Replacement Myocardial Fibrosis in Patients With Mitral Valve Prolapse: Relation to Mitral Regurgitation, Ventricular Remodeling, and Arrhythmia.

BACKGROUND: Mitral valve prolapse (MVP) is a frequent disease that can be complicated by mitral regurgitation (MR), heart failure, arterial embolism, rhythm disorders, and death. Left ventricular (LV) replacement myocardial fibrosis, a marker of maladaptive remodeling, has been described in patients with MVP, but the implications of this finding remain scarcely explored. We aimed at assessing the prevalence, pathophysiological and prognostic significance of LV replacement myocardial fibrosis through late gadolinium enhancement (LGE) by cardiac magnetic resonance in patients with MVP. METHODS: Four hundred patients (53±15 years of age, 55% male) with MVP (trace to severe MR by echocardiography) from 2 centers, who underwent a comprehensive echocardiography and LGE cardiac magnetic resonance, were included. Correlates of replacement myocardial fibrosis (LGE+), influence of MR degree, and ventricular arrhythmia were assessed. The primary outcome was a composite of cardiovascular events (cardiac death, heart failure, new-onset atrial fibrillation, arterial embolism, and life-threatening ventricular arrhythmia). RESULTS: Replacement myocardial fibrosis (LGE+) was observed in 110 patients (28%; 91 with myocardial wall including 71 with basal inferolateral wall, 29 with papillary muscle). LGE+ prevalence was 13% in trace-mild MR, 28% in moderate MR, and 37% in severe MR, and was associated with specific features of mitral valve apparatus, more dilated LV and more frequent ventricular arrhythmias (45% versus 26%, P<0.0001). In trace-mild MR, despite the absence of significant volume overload, abnormal LV dilatation was observed in 16% of patients and ventricular arrhythmia in 25%. Correlates of LGE+ in multivariable analysis were LV mass (odds ratio, 1.01 [95% CI, 1.002-1.017], P=0.009) and moderate-severe MR (odds ratio, 2.28 [95% CI, 1.21-4.31], P=0.011). LGE+ was associated with worse 4-year cardiovascular event-free survival (49.6±11.7 in LGE+ versus 73.3±6.5% in LGE-, P<0.0001). In a stepwise multivariable Cox model, MR volume and LGE+ (hazard ratio, 2.6 [1.4-4.9], P=0.002) were associated with poor outcome. CONCLUSIONS: LV replacement myocardial fibrosis is frequent in patients with MVP; is associated with mitral valve apparatus alteration, more dilated LV, MR grade, and ventricular arrhythmia; and is independently associated with cardiovascular events. These findings suggest an MVP-related myocardial disease. Last, cardiac magnetic resonance provides additional information to echocardiography in MVP.

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.

Treatment of Mitral Valve Regurgitation with an Open Rigid Annuloplasty Ring.

BACKGROUND AND AIM OF THE STUDY: Annuloplasty constitutes a major operative step in the surgical treatment of degenerative mitral valve regurgitation (MR). The choice of ring structure to obtain an adequate remodeling of the mitral orifice and to respect the motion of the mitral apparatus remains the subject of debate. The study aim was to determine the clinical and echocardiographic outcome when using an open rigid ring to treat MR. METHODS: A total of 129 patients (94 men, 35 women; mean age 64.5 ± 11.7 years) was referred to the authors' institution between 1997 and 2011 for the surgical management of severe MR. Patients were implanted with a modified open rigid annuloplasty ring, and also underwent anterior and/or posterior leaflet repair. The occurrence of any major adverse cardiac and cerebrovascular event (MACCE) was considered as the primary end-point and was retrospectively collected along with echocardiographic data. RESULTS: The perioperative mortality was 1.6%. The cardiopulmonary bypass and cross-clamp times were 73.3 ± 17.1 min and 51.6 ± 13.0 min, respectively. There was one case (0.7%) of postoperative mitral systolic anterior motion. During a mean follow up period of 6.0 ± 3.1 years, 25 patients (19%) presented a MACCE. MACCE-free survival at one, five and 10 years was respectively 96.8%, 91.3%, and 61.4%. Preoperative determinants of MACCE were paroxysmal/persistent atrial fibrillation (HR 2.53; 95% CI: 1.06-6.01; p = 0.035) and age (HR 1.05; 95% CI: 1-1.09; p = 0.035). CONCLUSIONS: Mitral valve repair with an open-rigid ring offers satisfactory long-term results with a low rate of subsequent MR recurrence and reintervention. Preoperative AF is the main determinant of long-term adverse outcome.

