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Ambulatory electrocardiographic monitoring is still a useful tool in the hands of the clinical cardiologist, for both the diagnosis of many pathologies and the management of long-term therapy. The evolution of the instrumentation, which has become sophisticated but at the same time more manageable and easy to use, has made it possible to evaluate many parameters and data. The aim of this review is to provide a general overview of this old, but not obsolete tool, to describe the main indications for its use in the light of new scientific evidence and to offer a practical guide for its appropriate use and reporting.

To test whether two-dimensional longitudinal strain (2DSE) performed after revascularization by percutaneous coronary intervention (PCI) could predict left ventricular (LV) remodeling in patients with recent non-ST elevation myocardial infarction (NSTEMI).In 70 patients (62.7 ± 8.7 years) with recent NSTEMI (between 72 hours and 14 days), undergoing coronary angiography for recurrent angina, myocardial deformation parameters were measured by 2DSE before and 24 hours after reperfusion therapy. Strain in all LV segments was averaged to obtain a global value (Global longitudinal Strain--GLS). Infarct size was estimated by clinical parameters and cardiac markers. After 6 months from intervention, LV negative remodeling was defined as lack of improvement of LV function, with increase in LV end-diastolic volume of greater than or equal than 15%.At follow-up, patients were subdivided into remodeled (n=32) and non-remodeled (n = 38) groups. Patients with negative LV remodeling had significantly lower baseline LV ejection fraction (44.8±6.9 vs. 48.7 ± 5.5 %; p0.05), higher peak troponin I (p0.001) and reduced GLS (- 10.6±6.1 vs - 17.6 ± 6.7 % p0.001) than those without LV remodeling. GLS showed a close correlation with peak troponin I after PCI (r = 0.64, P0.0001) and LV WMSI (r = 0.42, p0.01). By multivariable analysis, diabetes mellitus (P0.005), peak of Troponin I after PCI (P0.0005), GLS at baseline (OR: 4.3; p0.0001), and lack of improvement of GLS soon after PCI (OR: 1.45, P0.01) were powerful independent predictors of negative LV remodelling at follow-up. In particular, a GLS ≤ 12 % showed a sensitivity and a specificity respectively of 84.8% and 87.8% to predict negative LV remodelling at follow-up.in patients with recent NSTEMI, longitudinal LV global and regional speckle-tracking strain measurements are powerful independent predictors of LV remodeling after reperfusion therapy.

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.

Objective: In dilated cardiomyopathy (DCM), right ventricular (RV) dysfunction has been reported and attributed both to altered loading conditions and to RV involvement in the myopathic process. The aim of the study was to detect RV myocardial function in DCM using two-dimensional (2D) strain echocardiography and to assess the effects of cardiac resynchronization therapy (CRT) on RV myocardial strain during a 6-month follow-up. Methods and Results: A total of 110 patients (mean age: 55.4 ± 11.2 years) with either idiopathic (n = 60) or ischemic (n = 50) DCM, without overt clinical signs of RV failure, underwent standard echo and 2D strain analysis of RV longitudinal strain in RV septal and lateral walls. The two groups were comparable for clinical variables (New York Heart Association class III in 81.8%). Left ventricular volumes, ejection fraction, stroke volume, and mitral valve effective regurgitant orifice were similar between the two groups. No significant differences were evidenced in Doppler mitral and tricuspid inflow measurements. RV diameters were mildly increased in patients with idiopathic DCM, while RV tricuspid annulus systolic excursion and Tei-index were comparable between the two groups. RV global longitudinal strain and regional peak myocardial strain were significantly impaired in patients with idiopathic DCM compared with those having ischemic DCM (all P < 0.001). Using left ventricular end-systolic volume as marker for response to CRT, 70 patients (63.3%) were long-term responders. Ischemic DCM patient responders to CRT showed a significant improvement in RV peak systolic strain. Conversely, in patients with idiopathic DCM and in ischemic patients nonresponders to CRT, no improvement in RV function was evidenced. By multivariable analysis, in the overall population, ischemic etiology of DCM (P < 0.0001), positive response to CRT (P < 0.001), and longitudinal intraventricular dyssynchrony (P

Background and aim Most but not all studies in children, adolescents and young adults with a family history of coronary artery disease have reported an increase in lipoprotein(a) (Lp(a)) concentrations. The aim of this study was to assess if healthy children, adolescents and young adults with a parental history of premature myocardial infarction (PHPMI) have increased Lp(a) levels and are at higher risk of elevated (>30mg/dl) Lp(a) concentrations. Methods and results One hundred fifty healthy children, adolescents and young adults with PHPMI (55% males; age 18±6.7years) and 150 age- (±1year) and gender-matched control subjects participated in the study. Concentrations of total plasma cholesterol, low-density lipoprotein (LDL)-cholesterol, high density lipoprotein (HDL)-cholesterol, apolipoprotein (Apo) A-I and B, triglycerides and Lp(a) were determined after fasting for 14h. Participants with PHPMI had higher concentrations of LDL-cholesterol (107.9±31.1 vs. 99.2±28.7mg/dl, p =0.01), Apo B (89.6±26.4 vs. 82.8±20.2mg/dl, p =0.011) and Lp(a) (26.7±34.0 vs. 19.2±23.2mg/dl, p =0.012) and lower HDL-cholesterol concentrations (47.9±11.3 vs. 50.7±13.9mg/dl, p =0.038) than participants without PHPMI. Thirty percent of PHPMI positive subjects had elevated Lp(a) concentrations vs. 16.7% of PHPMI negative subjects ( p =0.009; relative risk 2.14; 95% CI 1.23–3.73). In a conditional logistic regression analysis, Lp(a) concentration was significantly and independently associated with PHPMI. Conclusions Healthy young subjects with PHPMI have increased Lp(a) levels, a higher risk for elevated Lp(a) concentrations within an unfavourable lipid profile.

