BACKGROUND Obesity is a well-established risk factor for heart failure (HF). However, implications of pericardial fat on incident HF is unclear. OBJECTIVES This study sought to examine the association between pericardial fat volume (PFV) and newly diagnosed HF. METHODS This study ascertained PFV using cardiac computed tomography in 6,785 participants (3,584 women and 3,201 men) without pre-existing cardiovascular disease from the MESA (Multi-Ethnic Study of Atherosclerosis). Cox proportional hazards regression was used to evaluate PFV as continuous and dichotomous variable, maximizing the J-statistic: (Sensitivity + Specificity - 1). RESULTS In 90,686 person-years (median: 15.7 years; interquartile range: 11.7 to 16.5 years), 385 participants (5.7%; 164 women and 221 men) developed newly diagnosed HF. PFV was lower in women than in men (69 +/- 33 cm(3) vs. 92 +/- 47 cm(3); p < 0.001). In multivariable analyses, every 1-SD (42 cm(3)) increase in PFV was associated with a higher risk of HF in women (hazard ratio [HR]: 1.44; 95% confidence interval [CI]: 1.21 to 1.71; p < 0.001) than in men (HR: 1.13; 95% CI: 1.01 to 1.27; p = 0.03) (interaction p = 0.01). High PFV (>= 70 cm(3) in women; >= 120 cm(3) in men) conferred a 2-fold greater risk of HF in women (HR: 2.06; 95% CI: 1.48 to 2.87; p < 0.001) and a 53% higher risk in men (HR: 1.53; 95% CI: 1.13 to 2.07; p = 0.006). In sex-stratified analyses, greater risk of HF remained robust with additional adjustment for anthropometric indicators of obesity (p <= 0.008), abdominal subcutaneous or visceral fat (p <= 0.03) or biomarkers of inflammation and hemodynamic stress (p < 0.001) and was similar among Whites, Blacks, Hispanics, and Chinese (interaction p = 0.24). Elevated PFV predominantly augmented the risk of HF with preserved ejection fraction (p < 0.001) rather than reduced ejection fraction (p = 0.31). CONCLUSIONS In this large, community-based, ethnically diverse, prospective cohort study, pericardial fat was associated with an increased risk of HF, particularly HF with preserved ejection fraction, in women and men. (C) 2021 the American College of Cardiology Foundation. Published by Elsevier. All rights reserved.

Evidence linking cocaine to the risk of pulmonary hypertension (PH) is limited and inconsistent. We examined whether cocaine use, in the absence of other known causes of PH, was associated with elevated systolic pulmonary artery pressure (sPAP) and increased probability of PH. We compared patients with documented cocaine use to a randomly selected age, sex, and race-matched control group without history of cocaine use. All participants had no known causes of PH and underwent echocardiography for noninvasive estimation of sPAP. We used routinely reported echocardiographic parameters and contemporary guidelines to grade the probability of PH. In 88 patients with documented cocaine use (mean age +/- standard deviation 51.7 +/- 9.5 years), 33% were women and 89% were of Black race. The commonest route of cocaine use was smoking (74%). Cocaine users compared with the control group had significantly higher sPAP (mean +/- standard deviation, 30.1 +/- 13.1 vs 22.0 +/- 9.8 mm Hg, p <0.001) and greater likelihood of PH (25% vs 10%, p = 0.012). In multivariable analyses adjusted for potential confounders including left ventricular diastolic dysfunction, cocaine use conferred a fivefold greater odds of echo cardiographic PH (p = 0.006). Additionally, a stepwise increase in the likelihood of PH was noted across cocaine users with negative or no drug screen on the day of echocardiography to cocaine users with a positive drug screen (multivariable p for trend = 0.008). In conclusion, cocaine use was associated with a higher sPAP and an increased likelihood of echocardiographic PH with a probable acute-on-chronic effect. Published by Elsevier Inc.

