Pathophysiology-Based Management of Acute Heart Failure.

Even though acute heart failure (AHF) is one of the most common admission diagnoses globally, its pathogenesis is poorly understood, and there are few effective treatments available. Despite an heterogenous onset, congestion is the leading contributor to hospitalization, making it a crucial therapeutic target. Complete decongestion, nevertheless, may be hard to achieve, especially in patients with reduced end organ perfusion. In order to promote a personalised pathophysiological-based therapy for patients with AHF, we will address in this review the pathophysiological principles that underlie the clinical symptoms of AHF as well as examine how to assess them in clinical practice, suggesting that gaining a deeper understanding of pathophysiology might result in significant improvements in HF therapy.

Levosimendan as a "Bridge to Optimization" in Patients with Advanced Heart Failure with Reduced Ejection-A Single-Center Study.

Background: Patients with advanced heart failure with reduced ejection fraction often cannot tolerate target doses of guideline-directed medical therapy due to symptomatic hypotension, renal dysfunction, and associated electrolyte abnormalities. While levosimendan can facilitate the titration of ß-blockers in patients with advanced HFrEF, it is unclear whether ambulatory levosimendan infusions would offer the same benefit. In this prospective study, we investigate the effects of intermittent ambulatory levosimendan infusions on the uptitration of disease-modifying drugs. Methods: We enrolled 37 patients with advanced HFrEF who received repeated ambulatory infusions of levosimendan between January 2018 and January 2021. The demographic, clinical, and laboratory data were acquired 24 h before the first and the last ambulatory levosimendan infusion. Results: At the 1 year follow-up, the enrolled patients were on significantly higher doses of guideline-directed medical therapy, including bisoprolol (3.2 ± 2.8 mg vs. 5.9 ± 4.1 mg; p = 0.02), sacubitril/valsartan (41.67 ± 32.48 mg vs. 68.5 ± 35.72 mg; p = 0.01), and eplerenone (12.7 ± 8.5 mg vs. 22.8 ± 13.6 mg; p = 0.03). Furthermore, a substantial decrease in the furosemide dose was observed (123.2 ± 32.48 mg vs. 81.6 ± 19.47 mg; p < 0.0001). Conclusions: Levosimendan facilitates the optimization of disease-modifying heart failure medications in previously intolerant advanced HFrEF patients.

Echocardiography in Advanced Heart Failure for Diagnosis, Management, and Prognosis.

Advanced heart failure, an end-stage disease characterized by high mortality and morbidity despite standard medical therapy, requires various therapeutic strategies like heart transplant and long-term mechanical circulatory support. Echocardiography is the main imaging technique to identify transitions to advanced stages of disease and guide risk stratification and therapeutic decision-making processes. Progressive development of advanced echocardiographic techniques allows more comprehensive assessment of the hemodynamic and structural profiles of patients with advanced heart failure, and its use in clinical practice continues to expand. This article provides an overview of basic and emerging echocardiographic tools to assess patients with advanced heart failure.

Use of sacubitril/valsartan as 'bridge to transplant' in patients with end-stage hypertrophic cardiomyopathy.

The end stage or burned-out phase is an uncommon but challenging clinical evolution of hypertrophic cardiomyopathy (HCM). The management of end-stage HCM is empirically based on the use of drugs approved for heart failure with reduced ejection fraction; however, cardiac transplantation often represents the best option to improve survival. In our case, we describe the use of sacubitril/valsartan as a 'bridge to transplant' in a patient with end-stage HCM. After introducing the drug, enhancements in functional capacity, a reduction in natriuretic peptides and an increase in left ventricular ejection fraction occurred. Given their improved volume of oxygen consumption (VO2) peak and hemodynamic parameters, our patient was left off the waiting list for cardiac transplant and continues to be regularly followed-up with every 3 months.

Exercise-based rehabilitation strategies in heart transplant recipients: Focus on high-intensity interval training.

Despite progressive improvement in medical therapy and standard care, the exercise capacity of heart transplant recipients is reduced compared with age-matched healthy individuals. Exercise-based rehabilitation programs have been shown to improve the exercise capacity of transplant patients through a multifactorial effect. In this context, high-intensity interval exercise is a growing field of research, with current evidence suggesting a major benefit in heart transplant recipients compared with a conventional training protocol. Therefore, this study aimed to provide an overview of the mechanisms involved in the reduced exercise capacity of heart transplant patients and a review of current rehabilitation strategies with a special focus on the mechanisms and clinical effects of high-intensity interval training exercise.

