Disproportionate Mitral Regurgitation Determines Survival in Acute Heart Failure.

Objectives: To assess the prevalence and impact of mitral regurgitation (MR) on survival in patients presenting to hospital in acute heart failure (AHF) using traditional echocardiographic assessment alongside more novel indices of proportionality. Background: It remains unclear if the severity of MR plays a significant role in determining outcomes in AHF. There is also uncertainty as to the clinical relevance of indexing MR to left ventricular volumes. This concept of disproportionality has not been assessed in AHF. Methods: A total of 418 consecutive patients presenting in AHF over 12 months were recruited and followed up for 2 years. MR was quantitatively assessed within 24 h of recruitment. Standard proximal isovelocity surface area (PISA) and a novel proportionality index of effective regurgitant orifice/left ventricular end-diastolic volume (ERO/LVEDV) >0.14 mm2/ml were used to identify severe and disproportionate MR. Results: Every patient had MR. About 331/418 (78.9%) patients were quantifiable by PISA. About 165/418 (39.5%) patients displayed significant MR. A larger cohort displayed disproportionate MR defined by either a proportionality index using ERO/LVEDV > 0.14 mm2/ml or regurgitant volumes/LVEDV > 0.2 [217/331 (65.6%) and 222/345 (64.3%), respectively]. The LVEDV was enlarged in significant MR-129.5 ± 58.95 vs. 100.0 ± 49.91 ml in mild, [p < 0.0001], but remained within the normal range. Significant MR was associated with a greater mortality at 2 years {44.2 vs. 34.8% in mild MR [hazard ratio (HR) 1.39; 95% CI: 1.01-1.92, p = 0.04]}, which persisted with adjustment for comorbid conditions (HR; 1.43; 95% CI: 1.04-1.97, p = 0.03). Disproportionate MR defined by ERO/LVEDV >0.14 mm2/ml was also associated with worse outcome [42.4 vs. 28.3% (HR 1.62; 95% CI 1.12-2.34, p = 0.01)]. Conclusions: MR was a universal feature in AHF and determines outcome in significant cases. Furthermore, disproportionate MR, defined either by effective regurgitant orifice (ERO) or volumetrically, is associated with a worse prognosis despite the absence of adverse left ventricular (LV) remodeling. These findings outline the importance of adjusting acute volume overload to LV volumes and call for a review of the current standards of MR assessment. Clinical Trial Registration: https://clinicaltrials.gov/ct2/show/NCT02728739, identifier NCT02728739.

Right ventricular ejection fraction as predictor of outcome in acute heart failure using RV ellipsoid model: A retrospective analysis of a prospective cross-sectional study.

OBJECTIVES: The right ventricular (RV) function is an important prognostic factor in acute and chronic heart failure (HF). Echocardiography is an essential imaging modality with established parameters for RV function which are useful and easy to perform. However, these fail to reflect global RV volumes due to reliability on one acoustic window. It is therefore attractive to calculate RV volumes and ejection fraction (RVEF/E) using an ellipsoid geometric model which has been validated against MRI in healthy adults but not in the HF patients. DESIGN: This is a retrospective analysis of a prospective cross-sectional study enrolling 418 consecutive patients with symptoms of HF according to a predefined study protocol. All patients underwent echocardiographic assessment of RV function using Tricuspid Annular Plane Systolic Excursion (TAPSE) and RV fractional area change (RVFAC) and RVEF/E. SETTING: Single centre study with multiple locations for acute in-patients including high dependency units. PARTICIPANTS: Patients with acute or exacerbation of chronic HF older than 18 y.o. MAIN OUTCOME MEASURES: Ability of RVEF/E to predict patient outcomes compared with two established parameters of RV function over two-year follow-up period. Primary outcome measure was all-cause mortality. RESULTS: RVEF/E is equal to TAPSE & RVFAC in predicting outcome (p ≤ 0.01 vs p ≤ 0.01) and provides additional benefit of RV volume estimation based on standard 2D echo measurements. CONCLUSIONS: In this study we have shown that RVEF/E derived from ellipsoid model is not inferior to well established measures of RV function as a prognostic indicator of outcome in the acute HF.

Sex differences in the agreement between left ventricular ejection fraction measured by myocardial perfusion scintigraphy and by echocardiography.

