Background: The appropriateness use criteria (AUC) offers guidance to assist with the appropriate use of cardiac imaging. The recent AUC consensus is that follow-up radionuclide myocardial perfusion imaging (MPI) within 2-years of a normal MPI is rarely appropriate in asymptomatic patients or in those with stable symptoms. The utility of repeat testing in a patient with new or progressive symptoms has not been studied. Methods: After IRB approval, records from veterans who underwent multiple MPI stress testing within 2-years of a negative MPI, between 2013 and 2016, at our VA Medical Center were accessed and variables of interest collected. Descriptive analysis as well as direct comparison by means of χ2 for dichotomous variables was conducted. Results: A total of 318 male veterans underwent repeat MPI within 2-years of a normal MPI. The median age was 65 [IQR, 59-70]. Among this group, repeat testing for new or progressive symptoms was done in 206 veterans (65%), compared to 112 (35%) veterans without symptoms. 50 cases had reversible ischemia on repeat MPI. Of these, 37 (18%) were symptomatic. Among asymptomatic veterans with a positive repeat MPI, 3 out of the 11 (27%) were noted to have obstructive coronary artery disease (CAD) on coronary angiogram. In contrast, 24 out of 37 veterans with symptoms underwent coronary angiogram, with 15 (40.6%) found to have obstructive CAD. Overall, 2.6% of asymptomatic veterans who underwent repeat MPI had obstructive CAD on coronary angiogram, compared to 7.2% of veterans who had repeat testing for new or progressive symptoms. Comparison of angiogram findings for abnormal MPIs based on the presence of symptoms on presentation did not reach statistical significance (p=0.053). Conclusion: Among asymptomatic veterans who underwent repeat MPI, < 3% of veterans had obstructive CAD. These findings support the AUC’s position that for asymptomatic patients, repeat MPI within 2-years of a normal study is rarely appropriate. However, among veterans with symptoms, 7 % were found to have obstructive CAD, but the difference between asymptomatic and symptomatic patients did not reach statistical significance. In the setting of symptoms, a negative MPI within 2-years is possibly a marker of low risk for obstructive CAD.

The heart and kidney are invariably intertwined. Heart failure is associated with the important alterations in renal hemodynamics and function that constitute a major problem of clinical management. Conversely, in chronic renal disease, rarely does the heart escape consequences. Cardiovascular complications comprise the major cause of death in the end-stage renal disease (ESRD) population. The effects of chronic renal failure on the heart are diverse and involve numerous anatomical and functional aspects of the cardiovascular system.

Background In response to growth in cardiac imaging, medical societies have published appropriateness use criteria (AUC) and payers have introduced preauthorization mandates, largely through radiology benefits managers (RBM). The correlation of algorithms used to determine preauthorization with the AUC is unknown. In addition, studies applying the 2007 AUC for transthoracic echocardiography revealed that many echocardiograms could not be classified. We sought to examine the impact of the revised 2010 AUC on appropriateness ratings of transthoracic echocardiograms previously classified by the 2007 AUC and the relationship of preauthorization determination to AUC rating.Methods We reclassified indications for transthoracic echocardiography as appropriate, inappropriate, uncertain, or unclassifiable using the 2010 AUC in the same 625 patients previously reported using 2007 AUC. We also evaluated the relationship between preauthorization status by 2 RBM precertification algorithms and appropriateness rating by 2007 AUC.Results The appropriateness classification of 148 (24%) transthoracic echocardiograms was changed by the updated AUC (P < .001). The number of unclassifiable echocardiograms was markedly reduced from 99 (16%) to 8 (1%), and more echocardiograms were classified as inappropriate (95 [15%] vs 45 [7%]) or uncertain (43 [7%] vs 0 [0%]). Limited correlation between the 2007 AUC rating and RBM preauthorization determinations was noted, with only moderate agreement with RBM no. 1 (90%, K = 0.480, P < .001) and poor agreement with RBM no. 2 (72%, K = 0.177, P < .001).Conclusion The updated AUC (2010) provide enhanced clinical value compared with 2007 AUC. There is limited agreement between RBM preauthorization determination and 2007 AUC rating. (Am Heart J 2011; 162: 772-9.)