BACKGROUND:Heart failure (HF) is a major global health problem. Clinical trials test efficacy, effectiveness, and safety of novel and emerging therapies in HF. We sought to determine the salient features of ongoing interventional clinical trials in HF.METHODS AND RESULTS:We accessed the ClinicalTrials.gov registry of the National Institutes of Health (NIH) and the International Clinical Trials Registry Platform of the World Health Organization on January 1, 2017, and extracted pertinent information on current HF clinical trials for systematic review. Of 794 HF trials that met our inclusion criteria, almost one-half (49.1%) evaluated clinical end points and one-third (32.8%) examined imaging end points as primary outcomes. One-fourth (24.8%) were industry sponsored and one-third (35.6%) were university sponsored. The NIH and other United States federal agencies funded only 14 trials (1.8% of all trials; 10.7% of trials in the US). Among 536 HF trials with specified left ventricular ejection fraction status, 434 (81.0%) focused on HF with reduced ejection fraction (HFrEF) and only 102 (19.0%) trials targeted HF with preserved ejection fraction (HFpEF).CONCLUSIONS:Ongoing HF trials are predominantly sponsored by nongovernmental funding agencies. Although HFpEF occurs as commonly as HFrEF in the community, the number of clinical trials targeting HFpEF is substantially lower compared with HFrEF.

•Janeway lesions and Osler's nodes were clinical clues for the diagnosis of endocarditis.•The Chiari network, a benign right atrial structure, served as a nidus of infection.•Chiari network endocarditis occurred without tricuspid valve involvement.•Bilateral endocarditis was associated with both pulmonary and systemic emboli.•Large Chiari network vegetation resolved with antibiotic therapy alone (no surgery).

(p for interaction < 0.0001). 3 Lower BMI was associated with a greater risk of cardiovascular death and noncardiovascular death. Baseline BMI did not influence the risk of hospitalization for worsening heart failure or due to all causes.

Introduction: Heart failure (HF) is a global health problem. We sought to examine the focus of ongoing clinical trials in HF and compare ongoing trials with population prevalence of HF with preserv...

In the latter half of the 20th century, among participants of the Framingham Heart Study, incidence of heart failure (HF) has declined by about a third in women but not in men and survival after the onset of HF has improved in both sexes; however, HF remains highly lethal with over 50 % dying within 5 years after onset of HF. Overall, the 8-year relative risk of HF is 24 % lower in women compared with men. The 8-year incidence rates of HF with preserved ejection fraction (HFPEF; EF >45 %) and HF with reduced EF (HFREF; EF ≤45 %) in women and HFPEF in men are similar; however, men have a 2-fold higher cumulative incidence of HFREF than HFPEF. The lifetime risk of HF is about 20 % in both women and men at 40, 50, 60, 70, and 80 years of age. Contribution of hypertension and diabetes mellitus to the risk of HF was more prominent in women than in men. Serum levels of several biomarkers were distinctly different in women compared with men and had differential effects on left ventricular structure and function; however, the strength and direction of the association between biomarkers levels and HF risk were generally similar in women and men. In individuals with HF, about two-thirds of the underlying cause of death and about one-half of the immediate cause of death were due to cardiovascular causes. Non-cardiovascular underlying and immediate causes of death were more evident in HFPEF.

OBJECTIVE:To investigate secular trends in echocardiographically determined left ventricular mass (LVM). DESIGN, SETTING AND PARTICIPANTS:Longitudinal community-based cohort study in Framingham, Massachussetts. LVM was calculated from routine echocardiography in 4320 participants (52% women) of the Framingham offspring cohort at examination cycles 4 (1987-1991), 5 (1991-1995), 6 (1995-1998) and 8 (2005-2008), totalling 13 971 person-observations. MAIN OUTCOME MEASURES:Sex-specific trends in mean LVM (and its components, LV diastolic diameter (LVDD) and LV wall thickness (LVWT)), and LVM indexed to body surface area (BSA). RESULTS:In men, age-adjusted LVM modestly increased from examination 4 to 8 (192 g to 198 g, p-trend=0.0005), whereas, in women it decreased from 147 g at examination 4 to 140 g at examination 8 (p-trend<0.0001). The trend for increasing LVM in men tracked with an increasing LVDD (p-trend=0.0002), whereas the decline in LVM in women was accompanied by a decrease in LVWT (p-trend<0.0001). Indexing LVM to BSA abolished the increasing trend in men (p-trend=0.49), whereas, the decreasing trend in women was maintained. CONCLUSIONS:In our longitudinal analysis of a large community-based sample spanning two decades, we observed sex-related differences in trends in LVM, with a modest increase of LVM in men (likely attributable to increasing body size), but a decrease in women. Additional studies are warranted to elucidate the basis for these sex-related differences.

