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Aims: To identify independent electrocardiogram (ECG) predictors of long-term clinical outcome based on standardized analysis of the surface ECG in a large multicentre cohort of patients with sarcomeric hypertrophic cardiomyopathy (HCM)., Methods and Results: Retrospective observational study from the REMY French HCM clinical research observatory. Primary endpoint was a composite of all-cause mortality, major non-fatal arrhythmic events, hospitalization for heart failure (HF), and stroke. Secondary endpoints were components of the primary endpoint. Uni- and multivariable Cox proportional hazard regression analysis was performed to identify independent predictors. Among 994 patients with HCM, only 1.8% had a strictly normal baseline ECG. The most prevalent abnormalities were inverted T waves (63.7%), P-wave abnormalities (30.4%), and abnormal Q waves (25.5%). During a mean follow-up of 4.0 ± 2.0 years, a total of 272 major cardiovascular events occurred in 217 patients (21.8%): death or heart transplant in 98 (9.8%), major arrhythmic events in 40 (4.0%), HF hospitalization in 115 (11.6%), and stroke in 23 (2.3%). At multivariable analysis using ECG covariates, prolonged QTc interval, low QRS voltage, and PVCs of right bundle branch block pattern predicted worse outcome, but none remained independently associated with the primary endpoint after adjustment on main demographic and clinical variables. For secondary endpoints, abnormal Q waves independently predicted all-cause death [hazard ratio (HR) 2.35, 95% confidence interval (CI) 1.23-4.47; P = 0.009] and prolonged QTc the risk of HF hospitalization (HR 1.006, 95% CI 1.001-1.011; P = 0.024)., Conclusion: The 12-lead surface ECG has no independent value to predict the primary outcome measure in patients with HCM. The 12-lead surface ECG has been widely used as a screening tool in HCM but its prognostic value remains poorly known. The value of baseline surface ECG to predict long-term clinical outcomes was studied in a cohort of 994 patients with sarcomeric HCM. The surface ECG has no significant additional value to predict outcome in this patient population., (Published on behalf of the European Society of Cardiology. All rights reserved. © The Author(s) 2019. For permissions, please email: journals.permissions@oup.com.)

Aims: Strain delay index (SDI) allows quantification of the wasted contraction or gain of myocardial contractility expected after cardiac resynchronization therapy (CRT). The present multicentre prospective study aimed to assess the accuracy of the SDI in predicting responses to CRT in real-life patients with wide and narrow (<130 ms) QRS complexes., Methods and Results: Implantation of a CRT device was performed in 235 heart failure patients and echocardiography data were analysable in 80% (n= 189) of patients (age 65 ± 12 years, left ventricular ejection fraction = 26 ± 8%, 63 ischaemic, 51 with narrow QRS complexes). Mechanical dyssynchrony before CRT was quantified by the 12-segment standard deviation of peak longitudinal strain by speckle tracking (12SD-ε, 12 standard deviation of time to peak strain by speckle tracking), and SDI, defined as the sum of difference between end-systolic and peak-ε across the 16 segments. Response to CRT was defined as an end-systolic volume reduction (ESVR) at 6 months >15%. After CRT, ESVR>15% was observed in 60% (n= 114/189) of patients, and was greater in non-ischaemic (68 vs. 44%, P= 0.003) and wide QRS patients (65 vs. 49%, P= 0.04). Correlation between 12SD-ε and ESVR was poor (r = 0.18, P= 0.01). In contrast, SDI correlated with reverse remodelling (r = 0.61, P< 0.0001 for all) in both wide and narrow QRS patients and ischaemic and non-ischaemic patients. Decrease in SDI after CRT was greater in responders and correlated with ESVR. Finally, SDI > 25% identified responders to CRT (positive and negative predictive value of 80 and 84%, respectively) with 6% inter-observer variability., Conclusion: The present multicentre study suggests that SDI may identify responders to CRT in ischaemic and non-ischaemic patients.

Aims: A recent study suggested that no single echocardiographic index of cardiac dyssynchrony can reliably identify candidates for cardiac resynchronization therapy (CRT). We examined the value of three simple echocardiographic indices for predicting the 6-month clinical and echocardiographic responses to CRT., Methods and Results: We analysed data from 75 CRT-D system recipients. Standard echocardiography was used to measure aortic pre-ejection delay (APED), interventricular mechanical delay (IVMD), and delayed activation of the left ventricular (LV) infero-lateral wall (OVERLAP). Clinical responders were defined as patients who had an improved status, based on rehospitalization for heart failure, NYHA class, and peak oxygen consumption. Echocardiographic responders had a > or =10% decrease in LV end-systolic volume. During the study, one patient died and five were lost to follow-up. Of the remaining 69 analysable patients, 50 (72.5%) were classed as clinical responders and 41 (59.4%) as echocardiographic responders to CRT. Before CRT implantation, APED, IVMD, and OVERLAP were similar in responders and non-responders. The value of these indices of dyssynchrony as single or combined predictors of the clinical or echocardiographic response to CRT was low, with sensitivities ranging between 4 and 63%, and specificities between 37 and 100%., Conclusion: Simple echocardiographic indices of dyssynchrony were poor predictors of response to CRT.