We compared adherence to appropriateness criteria for transthoracic echocardiography in a Veterans Administration Medical Center (VAMC) and an academic practice and, within the VAMC, between physicians and mid-level providers. We reviewed 201 outpatient echocardiograms performed in the laboratory of an academic practice and 424 outpatient and inpatient studies performed at a VAMC. Echocardiographic examinations requested for indications addressed in the criteria were considered classified, and those for indications not addressed were considered unclassified. Classified studies were further rated as appropriate or inappropriate. Of 625 echocardiograms reviewed, 99 (16%) were unclassified. Approximately 80% of the indications for these could be assigned to 4 categories. Of the remaining 526 echocardiograms, indications were appropriate in 481 (91.4%) and inappropriate in 45 (8.6%). Among classified outpatient studies at the VAMC, mid-level providers requested significantly more studies for inappropriate indications than physicians (16.0% vs 7%, P = .024). There was no significant difference in the frequency of outpatient studies requested for inappropriate indications by VAMC and academic practice physicians (7.0% vs 9.5%, P = .558). The appropriateness criteria perform reasonably well at evaluating variations in use of echocardiography between health care systems and providers. The large majority of studies are requested for appropriate indications, although there is room for improvement.

We report a case of subacute bacterial endocarditis associated with small vessel vasculitis and a strongly positive cytoplasmic antineutrophil cytoplasmic antibody (c-ANCA) test. It is important to recognize this cause of positive c-ANCA because infectious endocarditis may closely mimic the clinical manifestations of ANCA-associated vasculitides such as Wegener granulomatosis or microscopic polyangiitis. Furthermore, ANCA-associated vasculitis may result in noninfectious endocarditis, which may be confused with bacterial endocarditis. In this paper, we review reported cases of ANCA-positive bacterial endocarditis and compare them to the reported cases of ANCA-associated idiopathic vasculitis with endocardial compromise.

EchocardiographyVolume 24, Issue 6 p. 656-657 Extensive Left Atrial Thrombus in a Cocaine User with a Bioprosthetic Mitral Valve, Sinus Rhythm, and Left Ventricular Dysfunction Howard J. Willens M.D., Howard J. Willens M.D. Department of Medicine, Division of Cardiology, University of Miami Miller School of Medicine, Miami VAMC, Miami, FloridaSearch for more papers by this authorGustavo Morales M.D., Gustavo Morales M.D. Department of Medicine, Division of Cardiology, University of Miami Miller School of Medicine, Miami VAMC, Miami, FloridaSearch for more papers by this authorRobert B. Stang M.D., Robert B. Stang M.D. Department of Medicine, Division of Cardiology, University of Miami Miller School of Medicine, Miami VAMC, Miami, FloridaSearch for more papers by this authorCheryl Postel R.D.C.S., Cheryl Postel R.D.C.S. Department of Medicine, Division of Cardiology, University of Miami Miller School of Medicine, Miami VAMC, Miami, FloridaSearch for more papers by this authorJoshua M. Hare M.D., Joshua M. Hare M.D. Department of Medicine, Division of Cardiology, University of Miami Miller School of Medicine, Miami VAMC, Miami, FloridaSearch for more papers by this authorSimon C. Chakko M.D., Simon C. Chakko M.D. Department of Medicine, Division of Cardiology, University of Miami Miller School of Medicine, Miami VAMC, Miami, FloridaSearch for more papers by this author Howard J. Willens M.D., Howard J. Willens M.D. Department of Medicine, Division of Cardiology, University of Miami Miller School of Medicine, Miami VAMC, Miami, FloridaSearch for more papers by this authorGustavo Morales M.D., Gustavo Morales M.D. Department of Medicine, Division of Cardiology, University of Miami Miller School of Medicine, Miami VAMC, Miami, FloridaSearch for more papers by this authorRobert B. Stang M.D., Robert B. Stang M.D. Department of Medicine, Division of Cardiology, University of Miami Miller School of Medicine, Miami VAMC, Miami, FloridaSearch for more papers by this authorCheryl Postel R.D.C.S., Cheryl Postel R.D.C.S. Department of Medicine, Division of Cardiology, University of Miami Miller School of Medicine, Miami VAMC, Miami, FloridaSearch for more papers by this authorJoshua M. Hare M.D., Joshua M. Hare M.D. Department of Medicine, Division of Cardiology, University of Miami Miller School of Medicine, Miami VAMC, Miami, FloridaSearch for more papers by this authorSimon C. Chakko M.D., Simon C. Chakko M.D. Department of Medicine, Division of Cardiology, University of Miami Miller School of Medicine, Miami VAMC, Miami, FloridaSearch for more papers by this author First published: 11 April 2007 https://doi.org/10.1111/j.1540-8175.2007.00457.xCitations: 1 Address for correspondence and reprint requests: Howard J. Willens, M.D., 3513 Greenleaf Circle, Hollywood, FL 33021-8437. Fax: 305-243-7244; E-mail: hjwillens@bellsouth.net Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat No abstract is available for this article.Citing Literature Volume24, Issue6July 2007Pages 656-657 RelatedInformation