BACKGROUND: Left ventricular ejection fraction (LVEF) is generally measured by echocardiography but is increasingly available with myocardial perfusion scintigraphy. With myocardial perfusion scintigraphy, the threshold of LVEF below which there is a risk for myocardial infarct or sudden cardiac death is higher for women (51%) than for men (43%). We tested the hypothesis that such a sex difference may also occur with echocardiography and myocardial perfusion scintigraphy. METHODS: Four hundred and four men, mean age = 67.7 ± SD = 12.3 yr; 339 women, 67.7 ± 11.7 yr had separate myocardial perfusion scintigraphy and echocardiography examinations within six months. A subset of 327 of these patients (181 men, 68.8 ± 12.1 yr; 146 women, 66.4 ± 12.1 yr) had examinations within one month and were additionally analysed as this sub-group. Myocardial perfusion scintigraphy and echocardiography were used to measure LVEF at rest and their agreement (neither considered as a reference method) was assessed by Bland-Altman plots: LVEF difference (myocardial perfusion scintigraphy minus echocardiography ) against average LVEF ( MPS + Echo 2 ). RESULTS: Of patients who had myocardial perfusion scintigraphy and echocardiography performed within six months, mean LVEF difference = +1.1% (95% limits of agreement: -19.3 to +21.6) in men but +10.9% (-10.7 to +32.5) in women. LVEF difference diverged from zero marginally in men (mean difference = +1.1, 95%CI = +0.1 to +2.1, p = 0.028) but more in women (+10.9, +9.8 to +12.1, p < 0.001). The LVEF difference correlated with average LVEF itself in both men (r = 0.305, p < 0.001) and women (r = 0.361, p < 0.001), and with age in women (r = 0.117, p = 0.031). Similar results were observed for the subset. CONCLUSIONS: Caution should be taken when interpreting LVEF measured by different techniques due to their wide limits of agreement and systematic bias, more markedly in women.

Non-genetic and genetic risk factors for adult cerebral venous thrombosis.

INTRODUCTION: A wide variety of non-genetic and genetic factors have been shown to associate with increased risk for cerebral venous thrombosis (CVT). However, there is a paucity of risk factor data and conclusions about their impact are often conflicting. Herein, we quantified the associations of non-genetic and genetic risk factors for CVT in adults. MATERIALS AND METHODS: Electronic databases were searched up to January 2017. Meta-analyses were performed (RevMan v5.3) to determine pooled odds ratios (ORs and 95% CIs) for risk factors, interstudy heterogeneity and publication bias. RESULTS: Twenty non-genetic (n = 2314) and 33 genetic (n = 2117) studies up to January 2017 met the selection criteria. For non-genetic factors, CVT risk increased in the presence of glucocorticosteroid therapy by 18.3-fold (3.3-102.6), alcohol consumption 2.7-fold (1.8-3.9), infection 7.5-fold (2.6-21.6), surgery 9.6-fold (1.1-83.5), hypercholesterolaemia 2.4-fold (1.3-4.4), hyperhomocysteinaemia 3.1-fold (2.1-4.6), antiphospholipid antibodies 7.0-fold (2.1-23.6), autoimmune diseases 5.6-fold (2.3-13.6), anaemia 4.0-fold (2.1-7.9), malignancy 3.2-fold (1.4-7.1) and pregnancy/puerperium 11.4-fold (5.7-24.3). Smoking, hypertension and diabetes did not associate with CVT risk. For genetic factors, CVT risk increased in the presence of factor V Leiden (G1691A) by 2.5-fold (1.9-3.3), protein C deficiency 10.7-fold (3.1-37.7), protein S deficiency 5.7-fold (1.4-22.4), antithrombin deficiency 3.8-fold (1.0-13.8), prothrombin (G20210A) 5.5-fold (4.0-7.27) and TAFI gene variant (C1040T) 1.6-fold (1.0-2.4). Prothrombin G20210A and factor V Leiden polymorphisms tended to have higher ORs for CVT than for ischaemic stroke. CONCLUSIONS: We provide quantitative data supporting a strong basis for genetic and non-genetic risk factors in CVT. Its genetic liability seems higher when compared with sporadic ischaemic stroke.