Effects of Sacubitril/Valsartan on the Right Ventricular Arterial Coupling in Patients with Heart Failure with Reduced Ejection Fraction.

BACKGROUND: right ventricle-pulmonary artery (RV-PA) coupling assessed by measuring the tricuspid anular plane systolic excursion (TAPSE)/pulmonary artery systolic pressure (PASP) ratio has been recently proposed as an early marker of right ventricular dysfunction in patients with heart failure with a reduced ejection fraction (HFrEF). METHODS: As the effects of sacubitril/valsartan therapy on RV-PA coupling remain unknown, this study aimed to analyse the effect of this drug on TAPSE/PASP in patients with HFrEF. We retrospectively analysed all outpatients with HFrEF referred to our unit between October 2016 and July 2018. RESULTS: At the 1-year follow-up, sacubitril/valsartan therapy was associated with a significant improvement in TAPSE (18.26 ± 3.7 vs. 19.6 ± 4.2 mm, p < 0.01), PASP (38.3 ± 15.7 vs. 33.7 ± 13.6, p < 0.05), and RV-PA coupling (0.57 ± 0.25 vs. 0.68 ± 0.30 p < 0.01). These improvements persisted at the 2-year follow-up. In the multivariable analysis, the improvement in the RV-PA coupling was independent of the left ventricular remodelling. CONCLUSIONS: in patients with HFrEF, sacubitril/valsartan improved the RV-PA coupling; however, further trials are necessary to evaluate the role of sacubitril/valsartan in the treatment of right ventricle (RV) dysfunction either associated or not associated with left ventricular dysfunction.

Berlin Heart EXCOR® pediatric ventricular assist device in a patient with Sotos syndrome: a case report.

INTRODUCTION: Berlin Heart EXCOR® pediatric ventricular assist device is a mechanical circulatory support device currently used in pediatric patients. Sotos syndrome is a well-described multiple anomaly syndrome characterized by overgrowth, distinctive craniofacial appearance, cardiac abnormalities, and variable learning disabilities. CASE PRESENTATION: We describe a 7-year-old female Caucasian child with classic Sotos syndrome features subjected to implantation of Berlin Heart EXCOR® pediatric biventricular assist device mechanical support. A heart transplant was carried out after a support time of 459 days. After 5 years of follow-up, our patient is clinically stable and the performance of the transplanted heart is excellent. CONCLUSION: This case confirms that Berlin Heart EXCOR® pediatric ventricular assist device can provide satisfactory and safe circulatory support for children with end-stage heart diseases, even in those with Sotos syndrome. The syndrome is not a contraindication to implantation, since the complications are the same as those observed in patients without the syndrome and the prognosis is not affected by the disease.

Beta Blockers Up-Titration in Patients with Heart Failure Reduced Ejection Fraction and Cardiac Resynchronization Therapy, a Single Center Study.

Clinical trials have shown the benefits of ß-blockers therapy in patients with heart failure reduced ejection fraction. These benefits include improved survival and a reduced need for hospitalization. Cardiac resynchronization therapy has emerged as an essential device-based therapy for symptomatic patients with heart failure reduced ejection fraction despite optimal pharmacologic treatment. The extent to which ß-blockers are being utilized in patients receiving cardiac resynchronization therapy is not well known. In this study, we evaluate the possibility of increasing ß-blockers doses in an unselected cohort of heart failure reduced ejection patients after cardiac resynchronization therapy capable defibrillator system implantation and the correlation between ß-blockers treatments and clinical outcome. Methods and results: Patients with heart failure reduced ejection fraction in ß-blockers therapy that underwent cardiac resynchronization therapy capable defibrillator system implantation between July 2008, and December 2016 were enrolled in the study. The ß-blockers dose was determined at the time of discharge and during follow-up. Cardiovascular mortality, hospitalization for worsening heart failure or arrhythmic storm and appropriate intervention of the device, were recorded. The study cohort included 480 patients, 289 patients (60.3%) had ß-blockers doses equal to the dose before CRT (Group 1), 191 patients (39.7%) had higher ß-blockers doses than those before the CRT implant (Group 2). Comparing the two groups, Group 2 have lower cardiovascular mortality, heart failure-related hospitalization, and arrhythmic events than Group 1. Conclusion: After initiating CRT, ß-blockers could be safely up-titrated at higher doses with the reduction in mortality, heart failure-related hospitalization, and arrhythmic events.

