Search

Impact of the gestational changes on cardiac contractility is not clearly defined. Our aim was to evaluate subtle changes of the right ventricular systolic function during pregnancy, assessed by new echocardiographic techniques, in a population tested for inherited thrombophilia. 87 pregnant women, with a mean age of 32 ± 4 years, genetically tested for inherited thrombophilia (22 with high-risk inherited thrombophilia and 65 control group) were included. All participants had four echocardiographic assessments, three during pregnancy (one in each trimester) and the forth at 6 months after giving birth. The right ventricular (RV) systolic function was assessed by fractional area change, ejection fraction (EF) by 3D echocardiography, tricuspid annular velocity by tissue Doppler, tricuspid annular plane systolic excursion, and strain by speckle tracking. Pulmonary artery pressure was estimated using the pressure gradient between right atrium and RV. Parameters of RV systolic function, at visits 2-4, had lower values compared with the first visit and were significantly lower in the high-risk thrombophilia group. Tricuspid regurgitation and pressure gradient between the right atrium and the RV had a significant increase during pregnancy for all subjects. At visit 1, there were no differences between groups, but at the next three visits there were higher values of the gradient in the high-risk thrombophilia group. High-risk inherited thrombophilia impacts the RV contractility, with higher pulmonary artery pressure. Further studies are needed to assess long-term impact on RV of high-risk inherited thrombophilia.

Background 2D speckle tracking echocardiography (2DSTE) was proved to be accurate for the assessment of the RV function. However, normal values for RV strain refer mostly to 3- or 6-segment models, excluding the contribution of other RV walls to RV function. We analyze RV function by 2DSTE in a normal population, using parasternal two-(2C) and apical four-chamber (4C) RV views, and creating a new 12-segment model for a potential better definition of RV function. Methods We prospectively evaluated 100 normals using 2DE and STE. We assessed the RV systolic function from regional strain (basal, mid, and apical), and at the level of each wall: lateral (LS), septal (SS), inferior (IS), and anterior (AS), and also global strain for 4C (4CGS), and 2C (2CGS). Global systolic strain rate (SRs) was measured from 2C and 4C views. Diastolic function was assessed from early (SRe) and late global strain rate (SRl), for both views. Results A total of 70 healthy individuals (48±15 years, 34 men) were suitable for concomitant 4C and 2CRV analysis. Feasibility of the STE analysis was 87.8%. We found significantly lower SS by comparison with LS, AS, and IS (P

Background: Patients with uncomplicated diabetes have reduced left ventricular long-axis function, related to poor glycemic control and increased conduit arterial stiffness, with increased radial function. It is unknown if improved control of risk factors can reverse these subclinical changes. Patients and methods: We studied 27 patients with type 2 diabetes (18 men) 57 ± 1 months (mean ± SD) after an initial visit when they were compared with healthy age- and sex-matched controls. On both visits patients had detailed echocardiographic studies including tissue Doppler, noninvasive tests of conduit arterial function, and metabolic and lipid profiling. Results: Mean age at this second review was 63.4 ± 8.1 years; 48% of patients received insulin. Mean HbA1c had decreased by 13% to 8 ± 1.6% and cholesterol by 17% to 4.3 ± 1.3 mmol/L (both, P < 0.01), but long-axis systolic and early diastolic myocardial velocities had also declined, by 13% and 20%, respectively (both, P < 0.001). Body mass index had increased by 4%, arterial pulse pressure by 17% (both P < 0.01), and carotid arterial stiffness by 49% (P < 0.01). Fractional shortening (by 21%, P < 0.001), radial systolic velocity (by 13%, P < 0.05), and ejection fraction (by 9% to 68 ± 7%, P < 0.01) had all declined. Reductions in longitudinal function were best predicted by its baseline measurements, duration of diabetes, fasting triglycerides, and arterial stiffness (epsilon index). Conclusions: Despite improved diabetic control, subclinical left ventricular dysfunction progressed over 5 years. Radial compensation was reversed. Prevention of subclinical myocardial dysfunction in diabetes might require more intensive control of net cardiovascular risk.