Background/objective: Increased carotid intima-media thickness (IMT) is an early manifestation of atherosclerosis. Our group has previously demonstrated that a parental history of premature myocardial infarction (PHPMI) is associated with an increase in carotid IMT in children-adolescents (mean age 13 years) and young adults (mean age 24 years). The aim of the present study was to evaluate if carotid structural changes are detectable in young children with PHPMI. Methods: 26 healthy children (9 males and 17 females; 5–12 years, mean age 9.1 (2.5) years) with PHPMI and 26 age-matched (plus or minus 1 year), sex-matched and body mass index-matched (BMI; plus or minus 20%) control subjects were enrolled in the study. They underwent high resolution B-mode ultrasonographic evaluation of common carotid artery IMT. Lipid profile, resting blood pressure and BMI were also evaluated. Results: Compared to controls, subjects with PHPMI had increased IMT of common carotid arteries (mean of combined sites: 0.444 (0.076) mm versus 0.382 (0.062) mm in controls, p = 0.001). Offspring of coronary patients showed an unfavourable lipid profile compared to controls; however, the association between a PHPMI and carotid IMT was independent of lipids, apolipoproteins and other traditional risk factors. Conclusions: Vascular structural changes are detectable in subjects with PHPMI at a young age and occur independently of several traditional cardiovascular risk factors.

Aims In dilated cardiomyopathy (DCM), attenuation of left atrial (LA) booster pump function has been observed, and attributed both to altered LA loading conditions owing to left ventricular (LV) diastolic dysfunction and to LA involvement in the myopathic process. The aim of the present study was to detect LA systolic dysfunction in DCM using speckle-tracking two-dimensional strain echocardiography (2DSE), and to assess the effects of cardiac resynchronization therapy (CRT) on LA myocardial strain during 6 month follow-up. Methods and results A total of 90 patients (aged, 52.4+10.2 years) with either idiopathic (n = 47) or ischaemic (n = 43) DCM underwent standard Doppler echo and 2DSE analysis of atrial longitudinal strain in the basal segments of LA septum and LA lateral wall, and in LA roof. The two groups were comparable for clinical variables (NYHA class: III in 72.2%; IV in 27.8%). LV volumes, ejection fraction, stroke volume, and mitral valve effective regurgitant orifice were similar between the two groups. No significant differences were evidenced in Doppler transmitral inflow measurements. LA diameter and maximal volume were also similar between the two groups. Conversely, LA active emptying volume and fraction were both lower in patients with idiopathic DCM. Peak systolic myocardial atrial strain was significantly compromised in patients with idiopathic DCM compared with ischaemic DCM in all the analysed atrial segments (P , 0.001). At follow-up, 64 patients (71.1%) (37 idiopathic and 27 ischaemic) were responders, and 26 (28.9%) (10 idiopathic; 16 ischaemic) were non-responders to CRT (responder: decrease of LV end-systolic volume .15%). A significant improvement in LA systolic function was obtained only in patients with ischaemic DCM responders to CRT (P , 0.001). By multivariable analysis, in the overall population, it was found that ischaemic aetiology of DCM (b-cofficient = 0.62; P , 0.0001) and positive response to CRT (b-cofficient = 0.42; P , 0.01) were the only independent determinants of LA lateral wall systolic strain. Conclusions Two-dimensional strain represents a promising non-invasive technique to assess LA atrial myocardial function in patients with DCM. LA pump and reservoir function at baseline and after CRT are more depressed in idiopathic compared with ischaemic DCM patients. Future longitudinal studies are warranted to understand further the natural history of LA myocardial function, the extent of reversibility of LA dysfunction with CRT, and the possible prognostic impact of such indexes in patients with congestive heart failure.

Athletes heart is a left ventricular adaptation to long-term, intensive training which includes changes as increased cavity diameter, wall thickness and mass. Even if the standard 2-dimensional echocardiography represents an irreplaceable method in the evaluation of cardiac adaptations to physical exercise, the data currently available suggests the usefulness of Doppler Myocardial Imaging (DMI) in the assessment of the myocardial systolic and diastolic function of the athletes heart. In particular, DMI analysis in the trained subject has demonstrated interesting prospective for : 1) the differential diagnosis from pathological left ventricular hypertrophy due to Hypertrophic Cardiomyopathy (HCM); 2) the prediction of cardiac performance during physical effort; 3) the evaluation of the bi-ventricular interaction; 4) the analysis of the myocardial adaptations to various training protocols; 5) the early identification of specific genotypes associated with cardiomyopathies. Such a combined use of standard 2-D echo and DMI may be taken into account for a valid noninvasive and easy-repeatable evaluation of both physiological and pathological ventricular hypertrophy.

Background Conflicting data have been reported about the nature (physiologic versus pathologic) of left ventricular (LV) hypertrophy in master athletes. Aim of the study To analyze LV and right ventricular (RV) myocardial function in master athletes with LV hypertrophy induced by either endurance or strength training. Methods Standard Doppler echo and colour Doppler Myocardial Imaging (DMI) of LV and of RV basal lateral walls were performed in 40 competitive master (>45years) endurance athletes (ATE), in 20 master strength-trained athletes (ATS) and 25 age-matched healthy sedentary subjects, all males. By use of DMI, the following parameters of myocardial function were assessed: systolic peak velocities, precontraction time, contraction time, early (E m ) and late ( A m ) diastolic peak velocities, E m / A m ratio, relaxation time. Results The two groups were comparable for age, but ATS at rest showed higher heart rate, systolic blood pressure, and body surface area. LV mass index did not significantly differ between the two groups of athletes. However, ATS showed increased wall thickness and relative wall thickness, while LV stroke volume and both LV and RV end-diastolic diameters were greater in ATE. All transmitral and transtricuspid Doppler indexes were higher in ATE. DMI analysis showed in ATE higher E m and E m / A m ratio at the level of both RV and LV lateral walls. In the overall population of athletes, linear regression models evidenced independent positive association of RV peak E m velocity with both LV stroke volume and maximal workload achieved by bicycle ergometer (both p Conclusions RV early diastolic myocardial function is positively influenced by preload increase in master athletes and represents an independent determinant of cardiac performance during physical effort. Therefore, colour DMI may be taken into account to distinguish different cardiac adaptation to either endurance or strength sport training in master athletes.

