Elisabetta Palmerini

Feasibility and reference values of left atrial longitudinal strain imaging by two-dimensional speckle tracking

BackgroundThe role of speckle tracking in the assessment of left atrial (LA) deformation dynamics is not established. We sought to determine the feasibility and reference ranges of LA longitudinal strain indices measured by speckle tracking in a population of normal subjects.MethodsIn 60 healthy individuals, peak atrial longitudinal strain (PALS) and time to peak longitudinal strain (TPLS) were measured using a 12-segment model for the left atrium. Values were obtained by averaging all segments (global PALS and TPLS) and by separately averaging segments measured in the two apical views (4- and 2-chamber average PALS and TPLS).ResultsAdequate tracking quality was achieved in 97% of segments analyzed. Inter and intra-observer variability coefficients of measurements ranged between 2.9% and 5.4%. Global PALS was 42.2 ± 6.1% (5–95° percentile range 32.2–53.2%), and global TPLS was 368 ± 30 ms (5–95° percentile range 323–430 ms). The 2-chamber average PALS was slightly higher than the 4-chamber average PALS (44.3 ± 6.0% vs 40.1 ± 7.9%, p < 0.0001), whereas no differences in TPLS were found (p = 0.93).ConclusionSpeckle tracking is a feasible technique for the assessment of longitudinal myocardial LA deformation. Reference ranges of strain indices were reported.

Early Detection of Left Atrial Strain Abnormalities by Speckle-Tracking in Hypertensive and Diabetic Patients with Normal Left Atrial Size

BACKGROUND Systemic hypertension and type 2 diabetes mellitus are associated with impaired left atrial (LA) function, but whether LA functional abnormalities also occur in patients with hypertension and diabetes who have normal LA sizes is unknown. The aim of this study was to explore LA strain using speckle-tracking echocardiography in patients with hypertension or diabetes and normal LA size. METHODS LA strain was studied by speckle-tracking echocardiography in 155 patients with hypertension or diabetes with LA volume indexes < 28 mL/m(2) (83 with hypertension, 34 with diabetes, and 38 with both diabetes and hypertension) and 36 age-matched controls. The following indexes were measured: peak atrial longitudinal strain, time to peak atrial longitudinal strain, atrial longitudinal strain during early diastole and late diastole, and peak LA strain rate during ventricular systole, early diastole, and late diastole. RESULTS Peak atrial longitudinal strain was lower in patients with hypertension (29.0 ± 6.5%) and those with diabetes (24.7 ± 6.4%) than in controls (39.6 ± 7.8%) and further reduced in patients with diabetes and hypertension (18.3 ± 5.0%) (P < .0001). Similar results were found for atrial longitudinal strain during early diastole, atrial longitudinal strain during late diastole, and peak LA strain rate during ventricular systole and early diastole (P < .0001 for all). An inverse trend was found for time to peak atrial longitudinal strain, whereas no differences in peak LA strain rate during late diastole were observed. Two-way analysis of variance showed no interactions between hypertension and diabetes. In multivariate analyses, hypertension and diabetes were both independently associated with decreases in all LA strain and strain rate indexes, with the exception of peak LA strain rate during late diastole. CONCLUSIONS LA deformation mechanics are impaired in patients with hypertension or diabetes with normal LA size. The coexistence of both conditions further impairs LA performance in an additive fashion. Speckle-tracking echocardiography may be considered a promising tool for the early detection of LA strain abnormalities in these patients.

Acute effects of caffeine and cigarette smoking on ventricular long-axis function in healthy subjects