Aims In asymptomatic patients with severe primary mitral regurgitation (PMR), early detection of left ventricular (LV) dysfunction indicates the optimal timing of mitral valve surgery; however, normal ejection fraction (EF) and end-systolic diameter (ESD) can mask significant LV impairment. Methods We studied 28 asymptomatic patients (59 ± 13 years, 18 male) with severe PMR, EF > 60%, and ESD 10% (13 patients) and IB, with an EF reduction Results Patients with PMR had longitudinal dysfunction and decreased radial systolic deformation, by comparison with controls, although EF and ESD were similar. Subgroup IA had significantly lower S(TVI) , LS, and RS than IB (7.3 ± 0.9 vs 10.8 ± 1.5 m/s; -16.0 ± 4.2% vs -21.7 ± 2.1%; and 37.4 ± 2.5% vs 41.6 ± 2.4%; all p 10% (r(2) = 0.52, p Conclusion Myocardial systolic velocities as well as radial and longitudinal LV deformation assessed by speckle tracking can detect subclinical LV dysfunction and predict impaired postoperative LV function in asymptomatic patients with severe PMR.

Background: The risk factors that contribute to atherosclerosis also predict clinical heart failure, but it is unclear how they affect myocardial function. Aims were to assess if major cardiovascular risk factors cause subclinical myocardial dysfunction in asymptomatic subjects. Methods: We measured regional left ventricular (LV) function at rest and during dobutamine stress echocardiography in 246 subjects (54 ± 12 years, 54% men) analyzed in five groups according to the presence of six risk factors (diabetes, hypertension, obesity, dyslipidemia, smoking, and family history; age was similar in the five groups). LV longitudinal function was assessed from the mean velocities of four basal segments, and radial function from the velocities of the basal posterior wall. Results: Risk factors did not affect LV ejection fraction, but longitudinal systolic velocity decreased progressively with the number of risk factors, at rest (6.8 ± 1.3 vs. 6.2 ± 1.6 vs. 5.8 ± 1.5 vs. 5.4 ± 1.3 vs. 5.3 ± 1.3 cm/sec, for the five groups, respectively) and at peak stress (14.3 ± 3.3 vs. 12.9 ± 3.2 vs. 11.8 ± 3.4 vs. 11.3 ± 2.6 vs. 11.1 ± 2.3 cm/sec) (both P < 0.0001). Radial systolic velocity increased according to the number of risk factors (P < 0.01). By multivariate regression, determinants of reduced longitudinal systolic velocity at rest were body mass index, diastolic blood pressure, age, and fasting plasma glucose (r = 0.57, r2 = 0.32, P < 0.0001). Conclusion: Asymptomatic subjects have impaired LV long-axis function at rest and during stress, according to their number of major cardiovascular risk factors. Global LV systolic function is maintained by compensatory increases in radial function. These changes provide new targets for preclinical diagnosis and for monitoring responses to preventive strategies. Echocardiography 2011;28:813-820)

Diastolic mitral regurgitation (DMR) has been reported in patients with AV block, aortic regurgitation, cardiomyopathies, and in patients with long filling periods in atrial tachyarrhythmias. The mechanism for DMR is a reversal in the atrioventricular gradient during diastole. However, because of its relatively low velocity, it may be difficult to diagnose noninvasively. We present three different cases of diastolic MR in 2:1 second-degree AV block, atrial flutter, and dilated cardiomyopathy, with different locations in diastole. Diastolic tricuspid regurgitation commonly accompanies DMR. Careful analysis of echocardiographical images related with online ECG is very important in order to delineate systolic and DMR, and their timing in systole and diastole.