Aims The present study was designed to test whether early carotid structural changes are demonstrable (by high resolution B-mode ultrasound) in children, adolescents and young adults with a history of premature parental myocardial infarction. Methods and Results One hundred and fourteen healthy young (5 to 30 years) subjects with a parental history of premature myocardial infarction and 114 age- and sex-matched control subjects were enrolled in the study. They were divided into two age groups: children and adolescents (age 5 to 18 years) (54 individuals with a parental history of premature myocardial infarction and their control subjects; mean age 12·8±3·8 years) and young adults (age 19 to 30 years) (60 individuals with a parental history and their controls; mean age 23·8±3·3 years). All subjects underwent high resolution B-mode ultrasonographic evaluation of common carotid artery intima–media thickness. Lipid profile, resting blood pressure, body mass index and smoking status were also evaluated. In both age groups, compared to controls, subjects with a parental history of premature myocardial infarction had increased intima–media thickness of common carotid arteries (mean of combined sites: age 5–18 years: 0·45±0·076mm vs 0·40±0·066mm in controls, P =0·008; age 19–30 years: 0·48±0·077mm vs 0·45±0·078mm in controls, P =0·007) Offspring of coronary patients showed an unfavourable lipid profile, however, the association between a parental history of premature myocardial infarction and carotid intima–media thickness was independent of lipids, apolipoproteins and other traditional risk factors. Conclusions Vascular structural changes associated with a parental history of premature myocardial infarction are already detectable in childhood and adolescence and occur independently of several traditional cardiovascular risk factors. Copyright 2002 The European Society of Cardiology. Published by Elsevier Science Ltd. All rights reserved .

Findings from epidemiologic and autopsy studies suggest that the offspring of patients with premature coronary disease may be at increased risk for atherosclerosis. We undertook a study to determine whether changes in brachial-artery reactivity and thickness of the carotid intima and media, two markers of early atherosclerosis, are present in adolescents and young adults with a parental history of premature myocardial infarction.We enrolled 40 healthy young people whose parents had had premature myocardial infarction (48 percent male; mean [+/-SD] age, 19.0+/-5.2 years) and 40 control subjects who were matched with the first group according to age and sex. All the subjects underwent high-resolution B-mode ultrasound examinations for the measurement of the brachial-artery vasodilatory response after arterial occlusion (i.e., reactive hyperemia) and the intima-media thickness of the distal common carotid arteries. Lipid profiles, blood pressure while at rest, body-mass index, and smoking status were also determined.As compared with the control subjects, the offspring of patients with premature myocardial infarction had lower flow-mediated reactivity of the brachial arteries (5.7+/-5.0 percent, vs. 10.2+/-6.6 percent in the control subjects; P=0.001) and greater mean intima-media thickness of the common carotid artery (0.49+/-0.08 mm, vs. 0.44+/-0.07 mm in the control subjects, P=0.004). In the subjects with a parental history of premature myocardial infarction, an inverse association was found between brachial-artery reactivity and carotid intima-media thickness (r=-0.46, P=0.003). In a conditional logistic-regression analysis, both brachial-artery reactivity and carotid intima-media thickness were significantly and independently correlated with a parental history of premature myocardial infarction.Structural and functional changes are present at an early age in the arteries of persons with a parental history of premature myocardial infarction.

Background:QT interval dispersion has been proposed as a simple noninvasive predictor of ventricular arrhythmias and sudden death. Patients with thalassemia major are at increased risk for sudden death. However, the independent effect of increased QT dispersion on the risk of sudden death in thalassemia major is not known. This study sought to test the hypothesis that an abnormal QT dispersion predicts sudden death in patients with thalassemia major. Methods:QT dispersion was measured in 13 consecutive patients with thalassemia major who had sudden death at a mean age of 16.1 ± 2.8 years, and in 13 survivors matched for age, gender, examination year, and transfusion therapy. Results:Patients who died suddenly had significantly greater QT dispersion (59 ± 29 ms) than patients who survived (29 ± 13 ms; P = 0.002). A cut-off value of 50 ms for QT dispersion had a sensitivity of 54%, a specificity of 92%, a positive predictive value of 87%, a negative predictive value of 67% and a predictive accuracy of 73% in identifying patients at risk of sudden death. With multiple regression analysis, QT dispersion was the only independent predictor of sudden death. Conclusions:QT dispersion is a useful marker of risk of sudden death in patients with thalassemia major. A.N.E. 1999;4(3):295–300

Objectives: To explore the full range of right heart dimensions and the impact of long-term intensive training in athletes. Background: Although echocardiography has been widely used to distinguish the athlete's heart from pathologic left ventricular (LV) hypertrophy, only few reports have described right ventricular (RV) and right atrial (RA) adaptations to extensive physical exercise. Methods: 650 top-level athletes [395 endurance-(ATE) and 255 strength-trained (ATS); 410 males (63.1%); mean age 28.4 +/- 10.1; 18-40 years] and 230 healthy age-and sex-comparable controls underwent a transthoracic echocardiographic exam. Along with left heart parameters, right heart measurements included: RV end-diastolic diameters at the basal and mid-cavity level; RV base-to-apex length; RV proximal and distal outflow tract diameters; RA long and short diameters; and RA area. Tricuspid annular plane systolic excursion and RV tissue Doppler systolic peak velocity were assessed as indexes of RV systolic function. Pulmonary artery systolic pressure (PASP) was estimated from the peak tricuspid regurgitant velocity. Results: ATS showed increased sum of wall thickness and relative wall thickness, whereas left atrial volume, LV end-diastolic volume, LV stroke volume and PASP were significantly higher in ATE. RV and RA measurements were all significantly greater in ATE than in ATS and controls. ATE also showed improved early diastolic RV function, whereas RV systolic indexes were comparable among groups. On multivariate analysis, type and duration of training (p

