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ObjectivesThe aim of this study was to demonstrate the physiologic effects of percutaneous mitral paravalvular leak (PVL) closure through pre‐ and post‐closure left and right heart catheterization.BackgroundMitral PVL represents a significant source of morbidity and mortality following mitral valve repair and replacement. Although percutaneous PVL closure is an effective treatment with improvements in symptoms and mortality, data regarding the acute hemodynamic effects of such closure are lacking.MethodsConsecutive patients with clinically significant heart failure and/or hemolysis attributed to mitral PVL underwent percutaneous mitral PVL closure with pre‐ and post‐procedural right and left heart catheterization. Hemodynamic measurements of cardiovascular function obtained in this manner were compared and stratified according to pre‐ and post‐procedural echocardiographic severity of PVL.ResultsTwenty‐four patients (age 68 ± 9.4 years, 75% male) underwent percutaneous mitral PVL closure. Significant improvements were found in left atrial pressure (LAP) (mean LAP lowered from 21 ± 4 to 19 ± 3 mm Hg, P = 0.005), pulmonary artery pressure (PAP) (mean PAP lowered from 36 ± 11 to 33 ± 9, P = 0.04), and cardiac index (increased from 2.8 ± 0.8 to 3.0 ± 0.7 L/min/m2, P = 0.01). Left atrial v‐wave reduction of 20% was associated with ≤ mild residual PVL by transesophageal echocardiography (P = 0.09).ConclusionsPercutaneous mitral PVL closure is associated with significant reductions in LAP and PAP and an increase in cardiac index. These hemodynamic effects underlie the clinical benefits of PVL closure and may be a useful tool for intraprocedural guidance. © 2017 Wiley Periodicals, Inc.

Background: Heart failure (HF) with preserved ejection fraction (HFpEF) is a heterogeneous syndrome. Phenotyping patients into pathophysiologically homogeneous groups may enable better targeting of treatment. Obesity is common in HFpEF and has many cardiovascular effects, suggesting that it may be a viable candidate for phenotyping. We compared cardiovascular structure, function, and reserve capacity in subjects with obese HFpEF, those with nonobese HFpEF, and control subjects. Methods: Subjects with obese HFpEF (body mass index ≥35 kg/m 2 ; n=99), nonobese HFpEF (body mass index <30 kg/m 2 ; n=96), and nonobese control subjects free of HF (n=71) underwent detailed clinical assessment, echocardiography, and invasive hemodynamic exercise testing. Results: Compared with both subjects with nonobese HFpEF and control subjects, subjects with obese HFpEF displayed increased plasma volume (3907 mL [3563–4333 mL] versus 2772 mL [2555–3133 mL], and 2680 mL [2380–3006 mL]; P <0.0001), more concentric left ventricular remodeling, greater right ventricular dilatation (base, 34±7 versus 31±6 and 30±6 mm, P =0.0005; length, 66±7 versus 61±7 and 61±7 mm, P <0.0001), more right ventricular dysfunction, increased epicardial fat thickness (10±2 versus 7±2 and 6±2 mm; P <0.0001), and greater total epicardial heart volume (945 mL [831–1105 mL] versus 797 mL [643–979 mL] and 632 mL [517–768 mL]; P <0.0001), despite lower N-terminal pro-B-type natriuretic peptide levels. Pulmonary capillary wedge pressure was correlated with body mass and plasma volume in obese HFpEF ( r =0.22 and 0.27, both P <0.05) but not in nonobese HFpEF ( P ≥0.3). The increase in heart volumes in obese HFpEF was associated with greater pericardial restraint and heightened ventricular interdependence, reflected by increased ratio of right- to left-sided heart filling pressures (0.64±0.17 versus 0.56±0.19 and 0.53±0.20; P =0.0004), higher pulmonary venous pressure relative to left ventricular transmural pressure, and greater left ventricular eccentricity index (1.10±0.19 versus 0.99±0.06 and 0.97±0.12; P <0.0001). Interdependence was enhanced as pulmonary artery pressure load increased ( P for interaction <0.05). Compared with those with nonobese HFpEF and control subjects, obese patients with HFpEF displayed worse exercise capacity (peak oxygen consumption, 7.7±2.3 versus 10.0±3.4 and12.9±4.0 mL/min·kg; P <0.0001), higher biventricular filling pressures with exercise, and depressed pulmonary artery vasodilator reserve. Conclusions: Obesity-related HFpEF is a genuine form of cardiac failure and a clinically relevant phenotype that may require specific treatments.