Objective: Athlete’s heart is associated with left ventricular (LV) hypertrophy (LVH), and “supranormal” cardiac function, suggesting that this is a physiological process. Hypertrophy alone cannot explain increase in cardiac function, therefore, other mechanisms, such as better ventriculo-arterial coupling might be involved. Methods: We studied 60 male (21 ± 3 years) subjects: 27 endurance athletes, and a control group of 33 age-matched sedentary subjects. We assessed global systolic and diastolic LV function, short- and long-axis myocardial velocities, arterial structure and function and ventriculo-arterial coupling, endothelial function by flow-mediated dilatation, and amino-terminal pro-brain natriuretic peptide (NT-proBNP) and biological markers of myocardial fibrosis and of oxidative stress. Results: Athletes had “supranormal” LV longitudinal function (12.4 ± 1.0 vs 10.1 ± 1.4 cm/s for longitudinal systolic velocity, and 17.4 ± 2.6 vs 15.1 ± 2.4 cm/s for longitudinal early diastolic velocity, both P < 0.01), whereas ejection fraction and short-axis function were similar to controls. Meanwhile, they had better endothelial function (16.7 ± 7.0 vs 13.3 ± 5.3%, P < 0.05) and lower arterial stiffness (pulse wave velocity 7.1 ± 0.6 vs 8.8 ± 1.1 m/s, P = 0.0001), related to lower oxidative stress (0.259 ± 0.71 vs 0.428 ± 0.88 nmol/mL, P = 0.0001), with improved ventriculo-arterial coupling (37.1 ± 21.5 vs 15.5 ± 13.4 mmHg.m/s 3 × 10 3 ,P = 0.0001). NT-proBNP and markers of myocardial fibrosis were not different from controls. LV longitudinal function was directly related to ventriculo-arterial coupling, and inversely related to arterial stiffness and to oxidative stress. Conclusions: “Supranormal” cardiac function in athletes is due to better endothelial and arterial function, related to lower oxidative stress, with optimized ventriculo-arterial coupling; athlete’s heart is purely a physiological phenomenon, associated with “supranormal” cardiac function, and there are no markers of myocardialfibrosis. (Echocardiography 2010;27:659-667)

To determine if global ventricular function can be assessed from the long-axis contraction of the left ventricle, we compared pulsed-wave Doppler myocardial imaging of mitral annular motion to radionuclide ventriculography.We studied 51 patients (56 +/- 10 years, 11 women) with a radionuclide ejection fraction of 52 +/- 13% (15%-70%). Peak systolic velocities of medial and lateral mitral annular motion correlated with ejection fraction (0.55 and 0.54, respectively; P0.001), as did the time-velocity integrals (0.57 and 0.58, respectively; P0.001). Correlations were higher in normal ventricles (0.62-0.69) than in patients with previous myocardial infarction (0.39-0.64). Patients with anterior myocardial infarction had the lowest correlations (0.39-0.46). The best differentiation of normal (or = 50%) from abnormal (50%) ejection fraction was provided by peak systolic velocityor = 8 cm/sec for the medial (sensitivity 80%, specificity 89%) or lateral (sensitivity 80%, specificity 92%) mitral annulus.Global left ventricular function can be estimated by recording mitral annular velocity. The implementation of a cutoff limit of 8 cm/sec gave a simple guide for differentiating between normal and abnormal left ventricular systolic function that might be useful clinically in patients without regional wall-motion abnormalities. However, in patients with important segmental wall-motion abnormalities during systole, left ventricular longitudinal shortening is an imperfect surrogate for ejection fraction.

A 56-year-old man received thrombolysis for an anterior myocardial infarction after chest pain for 18 hours. Ten days later he was readmitted with fever and hemodynamic deterioration. Transesophageal echocardiography demonstrated a thin-walled cavity at the apex of the left ventricle. At operation he was found to have a myocardial abscess, and after excision and antibiotics his subsequent clinical course was uneventful. We review the echocardiographic diagnosis and clinical features of myocardial abscess complicating acute infarction. Presumed etiologic factors in our patient included late thrombolysis, mural thrombus, and poor dental hygiene leading to septicaemia.