OBJECTIVES: To detect right ventricular myocardial function in dilated cardiomyopathy (DCM) using two-dimensional strain echocardiography (2DSE) and to evaluate the relationship between right ventricular dysfunction and response to cardiopulmonary exercise test (CPET). METHODS: Seventy-five DCM patients (44 idiopathic and 31 ischemic) without clinical signs of right ventricular failure underwent standard echo, 2DSE analysis of right ventricle and bicycle CPET. RESULTS: The two groups were comparable for clinical and standard two-dimensional echocardiographic and Doppler variables, except for right ventricular diameters that were mildly increased in patients with idiopathic DCM. Right ventricular global longitudinal strain (RV GLS) and regional peak myocardial right ventricular strain were significantly impaired in patients with idiopathic DCM compared with ischemic DCM (both P

AIMS: To analyse right ventricular (RV) myocardial deformation in patients with left ventricular (LV) hypertrophy secondary to either hypertrophic cardiomyopathy (HCM) or athlete's competitive endurance training. METHODS AND RESULTS: Standard Doppler echo, exercise stress echo, and 2D speckle-tracking strain echocardiography (2DSE) of RV longitudinal deformation in RV septal and lateral walls were performed in 50 top-level endurance athletes and in 35 patients with HCM, all men, having evidence of LV hypertrophy. Right ventricular global longitudinal strain (GLS) was calculated by averaging local strains along the entire right ventricle. The two groups were comparable for age and blood pressure, whereas athletes showed lower heart rate and increased body surface area than HCM. Interventricular septal thickness was higher in HCM, whereas both LV and RV end-diastolic diameters (LVEDD and RVEDD) and LV stroke volume were increased in athletes. Right ventricular tricuspid annulus systolic excursion was comparable between the two groups. Conversely, RV GLS and regional peaks of RV myocardial strain were significantly impaired in patients with HCM (all P < 0.001). Multiple linear regression models detected an independent association between RV GLS and LVEDD (beta-coefficient = -0.68, P < 0.0001) in athletes, as well as an independent correlation of the same RV GLS with septal thickness (beta = 0.63, P < 0.0001) in HCM. An RV GLS cut-off value of -0.16% differentiated athletes and HCM with an 86% sensitivity and a 92% specificity. Furthermore, in the overall population, RV GLS (beta = 0.51, P < 0.0001) was a powerful independent predictor of maximal workload during exercise stress echo. CONCLUSION: Right ventricular myocardial systolic deformation is positively influenced by preload increase in athletes and negatively associated with increased septal thickness in HCM. Therefore, 2DSE may represent a useful tool in the differential diagnosis between athlete's heart and HCM, underlining the different involvement of RV myocardial function in either physiological or pathological LV hypertrophy.

Although cardiac adaptation to different sports has been extensively described, the potential effect of top-level training on the aortic root dimension remains not investigated fully. To explore the full range of aortic root diameters in athletes, 615 elite athletes (370 endurance-trained athletes and 245 strength-trained athletes; 410 men; mean age 28.4 +/- 10.2 years, range 18 to 40) underwent transthoracic echocardiography. The end-diastolic aortic diameters were measured at 4 locations: (1) the aortic annulus, (2) the sinuses of Valsalva, (3) the sinotubular junction, and (4) the maximum diameter of the proximal ascending aorta. Ascending aorta dilation at the sinuses of Valsalva was defined as a diameter greater than the upper limit of the 95% confidence interval of the overall distribution. The left ventricular (LV) mass index and ejection fraction did not significantly differ between the 2 groups. However, the strength-trained athletes had an increased body surface area, sum of wall thickness (septum plus LV posterior wall), LV circumferential end-systolic stress, and relative wall thickness. In contrast, the left atrial volume index, LV stroke volume, and LV end-diastolic diameter were greater in the endurance-trained athletes. The aortic root diameter at all levels was significantly greater in the strength-trained athletes (p

An increased carotid intima-media thickness (IMT) is detectable in young subjects with parental history of premature myocardial infarction (PHPMI) or hypertension (PHH). In this study we evaluated if PHPMI and PHH exert a different influence on carotid IMT and if their conjunction produces additive effects. High-resolution B-mode ultrasonographic evaluation of common carotid artery IMT was acquired from 48 subjects without PHPMI and PHH (22 males, 26 females; mean age 22.1±4.9 years; controls), 24 age- (±1 year) and sex-matched subjects with PHH without PHPMI (PHH-positive/PHPMI-negative subjects), 24 age- and sex-matched subjects with PHPMI without PHH (PHH-negative/PHPMI-positive subjects) and 24 age- and sex-matched subjects with both PHPMI and PHH (PHH/PHPMI-positive subjects). Lipid profile, resting blood pressure, smoking behaviour and body mass index (BMI) were also assessed. Carotid IMT was smaller in controls (0.41±0.07mm) compared to PHH-positive/PHPMI-negative subjects (0.47±0.10, p=0.023), to PHH-negative/PHPMI-positive subjects (0.54±0.11, p0.001) and to PHH/PHPMI-positive subjects (0.52±0.10mm, p0.001). Carotid IMT was greater in PHH-negative/PHPMI-positive (p=0.006) and in PHH/PHPMI-positive (p=0.031) than in PHH-positive/PHPMI-negative subjects. No difference in carotid IMT was evident between PHH-negative/PHPMI-positive and PHH/PHPMI-positive subjects (p=0.549). In the comparison among subjects using multiple regression analysis, only PHPMI, age and BMI were independently associated with carotid IMT. In healthy young subjects with PHPMI and/or PHH, carotid IMT is increased. PHPMI is a stronger predictor of increased carotid IMT than PHH. PHH in conjunction with PHPMI does not add any further detrimental effect on carotid IMT.