Background: To assess the value of scores based on the presence of comorbid conditions for mortality risk-stratification in patients with coronary artery disease (CAD).Methods: We prospectively followed 305 males with CAD undergoing coronary angiography for 58 months. We correlated the modified Charlson Index (MCI) and the recently proposed CAD-specific index (CSI) with the risk of all-cause mortality.Results: The odds ratio (OR) for death increased by 31% per point increase in the MCI (95% CI = 17-46%; p < 0.0001). The OR for death increased by 16% per point increase in the CSI (95% CI = 8.5-25%; p < 0.0001). In logistic regression models that adjusted for age, left ventricular ejection fraction, and the number of vessels involved with CAD, both the MCI and the CSI were the strongest predictors of mortality according to the chi(2) value for each term, with the MCI having the highest value. The adjusted OR per point increase in the MCI was 1.32 (95% CI = 1. 17-1.48; p < 0.0001); the corresponding adjusted OR per point increase in the CSI was 1.17 (95% CI = 1.09-1.26; p < 0.0001). The model including the MCI had a slightly higher chi(2) value (45.1 vs. 39.1) and area under the receiver operator characteristic curve (0.742 vs. 0.727) than the model including the CSI.Conclusion: The MCI and the newly proposed CSI are powerful tools to predict all-cause mortality in patients with established CAD. Although the CSI was not superior to the MCI, its simplicity might make it useful in populations with a low prevalence of comorbidities not included in this score. (c) 2006 Elsevier Ireland Ltd. All rights reserved.

Background: Resting pulse rate (RPR) and obesity are both strong indicators of cardiovascular mortality and the risk of incident heart failure. Obesity is independently associated with increased RPR. Decreased physical activity, insulin resistance, subclinical inflammation and sympathetic activation have been implicated in this association. Leptin has recently been proposed as possible mediator of obesity-induced increased RPR through sympathetic activation and direct effects on the heart. In this study, we aimed to assess the independent relationship between leptin and RPR in the US population. Methods: We used weighted multiple regression to examine the relation between RPR and serum leptin levels among 2264 males and 2545 females enrolled in the Third US National Health and Nutrition Examination Survey. Results: In both males and females, leptin was positively associated with RPR. After adjustment for age, ethnicity, physical activity, body mass index, insulin resistance, triglycerides, HDL cholesterol, C-reactive protein and creatinine clearance, leptin independently predicted RPR in both males (β=6.7; 95%CI = 2.8-10.6; p<0.0001) and females (β=5.97; 95%CI = 2.8-9.4; p<0.0001). Lower physical activity was associated with higher RPR in both males and females. The homeostatic model assessment score for insulin resistance (HOMA-IR) predicted RPR in females but not in males, whereas the opposite was true for C-reactive protein levels. Conclusions: Our study demonstrates a positive correlation between RPR and serum leptin in the general adult US population, which is independent of body mass index, physical activity, metabolic and inflammatory factors and support the role of leptin as a mediator of obesity-related increase in RPR. Further studies are required to evaluate the independent role of RPR and hyperleptinemia as determinants of the risk of incident heart failure. Tabled 1 Estimate (Beta) 95% Confidence Interval P value Males (n = 2264) (Log) Leptin 6.67 2.75 to 10.6 0.001 (Log) CRP (mg/dL) 5.52 2.64 to 8.39 <0.001 HOMA-IR 0.29 −0.22 to 0.8 0.26 Physical Activity −0.007 −0.012 to −0.002 0.006 Females (n = 2545) (Log) Leptin 5.97 2.8 to 9.14 <0.001 (Log) CRP (mg/dL) 1.41 −0.99 to 3.81 0.24 HOMA-IR 0.55 0.23 to 0.86 0.001 Physical Activity −0.008 −0.014 to −0.002 0.007 Open table in a new tab

