applied to treatment recommendations. Tables also have been included that provide input on the use of echocardiography during diagnosis and treatment of infective endocarditis, evaluation and treatment of culture-negative endocarditis, and short-term and long-term management of patients during and after completion of antimicrobial treatment. To assist physicians who care for children, pediatric dosing was added to each treatment regimen. Conclusions— The recommendations outlined in this update should assist physicians in all aspects of patient care in the diagnosis, medical and surgical treatment, and follow-up of infective endocarditis, as well as management of associated complications. Clinical variability and complexity in infective endocarditis, however, dictate that these guidelines be used to support and not supplant physician-directed decisions in individual patient management.

More than a century ago, Osler took numerous syndrome descriptions of cardiac valvular infection that were incomplete and confusing and categorized them into the cardiovascular infections known as infective endocarditis. Because he was both a clinician and a pathologist, he was able to provide a meaningful outline of this complex disease. Technical advances have allowed us to better subcategorize infective endocarditis on the basis of microbiological etiology. More recently, the syndromes of infective endocarditis and endarteritis have been expanded to include infections involving a variety of cardiovascular prostheses and devices that are used to replace or assist damaged or dysfunctional tissues (Table 1). Taken together, infections of these novel intracardiac, arterial, and venous devices are frequently seen in medical centers throughout the developed world. In response, the American Heart Association’s Committee on Rheumatic Fever, Endocarditis, and Kawasaki Disease wrote this review to assist and educate clinicians who care for an increasing number of patients with nonvalvular cardiovascular device–related infections. Because timely guidelines1,2 exist that address the prevention and management of intravascular catheter–related infections, these device-related infections are not discussed in the present Statement. View this table: TABLE 1. Nonvalvular Cardiovascular Device–Related Infections This review is divided into two broad sections. The first section examines general principles for the evaluation and management of infection that apply to all nonvalvular cardiovascular devices. Despite the marked variability in composition, structure, function, and frequency of infection among the various types of nonvalvular cardiovascular devices reviewed in this article, there are several areas of commonality for infection of these devices. These include clinical manifestations, microbiology, pathogenesis, diagnosis, treatment, and prevention. The second section addresses each device and describes unique clinical features of infection. Each device is placed into one of 3 categories—intracardiac, arterial, or venous—for discussion. ### Clinical Manifestations The specific signs and symptoms associated with an infection of a …

Background — Although single case reports have described acute aortic dissection in relation to cocaine use, this condition is not widely recognized, and the features of cocaine-related aortic dissection have not been defined. Methods and Results — We reviewed all available hospital charts from 1981 to 2001 with the ICD-9 diagnosis of aortic dissection. Among the 38 cases of acute aortic dissection, 14 (37%) were related to cocaine use. Crack cocaine was smoked in 13 cases and powder cocaine was snorted in 1 case. The mean interval between cocaine use and the onset of symptoms was 12 hours (range, 0 to 24). Patients with cocaine-related dissection were much younger and more likely to undergo surgery compared with patients with aortic dissection without cocaine use. Most in the cocaine group were black, with a history of untreated hypertension. However, the two groups did not differ in other respects, including dissection type. Conclusions — In an inner city population, acute aortic dissection in the setting of crack cocaine use is common, presumably as a consequence of abrupt, transient, severe hypertension and catecholamine release. This diagnosis should be considered in cocaine users with severe chest pain.

Introduction: Rheumatic heart disease (RHD) strikes young adults at their peak economic productivity. Defining the global economic burden of RHD may motivate investments in research and prevention, yet prior approaches considering only medical costs may have underestimated the cost of illness. Objectives: To estimate the clinical and economic burden of RHD in India and Uganda. Outcomes were disability-adjusted life years (DALYs), direct medical costs, and indirect costs due to disability and premature mortality (2012 USD). Methods: We used a discrete-state Markov model to simulate the natural history of RHD using country-, age-, and gender-specific estimates from the literature and census data. We estimated direct medical costs from WHO-CHOICE and Disease Control and Prevention 3 publications. We conservatively estimated indirect costs (lost earnings and imputed caregiver costs) from World Bank data using novel economic methods. Results: In 2012, RHD generated 6.1 million DALYs in India and cost USD 10.7 billion (Table 1), including 1.8 billion in direct medical costs and 8.9 billion in indirect costs. During the same period, RHD produced 216,000 DALYs in Uganda, and cost USD 414 million, and, as in India, indirect costs represented the majority (88%) of the cost of illness. In both countries, women accounted for the majority (71-80%) of the DALYs; in Uganda, women bore 75% of the total cost. In sensitivity analyses, higher progression rates for subclinical disease doubled direct costs and DALYs. Conclusion: RHD exacts an enormous toll on the populations of India and Uganda, and its economic burden may be grossly underestimated if indirect costs are not systematically included. Women bear a disproportionate clinical burden from pregnancy-related complications. These results suggest that effective prevention and screening of RHD may represent a sound public health investment, particularly if targeted at high-risk subgroups such as young women.