Several reports suggest that noninvasive measurements of coronary flow reserve (CFR) by use of echocardiography may support decision making in intermediate stenosis of the left anterior descending coronary artery (LAD). The aim of the present study was therefore to analyze the clinical outcome in patients with intermediate stenosis of LAD after deferral of coronary revascularization on the basis of noninvasive CFR measurement.the study population included 280 patients with intermediate LAD stenosis (50-70% by angiography) (62.2 +/- 9.6 years). All the patients underwent transthoracic CFR assessment of LAD (after dipyridamole infusion) within 2 weeks from coronary angiography. If CFR of LAD wasor = 2, PTCA was recommended; if CFR was2, medical treatment was chosen. Primary end points were cardiac death, myocardial infarction, coronary revascularization procedure, and unstable angina.mean follow-up was 43 +/- 11 months (range 12-52 months). In 150 patients (53.6%) (CFRor = 2), coronary artery revascularization was performed (PTCA group); the remaining 130 patients (46.4%) (CFR2) were medically treated (medical group). Survival from cardiac death was 94% in the PTCA group and 92.4% in the medical group (P = 0.56). As for all cardiac events, the Kaplan-Meier percentage survival from cardiac events was 88.3% in the PTCA group and 86.4% in the medical group (P = 0.36).even if CFR as a "stand-alone" diagnostic criterion suffers from several structural limitations, a combined strategy including also other clinical and instrumental measurements before undergoing interventional procedures could improve the cost-benefit practice, in particular, for the management of patients with intermediate LAD stenosis.

OBJECTIVE: In dilated cardiomyopathy (DCM), right ventricular (RV) dysfunction has been reported and attributed both to altered loading conditions and to RV involvement in the myopathic process. The aim of the study was to detect RV myocardial function in DCM using two-dimensional (2D) strain echocardiography and to assess the effects of cardiac resynchronization therapy (CRT) on RV myocardial strain during a 6-month follow-up. METHODS AND RESULTS: A total of 110 patients (mean age: 55.4 +/- 11.2 years) with either idiopathic (n = 60) or ischemic (n = 50) DCM, without overt clinical signs of RV failure, underwent standard echo and 2D strain analysis of RV longitudinal strain in RV septal and lateral walls. The two groups were comparable for clinical variables (New York Heart Association class III in 81.8%). Left ventricular volumes, ejection fraction, stroke volume, and mitral valve effective regurgitant orifice were similar between the two groups. No significant differences were evidenced in Doppler mitral and tricuspid inflow measurements. RV diameters were mildly increased in patients with idiopathic DCM, while RV tricuspid annulus systolic excursion and Tei-index were comparable between the two groups. RV global longitudinal strain and regional peak myocardial strain were significantly impaired in patients with idiopathic DCM compared with those having ischemic DCM (all P < 0.001). Using left ventricular end-systolic volume as marker for response to CRT, 70 patients (63.3%) were long-term responders. Ischemic DCM patient responders to CRT showed a significant improvement in RV peak systolic strain. Conversely, in patients with idiopathic DCM and in ischemic patients nonresponders to CRT, no improvement in RV function was evidenced. By multivariable analysis, in the overall population, ischemic etiology of DCM (P < 0.0001), positive response to CRT (P < 0.001), and longitudinal intraventricular dyssynchrony (P

Aims To evaluate whether quantification of the extent of scarred left ventricular (LV) tissue by speckle-tracking strain echo (2DSE) can predict response to cardiac resynchronization therapy (CRT) in patients with ischaemic dilated cardiomyopathy (DCM). Methods and results Forty-five patients (58.3 ± 8.3 years; 24 males) with ischaemic DCM scheduled for CRT, and 25 controls were studied. A week before implantation all the patients underwent standard Doppler echo, 2DSE, and contrast-enhanced magnetic resonance (MR). Clinical and echocardiographic evaluation was repeated 6 months after CRT. The patients were considered as responders to CRT if LV end-systolic volume decreased by 15%. In DCM patients, LV ejection fraction was 29.2 ± 5.1%. By evaluating the 765 segments with MR, subendocardial infarct was identified in 17.0% and transmural infarct in 18.3%. With 2DSE, the average global longitudinal strain (GLS) was −23.1 ± 3.6% in controls and −15.1 ± 5.1% in DCM (P = 0.001). GLS showed a close correlation with total scar burden using MR (r = 0.64, P < 0.001). At follow-up, patients were subdivided into responders (n = 30; 66.7%) and non-responders (n = 15; 33.3%) to CRT. GLS was significantly different in non-responders than in responders (GLS: −10.4 ± 5.1 in non-responders vs. −18.4 ± 14% in responders, P < 0.001). In a multivariable analysis, GLS (P < 0.0001) and radial intraventricular dyssynchrony (P < 0.001) were powerful independent determinants of response to CRT. Conclusion GLS is strongly associated with total scar burden assessed by MR, and is an excellent independent predictor of response to CRT.

