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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.

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.

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, …

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.

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— 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.

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 …

Human immunodeficiency virus (HIV)–infected individuals are living longer in the era of antiretroviral therapy. As a result, they are increasingly prone to the development of concomitant chronic disease. Coronary heart disease (CHD) is the leading cause of death in the United States and Europe. Recent studies suggest that CHD rates may be increasing among HIV-infected patients (see Epidemiological Evidence for Cardiovascular Disease in HIV-Infected Patients and Relationship to Highly Active Antiretroviral Therapy, Working Group 2), and thus appropriate screening strategies for CHD in this population are needed. Recently, approaches to screening and assessment of cardiovascular disease (CVD) in HIV-infected individuals were discussed at a State of the Science Conference. Although insufficient evidence now exists to recommend a screening strategy for CHD in HIV that differs from that recommended in the non-HIV population, emerging risk factors and surrogate markers for atherosclerosis unique to the HIV population suggest specific strategies that may be useful in this population. Two broad screening categories are discussed here. The first screening strategy seeks to define the pretest likelihood of disease by identifying the presence of predisposing risk factors such as hypertension, elevated serum cholesterol, cigarette smoking, and physical inactivity. The second screening strategy aims at the detection of established CHD, even in its earliest stages. The currently available recommendations and guidelines for screening for the presence of cardiovascular risk factors in the general, non–HIV-infected population are detailed in Table 1.1–7 View this table: Table 1. Recommendations and Guidelines for Screening for Cardiovascular Risk Factors in the General Population The currently available recommendations and guidelines for screening for the presence of CVD risk factors in persons with HIV infection are detailed in Table 2. These recommendations take into account the evidence for dyslipidemia, insulin resistance, and changes in body fat distribution that have been shown to occur …

Background—The purpose of this statement is to update the recommendations by the American Heart Association (AHA) for the prevention of infective endocarditis that were last published in 1997.Methods and Results—A writing group was appointed by the AHA for their expertise in prevention and treatment of infective endocarditis, 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 infective endocarditis. The recommendations in this document reflect analyses of relevant literature regarding procedure-related bacteremia and infective endocarditis, in vitro susceptibility data of the most common microorganisms that cause infective endocarditis, results of prophylactic studies in animal models of experimental endocarditis, and retrospective and prospective studies of prevention of infective endocarditis. MEDLINE database searches from 1950 to 2006 were done for English-language papers 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 papers were also searched. We 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 paper was subsequently 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 infective endocarditis might be prevented by antibiotic prophylaxis for dental procedures even if such prophylactic therapy were 100% effective. (2) Infective endocarditis prophylaxis for dental procedures is reasonable only for patients with underlying cardiac conditions associated with the highest risk of adverse outcome from infective endocarditis. (3) For patients with these underlying cardiac conditions, prophylaxis is reasonable 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 infective endocarditis. (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 infective endocarditis prophylaxis is or is not recommended and to provide more uniform and consistent global recommendations.

Background— The contribution of anterior mitral leaflet second-order (“strut”) chordae tendineae to left ventricular (LV) systolic mechanics is debated; we measured the in vivo contribution of anterior chordae tendineae (ACT) and posterior chordae tendineae (PCT) to regional and global LV contractile function. Methods and Results— Eight sheep had radiopaque markers implanted in the LV epicardium, partitioning the ventricle into 12 regions. Microminiature force transducers and snares were sutured to anterior leaflet “strut” chordae originating from ACT and PCT papillary muscles. Chordal tension, marker images, and hemodynamic data were acquired before and after (CUT) severing ACT and PCT. Fractional area shrinkage and slope of the regional end-diastolic area–regional stroke work relation (r-PRSW) were computed for each LV region. CUT did not affect global LV systolic function but reduced FAS in LV segments near the PCT insertion site: equatorial posterior lateral (19±2% versus 16±2%, P P P P P P P N , P Conclusions— Dividing anterior leaflet strut chordae in sheep was associated acutely with regional LV systolic dysfunction near the chordal insertion sites. Caution is necessary when embarking on procedures that cut second-order chordae to treat ischemic mitral regurgitation, since this may compromise LV systolic function in ventricles that are already impaired.

