Clément Venner

All you need to know about the tricuspid valve: Tricuspid valve imaging and tricuspid regurgitation analysis

The acknowledgment of tricuspid regurgitation (TR) as a stand-alone and progressive entity, worsening the prognosis of patients whatever its aetiology, has led to renewed interest in the tricuspid-right ventricular complex. The tricuspid valve (TV) is a complex, dynamic and changing structure. As the TV is not easy to analyse, three-dimensional imaging, cardiac magnetic resonance imaging and computed tomography scans may add to two-dimensional transthoracic and transoesophageal echocardiographic data in the analysis of TR. Not only the severity of TR, but also its mechanisms, the mode of leaflet coaptation, the degree of tricuspid annulus enlargement and tenting, and the haemodynamic consequences for right atrial and right ventricular morphology and function have to be taken into account. TR is functional and is a satellite of left-sided heart disease and/or elevated pulmonary artery pressure most of the time; a particular form is characterized by TR worsening after left-sided valve surgery, which has been shown to impair patient prognosis. A better description of TV anatomy and function by multimodality imaging should help with the appropriate selection of patients who will benefit from either surgical TV repair/replacement or a percutaneous procedure for TR, especially among patients who are to undergo or have undergone primary left-sided valvular surgery.

Right ventricular dysfunction in patients with idiopathic dilated cardiomyopathy: Prognostic value and predictive factors

BACKGROUND Right ventricular (RV) dysfunction is an important predictor of impaired prognosis in idiopathic dilated cardiomyopathy. AIMS To determine the prognostic role of RV dysfunction, independent of left ventricular (LV) dysfunction. METHODS A total of 136 consecutive patients (73% men; mean age 59.0±13.2 years) with idiopathic dilated cardiomyopathy (LV ejection fraction ≤ 45%) were enrolled retrospectively. Thirty-four patients (25%, group 1) presented with RV dysfunction, defined as tricuspid annular plane systolic excursion (TAPSE) ≤ 15 mm; 102 patients (group 2) had preserved RV function. RESULTS Mean LV ejection fraction was 27.5±8.7%. Mean TAPSE was 18.6±5.4 mm (15-21.8 mm). Multivariable predictors of RV dysfunction were LV outflow tract time-velocity integral (odds ratio 0.8, 95% confidence interval [CI] 0.7-0.9; P=0.003) and E-wave deceleration time ≤ 145 ms (odds ratio 4.1, 95% CI 1.3-12.8; P=0.017). Major adverse cardiac event-free survival rates at 1 and 2 years were 64% and 55%, respectively, in group 1 and 87% and 79%, respectively, in group 2 (P=0.002). Both by multivariable analysis and after stratification using a propensity score, RV dysfunction emerged as an independent predictor for major adverse cardiac events (hazard ratio 3.2, 95% CI 1.3-7.6; P=0.009), along with right atrium area and age. CONCLUSION In idiopathic dilated cardiomyopathy, RV dysfunction with TAPSE ≤ 15 mm offers additional prognostic information, independent of the extent of LV dysfunction.

Possible relationship between antiphospholipid antibodies and embolic events in infective endocarditis

Objective Antiphospholipid (aPL) antibodies may activate platelets and contribute to vegetation growth and embolisation in infective endocarditis (IE). We aimed to determine the value of aPL as predictors of embolic events (EE) in IE. Methods We studied 186 patients with definite IE (Duke-Li criteria, all types of IE) from the Nanc-IE prospective registry (2007–2012) who all had a frozen blood sample and at least one imaging procedure to detect asymptomatic or confirm symptomatic EE. Anticardiolipin (aCL) and anti-β2-glycoprotein I (β2GPI) antibodies (IgG and IgM) were assessed after the end of patients’ inclusion. The relationship between antibodies and the detection of EE after IE diagnosis were studied with Kaplan-Meier and Cox multivariate analyses. Results At least one EE was detected in 118 (63%) patients (52 cerebral, 95 other locations) after IE diagnosis in 80 (time interval between IE and EE diagnosis: 5.9±11.3 days). At least one aPL antibody was found in 31 patients (17%). Detection of EE over time after IE diagnosis was more frequent among patients with anti-β2GPI IgM (log-rank P=0.0036) and that of cerebral embolisms, among patients with aCL IgM and anti-β2GPI IgM (log-rank P=0.002 and P<0.0001, respectively). Factors predictive of EE were anti-β2GPI IgM (HR=3.45 (1.47–8.08), P=0.0045), creatinine (2.74 (1.55–4.84), P=0.0005) and vegetation size (2.41 (1.41–4.12), P=0.0014). Those of cerebral embolism were aCL IgM (2.84 (1.22–6.62), P=0.016) and anti-β2GPI IgM (4.77 (1.79–12.74), P=0.0018). Conclusion The presence of aCL and anti-β2GPI IgM was associated with EE, particularly cerebral ones, and could contribute to assess the embolic risk of IE.

