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The usefulness of β-blockers in heart failure (HF) patients with permanent atrial fibrillation (AF) has been questioned. Background: The usefulness of β-blockers in heart failure (HF) patients with permanent atrial fibrillation (AF) has been questioned. Methods and results: We analyzed data from HF patients (958 patients (801 males, 84%, age 67 ± 11 years)) with AF enrolled in the MECKI score database. We evaluated prognosis (composite of cardiovascular death, urgent heart transplant, or left ventricular assist device) of patients receiving β-blockers (n = 777, 81%) vs. those not treated with β-blockers (n = 181, 19%). We also analyzed the role β1-selectivity and the role of daily β-blocker dose. To account for different HF severity, Kaplan-Meier survival curves were normalized for relevant confounding factors and for treatment strategies. Dose was available in 629 patients. Median follow-up was 1312 (577–2304) days in the entire population, 1203 (614–2420) and 1325 (569–2300) days in patients not receiving and receiving β-blockers. 224 (23%, 54/1000 events/year), 163 (21%, 79/1000 events/year), and 61 (34%, 49/1000 events/year) events were recorded, respectively. At 10-year patients treated with β-blockers had a better outcome (HR 0.447, p < 0.01) with no effects as regards β1selective drugs (53%) vs. β1-β2 blockers (47%). Survival improved in parallel with β-blocker dose increase (HR 0.296, 0.496, 0.490 for the high, medium, and low dose vs. no β-blockers, p < 0.0001). Conclusion: HF patients with AF taking a β-blocker have a better outcome (with a survival improvement in parallel with daily dose but no differences as regards β1 selectivity) but this does not mean that β-blockers improve outcomes in these patients as we cannot control for all the potential confounders associated with β-blocker use.

fraction. Rev Esp Cardiol 2013;66:261–8. [9] Herrmann HC, Pibarot P, Hueter I, et al. Predictors of mortality and outcomes of therapy in low-flow severe aortic stenosis: a Placement of Aortic Transcatheter Valves (PARTNER) Trial analysis. Circulation 2013;127:2316–26. [10] Ozkan A, Hachamovitch R, Kapadia SR, Tuzcu EM,Marwick TH. Impact of aortic valve replacement on outcome of symptomatic patients with severe aortic stenosis with low gradient and preserved left ventricular ejection fraction. Circulation 2013;128(6):622–31.

Aims: To evaluate the role of bisoprolol to control symptoms and left ventricular outflow tract obstruction (LVOTO) in a consecutive cohort of adults with hypertrophic cardiomyopathy (HCM). Methods and results: In this retrospective study, patients with HCM with an LVOT gradient ≥50 mmHg after Valsalva manoeuvre and New York Heart Association (NYHA) class II-III symptoms were assigned to receive bisoprolol (starting at 1.25 mg daily). The initial dose was increased every two weeks to achieve the target in LVOT gradient

Introduction: We sought to determine prevalence and predictive accuracy of clinical markers (red flags, RF), known to be associated with specific systemic disease in a consecutive cohort of patients with hypertrophic cardiomyopathy (HCM). Methods: We studied 129 consecutive patients (23.7 ± 20.9 years, range 0–74 years; male/female 68%/32%). Pre-specified RF were categorized into five domains: family history; signs/symptoms; electrocardiography; imaging; and laboratory. Sensitivity (Se), specificity (Sp), negative predictive value (NPV), positive predictive value (PPV), and predictive accuracy of RF were analyzed in the genotyped population. Results: In the overall cohort of 129 patients, 169 RF were identified in 62 patients (48%). Prevalence of RF was higher in infants (78%) and in adults >55 years old (58%). Following targeted genetic and clinical evaluation, 94 patients (74%) had a definite diagnosis (sarcomeric HCM or specific causes of HCM). We observed 14 RF in 13 patients (21%) with sarcomeric gene disease, 129 RF in 34 patients (97%) with other specific causes of HCM, and 26 RF in 15 patients (45%) with idiopathic HCM (p < 0.0001). Non-sarcomeric causes of HCM were the most prevalent in ages 55yo. Se, Sp, PPV, NPV and PA of RF were 97%, 70%, 55%, 98% and 77%, respectively. Single and clinical combination of RF (clusters) had an high specificity, NPV and predictive accuracy for the specific etiologies (syndromes/metabolic/infiltrative disorders associated with HCM). Conclusions: An extensive diagnostic work up, focused on analysis of specific diagnostic RF in patients with unexplained LVH facilitates a clinical diagnosis in 74% of patients with HCM.