Left Atrial Volume during Stress Is Associated with Increased Risk of Arrhythmias in Patients with Hypertrophic Cardiomyopathy.

INTRODUCTION: In patients affected by hypertrophic cardiomyopathy (HCM), left atrial volume index (LAVi) is associated with an increased risk of tachyarrhythmias and major clinical events. To date, the clinical meaning of LAVi measured during exercise (stress LAVi [sLAVi]) has not yet been investigated in HCM. This study sought to evaluate the correlation between LAVi/sLAVi and clinical outcome (risk of arrhythmias and heart failure [HF]) in patients with HCM. METHODS AND RESULTS: We enrolled a total of 51 consecutive patients with HCM (39 men; mean age: 39.41 ± 17.9 years) who underwent standard and stress echocardiography, following a common protocol. During follow-up (median follow-up was 1.82 years), the following composite endpoints were collected: ARRHYT endpoint (atrial fibrillation, paroxysmal supraventricular tachycardia, nonsustained ventricular tachycardia (VT), sustained VT, ventricular fibrillation, syncope of likely cardiogenic nature, and sudden cardiac death) and HF endpoint (worsening of functional class and left ventricular ejection fraction, hospitalization, and death for end-stage HF). Eight patients were lost at follow-up. ARRHYT endpoint occurred in 13 (30.2%) patients (8, 18.6%, supraventricular and 10, 23.2%, ventricular arrhythmias), whereas HF endpoint occurred in 5 (11.6%) patients. sLAVi (mean value of 31.16 ± 10.15 mL/m2) performed better than rLAVi as a predictor of ARRHYT endpoint (Akaike Information Criterion: 48.37 vs. 50.37, if dichotomized according to the median values). A sLAVi value of 30 mL/m2 showed a predictive accuracy of 72.1% (C-statistics of 0.7346), with a high negative predictive value (87.5%). CONCLUSION: These findings encourage future studies on sLAVi, as a potential predictor of arrhythmias and adverse outcome in patients with HCM.

Risk Stratification of Sudden Cardiac Death in Patients with Heart Failure: An update.

Heart failure (HF) is a complex clinical syndrome in which structural/functional myocardial abnormalities result in symptoms and signs of hypoperfusion and/or pulmonary or systemic congestion at rest or during exercise. More than 80% of deaths in patients with HF recognize a cardiovascular cause, with most being either sudden cardiac death (SCD) or death caused by progressive pump failure. Risk stratification of SCD in patients with HF and preserved (HFpEF) or reduced ejection fraction (HFrEF) represents a clinical challenge. This review will give an update of current strategies for SCD risk stratification in both HFrEF and HFpEF.

Diagnostic Clues for the Diagnosis of Nonsarcomeric Hypertrophic Cardiomyopathy (Phenocopies): Amyloidosis, Fabry Disease, and Mitochondrial Disease.

Hypertrophic cardiomyopathy (HCM) is the most common known inherited heart disorder, with a prevalence of 1:500 of the adult population. Etiology of HCM can be heterogeneous, with sarcomeric gene disease as the leading cause in up to 60% of the patients, and with a number of possible different diseases (phenocopies) in about 10%-15% of the patients. Early diagnosis of storage and infiltrative disorders, particularly those with specific treatments (i.e., Fabry disease and/or amyloidosis), means early management and treatment, with a significant impact on patients prognosis. Here, we report on four different cases of HCM, highlighting difficulties to make differential diagnosis of different forms of cardiomyopathies, and their potential impact on the management.

Management of Arrhythmias in Heart Failure.

Heart failure patients are predisposed to develop arrhythmias. Supraventricular arrhythmias can exacerbate the heart failure symptoms by decreasing the effective cardiac output and their control require pharmacological, electrical, or catheter-based intervention. In the setting of atrial flutter or atrial fibrillation, anticoagulation becomes paramount to prevent systemic or cerebral embolism. Patients with heart failure are also prone to develop ventricular arrhythmias that can present a challenge to the managing clinician. The management strategy depends on the type of arrhythmia, the underlying structural heart disease, the severity of heart failure, and the range from optimization of heart failure therapy to catheter ablation. Patients with heart failure, irrespective of ejection fraction are at high risk for developing sudden cardiac death, however risk stratification is a clinical challenge and requires a multiparametric evaluation for identification of patients who should undergo implantation of a cardioverter defibrillator. Finally, patients with heart failure can also develop symptomatic bradycardia, caused by sinus node dysfunction or atrio-ventricular block. The treatment of bradycardia in these patients with pacing is usually straightforward but needs some specific issue.