In patients with idiopathic dilated cardiomyopathy (DCM) a more depressed left atrial (LA) booster pump function has been observed compared to ischemic patients although under similar loading conditions, and attributed both to altered LA overload and to LA larger involvement in the myopathic process.To detect by speckle-tracking two-dimensional strain (2DSE) LA systolic dysfunction in patients with either idiopathic or ischemic DCM, and to assess in these patients possible correlation between LA myocardial function and exercise capacity during cardiopulmonary test.Three-hundred-fourteen patients (52.4+/-11.2 years) with either idiopathic (160 patients) or ischemic (154 patients) DCM underwent cardiopulmonary stress test, standard Doppler echo and 2DSE analysis of atrial longitudinal strain in the basal segments of LA septum and LA lateral wall, and in LA roof.The two groups were comparable for most of clinical variables. LV volumes, ejection fraction, stroke volume, and mitral valve effective regurgitant orifice were similar between the two groups. No significant differences were evidenced in Doppler transmitral inflow measurements. Also LA diameter and maximal volume were similar between the two groups. Conversely, LA active empting volume and fraction were both lower in patients with idiopathic DCM (0.001). Peak systolic myocardial atrial strain was significantly reduced in patients with idiopathic DCM compared with ischemic DCM at the level of all the analyzed atrial segments (p0.0001). By multivariable analysis, in the overall population, ischemic aetiology of DCM (p0.0001) and LA volume (p0.001) were the only independent determinants of LA lateral wall systolic strain. On the other hand, LA lateral wall systolic strain (p0.0001) and LA volume (p0.001) were powerful independent predictors of peak oxygen consumption during cardiopulmonary exercise testing.Two-dimensional strain represents a promising non-invasive technique to assess LA atrial myocardial function in patients with DCM. LA systolic deformation is more depressed in idiopathic compared with ischemic DCM, and is closely associated with functional capacity during effort. Future longitudinal studies are warranted to further our understanding of the natural history of LA myocardial function, the extent of reversibility of LA dysfunction with therapy, and the possible prognostic impact of such indexes in patients with congestive heart failure.

Atrial function is an integral part of cardiac function that is often neglected. The presence of left ventricule hypertrophy (LVH) due to arterial hypertension may impair atrial function. However, it has also been suggested that physical training attenuates the age-associated impairment of diastolic filling. This study investigated whether mechanical dysfunction in the left atrium (LA) is present in patients with either physiological or pathological LVH, using two-dimensional strain rate imaging (2D strain echocardiography; 2DSE).Standard echocardiography, exercise stress echo and 2DSE of the left atrium were performed in 40 patients with arterial hypertension, 45 age-matched elite athletes (40 years) and 25 healthy sedentary controls. Atrial longitudinal strain was performed from the apical views for the basal segments of the LA septum, lateral wall and roof.LV mass index and ejection fraction were comparable between patients with either physiological or pathological LVH. Elite athletes showed increased LV end-diastolic diameter, end-diastolic volume and stroke volume, whereas circumferential end-systolic stress was higher in patients with hypertension. LA diameter and maximum volume were increased but similar between the two groups of patients with LVH. LA active emptying volume and fraction were both higher in patients with hypertension. Conversely, peak systolic myocardial atrial strain was significantly reduced in patients with pathological LVH compared with controls and athletes for all the analysed atrial segments (p0.0001). Using multivariate analysis, LV end-diastolic volume/body surface area (BSA) (beta coefficient 0.52; p0.0001) and LV mass (beta = 0.48; p0.001) in athletes emerged as the only independent determinants of LA lateral wall peak systolic strain. In contrast, in patients with hypertension, an independent negative association of LA lateral wall peak systolic strain with both LV mass (beta = -0.42; p0.001) and circumferential end-systolic stress (beta = -0.43; p0.001) was found. In addition, in the overall population of patients with LVH, LA lateral wall systolic strain (beta = 0.49; p0.0001) was a powerful independent predictor of maximum workload during exercise testing.2DSE represents a promising, non-invasive, simple and reproducible technique to assess LA myocardial function in patients with either physiological or pathological LVH. LA myocardial deformation is impaired in patients with hypertension compared with age-matched sedentary controls and elite athletes, and is closely associated with functional capacity during effort.

Objectives: Systemic sclerosis (SSc) is a multisystem disorder characterized by widespread vascular lesions and fibrosis of skin and distinct internal organs. Cardiac involvement is a common finding in SSc, but often clinically occult. Aim of the study: To analyze possible associations of left ventricular (LV) myocardial function with coronary flow reserve (CFR) and endothelial function in asymptomatic patients with SSc. Methods: 30 healthy patients and 33 age- and sex-comparable asymptomatic patients classified as having either diffuse (18 patients) or limited form (15 patients) of SSc underwent standard Doppler Echo, Doppler myocardial imaging, Strain rate imaging of interventricular septum and LV lateral wall, transthoracic CFR of left anterior descending coronary vessel (after dipyridamole infusion), and brachial artery vasodilatation measurement (Vivid 7, GE Medical Systems Inc). Results: LV diameters and ejection fraction were comparable between the two groups, while systolic pulmonary pressure (P < 0.001) was increased in SSc. By chest-CT, 15 SSc patients showed interstitial pulmonary fibrosis. Serological antibodies analysis detected anti-centromere pattern in 14 SSc patients, and anti Scl-70 in 19 patients. In SSc, LV myocardial early diastolic peak velocity, peak systolic strain rate and strain were both reduced in basal and middle interventricular septum, and in basal and middle LV lateral wall. Both CFR (P < 0.0001) and endothelial flow-mediated dilatation (P < 0.001) were significantly lower in SSc patients. By stepwise forward multivariate analyses, CFR (P < 0.001) and endothelial function (P < 0.001) were powerful independent determinants of middle LV strain. Conclusions: Strain rate imaging, transthoracic CFR, and brachial artery flow-mediated dilatation are valuable noninvasive and easily repeatable tools for detecting LV myocardial and vascular involvement caused by SSc. Their combined use may be therefore useful for early identifying patients with more diffused and severe form of SSc, ideally in asymptomatic cases prior to the development of severe vasculopathy, when it may be most feasible to modify the disease process by new potential therapies.