Three-Dimensional Echocardiography for the Assessment of Right Ventriculo-Arterial Coupling

Background: The analysis of right ventriculo‐arterial coupling (RVAC) from pressure‐volume loops is not routinely performed. RVAC may be approached by the combination of right heart catheterization (RHC) pressure data and cardiac magnetic resonance (CMR)–derived right ventricular (RV) volumetric data. RV pressure and volume measurements by Doppler and three‐dimensional echocardiography (3DE) allows another way to approach RVAC. Methods: Ninety patients suspected of having pulmonary hypertension underwent RHC, 3DE, and CMR (RHC mean pulmonary artery pressure [mPAP] 37.9 ± 11.3 mm Hg; range, 15–66 mm Hg). Three‐dimensional (3D) echocardiography was performed in 30 normal patients (echocardiographic mPAP 18.4 ± 3.1 mm Hg). Pulmonary artery (PA) effective elastance (Ea), RV maximal end‐systolic elastance (Emax), and RVAC (PA Ea/RV Emax) were calculated from RHC combined with CMR and from 3DE using simplified formulas including mPAP, stroke volume, and end‐systolic volume. Results: Three‐dimensional echocardiographic and RHC‐CMR measures for PA Ea (3DE, 1.27 ± 0.94; RHC‐CMR, 0.71 ± 0.52; r = 0.806, P < .001), RV Emax (3DE, 0.72 ± 0.37; RHC‐CMR, 0.38 ± 0.19; r = 0.798, P < .001), and RVAC (3DE, 2.01 ± 1.28; RHC‐CMR, 2.32 ± 1.77; r = 0.826, P < .001) were well correlated despite a systematic overestimation of 3DE elastance parameters. Among the whole population, 3D echocardiographic PA Ea and 3D echocardiographic RVAC but not 3D echocardiographic RV Emax were significantly lower in patients with mPAP < 25 mm Hg (n = 41) than in others (n = 79). Among the 90 patients who underwent RHC, 3D echocardiographic PA Ea and 3D echocardiographic RVAC but not 3D echocardiographic RV Emax increased significantly with increasing levels of pulmonary vascular resistance. Conclusions: Three‐dimensional echocardiography–derived PA Ea, RV Emax, and RVAC correlated well with the reference RHC‐CMR measurements. Ea and RVAC but not Emax were significantly different between patients with different levels of afterload, suggesting failure of the right ventricle to maintain coupling in severe pulmonary hypertension. HIGHLIGHTS3D echo‐derived PA Ea, RV Emax, RVAC are correlated with those derived from RHC‐CMR.3D echo‐derived PA Ea and RVAC are significantly lower in patients with mPAP <25 mm Hg.3D echo‐derived PA Ea and RVAC increase significantly with severity of PH.3D echo‐derived RV Emax is not significantly influenced by levels of afterload.

Interactions between mitral valve and left ventricle analysed by 2D speckle tracking in patients with mitral valve prolapse: one more piece to the puzzle.

Aims Two‐dimensional echocardiography often reveals abnormal left ventricle (LV) lateral wall kinetics in patients presenting with mitral valve prolapse (MVP). However, relations between MVP and LV deformation are not clearly established. The aim of this study was to assess and quantify mitral valve chordae, leaflets, and LV myocardial interactions using speckle tracking echocardiography (STE). Methods and results Using STE‐derived longitudinal strain curves, LV peak longitudinal strain (PLS, %), post‐systolic index (PSI), and pre‐stretch index (PST) were analysed in 100 patients with MVP and normal LV ejection fraction. Global, regional, and segmental values were compared according to mitral regurgitation severity and MVP location. Twenty healthy subjects served as control patients. There was no significant difference among control and MVP group for global and regional PLS (−23.7 ± 3.2 vs. −23.1 ± 2.2). In contrast, patients with MVP had significantly higher values of global PST (3.2 ± 4.1 vs. 1.3 ± 1.2; P = 0.01) and global PSI (3.2 ± 0.4 vs. 1.7 ± 1.1; P = 0.05) compared with controls, located mainly in the lateral wall and basal segments. Both anterior and posterior MVPs were responsible for PSI in basal inferior segments and PST in anterior ones. Mid‐wall segmental deformation pattern changes were mainly observed at the level of the segments adjacent to the papillary muscle. Conclusion This study supports the hypothesis that pathological early‐systolic shortening and late systolic, post‐systolic deformation are attributed to an increased interaction between wall deformation and mitral valve events in patients with MVP. STE is a useful tool in the assessment of interplays between MV leaflets and myocardium and helps to demonstrate changes in temporal pattern of myocardial deformation.