One in seven US households cannot reliably afford food. Food budgets are more frequently exhausted at the end of a month than at other points in time. We postulated that this monthly pattern influenced health outcomes, such as risk for hypoglycemia among people with diabetes. Using administrative data on inpatient admissions in California for 2000–08, we found that admissions for hypoglycemia were more common in the low-income than the high-income population (270 versus 210 admissions per 1,000,000). Risk for hypoglycemia admission increased 27 percent in the last week of the month compared to the first week in the low-income population, but we observed no similar temporal variation in the high-income population. These findings suggest that exhaustion of food budgets might be an important driver of health inequities. Policy solutions to improve stable access to nutrition in low-income populations and raise awareness of the health risks of food insecurity might be warranted.

Endocarditis is a rare and highly variable disease, with a dramatic mortality that has not improved significantly despite progress in diagnosis and treatment. Strategies for prevention and management have generally been based on relatively small, usually single-center, experiences or, in the case of prophylaxis guidelines, been extrapolated from animal models of disease. Randomized controlled studies are unavailable and seem unlikely to inform our practices any time soon. How can we hope to make better therapeutic choices and improve outcome in their absence? Article see p 1005 The International Collaboration on Endocarditis—Prospective Cohort Study registry is an international collaborative effort among 61 centers in 28 countries that has compiled data from 2760 patients with definite infective endocarditis diagnosed according to the modified Duke criteria.1 Observational data from these patients creates the opportunity to examine some of the critical questions in endocarditis management, including the question whether surgical intervention during the acute hospitalized phase of endocarditis will improve survival. Lalani and colleagues address this topic in this issue of Circulation. 2 Surgical timing is one of the hardest clinical issues in treating patients with endocarditis. The traditional indications for surgery include heart failure, paravalvular extension of infection, and recurrent embolization.3,4 These have been based on observational studies and have generally been borne out by patient outcomes. As anyone who cares for these patients well understands, however, the decision to commit to a surgical procedure that might possibly be avoided is quite difficult for the patient, the surgeon, and the referring physician. An understanding of the degree of probable benefit of surgery would be extremely useful, if the benefit could be assessed in a way that was highly tailored to the individual patient’s circumstances. Because patients …

Endocarditis is a potentially life-threatening disease. Although it is rare, endocarditis is a common concern in the differential diagnosis of many day-to-day clinical situations, because its many manifestations can mimic other systemic infections and inflammatory states. The annual incidence of endocarditis is increasing, with 20,000 to 30,000 new cases per year, particularly among newborn and elderly patients. The implications for these patients are serious and lifelong, despite advances in antimicrobial therapy and diagnostic and surgical techniques. A time- and cost-efficient strategy for the detection of endocarditis is critical for avoiding long-term sequelae and for prompt management of major systemic complications, including mycotic aneurysms, splenic abscess, and focal ischemia secondary to embolism. Echocardiography is the primary technique for the detection of vegetations and cardiac complications that result from endocardial infection. As imaging has improved, the role of echocardiography in the diagnosis and management of patients with endocarditis has become defined clearly. Formal diagnostic criteria for endocarditis 13 recently have been developed to underscore the importance of echocardiographic findings in establishing or ruling out the presence of endocarditis.

Ultrasound-Doppler assessment of diastolic function is subject to velocity errors caused by angle sensitivity and a fixed location of the sample volume. We used 3-dimensional phase contrast magnetic resonance imaging (MRI) to evaluate these errors in 10 patients with hypertension and in 10 healthy volunteers. The single (Doppler) and triple (MRI) component velocity was measured at early (E) and late (A) inflow along Doppler-like sample lines or 3-dimensional particle traces generated from the MRI data. Doppler measurements underestimated MRI velocities by 9.4% +/- 8.6%; the effect on the E/A ratio was larger and more variable. Measuring early and late diastolic inflows from a single line demonstrated the error caused by their 3-dimensional spatial offset. Both errors were minimized by calculating the E/A ratio from maximal E and A values without constraint to a single line. Alignment and spatial offset are important sources of error in Doppler diastolic parameters. Improved accuracy may be achieved with the use of maximal E and A velocities from wherever they occur in the left ventricle.