Patients with type 2 diabetes mellitus are at increased risk for cardiovascular disease (CVD) and mortality. Beyond traditional CVD risk factors, novel measures reflecting additional aspects of disease pathophysiology, such as biventricular volume (BiVV), may be useful for risk stratification. The aim of this study was to examine the relationship between BiVV and risk for mortality in European Americans with type 2 diabetes mellitus from the Diabetes Heart Study (DHS). BiVV was calculated from 771 noncontrast computed tomographic scans performed to image coronary artery calcified plaque. Relationships between BiVV and traditional CVD risk factors were examined. Cox proportional-hazards regression was performed to determine risk for mortality (all-cause and CVD mortality) associated with increasing BiVV. Area under the curve analysis was used to assess BiVV utility in risk prediction models. During 8.4 +/- 2.4 years of follow-up, 23% of the patients died. In unadjusted analyses, BiVV was significantly associated with increasing body mass index, height, coronary artery calcified plaque, history of hypertension, and previous myocardial infarction (p <0.0001 to 0.012). BiVV was significantly associated with all-cause (hazard ratio 2.45, 95% confidence interval 1.06 to 5.67, p = 0.036) and CVD (hazard ratio 4.36, 95% confidence interval 1.36 to 14.03, p = 0.014) mortality in models adjusted for other known CVD risk factors. Area under the curve increased from 0.76 to 0.78 (p = 0.04) and from 0.74 to 0.77 (p = 0.02) for all-cause and CVD mortality with the inclusion of BiVV. In conclusion, in the absence of echocardiography or other noninvasive imaging modalities to assess ventricular volumes, or when such methods are contraindicated, BiVV from computed tomography may be considered a tool for the stratification of high-risk patients, such as those with type 2 diabetes mellitus. (C) 2013 Elsevier Inc. All rights reserved. (Am J Cardiol 2013;111:1152-1158)

Background The relations between subclinical atherosclerosis and inflammatory biomarkers have generated intense interest but their significance remains unclear. We sought to determine the association between a panel of biomarkers and subclinical aortic atherosclerosis in a community‐based cohort. Methods and Results We evaluated 1547 participants of the Framingham Heart Study Offspring cohort who attended the 7th examination cycle and underwent both cardiovascular magnetic resonance imaging ( CMR ) and assays for 10 biomarkers associated with atherosclerosis: high‐sensitivity C‐reactive protein, fibrinogen, intercellular adhesion molecule‐1, interleukin‐6, interleukin‐18, lipoprotein‐associated phospholipase‐A2 activity and mass, monocyte chemoattractant protein‐1, P‐selectin, and tumor necrosis factor receptor‐2. In logistic regression analysis, we found no significant association between the biomarker panel and the presence of aortic plaque (global P =0.53). Using Tobit regression with aortic plaque as a continuous variable, we noted a modest association between biomarker panel and aortic plaque volume in age‐ and sex‐adjusted analyses ( P =0.003). However, this association was attenuated after further adjustment for clinical covariates ( P =0.09). Conclusions In our community‐based cohort, we found no significant association between our multibiomarker panel and aortic plaque. Our results underscore the strengths and limitations of the use of biomarkers for the identification of subclinical atherosclerosis and the importance of traditional risk factors.