Myocardial deformation in malignant mitral valve prolapse: A shifting paradigm to dynamic mitral valve-ventricular interactions.

Objectives: This study sought to assess the value of myocardial deformation using strain echocardiography in patients with mitral valve prolapse (MVP) and severe ventricular arrhythmia and to evaluate its impact on rhythmic risk stratification. Background: MVP is a common valvular affection with an overly benign course. Unpredictably, selected patients will present severe ventricular arrhythmia. Methods: Patients with MVP as the only cause of aborted SCD (MVP-aSCD: ventricular fibrillation and monomorphic and polymorphic ventricular tachycardia) with no other obvious reversible cause were identified. Nonconsecutive patients referred for the echocardiographic evaluation of MVP were enrolled as a control cohort and dichotomized according to the presence or absence of premature ventricular contractions (MVP-PVC or MVP-No PVC, respectively). All patients had a comprehensive strain assessment of mechanical dispersion (MD), postsystolic shortening, and postsystolic index (PSI). Results: A total of 260 patients were enrolled (20 MVP-aSCD, 54 MVP-PVC, and 186 MVP-No PVC). Deformation pattern discrepancies were observed with a higher PSI value in MVP-aSCD than that in MVP-PVC (4.6 ± 2.0 vs. 2.9 ± 3.7, p = 0.014) and a higher MD value than that in MVP-No PVC (46.0 ± 13.0 vs. 36.4 ± 10.8, p = 0.002). In addition, PSI and MD increased the prediction of severe ventricular arrhythmia on top of classical risk factors in MVP. Net reclassification improvement was 61% (p = 0.008) for PSI and 71% (p = 0.001) for MD. Conclusions: In MVP, myocardial deformation analysis with strain echocardiography identified specific contraction patterns with postsystolic shortening leading to increased values of PSI and MD, translating the importance of mitral valve-myocardial interactions in the arrhythmogenesis of severe ventricular arrhythmia. Strain echocardiography may provide important implications for rhythmic risk stratification in MVP.

Left ventricular myocardial deformation pattern, mechanical dispersion, and their relation with electrocardiogram markers in the large population-based STANISLAS cohort: insights into electromechanical coupling.

AIMS: Mechanical alterations in patients with electrical conduction abnormalities are reported to have prognostic value in patients with left ventricular asynchrony or long QT syndrome beyond electrocardiogram (ECG) variables. Whether conduction and repolarization patterns derived from ECG are associated with speckle tracking echocardiography parameters in subjects without overt cardiac disease is yet to be investigated. To report ranges of longitudinal deformation according to conduction and repolarization values in a population-based cohort. METHODS AND RESULTS: One thousand, one hundred, and forty subjects (48.6 ± 14.0 years, 47.7% men) enrolled in the fourth visit of the STANISLAS cohort (Lorraine, France) were studied. Echocardiography strain was performed in all subjects. RR, PR, QRS, and QT intervals were retrieved from digitalized 12-lead ECG. Echocardiographic data were stratified according to quartiles of QRS and QTc duration values. Full-wall global longitudinal strain (GLS) was -21.1 ± 2.5% with a mechanical dispersion (MD) value of 34 ± 12 ms. Absolute GLS value was lower in the longest QRS quartile and shortest QTc quartile (both P < 0.001). Time-to-peak of strain was not significantly different according to QRS duration although significantly higher in patients with higher QTc (P < 0.001). MD was significantly greater in patients with longer QTc (32 ± 12 ms for QTc < 396 ms vs. 36 ± 12 ms for QTc > 421 ms; P = 0.002). CONCLUSION: Longer QTc is related to increased MD and better longitudinal strain values. In a population-based setting, QRS is not associated with MD, suggesting that echocardiography-based dyssynchrony does not largely overlap with ECG-based dyssynchrony.

[Complications and prognosis of infective endocarditis]. / Complications et pronostic de l'endocardite infectieuse.