The number of adults who have survived with congenital heart disease is increasing rapidly. Although prevalence studies have not been performed, estimates of expected numbers of people reaching adulthood with congenital heart disease (CHD) can now be made because birth prevalence has been studied and mortality rates have begun to stabilize. Birth prevalence for all forms of congenital heart disease detected in the first year of life is estimated at 8.1 per thousand live births on the basis of data from the Centers for Disease Control1; estimates for disease of sufficient severity to result in a catheterization, surgery, or death in the first year of life are 2.3 per thousand, using population-based data derived from the Pediatric Cardiac Care Consortium.2 In 1990, the National Center for Health Statistics reported the number of US live births to be 4 158 212.3 Age-specific mortality data were obtained from the complete life table for the US population4 and from population-based death rates during hospital admission using data from 6 states in 1992. Estimates of numbers of individuals reaching adulthood born in 1990 with congenital heart disease of sufficient severity to be diagnosed or treated during the first year of life are shown in the Figure. Disregarding all patients born before 1990 and those not diagnosed in the first year and assuming stable mortality in early adulthood, by 2020, nearly 760 000 individuals will have CHD, with 200 000 in the more severe subgroup. Number of children born after 1990 with congenital heart disease estimated to reach adulthood. □ indicates diagnosed in the first year of life; ⋄, undergoing catheterization or surgery in the first year of life. This striking increase in the estimated number of patients with congenital heart disease who will require competent care within the …

Infective endocarditis (IE) is associated with substantial morbidity and mortality. Although it is relatively rare in children, its incidence may be increasing.1 This paper focuses on the features that are particularly relevant to infants and children, including important issues for the primary care physician. The epidemiology of heart disease in children has changed over the past 3 to 4 decades. With the increased survival rate of children with congenital heart disease (CHD) and the overall decrease in rheumatic valvular heart disease in developed countries, CHD now constitutes the predominant underlying condition for IE in children over the age of 2 years in these countries. The complexities of management of neonatal and pediatric intensive care unit patients have increased the risks of catheter-related IE. In addition, postoperative IE is a long-term risk following correction of complex CHD. The proper use of the diagnostic microbiology laboratory is critical in the diagnosis and management of children with IE. Moreover, newer diagnostic guidelines have improved sensitivity for making the diagnosis of clinically definite IE. In addition, advances in noninvasive techniques such as two-dimensional (2D) echocardiography have enhanced our ability to diagnose IE. Newer antibiotics have become available that can be used in children with IE, and home intravenous (IV) therapy has become an acceptable approach for stable patients who are at low risk for embolization. Additionally, approaches to the prevention of endocarditis have been recently modified and are reviewed in this paper. IE occurs less commonly in children than in adults and accounts for approximately 1 in 1280 pediatric admissions per year.2 Although the reported hospitalization rates for IE vary considerably among published series, the frequency of endocarditis among children appears to have increased in recent years.3 This is due in part to improved survival among children who are at risk … Address correspondence to Kathryn A. Taubert, PhD, Vice President, Department of Science and Medicine, American Heart Association, 7272 Greenville Ave, Dallas, TX 75231. E-mail: ktaubert{at}heart.org