An active 60-year-old man presented with a 3-month history of palpitations and a sudden discomfort in the right foot with subsequent coolness and numbness of the right toes. The patient was in atrial flutter with a ventricular rate of 136 beats/min. An echocardiogram showed moderate to severe left ventricular (LV) systolic dysfunction with an ejection fraction of 30%. A spherical echo density measuring 2.2 cm was noted in the LV apex. This mass was suggestive of an LV thrombus. The patient was admitted to the hospital for anticoagulation using warfarin, enoxaparin, and aspirin. A cardiothoracic surgical consult was obtained to discuss the option of surgical removal of the thrombus or a course of anticoagulants, and a cardiovascular magnetic resonance imaging study was requested for tissue characterization of the mass. The cardiovascular magnetic resonance examination was started at 1:43 pm. Routine cine …

Meeting abs tracts - A single PDF containing all abstracts in this Supplement is available

Background Myocardial rupture is a relatively rare and usually fatal complication of myocardial infarction (MI). Early recognition of patients at greatest risk of myocardial rupture provides an opportunity for early intervention.Methods VALIANT was a double-blind, randomized, controlled trial comparing valsartan, captopril, and their combination in high-risk patients post-MI. Myocardial rupture was identified by autopsy (available in 138/589 patients dying within 30 days of index MI), echocardiography, direct surgical visualization, or presence of hemopericardium. An independent clinical end points committee reviewed medical records for all deaths or suspected nonfatal cardiovascular events.Results Rupture was identified in 45 (0.31%) patients enrolled in VALIANT, occurring 9.8 +/- 6.0 days after the qualifying MI. Rupture accounted for 7.6% (45/589) of all deaths occurring in the first 30 days of follow-up and 24% (33/138) of deaths in which autopsies were obtained. Compared with survivors, rupture was associated with increased age, hypertension, increased Killip class, lower estimated glomerular filtration rate, and Q wave MI, and inversely related to beta-blocker and diuretic use. Compared with patients who died of other causes within 30 days, patients with myocardial rupture were more likely to have had an inferior MI, Q wave MI, or hypertension; to have used oral anticoagulants; or to have received thrombolytic therapy.Conclusions Although rare, myocardial rupture accounted for nearly one fourth of all deaths within the first 30 days after high-risk MI, suggesting an estimated incidence of approximately 1% within the first 30 days. A number of clinical characteristics may identify post-MI patients at higher risk of myocardial rupture. (Am Heart J 2010; 160: 145-51.)

OBJECTIVE:The study objective was to describe the echocardiographic characteristics and investigate the clinical correlates and prognostic significance of left ventricular false tendons (LVFTs). Although LVFTs are generally considered as anatomic variants, they have been associated with innocent precordial murmurs and electrocardiographic abnormalities in small case series. The correlates of LVFTs in the community are unknown. METHODS:We compared 101 Framingham Study participants with LVFTs (mean age 56 years, 45% were women) on routine two-dimensional echocardiograms with 151 referents without LVFTs (mean age 57 years, 44% were women). We examined the cross-sectional clinical, electrocardiographic (rest and ambulatory), and echocardiographic correlates of LVFTs using logistic regression models and evaluated the prospective association between LVFTs and all-cause mortality using Cox proportional hazards regression models. RESULTS:A total of 107 LVFTs (94 simple with 2 points of attachment and 13 complex/branching type with 3 or more points of attachment) were identified in 101 participants. LVFTs were most commonly visualized in the apical 4-chamber view (81%) and predominantly localized to the apical third of the left ventricular cavity (78%). LVFTs were associated with the presence of innocent precordial murmurs (multivariable adjusted odds ratio [OR] 5.55, 95% confidence interval [CI], 1.40-21.94) and electrocardiographic left ventricular hypertrophy (OR 4.43; 95% CI, 1.08-18.25). Body mass index was inversely related to the presence of LVFTs (per kilogram/meters squared increment; OR 0.94; 95% CI, 0.88-0.99). LVFTs were not associated with QRS axis deviation, ventricular premature beats, or repolarization abnormalities (all P values > .20). During a mean (+/- standard deviation) follow-up of 7.7 (+/-1.6) years, 15 participants with LVFTs and 19 participants without LVFTs died. In multivariable analyses, the presence of LVFTs was not associated with the risk of death (P = .92). CONCLUSION:In our community-based sample of middle-aged to elderly white women and men, LVFTs were more likely to be identified in individuals with lower body mass index and cross-sectionally associated with the presence of innocent precordial murmurs and electrocardiographic left ventricular hypertrophy, but they were not associated with the risk of mortality.