Clinical manifestations of infective endocarditis may involve almost all body organs. They are usually classified as either cardiac or extra-cardiac complications. The first stage of infection is the development of intra-cardiac vegetation, which may further spread with an increase in size and number of vegetations, destructive valve lesions, and perivalvular extension of the infection. These anatomical lesions are responsible for hemodynamic disorders, mostly valvular regurgitation, and often lead to heart failure, which is the most frequent complication of IE. Embolic events may affect various vascular territories, the most frequent sites being brain, spleen and kidney for left-sided IE, and lung for right-sided IE. Cerebral complications may be of ischemic, hemorrhagic and/or infectious origin, are often the revealing symptoms of IE, and are well-recognized factors of poor prognosis. IE remains a dreadful disease with an in hospital mortality of 20%, a 5 year mortality of 40% and a significant morbidity.

[Treatment of infectious endocarditis]. / Traitement de l'endocardite infectieuse.

Antibiotic treatment of infective endocarditis is part of a multidisciplinary patient management that should be conducted within an "Endocarditis team". Initial antibiotic treatment of infective endocarditis should be parenteral and comply with current international guidelines. A switch to an oral antibiotic regimen may be considered after 2weeks of successful parenteral antibiotic treatment. Aminoglycosides should no longer be used for the initial treatment of native valve Staphylococcus aureus endocarditis. Valve surgery is required in almost half of the patients.

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.

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 (ß [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 Bazett's 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.

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.

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-ß2-glycoprotein I (ß2GPI) 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-ß2GPI IgM (log-rank P=0.0036) and that of cerebral embolisms, among patients with aCL IgM and anti-ß2GPI IgM (log-rank P=0.002 and P<0.0001, respectively).Factors predictive of EE were anti-ß2GPI 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-ß2GPI IgM (4.77 (1.79-12.74), P=0.0018). CONCLUSION: The presence of aCL and anti-ß2GPI IgM was associated with EE, particularly cerebral ones, and could contribute to assess the embolic risk of IE.

[New treatments for heart failure]. / Les nouveaux traitements de l'insuffisance cardiaque.

New direct oral anticoagulants are recommended as first-line therapy in case of atrial fibrillation within a heart failure. In the absence of atrial fibrillation, the role for new direct oral anticoagulants would have to be confirmed in the next years. Sacubitril/valsartan, angiotansin II receptor neprilysin inhibitor, presents with an efficacy superior to that of angiotensin converting enzyme inhibitors. It is now recommended in the treatment of heart failure as a third-line therapy. Modalities of prescription are strict, and safety is good.

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.

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.

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.

Myocardial deformation pattern in left ventricular non-compaction: Comparison with dilated cardiomyopathy.

INTRODUCTION: Left ventricular (LV) systolic dysfunction is the most frequent initial presentation of patient with LV noncompaction (NC). Our objectives were to evaluate myocardial contraction properties in patients with LVNC and the relationship of non-compacted segments with the degree of global and regional systolic deformation. METHODS: We included 50 LVNC with an echocardiography and speckle imaging calculation of peak longitudinal strain (PLS). Each of the 16 LV myocardial segments was defined as NC (ratio NC/compacted layer > 2), borderline (NC/C 0-2) and compacted (NC/C = 0). Basal, median and apical strain values were calculated as the average of segmental strain values. For comparison a group of 50 patients with dilated cardiomyopathy (DCM) underwent the same measurements. RESULTS: There was no statistical difference between the 2 groups for any conventional LV systolic parameters. A characteristic deformation pattern was observed in LVNC with higher strain values in the LV apical segments (- 12.8 ± 5.9 vs - 10.7 ± 5.7) and an apical-basal ratio (1.52 ± 0.73 vs 1.12 ± 0.42; p < 0.001). There was no correlation between LV function and the degree of NC. Among 726 segments, compacta thickness was thinner in NC vs C segments (6.4 ± 1.4 vs 7.7 ± 1.8 mm; p < 0.05). There was no difference in WMS but regional strain values were significantly higher in NC compared to C segments (- 13.1 ± 6.1 vs - 10.2 ± 6.3; p < 0.05). CONCLUSIONS: Compared to DCM, LVNC presented with relatively preserved apical deformation as compared to basal segments. Lower regional deformation values in compacted segments confirm the concept that LVNC is a phenotypic marker of an underlying diffuse cardiomyopathy involving both C and NC myocardium.