Aims: Cardiac resynchronization therapy (CRT) has become an attractive therapeutic option for patients with end-stage heart failure (HF). Currently, patients are selected for CRT on ECG and on echocardiographic criteria analysed at rest. Whether the physical effort may further increase myocardial dyssynchrony is not fully established. The aim of the study was to test by the use of Doppler myocardial imaging (DMI) if dynamic left ventricular (LV) dyssynchrony during physical effort may be a determinant of dynamic mitral regurgitation in patients with dilated cardiomyopathy and 'narrow' QRS. Methods and results: Sixty patients (62.3 ± 8.3 years) with idiopathic dilated cardiomyopathy and narrow QRS duration (< 120 ms) were selected. All the patients underwent standard Doppler echo, colour DMI, supine bicycle exercise stress echocardiography, and cardiopulmonary exercise testing. Cardiac synchronicity was assessed, at rest and at peak exercise, from measurements of time intervals (Ts) between the onset of the QRS complex and the peak myocardial systolic velocity, in a six-basal-six-mid-segmental model. Standard deviation of Ts of the 12 LV segments (Ts-SD-12) was also calculated. In baseline conditions, HF patients showed an LV ejection fraction of 30.1 ± 4%, and a significant electromechanical delay (Ts-SD-12 ≥ 34.4 ms) in 20 patients (33.3%). At peak of physical exercise, a significant electromechanical delay was detected in 35 patients (58.3%), whereas in 47 patients (78.3%) exercise-induced increase in mitral valve effective regurgitant orifice (ERO) was observed. By multivariable analysis, an independent positive association between changes in Ts-SD-12 and in mitral valve ERO (P < 0.0001), as well as an independent inverse correlation of the same changes in Ts-SD-12 with LV stroke volume (P < 0.0001) were detected. In addition, changes in Ts-SD-12 were also independent determinants of peak VO2 (P < 0.0001) during cardiopulmonary exercise testing. Conclusion: Colour DMI is an effective technique for assessing the severity of regional delay in activation of LV walls in HF patients with narrow QRS both at rest and during stress test. The increase in LV dyssynchrony during exercise strongly correlates with the increase in mitral regurgitation severity and with the impairment of LV stroke volume. © The European Society of Cardiology 2007. All rights reserved.

Preclinical abnormalities are detectable in young normotensive individuals with a positive parental history of hypertension (PHH).1 Increased carotid intima–media thickness (IMT) is considered an early and valuable predictor of atherosclerotic disease; however, information on the effect of PHH on potential vascular structural abnormalities in young normotensive healthy subjects is limited. The aim of this study was to evaluate the presence of carotid structural differences in normotensive young adults and children with and without PHH. The study population comprised 29 cases (healthy subjects with PHH, 45% males, mean (SD) age 23 (5) years) consecutively recruited among the offspring (age 11–30 years) of patients with essential hypertension who had been followed at the Hypertension Outpatient Clinic of the Department of Cardiology, Cardarelli Hospital of Naples, Italy. Parental hypertension was defined as a blood pressure of at least 140/90 mm Hg, measured on three different days in the supine position by sphygmomanometry. The control group consisted of 29 age-matched (+1 year) and sex-matched healthy subjects without PHH (parents not on antihypertensive drugs and blood pressure values

Systemic sclerosis (SSc) is a multi-system disorder characterized by widespread vascular lesions and fibrosis of skin and distinct internal organs. The aim of the present study was to analyze possible associations of left ventricular (LV) myocardial function with coronary flow reserve (CFR) and endothelial function in asymptomatic patients with SSc. Thirty healthy subjects and 33 age- and sex-comparable asymptomatic SSc patients underwent standard Doppler Myocardial Imaging, Strain Rate (SR) Imaging of interventricular septum (IVS) and LV lateral wall, transthoracic CFR of left anterior descending coronary vessel, and brachial artery vasodilatation measurement. In SSc patients, LV myocardial early diastolic peak velocity, peak systolic SR and strain were both reduced in basal and middle IVS, and in basal and middle LV lateral wall (p0.001). In addition, both CFR (p0.0001) and endothelial flow-mediated dilatation (p0.001) were significantly lower in SSc patients. By stepwise forward multivariate analyses, CFR (p0.001) and endothelial function (p0.001) were powerful independent determinants of middle LV strain of SSc patients. In conclusion, SR Imaging, transthoracic CFR and brachial artery flow-mediated dilatation are valuable non-invasive and easy-repeatable tools for detecting early LV myocardial and vascular involvement caused by SSc.

We sought to assess the indexes of myocardial activation delay, using Doppler myocardial imaging (DMI), as potential predictors of cardiac events in patients with hypertrophic cardiomyopathy (HCM). The distribution and magnitude of left ventricular (LV) hypertrophy are not uniform in patients with HCM, which results in heterogeneity of regional LV systolic function.The study population included 123 HCM patients (39.4+/-5.9 years) and 123 age- and sex-matched healthy subjects, followed up for 48.4+/-8.8 months. By use of pulsed DMI, the following regional parameters were evaluated in six different basal myocardial segments: myocardial peak velocities and systolic time-intervals; myocardial intraventricular (intra-V-Del) and interventricular (inter-V-Del) systolic delays. DMI analysis in HCM showed lower myocardial systolic and early-diastolic peak velocities of all the segments. As for time intervals, HCM showed significant inter- and intra-V delays (P0.0001), whereas homogeneous systolic activation of the ventricular walls was assessed in controls. During the follow-up, 16 cardiac deaths (12 sudden deaths) were observed in HCM patients. InHCM, DMI intra-V-Del was the most powerful independent predictor of sudden cardiac death (P0.0001). In particular, an intra-V-Del45 ms is identified with high sensitivity and specificity in HCM patients at higher risk of ventricular tachycardia and sudden cardiac death (test accuracy: 88.8%).In HCM patients, DMI indexes of intra-V-Del may provide additional information for selecting subgroups of HCM patients at increased risk of ventricular arrhythmias and sudden cardiac death at follow-up. Accordingly, such patients may be more actively identified for early intensive treatment and survey.