Background— Data on the clinical use of left atrial (LA) hemodynamic monitoring during MitraClip procedure are limited. This study evaluated the association between intraprocedural changes in LA pressure after MitraClip and improvement in exercise capacity as documented by 6-minute walk test (6MWT). Methods and Results— Study population included 50 patients who underwent MitraClip at the Mayo Clinic (Rochester, MN), between June 2014 and July 2016 and completed both baseline and 30-day follow-up 6MWT. Primary outcome for the current analysis was defined as 6MWT improvement above the median. Mean age of the study population was 79±10 years, and 34 (68%) were men. Baseline preprocedural 6MWT distance was 308 m (interquartile range [IQR], 234–394 m). Acute, intraprocedural change in LA pressure after MitraClip was 3 mm Hg (IQR, 1–6 mm Hg), and change in V wave was 11 mm Hg (IQR, 6–19 mm Hg). Median 6MWT improvement was 25 m (IQR, 19–47 m). Univariate analysis showed that patients with ≤ mild postprocedural mitral regurgitation were 4-fold more likely to experience an improvement in 6MWT ( P =0.02). Multivariate model demonstrated that each 5 mm Hg decrease in V wave was associated with 49% increased likelihood for improvement in 6-minute walk ( P =0.04). Similar model with V-wave change as a dichotomous variable showed that patients with a V-wave decrease of ≥11 mm Hg were 3.8× more likely to improve their 6MWT ( P =0.05). Conclusions— Acute changes in LA pressure after MitraClip procedure are associated with clinical improvement as measured by 6MWT. Continuous LA pressure monitoring may be a useful tool for procedural guidance during transcatheter mitral repair.

AbstractIntroductionThe pace of medical discovery is accelerating to the point where caregivers can no longer keep up with the latest diagnosis or treatment recommendations. At the same time, sophisticated and complex electronic medical records and clinical systems are generating increasing volumes of patient data, making it difficult to find the important information required for patient care. To address these challenges, Mayo Clinic established a knowledge management program to curate, store, and disseminate clinical knowledge.MethodsThe authors describe AskMayoExpert, a point‐of‐care knowledge delivery system, and discuss the process by which the clinical knowledge is captured, vetted by clinicians, annotated, and stored in a knowledge content management system. The content generated for AskMayoExpert is considered to be core clinical content and serves as the basis for knowledge diffusion to clinicians through order sets and clinical decision support rules, as well as to patients and consumers through patient education materials and internet content. The authors evaluate alternative approaches for better integration of knowledge into the clinical workflow through development of computer‐interpretable care process models.ResultsEach of the modeling approaches evaluated has shown promise. However, because each of them addresses the problem from a different perspective, there have been challenges in coming to a common model. Given the current state of guideline modeling and the need for a near‐term solution, Mayo Clinic will likely focus on breaking down care process models into components and on standardization of those components, deferring, for now, the orchestration.ConclusionA point‐of‐care knowledge resource developed to support an individualized approach to patient care has grown into a formal knowledge management program. Translation of the textual knowledge into machine executable knowledge will allow integration of the knowledge with specific patient data and truly serve as a colleague and mentor for the physicians taking care of the patient.

Abstract Aims Short-term studies have reported left ventricular (LV) dilatation following surgical creation of arteriovenous fistulas (AVF) or arteriovenous grafts (AVGs), but chronic cardiac structural and functional changes have not been examined or related to clinical outcomes following AVF/AVG. We sought to characterize the long-term changes in cardiac structure and function in patients undergoing shunt creation for haemodialysis. Methods and results A retrospective analysis was performed of patients undergoing echocardiography before and after surgical AVF/AVG creation for the initiation of haemodialysis. 137 patients underwent echocardiographic examinations prior to AVF and 2.6 years (median) after AVF creation. Following AVF and dialysis initiation, there were reductions in blood pressure, body weight and estimated plasma volume coupled with modest reverse LV remodelling. In contrast, AVF/AVG creation was associated with significant right ventricular (RV) dilatation and deterioration in RV function. Incident heart failure (HF) developed in 43% of patients in tandem with greater RV remodeling. The development of RV dilation following surgical AVF/AVG was independently associated with increased risk of death [HR 3.9, 95% CI (1.7–9.2), P = 0.001]. Conclusion In long-term follow-up, RV remodelling and dysfunction develop following AVF/AVG creation and dialysis initiation, despite improved control of LV pressure load through dialysis. Deleterious effects on right heart structure and function are coupled with development of incident HF and increased risk of death. Further study is required to identify patients at greatest risk for detrimental AVF/AVG changes who may benefit from alternate forms of dialysis or potentially ligation of existing AVF.