Background: Mitral annuloplasty is an important element of most mitral repairs, yet the effects of various types of annuloplasty rings on mitral annular dynamics are still debated. Recent studies suggest that flexible rings preserve physiologic mitral annular area change during the cardiac cycle, while rigid rings do not. Methods: To clarify the effects of mitral ring annuloplasty on mitral annular dynamic geometry, we sutured 8 radiopaque markers equidistantly around the mitral anulus in 3 groups of sheep (n = 7 each: no ring, Carpentier-Edwards semi-rigid Physio-Ring [Baxter Healthcare Corp, Edwards Division, Santa Ana, Calif], and Duran flexible ring [Medtronic, Inc, Minneapolis, Minn]). Ring sizes were selected according to anterior leaflet area and inter-trigonal distance (Physio-Ring 28 mm, n=7; Duran ring 31 mm, n=5, and 29 mm, n=2). After 8 ± 1 days of recovery, the sheep were sedated and studied by means of biplane videofluoroscopy. Mitral annular area was calculated from 3-dimensional marker coordinates without assuming circular or planar geometry. Results: In the no ring group, mitral annular area varied during the cardiac cycle by 11% ± 2% (mean ± SEM; maximum=7.6 ± 0.2, minimum=6.8 ± 0.2 cm 2 ; P ≤ .001). Mitral annular area was fixed in the Physio-Ring group (4.6 ± 0.1 cm 2 ) and, surprisingly, also static in the Duran ring group (4.8 ± 0.1 cm 2 ; P = .26 vs Physio-Ring). Furthermore, mitral annular 3-dimensional shape changed in the no-ring group during the cardiac cycle, but not in the Physio-Ring or Duran groups. Conclusions: Mitral annular area and shape did not change during the cardiac cycle after ring annuloplasty, regardless of ring type. Thus mitral annular area reduction, independent of intrinsic ring flexibility, is the chief mechanism responsible for the salutary effects of mitral ring annuloplasty. (J Thorac Cardiovasc Surg 1999;117:302-9)

Left ventricular (LV) wall stress is an important element in the assessment of LV systolic function; however, a reproducible technique to determine instantaneous local or regional wall stress has not been developed. Fourteen dogs underwent placement of twenty-six myocardial markers into the ventricle and septum. One week later, marker images were obtained using high-speed biplane videofluoroscopy under awake, sedated, atrially paced baseline conditions and after inotropic stimulation (calcium). With a model taking into account LV pressure, regional wall thickness, and meridional and circumferential regional radii of curvature, we computed average midwall stress for each of nine LV sites. Regional end-systolic and maximal LV wall stress were heterogeneous and dependent on latitude (increasing from apex to base, P < 0.001) and specific wall (anterior > lateral and posterior wall stresses; P = 0.002). Multivariate ANOVA demonstrated only a trend ( P = 0.056) toward increased LV stress after calcium infusion; subsequent univariate analysis isolated significant increases in end-systolic LV wall stress with increased inotropic state at all sites except the equatorial regions. The model used in this analysis incorporates local geometric factors and provides a reasonable estimate of regional LV wall stress compared with previous studies. LV wall stress is heterogeneous and dependent on the particular LV site of interest. Variation in wall stress may be caused by anatomic differences and/or extrinsic interactions between LV sites, i.e., influences of the papillary muscles and the interventricular septum.

To study the three-dimensional size, shape, and motion of the mitral leaflets and annulus, we surgically attached radiopaque markers to sites on the mitral annulus and leaflets in seven sheep. After 8 days of recovery, the animals were sedated, and three-dimensional marker positions were measured by computer analysis of biplane videofluorograms (60/s). We found that the oval mitral annulus became most elliptical in middiastole. Both leaflets began to descend into the left ventricle (LV) during the rapid fall of LV pressure (LVP), before leaflet edge separation. The anterior leaflet exhibited a compound curvature in systole and maintained this shape during opening. The central cusp of the posterior leaflet was curved slightly concave to the LV during opening. Markers at the border of the “rough zone” were separated by 10 mm during systole. We conclude that coaptation occurs very near the leaflet edges, that the annulus and leaflets move toward their open positions during the rapid fall of LVP, and that leaflet edge separation, the last event in the opening sequence, occurs near the time of minimum LVP.