Long-Term Outcome of Patients With Low/Intermediate Risk Myocarditis Is Related to the Presence of Left Ventricular Remodeling in Addition to the MRI Pattern of Delayed Gadolinium Enhancement

Acute myocarditis (AM) refers to a series of heterogeneous clinical manifestations, ranging from asymptomatic course, heart failure, arrhythmia, to cardiogenic shock. Low-risk patients according to conventional criteria remain the most common form, and 80% of patients are discharged from hospital

Heart failure with preserved ejection fraction: A systemic disease linked to multiple comorbidities, targeting new therapeutic options

Heart failure is a pathology associated with severe morbidity and mortality. In this large field, heart failure with preserved ejection fraction (HFpEF) appears to be an increasing global health problem; it should be considered as a progressive syndrome, characterized by complex mechanisms of systemic and cardiac adaptation that vary over time, particularly with ageing. Multiple biological phenotypes contribute to the heterogeneous clinical syndrome. HFpEF emerges as a model with proinflammatory cardiovascular and non-cardiovascular coexisting comorbidities, leading to systemic inflammation and subsequent fibrosis and to diverse clinical HFpEF phenotypes. All of these aspects are often present in the elderly population, bordering on the emergence of a true geriatric syndrome. The therapeutic approach cannot be uniform, and must involve management of the different comorbidities according to a phenotype treatment strategy, respecting the pharmacological approaches to the biological pathways involved in the proinflammatory comorbidity-related status. Future studies should consider these multiple distinct HFpEF phenotypes in the development of large morbimortality trials adapted to comorbidities or specific risk factors.

Can MRI detect pulmonary hypertension in a population pre-selected by echocardiography?

Background The place of magnetic resonance imaging (MRI) in the assessment of pulmonary hypertension (PH) remains controversial. Several studies proposed to use MRI to assess pulmonary pressure but the level of proof is low. Purpose To evaluate the diagnostic power of cardiac MRI within a non-selected population of patients suspected of PH after an echocardiography. Material and Methods Fifty-six consecutive patients, suspected of PH after an echocardiography, were assessed with right heart catheterization and cardiac MRI (including a high temporal resolution pulmonary flow curve). We extracted from the MRI data the main parameters proposed by all precedent studies available in the literature. We looked for multivariate linear relations between those parameters and the mean pulmonary arterial pressure (mPAP), and eventually assessed with a logit regression the ability of those parameters to diagnose PH in our population. Results The multivariate model retained only two parameters: the right ventricle ejection fraction and the pulmonary trunk minimum area. The prediction of mPAP (r2 = 0.5) yielded limits of agreement of 15 mmHg. However, the prediction of PH within the population was feasible and the method yielded a specificity of 80% for a sensitivity of 100%. Conclusion The performance of MRI to assess mPAP is too low to be used as a replacement for right heart catheterization but MRI could be used as second line examination after echocardiography to avoid right heart catheterization for normal patients.

Electrocardiographic patterns and long-term training-induced time changes in 2484 elite football players

BACKGROUND High-level physical training induces cardiac structural and functional changes, including 12-lead electrocardiogram modifications. OBJECTIVES The purpose of this cross-sectional longitudinal study was to establish a quantitative electrocardiographic profile in highly trained football players. Initial and serial annual electrocardiogram monitoring over subsequent years allowed us to investigate the long-term effects of exercise on cardiac conduction and electrophysiological remodelling. METHODS Between 2005 and 2015, serial evaluations, including 12-lead electrocardiograms, were performed in 2484 elite male football players from the French Professional Football League. A total of 6247 electrocardiograms were performed (mean 2.5±1.8 electrocardiograms/player). Heart rate (beats/min), atrioventricular delay (PR, ms), intraventricular conduction delay (QRS, ms), corrected QT delay (QTc) and electrical left ventricular hypertrophy (LVH) (Sokolow-Lyon index, mm) were measured, and the fixed effect of time was evaluated using panel data analysis (β [95% confidence interval] change between two visits). RESULTS According to European Society of Cardiology and Seattle criteria, 15% of the electrocardiogram intervals were considered abnormal. We observed 17% sinus bradycardia<50 beats/min (mean heart rate 60±11 beats/min), 8% first-degree atrioventricular block>200ms (mean PR 170±27ms), 1.5% QRS>120ms (mean QRS 87±19ms) and 3% prolonged QT interval (mean QTc using Bazetts formula [QTcB] 395±42ms). Electrical LVH (mean Sokolow-Lyon index 34±10mm) was noted in 37% of players. Over time, electrocardiogram changes were noted, with a significant remodelling trend in terms of decreased heart rate (-0.41 [-0.55 to -0.26] beats/min), QRS duration (-2.4 [-2.7 to -2.1] ms) and QTcB delay (-1.2 [-1.9 to -0.5] ms) (all P<0.001). CONCLUSIONS This study describes usual electrocardiographic training-induced changes in a large series of football players over the follow-up timeframe. The most frequent outliers were electrical LVH and sinus bradycardia. These results have important implications for optimizing electrocardiogram interval measurements in initial screening and during follow-up of football players, with potential cost-effective implications.

Perivalvular extension of native mitral valve infective endocarditis with annular fistula and preserved valve function.

Perivalvular extension is a rare but severe complication mainly of aortic and prosthetic valve infective endocarditis (IE). In mitral IE, the extension is usually located posteriorly or laterally to the annulus. This case enlightens the value of multimodality imaging in this context. A 23-year-old male with no medical history presented an inaugural acute …