Exercise speckle-tracking strain imaging demonstrates impaired right ventricular contractile reserve in hypertrophic cardiomyopathy.

AIMS: To analyse right ventricular (RV) systolic function in patients with hypertrophic cardiomyopathy (HCM) at rest and during exercise, and its possible correlation with left ventricular(LV) morphology and function. METHODS AND RESULTS: Standard echo, exercise stress echo, and RV 2D speckle-tracking strain (2DSE) were performed in 45 patients with HCM and in 45 age- and sex-comparable healthy controls. RV global longitudinal strain (GLS) was calculated by averaging local strains along the entire right ventricle. LV mass index and IVS wall thickness were significantly increased in HCM, while LV ejection fraction, RV diameters, RV tissue Doppler systolic peak and the RV end-systolic pressure-area relationship at rest were comparable between the two groups. Conversely, all transmitral Doppler indexes were significantly impaired in HCM. In addition, RV GLS and regional peak myocardial RV strains were significantly reduced in patients with HCM (all P<0.001). During physical effort, LV ejection fraction was comparable between the two groups. Conversely, LV E/Em ratio was significantly increased in HCM. Increase in TAPSE and RV tissue Doppler Sm peak velocity during effort were similar between the two groups. Conversely, increases of RV end-systolic pressure-area, regional and global RV strain were significantly lower in HCM patients (RV lateral strain: 10.3±3.5% of increase in HCM vs 20.5±4.5% in controls; p<0.0001). Multivariable analysis detected independent associations of RV lateral strain at peak stress with LV IVS thickness, maximal workload during exercise, and LV E/Em ratio during effort (all p<0.0001). An RV lateral 2DSE cut-off point of -14% differentiated controls and HCM with an 86%sensitivity and a 92% specificity. CONCLUSIONS: RV contractile reserve for HCM is impaired and this suggests that the lower resting values of RV in HCM may represent early subclinical myocardial damage, closely associated with exercise capacity.

Non sustained ventricular tachycardia in hypertrophic cardiomyopathy and new ultrasonic derived parameters.

BACKGROUND: The mechanism of sudden death in hypertrophic cardiomyopathy (HCM) is ventricular tachyarrhythmia emanating from myocyte disarray, fibrosis, and inhomogeneity in intramyocardial activation. Tissue synchronization imaging (TSI) allows the measurement of regional delay, while two-dimensional strain can be used to identify myocardial fibrosis. The aim of this study was to assess the relationship between new ultrasonically derived parameters and nonsustained ventricular tachycardia (NSVT) in patients with HCM. METHODS: Ninety-three patients with HCM (mean age, 36 +/- 16 years) and 30 patients with hypertension with secondary left ventricular (LV) hypertrophy (mean age, 42 +/- 10 years; 65% men) were studied. All underwent standard echocardiographic, TSI, and two-dimensional strain examinations. Patients were followed every 3 months for 2 years. Holter monitoring was performed every 3 months. The primary endpoint was the occurrence of NSVT. RESULTS: Twenty-four patients (26%) had >or=1 episode of NSVT. Patients with NSVT had a higher value of maximal LV thickness (22 +/- 6 vs 19 +/- 5 mm, P = .04). There were no significant associations between NSVT on Holter monitoring and LV outflow gradient, New York Heart Association class, syncope, and medical therapy. N-terminal pro-brain natriuretic peptide values were significantly (P = .01) higher in patients with NSTV (1034 +/- 1088 vs 561 +/- 593 pg/mL). Patients with HCM and NSVT had (1) similar values on TSI-studied parameters to patients without NSVT, (2) significant reductions in basal and mid septal strain and in basal anterior-septal strain, and (3) more frequently peak systolic strain >or= -10% (P < .0001). In multivariate analysis, the presence of >3 LV segments with longitudinal two-dimensional strain >or= -10% (sensitivity, 81%; specificity, 97.1%; area under the curve, 0.944; P < .0001) was an independent predictor of NSVT. CONCLUSIONS: Using a simple, inexpensive, easily available, and bedside-usable tool, it was possible to recognize with good sensitivity and specificity patients with HCM at higher risk for NSVT.