Objective To update recommendations issued by the American Heart Association last published in 1990 for the prevention of bacterial endocarditis in individuals at risk for this disease. Participants An ad hoc writing group appointed by the American Heart Association for their expertise in endocarditis and treatment with liaison members representing the American Dental Association, the Infectious Diseases Society of America, the American Academy of Pediatrics, and the American Society for Gastrointestinal Endoscopy. Evidence The recommendations in this article reflect analyses of relevant literature regarding procedure-related endocarditis, in vitro susceptibility data of pathogens causing endocarditis, results of prophylactic studies in animal models of endocarditis, and retrospective analyses of human endocarditis cases in terms of antibiotic prophylaxis usage patterns and apparent prophylaxis failures. MEDLINE database searches from 1936 through 1996 were done using the root words endocarditis, bacteremia, and antibiotic prophylaxis. Recommendations in this document fall into evidence level III of the US Preventive Services Task Force categories of evidence. Consensus Process The recommendations were formulated by the writing group after specific therapeutic regimens were discussed. The consensus statement was subsequently reviewed by outside experts not affiliated with the writing group and by the Science Advisory and Coordinating Committee of the American Heart Association. These guidelines are meant to aid practitioners but are not intended as the standard of care or as a substitute for clinical judgment. Conclusions Major changes in the updated recommendations include the following: (1) emphasis that most cases of endocarditis are not attributable to an invasive procedure; (2) cardiac conditions are stratified into high-, moderate-, and negligible-risk categories based on potential outcome if endocarditis develops; (3) procedures that may cause bacteremia and for which prophylaxis is recommended are more clearly specified; (4) an algorithm was developed to more clearly define when prophylaxis is recommended for patients with mitral valve prolapse; (5) for oral or dental procedures the initial amoxicillin dose is reduced to 2 g, a follow-up antibiotic dose is no longer recommended, erythromycin is no longer recommended for penicillin-allergic individuals, but clindamycin and other alternatives are offered; and (6) for gastrointestinal or genitourinary procedures, the prophylactic regimens have been simplified. These changes were instituted to more clearly define when prophylaxis is or is not recommended, improve practitioner and patient compliance, reduce cost and potential gastrointestinal adverse effects, and approach more uniform worldwide recommendations.

Continuous-wave Doppler signal intensity is commonly expected to reflect the severity of mitral regurgitation. Physical principles predict that alignment of the imaging beam, flow velocity, and turbulence can also be important or even dominant determinants of continuous-wave Doppler signal intensity. The reliability of tracking regurgitant severity with continuous-wave Doppler signal intensity was assessed in vitro with varying volume, velocity, turbulence, and beam alignment. The conditions wherein continuous-wave Doppler signal intensity increased with regurgitant volume were specific but poorly predictable combinations of orifice size, flow volume, and perfect beam alignment. Under other conditions flow velocity and turbulence effects dominated, and continuous-wave Doppler signal intensity did not reflect changing regurgitant volume. Continuous-wave Doppler signal intensity-based impressions of regurgitant severity may be unreliable and even misleading under some circumstances.

Aims : Patients with mild heart failure (HF) who are clinically compensated may have normal left ventricular (LV) stroke volume (SV). Despite this, altered intra-ventricular flow patterns have been recognized in these subjects. We hypothesized that, compared with normal LVs, flow in myopathic LVs would demonstrate a smaller proportion of inflow volume passing directly to ejection and diminished the end-diastolic preservation of the inflow kinetic energy (KE). Methods and results : In 10 patients with dilated cardiomyopathy (DCM) (49 ± 14 years, six females) and 10 healthy subjects (44 ± 17 years, four females), four-dimensional MRI velocity and morphological data were acquired. A previously validated method was used to separate the LV end-diastolic volume (EDV) into four flow components based on the blood's locations at the beginning and end of the cardiac cycle. KE was calculated over the cardiac cycle for each component. The EDV was larger (P = 0.021) and the ejection fraction smaller (P < 0.001) in DCM compared with healthy subjects; the SV was equivalent (DCM: 77 ± 19, healthy: 79 ± 16 mL). The proportion of the total LV inflow that passed directly to ejection was smaller in DCM (P = 0.000), but the end-diastolic KE/mL of the direct flow was not different in the two groups (NS). Conclusion : Despite equivalent LVSVs, HF patients with mild LV remodelling demonstrate altered diastolic flow routes through the LV and impaired preservation of inflow KE at pre-systole compared with healthy subjects. These unique flow-specific changes in the flow route and energetics are detectable despite clinical compensation, and may prove useful as subclinical markers of LV dysfunction.

Background Blood flow within the cardiovascular system is driven by pressure differences, where blood accelerates from higher to lower pressure areas. Invasive methods of pressure measurement, which are commonly applied to assessment of diastolic function, may not capture the heterogeneity of regional intracardiac pressure differences. We utilized pressure fields based on time-resolved 3D CMR data to investigate the timing and distribution of intracardiac pressure gradients in the left heart throughout diastole.

Background Turbulent blood flow is a cause of energy loss in the cardiovascular system, and can thus be seen as a measure of flow inefficiency. Novel 4D flow CMR methods permit estimation of intracardiac turbulent kinetic energy (TKE). On the basis of the Reynolds number, one might expect that larger left ventricular (LV) size would promote higher TKE values, and thus lower flow efficiency. In this study, we hypothesized that the TKE of diastolic inflow would be larger in the dilated LVs of heart failure patients compared to normal LVs.