Background —Recently, renewed interest in allograft and stentless “freehand” bileaflet xenograft mitral valve replacement has arisen. The variability of human papillary tip anatomy and scarcity of donors limit allograft availability, making xenograft mitral valves an attractive alternative; however, these valves require new surgical implantation techniques, and assessment of their hemodynamics and functional geometry is lacking. Methods —Seven sheep underwent implantation of a new stentless, glutaraldehyde-preserved porcine mitral valve (Physiological Mitral Valve [PMV], Medtronic) and were studied acutely under open-chest conditions. A new method of retrograde cardioplegia was developed. Hemodynamic valve function was assessed by epicardial Doppler echocardiography. 3D motion of miniature radiopaque markers sutured to the valve leaflets, annulus, and papillary tips was measured. Six other sheep with implanted markers served as controls. Results —Both papillary muscle tips avulsed in the first animal, leaving 6 other animals. Mitral regurgitation was not observed in any xenograft valve. The peak and mean transvalvular gradients were 4.6±1.8 mm Hg and 2.6±1.5 mm Hg, respectively. The average mitral valve area was 5.7±1.6 cm 2 . Valve closure in the xenograft group occurred later (30±11 ms, P P P P P Conclusions —Successful freehand stentless porcine mitral valve implantation is feasible in sheep and was associated with excellent early postoperative hemodynamics. Physiological mitral valve annular contraction and functional leaflet closure mechanics were preserved. Long-term valve durability, calcification, and hemodynamic performance remain to be determined in models.

Background —Current surgical methods for treating aortic valve and aortic root pathology vary widely, and the basis for selecting one repair or replacement alternative over another continues to evolve. More precise knowledge of the interaction between normal aortic root dynamics and aortic valve mechanics may clarify the implications of various surgical procedures on long-term valve function and durability. Methods and Results —To investigate the role of aortic root dynamics on valve function, we studied the deformation modes of the left, right, and noncoronary aortic root regions during isovolumic contraction, ejection, isovolumic relaxation, and diastole. Radiopaque markers were implanted at the top of the 3 commissures (sinotubular ridge) and at the annular base of the 3 sinuses in 6 adult sheep. After a 1-week recovery, ECG and left ventricular and aortic pressures were recorded in conscious, sedated animals, and the 3D marker coordinates were computed from biplane videofluorograms (60 Hz). Left ventricular preload, contractility, and afterload were independently manipulated to assess the effects of changing hemodynamics on aortic root 3D dynamic deformation. The ovine aortic root undergoes complex, asymmetric deformations during the various phases of the cardiac cycle, including aortoventricular and sinotubular junction strain and aortic root elongation, compression, shear, and torsional deformation. These deformations were not homogeneous among the left, right, and noncoronary regions. Furthermore, changes in left ventricular volume, pressure, and contractility affected the degree of deformation in a nonuniform manner in the 3 regions studied, and these effects varied during isovolumic contraction, ejection, isovolumic relaxation, and diastole. Conclusions —These complex 3D aortic root deformations probably minimize aortic cusp stresses by creating optimal cusp loading conditions and minimizing transvalvular turbulence. Aortic valve repair techniques or methods of replacement using unstented autograft, allograft, or xenograft tissue valves that best preserve this normal pattern of aortic root dynamics should translate into a lower risk of long-term cusp deterioration.

Background —Asymmetrical mitral annular (MA) dilatation and papillary muscle dislocation are implicated in the pathogenesis of functional mitral regurgitation (MR). Methods and Results —To determine the mechanism by which annular and papillary muscle geometric alterations result in MR, we implanted radiopaque markers in the left ventricle, mitral annulus, anterior and posterior mitral leaflets, and papillary muscle tips and bases in 2 groups of sheep. One group served as controls (CTL, n=7); an experimental group (EXP, n=9) underwent topical phenol application to obliterate anterior annular and leaflet muscle (confirmed histologically ex vivo). After 1 week of recovery, markers were imaged with biplane videofluoroscopy, and hemodynamic data were recorded. MA area (computed from 3-dimensional marker coordinates) was 11% to 13% larger in the EXP group than in the CTL group ( P 1 cm) increases in both the intercommissural and septolateral annular axes. The anterior papillary muscle tip in EXP was displaced from CTL by 2.9±0.23 mm toward the anterolateral left ventricle and 2.5±0.12 mm toward the mitral annulus at end systole; the posterior papillary muscle geometry was unchanged. Transthoracic echocardiography revealed MR only in the heart exhibiting biaxial annular enlargement. Conclusions —MA dilatation in the intercommissural dimension with anterior papillary muscle tip displacement toward the annulus is insufficient to produce MR in sheep. Functional MR may require MA dilatation in the septolateral axis, as observed with proximal circumflex coronary occlusion.

