Reddy, Yogesh N.V.

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.

VT Ablation in LVAD RecipientsBackgroundPatients with advanced heart failure (HF) are predisposed to ventricular arrhythmias (VAs), particularly following implantation of a left ventricular assist device (LVAD). There is minimal evidence for appropriate management strategies.ObjectivesThis study aimed to compare the burden of VA and response to ablation performed either before or following LVAD implantation.MethodsWe created a retrospective cohort of patients who underwent both VA ablation and Heart Mate II (Thoratec, Pleasanton, CA, USA) LVAD implantation at Mayo Clinic (Rochester, MN, USA). Patients were stratified based on whether they underwent VA ablation before (pre‐LVAD) or after LVAD (post‐LVAD) implantation. Descriptive analyses assessed 6‐month arrhythmia burden in relation to LVAD implantation and VA ablation.ResultsA total of 9 patients underwent both LVAD implantation and VA ablation. There were 3 and 6 patients, respectively, in the pre‐LVAD and post‐LVAD cohorts. Among patients in the pre‐LVAD cohort, the median number of VAs tended to increase after ablation (9 vs. 72) and decreased after LVAD implantation (72 vs. 63). Similarly among patients in the post‐LVAD cohort, the median burden of VAs increased after LVAD implantation (1 vs. 22) and the median burden decreased after ablation (22 vs. 13). Two of 6 patients had substrate related to the LVAD inflow cannula site, while other substrate was not related directly to the cannula.ConclusionsIn patients with progressive HF and LVAD implantation, ablation is associated with reduced VA rates. In LVAD patients, most VAs arise from substrate unrelated to the inflow cannula site.

Abstract Aims The goal of the study was to examine the prognostic impact, haemodynamic and clinical features associated with lung congestion in patients with chronic heart failure (HF). Methods and results HF patients (n = 186) and HF-free controls (n = 21) underwent right heart catheterization, echocardiography, pulmonary function testing and chest radiography that was blindly scored for the presence and severity of lung oedema. Lung congestion correlated directly with pulmonary vascular resistance (PVR, P = 0.004) and inversely with pulmonary artery (PA) compliance (P &lt; 0.001) and the diffusion limit for carbon monoxide (DLCO, P = 0.009). Compared with dry lung HF, wet lung HF patients (congestion score &gt; median) had 25% lower PA compliance and 25–35% higher PVR, transpulmonary gradients and PA pressures (40 vs. 32 mmHg, P &lt; 0.001) despite marginally higher PA wedge pressure (PAWP; 22 vs. 19 mmHg, P = 0.002). Wet lung HF patients displayed more right ventricular (RV) dilatation and dysfunction, more restrictive ventilation and greater reduction of DLCO. The strongest correlates of lung congestion were NT-proBNP, haemoglobin, albumin, and glomerular filtration, all surpassing PAWP. After a median of 333 days (interquartile range 80–875), 59 patients (32%) died. Lung congestion was associated with reduced survival (P &lt; 0.0001), even after adjusting for PAWP, NT-proBNP, anaemia, CAD and renal dysfunction. Conclusion Interstitial lung oedema is associated with pulmonary vascular disease, RV overload and dysfunction and increased mortality in HF. These data reinforce the importance of aggressive decongestion in HF and suggest that novel agents aimed at reducing lung water may help to deter progression of pulmonary vascular disease and biventricular HF.

The percutaneous Melody valve is occasionally used for the treatment of bioprosthetic valve dysfunction and is an attractive option for patients at high risk for repeat operation. Anticoagulation is not routinely recommended following Melody valve placement. We present the case of a young woman who developed subacute spontaneous thrombosis of her Melody valve 15 months after placement. Her clinical status was compromised by severe tricuspid prosthesis stenosis and right-to-left shunting across a small residual atrial septal defect. Surgical replacement was required. To our knowledge, this is the first reported case of spontaneous thrombosis of a Melody valve in the tricuspid position.

A 33-year-old male with systemic lupus erythematosus (SLE) presented with acute abdominal pain and was found to have lupus mesenteric vasculitis on imaging and during exploratory laparotomy. Post laparotomy he continued to have persistent nausea and dyspepsia and an electrocardiogram showed evidence of an inferior ST elevation myocardial infarction (STEMI). Emergency cardiac catheterization showed evidence of thrombotic right coronary artery occlusion. His coronaries were otherwise normal with no evidence of underlying coronary artery disease. Extensive workup with trans-esophageal echo, serologies for antiphospholipid antibody syndrome (APS) and bubble study was negative. This effectively ruled out Libman–Sacks endocarditis, APS-induced arterial thrombus and paradoxical emboli as potential causes of his STEMI. By exclusion of other causes, the etiology of his STEMI was felt to be secondary to in-situ coronary artery thrombosis in the setting of active SLE. To the best of our knowledge, this is the first report of a patient with SLE presenting with both lupus mesenteric vasculitis and in-situ coronary arterial thrombosis in the absence of APS.