BackgroundFew data exist regarding the direct effects of caffeine and smoking on cardiac function. We sought to explore the acute effects of caffeine assumption, cigarette smoking, or both on left ventricular (LV) and right ventricular (RV) function in a population of young normal subjects.MethodsForty-five healthy subjects aged 25 ± 2 years underwent echocardiography. Fifteen of them were non-smokers and habitual coffee consumers (group 1), 15 were smokers and not habitual coffee consumers (group 2), and 15 were smokers and habitual coffee consumers (group 3). Peak systolic (Sa), early diastolic Ea, and late diastolic (Aa) velocity of mitral annulus were measured by pulsed Tissue Doppler, and left atrioventricular plane displacement was determined by M-mode. Tricuspid annular velocities and systolic excursion (TAPSE) were also determined. Measurements were performed at baseline and after oral assumption of caffeine 100 mg in group 1, one cigarette smoking in group 2, and both in group 3.ResultsNo changes in ventricular function were observed in group 1 after caffeine administration. In group 2, cigarette smoking yielded an acute increase in mitral Aa (+12.1%, p = 0.0026), tricuspid Sa (+9.8%, p = 0.012) and TAPSE (+7.9%, p = 0.017), and a decrease in the mitral Ea/Aa ratio (-8.5%, p = 0.0084). Sequential caffeine assumption and cigarette smoking in group 3 was associated with an acute increase in mitral Aa (+13.0%, p = 0.015) and tricuspid Aa (+11.6%, p < 0.0001) and a reduction in mitral Ea/Aa ratio (-8.5%, p = 0.0084) tricuspid Ea (-6.6%, p = 0.048) and tricuspid Ea/Aa ratio (-9.6%, p = 0.0003). In a two-way ANOVA model controlling for hemodynamic confounding factors, changes in the overall population remained significant for mitral Aa and Ea/Aa ratio, and for tricuspid Aa and Ea/Aa ratio.ConclusionIn young healthy subjects, one cigarette smoking is associated to an acute impairment in LV diastolic function and a hyperdynamic RV systolic response. Caffeine assumption alone does not exert any acute effect on ventricular long-axis function, but potentiates the negative effect of cigarette smoking by abolishing RV supernormal response and leading to a simultaneous impairment in both LV and RV diastolic function.

Acute effects of low doses of red wine on cardiac conduction and repolarization in young healthy subjects.

BACKGROUND Moderate to high blood concentrations of ethanol have been shown to yield acute changes in cardiac electrophysiological properties, but the effect of low concentrations have never been assessed. The role of concomitant changes in clinical variables or cardiac dimensions is also still unknown. This study aimed at exploring the acute effects of low doses of ethanol, administered as Italian red wine, on conduction, depolarization, and repolarization electrocardiographic (ECG) intervals in a population of healthy subjects. METHODS Forty healthy young volunteers drank a low quantity of red wine (5 ml/kg), and an equal volume of fruit juice in separate experiments. Heart rate, P-wave duration, PR interval, QRS duration, QT interval, corrected QT interval, QT dispersion, and corrected QT dispersion were assessed at baseline and after 60 minutes from challenge. RESULTS Mean blood ethanol concentration after drinking was 0.48 +/- 0.06 g/l. Compared to the control challenge, significant changes after red wine intake were observed in P-wave duration (from 101 +/- 11 to 108 +/- 14 milliseconds, p = 0.0006), PR interval (from 153 +/- 15 to 167 +/- 17 milliseconds, p < 0.0001), QT interval (from 346 +/- 28 to 361 +/- 24 milliseconds, p < 0.0001), and corrected QT interval (from 388 +/- 24 to 402 +/- 30 milliseconds, p = 0.0006). None of these changes showed correlations with modifications in clinical or echocardiographic variables. In multivariate analyses aimed at exploring predictors of ECG changes, none of the variables entered the final models. CONCLUSIONS Low doses of red wine acutely slow cardiac conduction and prolong repolarization in normal individuals. These changes are poorly predictable. The potential arrhythmogenic impact of these effects is worthy of exploration.