Cardiomyopathies (CMPs) are an increasingly recognized cause of heart failure and sudden death, particularly in young patients. Since their original description, major advances were achieved in the phenotype knowledge, natural history, and nosography of CMPs leading to different classification systems and therapies. However, a deeper knowledge of different causes, genotype-phenotype link, and natural history in different disease stages (preclinical, overt disease, and end-stage disease) according to a recognized standard of care (ie, international guidelines) is needed. Clinical registries can fill gaps in our knowledge regarding the uncovered issues on cause, clinical course, and management of CMPs.

BACKGROUND: The aim of the study was to detect if right ventricular (RV) ejection fraction assessed by real-time 3-dimensional echocardiography (RT3DE) could predict patients with dilated cardiomyopathy (DCM) with greater functional impairment in response to cardiopulmonary exercise. METHODS AND RESULTS: Seventy chronic heart failure patients with DCM (55.5 ± 9.1 years; 48 males; 30 ischemic; New York Heart Association Class III: 48) underwent both left ventricular (LV) and RV analysis by RT3DE. Postprocessing software provided data of RT3DE systolic dyssynchrony index of 16 LV segments (systolic dyssynchrony index [SDI]) and of both LV and RV ejection fraction. Cardiac magnetic resonance was performed in a subgroup of 40 DCM patients to confirm RT3DE measurements. All the patients underwent also bicycle cardiopulmonary exercise test with evaluation of oxygen consumption (VO2) peak% (percentage of the predicted value), VE/VCO2 slope, and circulatory power (CP). Mean LV ejection fraction was 29.8 ± 4.6%. RT3DE LV SDI index was 8.4.4 ± 4.2, and RV ejection fraction was 51.3 ± 4.6%. By cardiopulmonary test, mean VO2 peak was 15.2 ± 4.4 mL·kg·min, and mean CP was 2.1 ± 0.8. By univariable analyses, significant correlations were detectable between SDI index and VO2 peak% (r = -0.56; P < .0001) and peak CP (r = -0.48; P < .0005). Also RV ejection fraction directly correlated with VO2 peak% (r = 0.58; P < .0001) and inversely with VE/VCO2 slope (r = -0.44; P < .001). By multivariable analysis, SDI index (β coefficient = -0.46; P < .001) and 3D RV ejection fraction (β coefficient = 0.42; P < .001) emerged as the only independent determinants of VO2 peak% during cardiopulmonary test. CONCLUSIONS: Increased LV electromechanical dyssynchrony and impaired RV function in DCM patients are independently associated with worse ability to perform aerobic exercise.

BACKGROUND: The aim of this study was to define the range of left ventricular (LV) velocities and deformation indexes in highly trained athletes, analyzing potential differences induced by different long-term training protocols. METHODS: Standard echocardiography, pulsed-wave tissue Doppler echocardiography, and two-dimensional strain echocardiography of the interventricular septum and lateral wall were performed in 370 endurance athletes and 280 power athletes. Using pulsed-wave tissue Doppler, the following parameters of myocardial function were assessed: systolic peak velocities (S(m)), early (E(m)) and late (A(m)) diastolic velocities, and the E(m)/A(m) ratio. By two-dimensional strain echocardiography, peaks of regional systolic strain and LV global longitudinal strain were calculated. RESULTS: LV mass index and ejection fraction did not significantly differ between the two groups. However, power athletes showed an increased sum of wall thicknesses (P < .01) and relative wall thickness, while LV stroke volume and LV end-diastolic diameter (P < .001) were greater in endurance athletes. By pulsed-wave tissue Doppler analysis, E(m) and E(m)/A(m) at both the septal and lateral wall levels were higher in endurance athletes. By two-dimensional strain echocardiography, myocardial deformation indexes were comparable between the two groups. E(m)/A(m) ratios ≥ 1 were found in the overall population, while 90 % of athletes had an E(m) ≥ 16 cm/sec, S(m) ≥ 10 cm/sec, and global longitudinal strain ≤ -16%. Multivariate analyses evidenced independent positive association between Em peak velocity and LV end-diastolic volume (P < .001) and an independent correlation of global longitudinal strain with the sum of LV wall thicknesses (P < .005). CONCLUSIONS: This study describes the full spectrum of systolic and diastolic myocardial velocities and deformation indexes in a large population of competitive athletes.