Introduction Moderate mitral regurgitation (MR) of ischemic etiology has been associated with worse outcomes after coronary artery bypass grafting (CABG). Studies comparing concomitant mitral valve replacement/repair (MVR/Re) with CABG and standalone CABG have reported conflicting results. We performed a systematic review and meta-analysis of the published literature. Patients and Methods We searched using PubMed, Cochrane, EMBASE, CINAHL, and Google scholar databases from January 1960 to June 2016 for clinical trials comparing CABG to CABG + MVR/Re for moderate MR. Pooled risk ratio or mean difference (MD) with 95% confidence intervals (CI) for individual outcomes were calculated using random effects model and heterogeneity was assessed using Cochrane's Q-statistic. Results A total of 11 studies were included. Mean follow-up was 35.3 months. All-cause mortality (Mantel–Haenszel [MH] risk ratio [RR]: 0.96, 95% CI: 0.75–1.24, p = 0.775), early mortality (MH RR: 0.65, 95% CI: 0.39–1.07, p = 0.092), and stroke rates (MH RR 0.65, 95% CI: 0.21–2.03, p = 0.464) were similar between CABG and CABG + MVR/Re groups. Adverse event at follow-up was lower with CABG (MH RR: 0.90, 95% CI: 0.61–1.32, p = 0.584). MD of change from baseline in left ventricular (LV) end-systolic dimension (MD: − 2.50, 95% CI: − 5.21 to − 0.21, p = 0.071) and LV ejection fraction (MD: 0.48, 95% CI: − 2.48 to 3.44, p = 0.750) were not significantly different between the groups. Incidence of moderate MR (MH RR: 3.24, 95% CI: 1.79–5.89, p < 0.001) was higher in the CABG only group. Conclusion Addition of MVR/Re to CABG in patients with moderate ischemic MR did not result in improvement in early or overall mortality, stroke risk, or intermediate markers of LV function when compared with CABG alone.

Background: Diagnosis of heart failure with preserved ejection fraction (HFpEF) is challenging and relies largely on demonstration of elevated cardiac filling pressures (pulmonary capillary wedge pressure). Current guidelines recommend use of natriuretic peptides (N-terminal pro-B type natriuretic peptide) and rest/exercise echocardiography (E/e′ ratio) to make this determination. Data to support this practice are conflicting. Methods: Simultaneous echocardiographic-catheterization studies were prospectively conducted at rest and during exercise in subjects with invasively proven HFpEF (n=50) and participants with dyspnea but no identifiable cardiac pathology (n=24). Results: N-Terminal pro-B type natriuretic peptide levels were below the level considered to exclude disease (≤125 pg/mL) in 18% of subjects with HFpEF. E/e′ ratio was correlated with directly measured pulmonary capillary wedge pressure at rest ( r =0.63, P <0.0001) and during exercise ( r =0.57, P <0.0001). Although specific, current guidelines were poorly sensitive, identifying only 34% to 60% of subjects with invasively proven HFpEF on the basis of resting echocardiographic data alone. Addition of exercise echocardiographic data (E/e′ ratio>14) improved sensitivity (to 90%) and thus negative predictive value, but decreased specificity (71%). Conclusions: Currently proposed HFpEF diagnostic guidelines on the basis of resting data are poorly sensitive. Adding exercise E/e′ data improves sensitivity and negative predictive value but compromises specificity, suggesting that exercise echocardiography may help rule out HFpEF. These results question the accuracy of current approaches to exclude HFpEF on the basis of resting data alone and reinforce the value of exercise testing using invasive and noninvasive hemodynamic assessments to definitively confirm or refute the diagnosis of HFpEF. Clinical Trial Registration: URL: http://www.clinicaltrials.gov . Unique Identifier: NCT01418248.