BACKGROUND:It is understood that coronary heart disease (CHD) is one cause of heart failure, and many risk factors are common to both entities. Hypercholesterolemia, however, being a well-recognized risk factor for CHD, has an unclear association with incident heart failure. METHODS:We evaluated the relations of total and high-density lipoprotein (HDL) cholesterol to incident heart failure and CHD in 10,813 US male physicians (mean age, 68 years). Total and HDL cholesterol were analyzed both as continuous and as categorical (in quartiles) variables. RESULTS:There were 222 incident heart failure cases on follow-up (mean, 6 years). In Cox models, after adjusting for traditional coronary risk factors, 1-SD increase in total cholesterol (36.7 mg/dL) and HDL cholesterol (15.3 mg/dL) was not related to incident heart failure with a hazard ratio and 95% CI of 0.91 (0.79-1.05) for total cholesterol and 0.95 (0.82-1.11) for HDL cholesterol. In categorical models, heart failure risk in second, third, and fourth quartiles of total and HDL cholesterol was statistically not different from those in the lowest quartile; hazard ratios with 95% CI were 0.72 (0.49-1.05), 0.76 (0.52-1.11), 0.73 (0.50-1.09) for total cholesterol, and 0.78 (0.53-1.15), 0.66 (0.43-1.00), and 1.03 (0.69-1.54), for HDL cholesterol. Further adjustment for CHD on follow-up or exclusion of individuals with CHD at baseline did not alter the results. In contrast, high total cholesterol and low HDL cholesterol increased the risk of incident CHD (P < .001). CONCLUSION:In healthy males, total and HDL cholesterol levels were not related to incident heart failure.