Coronary calcification with no flow limiting lesions: A potential cause for ischaemic dysfunction in syndrome X patients

Aim Exertional angina in patients with no coronary flow limiting lesions remains a clinical puzzle. We aimed to assess the extent of coronary artery calcification (CAC) and its relationship to ventricular wall motion function using stress echocardiography in a group of patients limited by exertional angina, but no obstructive lesions. Methods We compared CT coronary calcium score (CACS) and dobutamine stress echocardiography in 55 patients (age 64.7 ± 7.7 years), divided into Group 1 (CACS ≤ 100) and Group 2 (CACS > 100). No patient had LV ejection fraction-EF < 55%, pulmonary hypertension, arrhythmia, renal failure or parathyroid disease. Multiple linear regression analysis was used to test the association between gender-standardized continuous echocardiographic parameters and patient groups adjusted for age, body surface area, osteoporosis and CV risk factors and CACS. Results At rest, LV long axis ‘subendocardial’ function was reduced (amplitude: β − 1.11 SD, p < 0.05, R2 0.6 and systolic velocity: β − 1.08 SD, p < 0.05, R2 0.44), left atrial (LA) indexed volume was raised (β 1.06 SD, p < 0.05, R2 0.37) and its systolic velocity decreased (β − 1.05 SD, p < 0.05, R2 0.35) in Group 2. With stress, wall motion score index increased (p < 0.05) and long axis disturbances worsened only in the same group. Multivariate analysis demonstrated clear relationship between ischaemic LV disturbances, reduced long axis amplitude, global longitudinal systolic strain and early diastolic strain rate. Resting and stress RV lengthening velocity also correlated with CAC score. Conclusion In symptomatic patients with no obstructive coronary lesions and with more than mild CAC, long axis disturbances and wall motion score index rise occur with stress, at the time of symptom development and correlate with severity of arterial calcification. These findings suggest CAC as a potential mechanism for coronary wall stiffness and consequently exertional ischaemic changes as a result of limited flow reserve.

New onset of electrocardiographic abnormalities heralding hypertrophic cardiomyopathy in an adult athlete.

A 41‐year‐old male asymptomatic athlete with unremarkable personal and family history of heart disease underwent annual preparticipation screening. No abnormalities were noted on prior testing. On this occasion, a 12‐lead electrocardiogram showed diffused and marked repolarization abnormalities. He was therefore referred for echocardiography, which showed moderate asymmetric hypertrophy localized at the mid‐apical portions of the left ventricular anterolateral wall. Cardiac magnetic resonance confirmed the diagnosis of hypertrophic cardiomyopathy. Re‐evaluation of the electrocardiogram performed the previous year revealed a completely normal tracing.

Echocardiographic Assessment of Ebstein's Anomaly in a 60-Year-Old Man.

We present an echocardiographic evaluation of an elderly man affected with Ebsteins anomaly. In the natural history of this congenital disease only 5% of patients survive beyond the fifth decade. The patient presented severe right heart failure and he was refered to our institution for heart transplantation.

Effects of levosimendan on heart failure in normotensive patients: Does loading dose matter?

Abstract Background: Levosimendan is a calcium sensitizer and K+-ATP channel opener with inotropic and vasodilatatory effects irrespective of myocardial oxygen consumption, used for treatment of heart failure (HF). A loading dose is usually given by infusion for 12 h; however, profound lowering of blood pressure often disrupts or prolongs the infusion. The aim of this study was to assess clinical, biochemical and myocardial differences between different regimes of levosimendan therapy, with or without loading dose, and compared to standard therapy in heart failure. Methods: Fifty-seven patients (mean age ± SD: 60.9 ± 9.3 years, 45 males) with HF, New York Heart Association (NYHA) III–IV, reduced left ventricular ejection fraction (LVEF) were included. Twenty patients (NB group) were given levosimendan without loading dose, 14 patients (B group) were given levosimendan with loading dose, and 23 patients (C group) were given standard therapy. Clinical, biochemical and echocardiographic characteristics at baseline and one week after treatment were evaluated. Results: Groups were similar at baseline. After one week NHYA class (P < 0.001), NT pro-BNP (P < 0.001), LVEF (P = 0.045), E/A (P = 0.048) E/eʹ (P < 0.001), and PAPs (P < 0.001) decreased. DT (P = 0.011) and TAPSE (P = 0.035) increased in all groups. Conclusions: Levosimendan, as well as standard therapy, improves myocardial function and symptoms of HF, irrespective of the loading dose administration. Treatment options for patients with end-stage heart failure refractory to conventional medical therapy are limited. Inotropic drugs play an important role in heart failure (HF) (1–3).