Atrial myocardial deformation properties in obese nonhypertensive children.

BACKGROUND: Obesity in adulthood is associated with a higher occurrence of atrial arrhythmias. Obese children, without arterial hypertension, may be a unique clinical opportunity to evaluate the effect of obesity, per se, on atrial myocardial function, excluding the influence of possible comorbidities. We sought to define the preclinical effects of obesity on the atrial function of healthy children with excess weight who have no other clinically appreciable cause of heart disease, by using the more sensitive ultrasonic-derived strain (S) and S rate imaging. METHODS: We studied 320 children divided into two groups: obese children (group O; n = 160; age 12 +/- 3 years); and healthy lean children, comparable for age, sex, and pubertal stage (referents; n = 160; mean age 12 +/- 3 years). RESULTS: Systolic blood pressure (BP) and diastolic BP, as well as 24-hour systolic BP and 24-hour diastolic BP were comparable between groups. Left ventricular mass/height(2.7) and left atrial dimensions were increased (P < .0001) in group O (46 +/- 12 g/m(2.7)) compared with referents (31 +/- 14 g/m(2.7)). Standard echocardiographic indices of global left ventricular systolic function were similar in the two groups. Obese children showed atrial peak systolic S rate (2.5 +/- 1.2 (s-1)) values lower (P < .0001) than that of referents (4.9 +/- 1.6(s-1)) in both left and right atria. In multivariable analysis, average peak systolic atrial S was significantly correlated with glycemia (P < .05, coefficient -0.23), body mass index (P < .01, coefficient -0.19), and left ventricular mass (P < .05, coefficient -0.17). CONCLUSIONS: Our study demonstrated that obesity, in absence of hypertension, is associated with reduced atrial myocardial deformation properties already in childhood involving both right and left atria.

Abnormal regional myocardial deformation properties and increased aortic stiffness in normotensive patients with aortic coarctation despite successful correction: an ABPM, standard echocardiography and strain rate imaging study.

The long-term follow-up data subsequent to a successful repair of AoC (aortic coarctation) show that life expectancy remains reduced. Previous standard echocardiographic studies have demonstrated normal or increased systolic cardiac function in patients following successful repair of AoC. SR (strain rate) imaging is a new technique able to detect subclinical myocardial abnormalities. In the present study we investigated whether young patients (without hypertension, as assessed using ambulatory blood pressure monitoring and an exercise test) following successful AoC repair already have abnormal myocardial deformation properties, and the relationship of the deformation properties with aortic stiffness. We studied 166 subjects, 83 AoC non-hypertensive patients (mean age 12+/-4 years) a number of years after successful repair of AoC and 83 age- and sex-matched subjects as controls. Peak systolic SR (1/s) for both regional longitudinal and radial function was assessed. The aortic stiffness index was calculated from the echocardiographically derived thoracic aortic diameters, and the measurement of blood pressure was obtained by cuff sphygmomanometry. The LV (left ventricular) ejection fraction was significantly increased in AoC patients, whereas regional longitudinal SRs were significantly reduced (-1.1+/-0.9 compared with -2+/-0.5, P<0.0001) in patients. The aortic stiffness index was significantly increased in AoC patients (12+/-9, P<0.0001). At multilinear regression analysis, age at repair (P=0.005; coefficient, -0.201; S.E.M., 0.027) and the aortic stiffness index (P=0.0029; coefficient, 0.334; S.E.M., 0.423) predicted longitudinal SR. Despite the presence of a successful repair for AoC, in the absence of hypertension, longitudinal deformation properties were significantly impaired. Moreover, the degree of longitudinal SR impairment was correlated with age at repair and aortic stiffness. Early repair can delay the onset of hypertension in postcoarctectomy patients, but cannot prevent the innate structural and functional abnormalities of the aorta and their deleterious effect on myocardial deformation properties.

Left ventricle myocardial mechanics and textural properties in patients with Williams syndrome.