To determine whether the observed association between mitral annular calcification (MAC) and mortality is independent of the severity of coronary artery disease (CAD), we analyzed data from 134 male veterans (age 63 ± 10 years) followed for 5 years who had undergone diagnostic coronary angiography and transthoracic echocardiography within 6 months of each other. Echocardiograms were retrospectively reviewed for the presence of MAC. The relation of MAC to all‐cause mortality was analyzed using logistic regression, and odds ratios (OR) were calculated. MAC was present in 49 (37%) subjects. Over the 5‐year follow‐up period, 38 (28%) patients expired. Five‐year survival was 80% for subjects without MAC and 56% for subjects with MAC (P = 0.003). MAC (OR = 3.16, 95% confidence interval [CI]= 1.43–6.96, P = 0.003), ejection fraction (OR = 0.76, 95% CI = 0.59–0.97, P = 0.02), and left main CAD (OR = 2.70, 95% CI = 1.11–6.57, P = 0.02) were significantly associated with mortality in univariate analysis. After adjusting for left ventricular ejection fraction, number of obstructed coronary arteries and the presence of left main coronary artery stenosis, MAC significantly predicted death (OR = 2.48, 95% CI = 1.09–5.68, P = 0.03). Similarly, after adjusting for predictors of MAC, including ejection fraction, age, diabetes, peripheral vascular disease, and heart failure, MAC remained a significant predictor of death (OR = 2.38, 95% CI = 1.02–5.58, P = 0.04). MAC also predicted death independent of smoking status, hypertension, serum creatinine, low density lipoprotein cholesterol, high density lipoprotein cholesterol, and C‐reactive protein levels (OR = 3.98, 95% CI = 1.68–9.40, P = 0.001). MAC detected by two‐dimensional echocardiography independently predicts mortality and may provide an easy‐to‐perform and inexpensive way to improve risk stratification.

PURPOSE: Both the presence of diabetes mellitus (DM) and the presence and severity of coronary artery disease (CAD) predict recurrent major adverse cardiovascular events (MACE). The purpose of our study was to examine the correlation between DM, coronary angiographic findings and the risk of MACE among patients with established CAD.

Pulse pressure (PP), a marker of arterial stiffness, predicts cardiovascular risk. We aimed to determine whether augmentation pressure (AP) derived from the aortic pressure waveform predicts major adverse cardiovascular events (MACE) and death independently of PP in patients with established coronary artery disease (CAD). We prospectively followed-up 297 males undergoing coronary angiography for 1186±424 days. Ascending aortic pressure tracings obtained during catheterization were used to calculate AP (difference between the second and the first systolic peak). Augmentation index (AIx) was defined as AP as a percentage of PP. We evaluated whether AP and AIx can predict the risk of MACE (unstable angina, acute myocardial infarction, coronary revascularization, stroke, or death) and death using Cox regression. All models evaluating AP included PP to assess whether AP adds to the information already provided by PP. Both AP and AIx significantly predicted MACE. The hazard ratio (HR) per 10 mm Hg increase in AP was 1.20 (95% confidence interval [CI], 1.08 to 1.34; P <0.001); the HR for each 10% increase in AIx was 1.28 (95% CI, 1.11 to 1.48; P =0.004). After adjusting for other univariate predictors of MACE, age, and other potential confounders, AP remained a significant predictor of MACE (HR per 10 mm Hg increase=1.19; 95% CI, 1.06 to 1.34; P =0.002), as did AIx (adjusted HR, 1.28; 95% CI, 1.09 to 1.50; P =0.003). AP was a significant predictor of death (HR per 10 mm Hg increase=1.18; 95% CI, 1.02 to 1.39; P =0.03). Higher AIx was associated with a trend toward increased mortality (HR=1.22; 95% CI, 0.98 to 1.52; P =0.056). Aortic AP predicts adverse outcomes in patients with CAD independently of PP and other risk markers.