Background: Inflammatory processes play a critical role in myocarditis, dilated cardiomyopathy, and heart failure. The expression of the inflammatory chemokine osteopontin (OPN) is dramatically increased in cardiomyocytes and inflammatory cells during myocarditis and heart failure in human and animals. However, its role in the development of heart diseases is not known., Methods and Results: To understand whether OPN is involved in cardiomyopathies, we generated a transgenic mouse (MHC-OPN) that specifically overexpresses OPN in cardiomyocytes with cardiac-specific promoter-directed OPN expression. Young MHC-OPN mice were phenotypically indistinguishable from their control littermates, but most of them died prematurely with a half-life of 12 weeks of age. Electrocardiography revealed conduction defects. Echocardiography showed left ventricular dilation and systolic dysfunction. Histological analysis revealed cardiomyocyte loss, severe fibrosis, and inflammatory cell infiltration. Most of these inflammatory cells were activated T cells with Th1 polarization and cytotoxic activity. Autoantibodies against OPN, cardiac myosin, or troponin I, were not found in the serum of MHC-OPN mice., Conclusions: These data show that OPN expression in the heart induces in vivo T-cell recruitment and activation leading to chronic myocarditis, the consequence of which is myocyte destruction and hence, dilated cardiomyopathy. Thus, OPN might therefore constitute a potential therapeutic target to limit heart failure.

Aims: The mechanisms associated with cardiac resynchronization therapy (CRT) benefits have been elucidated in part, however little is known about the effects of biventricular pacing (BVP) on regional myocardial contractility., Methods and Results: Twenty patients with conventional CRT criteria were studied before and after device implantation. Speckle tracking strain analysis was performed from standard bidimensional acquisitions during different pacing configurations. Longitudinal and transverse strains were measured for the six basal left ventricular (LV) segments. Acute CRT improved LV end-diastolic and end-systolic volumes without significantly modifying LV ejection fraction. Moreover, CRT produced significant changes in regional strain. When compared with spontaneous rhythm, simultaneous BVP caused a significant increase in longitudinal septal strain (-4.8 vs. -7.3%, P = 0.003) and a significant decrease in longitudinal lateral strain (-8.2 vs. -5.9%, P = 0.03). Simultaneous BVP also induced a significant decrease in transverse lateral strain from 17.9 to 10.9% (P = 0.004)., Conclusion: In this acute echocardiographic study, BVP decreased lateral wall deformation while improving septal wall contraction, thus potentially improving LV contractile pattern.

Objectives: We sought to evaluate the impact of the left ventricular (LV) pacing site on hemodynamic response to cardiac resynchronization therapy (CRT)., Background: CRT reduces morbidity and mortality in heart failure patients. However, 20% to 40% of eligible patients may not fully benefit from CRT device implantation. We hypothesized that selecting the optimal LV pacing site could be critical in this issue., Methods: Thirty-five patients with nonischemic dilated cardiomyopathy referred for CRT device implantation were studied. Intraventricular dyssynchrony and latest activated LV wall were defined by tissue Doppler imaging analysis before the study. Eleven predetermined LV pacing sites were systematically assessed in random order: basal and mid-cavity (septal, anterior, lateral, inferior), apex, coronary sinus (CS), and the endocardial site facing the CS pacing site. For each patient, +dP/dT(max), -dP/dT(min), pulse pressure, and end-systolic pressure during baseline (AAI) and DDD LV pacing were compared. Two atrioventricular delays were tested., Results: Major interindividual and intraindividual variations of hemodynamic response depending on the LV pacing site were observed. Compared with baseline, LV DDD pacing at the best LV position significantly improved +dP/dT(max) (+31 +/- 26%, p < 0.001) and was superior to pacing the CS (+15 +/- 23%, p < 0.001), the lateral LV wall (+18 +/- 22%, p < 0.001), or the latest activated LV wall (+11 +/- 17%, p < 0.001)., Conclusions: The pacing site is a primary determinant of the hemodynamic response to LV pacing in patients with nonischemic dilated cardiomyopathy. Pacing at the best LV site is associated acutely with fewer nonresponders and twice the improvement in +dP/dT(max) observed with CS pacing., (Copyright 2010 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.)

Cardiac support device implantation is a new and promising therapy for refractory heart failure. If functional and echocardiographic modifications have largely been reported following this procedure, there is a paucity of information in the clinical setting about cellular abnormalities modifications during the 'reverse remodeling' process. We report for the first time a clinical measurement of cardiac sympathetic function using 123I-MIBG scintigraphy following cardiac support device implantation.