Infective endocarditis (IE) carries a high risk of morbidity and mortality. Rapid diagnosis, effective treatment, and prompt recognition of complications are essential to good patient outcome. Therapy of IE caused by the more commonly encountered organisms, including streptococci, enterococci, staphylococci, and the HACEK organisms ( Hemophilus parainfluenzae, Hemophilus aphrophilus, Actinobacillus [Hemophilus] actinomycetemcomitans, Cardiobacterium hominis, Eikenella species , and Kingella species), has been addressed previously by this committee.1 Likewise, the antimicrobial prevention of endocarditis has also been previously addressed.2 In this article, we review and update the current literature with respect to diagnostic challenges and strategies, difficult therapeutic situations, and management choices in patients with IE. This article focuses predominantly on adults with IE. A separate article, currently in preparation, will address the issues of IE in childhood. ### Clinical Criteria The diagnosis of IE is straightforward in those patients with classic oslerian manifestations: bacteremia or fungemia, evidence of active valvulitis, peripheral emboli, and immunologic vascular phenomena. In other patients, however, the classic peripheral stigmata may be few or absent.3 This may occur during acute courses of IE, particularly among intravenous drug abuse (IVDA) patients in whom IE is often due to Staphylococcus aureus infection of right-sided heart valves, or in patients with IE caused by microorganisms such as HACEK. Acute IE evolves too quickly for the development of immunologic vascular phenomena, which are more characteristic of subacute IE. In addition, acute right-sided IE valve lesions do not create the peripheral emboli and immunologic vascular phenomena that can result from left-sided valvular involvement.3 The variability in the clinical presentation of IE requires a diagnostic strategy that will be both sensitive for disease detection and specific for its exclusion across all the forms of the disease. In 1981, von Reyn et al4 proposed a scheme for strict case definitions of IE …

Background Left ventricular (LV) unloading with mechanical support devices alters biventricular geometry and impairs right ventricular (RV) contractility, but its effect on septal systolic function remains unknown. Methods and Results To evaluate the effects of LV volume and pressure unloading on septal geometry and function, LV preload was abruptly reduced by clamping left atrial pressure between 0 and −2 mm Hg in seven open-chest, anesthetized dogs by use of a pressure-control servomechanism to withdraw blood from the left atrium. With left atrial pressure clamping, maximal LV pressure decreased 30±12% (mean±SD) ( P P P P P P P P Conclusions LV unloading not only altered interventricular septal geometry but also reduced septal systolic thickening and output, all of which may contribute to impaired RV contractility during mechanical LV support.

To determine the value of transesophageal ultrasound in the assessment of cardiac valve prostheses, 14 patients with clinically suspected mitral prosthesis malfunction were studied by transthoracic and transesophageal two-dimensional imaging as well as by color Doppler flow velocity mapping (color Doppler). Patients underwent left ventricular angiography (n = 13), surgery (n = 11), or both angiography and surgery (n = 10). Nine patients had only mitral valve replacement, four patients had both mitral and aortic valve replacement, and one patient had mitral, aortic, and tricuspid valve replacement. There were 16 biological and four mechanical prostheses. The degree of mitral regurgitation was graded by both transthoracic and transesophageal color Doppler according to the area of the regurgitant jet visualized and was compared with a three-point classification of mitral regurgitation by left ventricular angiography judged by observers blinded to the echocardiographic results. All transesophageal studies were performed without complication and were well tolerated. The pathological morphology of the mitral prosthesis was additionally or more clearly visualized by transesophageal two-dimensional imaging and subsequently proven at surgery in three patients with flail leaflets and one patient with a vegetation compared with images obtained by the transthoracic approach. Valvular regurgitation was graded by the transthoracic approach as absent in four patients, mild in two patients, moderate in five patients, and severe in only three patients. The transesophageal assessment showed absence of mitral regurgitation in two patients, moderate regurgitation in two patients, and severe regurgitation in 10 patients.(ABSTRACT TRUNCATED AT 250 WORDS)