In a prospective study, we evaluated the hypothesis that QT variability is abnormal in multiple system atrophy. Time and frequency domain QT variability was assessed from 24-hour Holter monitoring. Three-channel Holter monitoring was performed in all subjects and was analyzed on a homemade analyzer. The 24-hour mean QT duration was similar in multiple system atrophy patients and in control subjects Unlike QT duration, several parameters of time and frequency domain QT variability were significantly increased in multiple system atrophy patients compared to healthy controls. Time domain measures of QT variability were significantly shorter while asleep than while awake in both groups. The nighttime % reduction in time-domain QT variability tended to be smaller in patients in comparison to control subjects, but this difference did not achieve statistical significance. This is the first reporting demonstrating that QT variability is abnormal in patients with multiple system atrophy

We sought to determine QT variability pattern in patients with hypertrophic cardiomyopathy (HCM) and its relationship with the risk of syncope. QT interval variability was assessed from 24-hour Holter monitoring in 10 HCM patients with history of syncope, 10 HCM patients without history of syncope, and 10 healthy subjects. QT variability was higher in patients with HCM, in particular in those with history of syncope, than in healthy controls. Time domain QT variability did not vary between waking and sleeping hours in HCM patients, whereas it was significantly shorter while asleep in the control group. Increased QT SDANN identified HCM patients with history of syncope with an accuracy of 75%. Our data show that QT variability is abnormal in HCM patients and indirectly support the concept that arrhythmia-related syncope in these patients may be, at least in part, related to an altered control of repolarization.

We correlated the incidence and degree of exercise induced ventricular arrhythmias (EIVA) with the angiographic severity of coronary artery disease (CAD) in 162 patients with a history of stable effort angina, all showing a positive exercise stress test for myocardial ischemia and a≥70% stenosis of a major coronary artery. Patients were grouped according to the following criteria: presence of electrocardiographic evidence of old transmural myocardial infarction (MI), number of significant coronary stenoses and number of left ventricular (LV) areas showing abnormal segmental wall motion (ASWM). The incidence of EIVA in patients with multivessel CAD was higher than in patients with single vessel CAD, but this difference was not statistically significant. The number of LV areas with ASWM was better correlated with the frequency of EIVA, which was 20.0% in patients with normal LV wall motion, 31.2% in patients with 1 area of ASWM, 54.0% in patients with 2 areas of ASWM (p

Summary We studied the influence of exercise level, severity of coronary artery disease (CAD), presence of previous myocardial infarction (MI), anterior or diaphragmatic, on the clinical value of exertional Q wave changes (Delta-Q). We retrospectively evaluated the exercise electrocardiograms of 62 patients without angiographic evidence of CAD and 133 patients with CAD; 28 of them had single (SVD) and 105 multivessel disease (MVD). Forty-one patients had a previous diaphragmatic MI and 23 anterior. The sensitivity specificity and predictive value of Delta-Q were compared to the ST criterion. The exercise level affected Delta-Q. ST and Delta-Q had similar specificity and predictive values. The extent of CAD did not affect the sensitivity of Delta-Q and this method was better than ST to detect SVD patients. The Delta-Q criterion was equally as efficient as ST in MVD patients without MI and with diaphragmatic MI. The loss of septal forces on resting electrocardiograms made useless Delta-Q analysis on patients with anterior MI. The improvement of sensitivity in SVD patients by Delta-Q might be of clinical value since these latter are frequently not diagnosed by the ST criterion.

The effects of changes in sympathetic tone on QT QS 2 ratio were studied in 10 healthy subjects aged 21 to 24 years. The subjects underwent a bicycle ergometer exercise, a tilt test, a decrease in carotid transmural pressure induced by means of pneumatic neck chamber, an i.v. injection of phenylephrine. A phonocardiogram and ECG were simultaneously recorded at a paper speed of 100 mm/s to evaluate QT and QS2 intervals in each test. In basal conditions, the QT QS 2 ratio was less than 1, whereas it increased progressively during the physical exercise and became greater than 1 at peak exercise. Both the upright position and the increase in neck-tissue pressure induced a significant increase in the QT QS 2 ratio as compared with the basal values, whereas i.v. administration of phenylephrine reduced significantly the QT QS 2 ratio. These results demonstrate that those stimuli which induce a rise in adrenergic activity may increase the QT QS 2 ratio. In contrast, the reflex inhibition of the adrenergic activity induced by phenylephrine is accompanied by a reduction in QT QS 2 ratio. Therefore, the QT QS 2 ratio might represent a reliable index of sympathetic cardiac tone.

In order to study whether different heart rates achieved at peak exercise by normal subjects and patients with coronary artery disease (CAD) affect the results of analysis of R-wave amplitude changes (delta R), we evaluated delta R at progressively increasing heart rate (HR) steps in 60 normal subjects with negative exercise tests (ET), in 130 patients with CAD, in 88 patients with true positive and 42 with false negative ET, and in 43 patients with no CAD and false positive ET. We found that the sensitivity and specificity of delta R were HR dependent, the former decreasing and the latter increasing with progressively increasing HR steps. Mean values of delta R did not discriminate among the four groups for HRs up to 150 bpm; significant differences were found between normal subjects and CAD patients, both with true positive and false negative stress tests, at HR greater than 150 bpm. False positive patients had mean delta R similar to those found in normal subjects. We hypothesize that quantitative delta R analysis could be useful in ECG diagnosis of false negative and false positive patients at HR greater than 150 bpm