We sought to analyze the prevalence, clinical course, and risk profile of left ventricular systolic dysfunction in adolescents with idiopathic dilated cardiomyopathy. Patients with clinical onset at 19 years (n = 14) of age and/or patients followed up for or =250 pg/ml (are under the curve 0.88) showed 100% sensitivity, 77% specificity, 62% positive predictive value, and 100% negative predictive value. In conclusion, compared to other clinical, echocardiographic, and biochemical parameters, the combination of advanced NYHA class, electrocardiographic atrial enlargement, and NT-pro-BNP > or =250 pg/ml seem to better predict the risk of adverse events in adolescent with long-term systolic dysfunction.

Previous reports have demonstrated that myocardial velocities are not sufficiently sensitive in fetal heart studies. Strain (S) and strain rate (SR) imaging is a new noninvasive ultrasonic technique able to quantify regional myocardial deformation properties. SR imaging has a superior sensitivity than myocardial velocity for noninvasive assessment of ventricular function, but this technique has not been used in the fetal heart. Our aim was to evaluate the feasibility of S/SR imaging in the fetal heart and to study characteristics of myocardial deformation properties and their changes with the gestational age in healthy fetuses. We studied 75 normal fetuses (weeks gestation 25 +/- 4, no evidence of structural cardiovascular disease by 2-D echo and Doppler study) using S/SR imaging. Left (LV) and right ventricle (RV) peak myocardial systolic, early diastolic and SR values during atrial contraction were obtained but, for S, we measured only peak systolic values. The sample volume was placed in the mid-segment of LV septal, lateral and RV free wall. S and SR curves were obtained in all the studied population. Peak longitudinal systolic deformation was homogeneous in all the walls studied. Moreover, fetal myocardial S and SR during diastole were characterized by a higher deformation during atrial contraction than during early filling. Peak systolic and peak diastolic ratios of regional myocardial deformation properties significantly correlated with the gestational age. Inter- and intraobserver variabilities for S and SR parameters were < 15%, < 18% and < 13%, < 15%, respectively. SR imaging is feasible in selected healthy fetuses, with a limited reproducibility; we presented normal values for the fetal heart; S/SR during fetal life are homogeneous in both LV and RV; and longitudinal myocardial deformation properties increase with the gestational age.

For the first time, peak systolic strain and strain rate (SR) were used to assess right ventricular (RV) and left ventricular (LV) regional function in children after transcatheter and surgical atrial septal defect (ASD) closure. Fifteen patients with successful ASD device closure (the ASD-D group, mean age 9 3 years), 15 age- and gender-matched patients with successful ASD surgical closure (the ASD-S group, mean age 9 3 years), and 15 age- and gender-matched controls were enrolled. Regional RV and LV longitudinal function was significantly reduced in the ASD-S group compared with controls in all the studied segments. The ASD-D group presented significantly (p

Cardiac arrhythmias and right chamber enlargement are well known long-term sequelae of atrial septal defect (ASD). Surgical ASD closure relieves patient symptoms but often fails to revert cardiac volume overload findings. Transcatheter ASD closure might be an attractive alternative to surgery, also because of the possibility to study the amount and time-course of the electro-geometric modifications following shunt disappearance. Between March 2000 and December 2002, 24 patients (age 22.7 +16.8 years) underwent percutaneous closure of large ASD (stretched diameter >20 mm and/or QP/QS ratio >1.5:1). ASD closure was performed with the Amplatzer Septal Occluder device (mean 25 +/- 7 mm), achieving a complete occlusion in all patients at 1 month. In 6 patients, right ventricular (RV) monophasic action potential was recorded during the procedure. All patients underwent standard 12-lead electrocardiography and transthoracic echocardiography before and at 24 hours and 1 month after ASD closure. After the procedure, monophasic action potential length increased from 359 +/- 27 to 372 +/- 27 ms (p

We describe an acute myocardial infarction in a young athlete with non-obstructive hypertrophic cardiomyopathy (HCM) and normal coronary arteries. A 18 year old athlete came to our attention for dispnoea and chest pain during effort. Echocardiography showed non-obstructive HCM, with restrictive physiology. Cardiac catheterization and coronary angiography showed elevated pulmonary artery pressure and normal coronary arteries. He was discharged on sotalol and diuretics. Nine months later, he was resuscitated from a cardiac arrest during mild effort. The ECG revealed a high rate of atrial fibrillation with significant ST-T changes, and echocardiography an akinesia of interventricular septum. Cardiac enzymes were elevated. The coronary angiogram showed normal coronary arteries. This case is important as a reminder that acute myocardial infarction is not only due to coronary artery disease, and that atrial fibrillation may represent a trigger of serious cardiovascular events in patients with HCM.