To evaluate the effects of substantial weight loss on tissue Doppler imaging parameters of right ventricular (RV) and left ventricular (LV) systolic and diastolic function, we performed standard echocardiography and tissue Doppler imaging in 17 patients with severe obesity before and after gastric bypass. Patients lost 39 +/- 10 kg over 7.6 +/- 3.6 months. Adjusted LV mass decreased (134 +/- 41 to 119 +/- 31 kg/m, p = 0.031). After weight loss, the ratios of early-to-late diastolic mitral and tricuspid inflow velocities increased (1.3 +/- 0.2 to 1.6 +/- 0.5, p = 0.02; 1.0 +/- 0.1 to 1.6 +/- 0.3, p = 0.003). Early diastolic tissue Doppler velocities increased at both the lateral and septal mitral annulus (7.6 +/- 1.5 to 9.3 +/- 2.5 cm/s, p = 0.009; and 6.6 +/- 1.4 to 7.7 +/- 1.7 cm/s; p = 0.028, respectively) and for their 2-site average (7.2 +/- 1.0 to 8.5 +/- 1.7 cm/s, p = 0.007). Early diastolic tricuspid annular velocity increased (7.2 +/- 2.8 to 10.6 +/- 2.3 cm/s, p <0.001) as did the ratio of early-to-late tricuspid annular diastolic velocity (0.9 +/- 0.4 to 1.1 +/- 0.2, p = 0.038). Tricuspid annular systolic velocity increased (8.6 +/- 2.5 to 10.3 +/- 2.7 cm/s, p = 0.037). In patients with severe obesity, significant weight loss results in an increase in tricuspid annular systolic and early diastolic velocities and mitral annular early diastolic velocities.

We prospectively followed 324 men, who underwent coronary angiography, for 1,161 +/- 418 days. We analyzed the association between ascending aortic pressures measured during cardiac catheterization and the risk of all-cause mortality and a combined end point of major adverse cardiovascular events (MACEs), including unstable angina pectoris, myocardial infarction, coronary revascularization, stroke, or death. Pulse pressure significantly predicted MACEs (hazard ratio [HR] per 10 nun Hg increase 1.09, 95% confidence interval [CI] 1.002 to 1.17, p = 0.04). Diastolic blood pressure (BP) inversely correlated with the risk of MACEs (HR per 10 mm Hg increase 0.85, 95% CI 0.74 to 0.98, p = 0.02). These correlations remained significant after adjusting for other predictors and potential confounders. The association between lower diastolic BP with the risk of MACEs was more pronounced in patients with triple-vessel coronary artery disease (p for interaction = 0.03). Peripheral diastolic BP (but not pulse pressure) correlated inversely with the risk of MACEs (HR 0.87 per 10 mm Hg increase, 95% CI 0.75 to 0.998, p = 0.047). Aortic pulse pressure significantly predicted death (HR per 10 mm Hg increase 1.18, 95% CI 1.05 to 1.33, p = 0.004), and aortic diastolic BP correlated inversely with the risk of death (HR 0.76, 95% CI 0.62 to 0.94, p = 0.01). (c) 2005 Elsevier Inc. All rights reserved.

Background— We evaluated whether cholesterol efflux activity of serum is associated with the presence of angiographic coronary artery disease (CAD) and the risk of major adverse cardiovascular events (MACE) and death. Methods and Results— We studied 168 men undergoing coronary angiography. Cholesterol efflux activity was measured in vitro by incubation of patient serum with human skin fibroblasts and defined as the ability of serum to decrease the pool of cholesterol available for esterification by the acylCoA:cholesterol acyl transferase (ACAT) reaction. We evaluated whether this activity was associated with the presence of CAD and the risk of MACE and death during a 4.5-year follow-up. Serum-induced changes in ACAT activity did not correlate with HDL levels or the presence of CAD. Patients in the highest tertile of change in ACAT activity had a significantly higher risk for MACE (HR, 2.15; 95% CI, 1.36 to 3.39; P=0.001) and death (HR, 2.23; 95% CI, 1.17 to 4.26; P=0.01). These correlations were independent of other risk markers including LDL, HDL, and C-reactive protein levels. Conclusions— Serum-induced depletion of cellular cholesterol available for esterification by ACAT was a strong, independent predictor of MACE and death. We speculate that the ability of serum to decrease ACAT activity depends on ATP binding cassette transporter A1 (ABCA1)–mediated efflux. Furthermore, serum samples that induce larger changes in ACAT activity contain increased levels of HDL particles that preferentially interact with ABCA1 and that these particles accumulate in the serum of patients because of low activity of ABCA1 in vivo preventing or limiting the extent of apoA-I lipidation.