OBJECTIVE: To study left ventricular mechanics and textural properties in patients with Williams syndrome to define the impact of left ventricular hypertrophy on the functional findings. METHODS: Echocardiography was performed in 16 Williams syndrome patients (aged 1-25 years, mean 10 +/- 6 years), four with associated supravalvular aortic stenosis and seven with systemic hypertension. Fifteen age- and body surface area-matched subjects were selected as control group. Particularly, left ventricular geometry, myocardial contractility [midwall rate-corrected circumferential fiber shortening/end-systolic meridional wall stress relationship (sigmaes)] and left ventricular diastolic function (mitral flow pattern and isovolumic relaxation time) were defined. In addition, integrated backscatter (IB) analysis intensity (IntIB) and cyclic variation (CVIB) were assessed for an ultrasonic myocardial characterization. RESULTS: Left ventricular hypertrophy was demonstrated in nine patients (56%) and abnormal left ventricular remodeling in ten patients (62%). Particularly seven of seven hypertensive patients and three of four patients with supravalvular aortic stenosis had abnormal remodeling; left ventricular geometry was normal in patients without hypertension or supravalvular aortic stenosis. In addition, midwall rate-corrected circumferential fiber shortening/(sigmaes) relationship was within the normal range in all patients. At integrated backscatter analysis, Williams syndrome patients showed, both at interventricular septum and posterior wall, reduced CVIB (9.36 +/- 2.16 versus 10.3 +/- 1.3 and 8.65 +/- 2 versus 10.5 +/- 1.1). Compared to Williams syndrome patients without left ventricular hypertrophy (7/16), those with left ventricular hypertrophy (9/16) showed decreased mitral E/A ratio (1.32 +/- 0.09 versus 1.62 +/- 0.02), increased isovolumic relaxation time (68 +/- 7 versus 53 +/- 7) and increased IntIBS at interventricular septum (-27.3 +/- 0.07 versus -34 +/- 5). CONCLUSIONS: Our data obtained in young Williams syndrome patients show that: (i) mild left ventricular functional and textural abnormalities may be detected also in absence of significant supravalvular aortic stenosis and/or hypertension; (ii) significant left ventricular hypertrophy may develop since childhood; (iii) differences in left ventricular remodeling and/or degree of left ventricular hypertrophy may occur. Further studies are required to define the real impact of the functional abnormalities on the natural history in patients with Williams syndrome.

Abnormal myocardial deformation properties in obese, non-hypertensive children: an ambulatory blood pressure monitoring, standard echocardiographic, and strain rate imaging study.

AIMS: The prevalence of obesity is increasing among children in the developed world. The association of obesity and abnormal cardiac function is still debated. The reported changes may reflect the role of comorbidities that contribute to ventricular dysfunction. Obese children, without arterial hypertension, may be a unique clinical opportunity to evaluate the effect of obesity, per se, on myocardial function, excluding the influence of possible comorbidities. We sought to define the preclinical effects of obesity on the cardiovascular system, of healthy children with excess weight who have no other clinically appreciable cause of heart disease, using the more sensitive ultrasonic-derived strain and strain rate (SR) imaging. METHODS AND RESULTS: We studied 300 subjects divided into two groups: (i) obese children (Group O: n=150; age, 12+/-3 years); (ii) healthy lean children comparable for age, sex, and pubertal stage (Referents: n=150; mean age, 12+/-3 years). Systolic (SBP) and diastolic blood pressure (DBP), as well as 24 h-SBP and 24 h-DBP were comparable between groups. Left ventricular (LV) mass/height(2.7) was increased (P<0.0001) in Group O (46+/-12 g/m(2.7)) when compared with Referents (31+/-14 gm(2.7)). Standard echocardiographic indices of global systolic function were similar in the two groups. Intima-media thickness measured at the common carotid artery was not significantly different (P=0.4) in obese children (0.46+/-0.09 mm) when compared with Referents (0.45+/-0.07 mm). Obese children showed regional longitudinal peak systolic myocardial deformation properties (SR=-1.4+/-0.7 s(-1)) lower (P<0.0001) than those of Referents (SR=-2.2+/-0.5) in both left and right ventricle. In multivariable analysis, average peak systolic SR was significantly correlated with homeostasis model assessment of insulin resistance (P<0.01; coefficient, 0.02; SE, 0.011), and insulin serum concentration (P<0.01; coefficient, 0.05; SE, 0.023). Average LV peak systolic strain was significantly correlated with body mass index (P=0.0001; coefficient, 0.06; SE, 0.016), LVM/H(2.7) (P=0.006; coefficient, 0.016; SE, 0.018). CONCLUSIONS: Our study demonstrated that obesity, in absence of hypertension, is associated with significant reduction in systolic myocardial deformation properties already in childhood involving both right and left ventricle. Obesity not only is a risk factor for later cardiovascular disease, but also is associated with contemporaneous and significant impairment of longitudinal myocardial deformation properties.