HomeCirculationVol. 117, No. 20Rotating Fibrocalcific Cast After Infected Pacemaker Lead Extraction Free AccessReview ArticlePDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissionsDownload Articles + Supplements ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toSupplemental MaterialFree AccessReview ArticlePDF/EPUBRotating Fibrocalcific Cast After Infected Pacemaker Lead Extraction Satish Kenchaiah, Mary J. Barnes, Roy Nambudripad, Kaveh Naemi and Serge Tobias Satish KenchaiahSatish Kenchaiah From the Memorial Heart and Vascular Institute (S.K., M.J.B., S.T.) and the Department of Pathology (R.N., K.N.), Long Beach Memorial Medical Center, Long Beach, Calif; and the Division of Cardiology (S.K., S.T.) and the Department of Pathology and Laboratory Medicine (R.N., K.N.), the University of California, Irvine Medical Center, Orange, Calif. , Mary J. BarnesMary J. Barnes From the Memorial Heart and Vascular Institute (S.K., M.J.B., S.T.) and the Department of Pathology (R.N., K.N.), Long Beach Memorial Medical Center, Long Beach, Calif; and the Division of Cardiology (S.K., S.T.) and the Department of Pathology and Laboratory Medicine (R.N., K.N.), the University of California, Irvine Medical Center, Orange, Calif. , Roy NambudripadRoy Nambudripad From the Memorial Heart and Vascular Institute (S.K., M.J.B., S.T.) and the Department of Pathology (R.N., K.N.), Long Beach Memorial Medical Center, Long Beach, Calif; and the Division of Cardiology (S.K., S.T.) and the Department of Pathology and Laboratory Medicine (R.N., K.N.), the University of California, Irvine Medical Center, Orange, Calif. , Kaveh NaemiKaveh Naemi From the Memorial Heart and Vascular Institute (S.K., M.J.B., S.T.) and the Department of Pathology (R.N., K.N.), Long Beach Memorial Medical Center, Long Beach, Calif; and the Division of Cardiology (S.K., S.T.) and the Department of Pathology and Laboratory Medicine (R.N., K.N.), the University of California, Irvine Medical Center, Orange, Calif. and Serge TobiasSerge Tobias From the Memorial Heart and Vascular Institute (S.K., M.J.B., S.T.) and the Department of Pathology (R.N., K.N.), Long Beach Memorial Medical Center, Long Beach, Calif; and the Division of Cardiology (S.K., S.T.) and the Department of Pathology and Laboratory Medicine (R.N., K.N.), the University of California, Irvine Medical Center, Orange, Calif. Originally published20 May 2008https://doi.org/10.1161/CIRCULATIONAHA.107.762245Circulation. 2008;117:e338–e339A 50-year-old man with a history of sick sinus syndrome had a dual-chamber pacemaker implanted 17 years ago. The pulse generator was replaced for battery depletion (end-of-service) about 12 years earlier and again 4 years earlier. He presented with a 4-month history of a skin lesion over the left subclavicular pacemaker pocket that began as a blister and progressed, despite topical and oral antibiotic therapy, to a partial erosion and exposure of a pacemaker lead.The pulse generator was explanted and the infected pacemaker pocket was debrided. The chronically implanted atrial and ventricular leads were extracted using a combined Excimer laser sheath (Spectranetics Inc, Colorado Springs, Colo) and Femoral Workstation (Cook Inc, Bloomington, Ind) approach. Fluoroscopy at the end of the procedure revealed no remnants of leads or stylets; however, 2-dimensional transesophageal echocardiography showed an echodense mass that was freely floating and rotating in a tumbling fashion inside the right atrium (Figure, A and Movie). A 35-mm Amplatz gooseneck snare (Microvena Corporation, White Bear Lake, Minn) was advanced through the femoral vein and the mass was grasped under transesophageal echocardiographic guidance and removed. Macroscopic examination of the mass revealed a 3.5×0.7×0.1-cm cast of the extracted lead (Figure, B). A histopathological section stained with hematoxylin and eosin showed benign fibrous tissue with prominent vasculature and focal calcifications (Figure, C). Download figureDownload PowerPointFigure. A, Transesophageal echocardiographic image obtained in bicaval view at the midesophageal level showing an echod- ense mass (arrowheads) in the right atrium. B, Macroscopic images of the luminal and adherent surface of the extracted pacemaker lead cast measuring 3.5×0.7×0.1 cm in size. C, Histopathological section (10× magnification) stained with hematoxylin and eosin showing benign fibrous tissue (arrowheads) with prominent vasculature (white arrows) and focal calcifications (black arrows).The patient's subsequent hospital course was uneventful, with no clinical evidence of pulmonary embolism. Cultures from the atrial lead grew Propionibacterium acnes, which was treated with intravenous vancomycin. Five days after extraction, a new dual-chamber pacemaker system was implanted with pulse generator embedded in the opposite subclavicular pocket. The patient was discharged the next day in good clinical condition with a 4-week course of parenteral antibiotic therapy. Three months later, he was in good health without recurrent infection.Disruption of the fibrotic attachments between the chronically implanted pacemaker leads and the vascular and intracardiac structures is an inherent part of lead extraction. In the present case, intraoperative transesophageal echocardiography was pivotal in the identification and retrieval of the free-floating, tumbling, radiolucent, and fibrocalcific pacemaker lead cast that likely averted a major complication downstream (pulmonary embolism).The online-only Data Supplement, which contains a movie, is available online with this article at http://circ.ahajournals.org/cgi/content/full/117/ 20/e338/DC1.DisclosuresNone.FootnotesCorrespondence to Satish Kenchaiah, MD, MPH, The Division of Cardiology, The University of California, Irvine Medical Center, 101 The City Dr South, Orange, CA 92868. E-mail [email protected] Previous Back to top Next FiguresReferencesRelatedDetailsCited By Jacobson A and Ailiani R (2019) Pseudoleads on Transesophageal Echocardiography, CASE, 10.1016/j.case.2018.08.001, 3:1, (35-38), Online publication date: 1-Feb-2019. May 20, 2008Vol 117, Issue 20 Advertisement Article InformationMetrics https://doi.org/10.1161/CIRCULATIONAHA.107.762245PMID: 18490528 Originally publishedMay 20, 2008 PDF download Advertisement SubjectsCatheter Ablation and Implantable Cardioverter-DefibrillatorEchocardiographyPacemaker