Anavekar, Nandan S.

Background— Constrictive pericarditis is a potentially reversible cause of heart failure that may be difficult to differentiate from restrictive myocardial disease and severe tricuspid regurgitation. Echocardiography provides an important opportunity to evaluate for constrictive pericarditis, and definite diagnostic criteria are needed. Methods and Results— Patients with surgically confirmed constrictive pericarditis (n=130) at Mayo Clinic (2008–2010) were compared with patients (n=36) diagnosed with restrictive myocardial disease or severe tricuspid regurgitation after constrictive pericarditis was considered but ruled out. Comprehensive echocardiograms were reviewed in blinded fashion. Five principal echocardiographic variables were selected based on prior studies and potential for clinical use: (1) respiration-related ventricular septal shift, (2) variation in mitral inflow E velocity, (3) medial mitral annular e' velocity, (4) ratio of medial mitral annular e' to lateral e', and (5) hepatic vein expiratory diastolic reversal ratio. All 5 principal variables differed significantly between the groups. In patients with atrial fibrillation or flutter (n=29), all but mitral inflow velocity remained significantly different. Three variables were independently associated with constrictive pericarditis: (1) ventricular septal shift, (2) medial mitral e', and (3) hepatic vein expiratory diastolic reversal ratio. The presence of ventricular septal shift in combination with either medial e'≥9 cm/s or hepatic vein expiratory diastolic reversal ratio ≥0.79 corresponded to a desirable combination of sensitivity (87%) and specificity (91%). The specificity increased to 97% when all 3 factors were present, but the sensitivity decreased to 64%. Conclusions— Echocardiography allows differentiation of constrictive pericarditis from restrictive myocardial disease and severe tricuspid regurgitation. Respiration-related ventricular septal shift, preserved or increased medial mitral annular e' velocity, and prominent hepatic vein expiratory diastolic flow reversals are independently associated with the diagnosis of constrictive pericarditis.

PurposeTo investigate the influence of portal pressure on the shear stiffness of the liver and spleen in a well‐controlled in vivo porcine model with magnetic resonance elastography (MRE). A significant correlation between portal pressure and tissue stiffness could be used to noninvasively assess increased portal venous pressure (portal hypertension), which is a frequent clinical condition caused by cirrhosis of the liver and is responsible for the development of many lethal complications.Materials and MethodsDuring multiple intraarterial infusions of Dextran‐40 in three adult domestic pigs in vivo, 3D abdominal MRE was performed with left ventricle and portal catheters measuring blood pressure simultaneously. Least‐squares linear regressions were used to analyze the relationship between tissue stiffness and portal pressure.ResultsLiver and spleen stiffness have a dynamic component that increases significantly following an increase in portal or left ventricular pressure. Correlation coefficients with the linear regressions between stiffness and pressure exceeded 0.8 in most cases.ConclusionThe observed stiffness–pressure relationship of the liver and spleen could provide a promising noninvasive method for assessing portal pressure. Using MRE to study the tissue mechanics associated with portal pressure may provide new insights into the natural history and pathophysiology of hepatic diseases and may have significant diagnostic value in the future. J. Magn. Reson. Imaging 2013;38:809–815. © 2013 Wiley Periodicals, Inc.

Background— The American Heart Association published updated guidelines for infective endocarditis (IE) prevention in 2007 that markedly restricted the use of antibiotic prophylaxis in certain at-risk patients undergoing dental and other invasive procedures. The incidence of IE caused by viridans group streptococci (VGS) in the United States after publication of the 2007 American Heart Association guidelines has not been reported. Methods and Results— We performed a population-based review of all definite or possible cases of VGS-IE using the Rochester Epidemiology Project of Olmsted County, Minnesota. Patient demographics and microbiological data were collected for all VGS-IE cases diagnosed from January 1, 1999, through December 31, 2010. We also examined the Nationwide Inpatient Sample hospital discharge database to determine the number of VGS-IE cases included between 1999 and 2009. We identified 22 cases with VGS-IE in Olmsted County over the 12-year study period. Rates of incidence (per 100 000 person-years) during time intervals of 1999–2002, 2003–2006, and 2007–2010 were 3.19 (95% confidence interval, 1.20–5.17), 2.48 (95% confidence interval, 0.85–4.10), and 0.77 (95% confidence interval, 0.00–1.64), respectively ( P =0.061 from Poisson regression). The number of hospital discharges with a VGS-IE diagnosis in the Nationwide Inpatient Sample database during 1999–2002, 2003–2006, and 2007–2009 ranged between 15 318 to 15 938, 16 214 to 17 433, and 14 728 to 15 479, respectively. Conclusions— On the basis of data complete through 2010, there has been no perceivable increase in the incidence of VGS-IE in Olmsted County, Minnesota, since the publication of the 2007 American Heart Association endocarditis prevention guidelines.

Background— The role of valve surgery in left-sided infective endocarditis has not been evaluated in randomized controlled trials. We examined the association between valve surgery and all-cause 6-month mortality among patients with left-sided infective endocarditis. Methods and Results— A total of 546 consecutive patients with left-sided infective endocarditis were included. To minimize selection bias, propensity score to undergo valve surgery was used to match patients in the surgical and nonsurgical groups. To adjust for survivor bias, we matched the follow-up time so that each patient in the nonsurgical group survived at least as long as the time to surgery in the respective surgically-treated patient. We also used valve surgery as a time-dependent covariate in different Cox models. A total of 129 (23.6%) patients underwent surgery within 30 days of diagnosis. Death occurred in 99 of the 417 patients (23.7%) in the nonsurgical group versus 35 deaths among the 129 patients (27.1%) in the surgical group. Eighteen of 35 (51%) patients in the surgical group died within 7 days of valve surgery. In the subset of 186 cases (93 pairs of surgical versus nonsurgical cases) matched on the logit of their propensity score, diagnosis decade, and follow-up time, no significant association existed between surgery and mortality (adjusted hazard ratio, 1.3; 95% confidence interval, 0.5 to 3.1). With a Cox model that incorporated surgery as a time-dependent covariate, valve surgery was associated with an increase in the 6-month mortality with an adjusted hazard ratio of 1.9 (95% confidence interval, 1.1 to 3.2). Because the proportionality hazard assumption was violated in the time-dependent analysis, we performed a partitioning analysis. After adjustment for early (operative) mortality, surgery was not associated with a survival benefit (adjusted hazard ratio, 0.92; 95% confidence interval, 0.48 to 1.76). Conclusions— The results of our study suggest that valve surgery in left-sided infective endocarditis is not associated with a survival benefit and could be associated with increased 6-month mortality, even after adjustment for selection and survivor biases as well as confounders. Given the disparity between the results of our study and those of other observational studies, well-designed prospective studies are needed to further evaluate the role of valve surgery in endocarditis management.