Showing papers by "Maurizio Galderisi published in 2000"

Pulsed Doppler tissue imaging in endurance athletes: relation between left ventricular preload and myocardial regional diastolic function.

Abstract: The aim of this study was to assess the effects of endurance training on myocardial regional systolic and diastolic function by pulsed Doppler tissue imaging (DTI). Twenty male water polo players and 20 male control subjects underwent standard Doppler echocardiography and pulsed DTI, performed in apical views by placing a sample volume on left ventricular (LV) basal septal and inferior walls. Age, body surface area, and blood pressure were comparable between the 2 groups, with lower heart rate in athletes (p <0.001). They had significantly increased LV mass index (due to both higher wall thickness and end-diastolic diameter), greater endocardial fractional shortening, higher transmitral early/atrial (E/A) peak velocities ratio. In athletes, DTI analysis showed significantly prolonged myocardial deceleration time and greater myocardial E/A peak velocity ratio of septal and inferior walls, whereas myocardial early peak velocity was increased (p <0.01) only at the inferior wall. In the overall group, we found univariate relations of septal and inferior E/A peak velocity ratio and myocardial deceleration time with LV mass levels, and, in particular, with the sum of wall thickness. By separate multivariate analyses, however, these relations disappeared, being dependent on heart rate degree. Another association found between LV end-diastolic diameter and myocardial early diastolic wave peak velocity of the inferior wall (r = 0.68, p <0.0001) remained significant (standardized beta coefficient 0.60, p <0.00001), even after adjusting for heart rate, body surface area, age, and stroke volume (R(2) = 0.71, p <0.00001). In conclusion, DTI is a useful tool for detecting regional changes in myocardial function induced by training, because athletes present with an improvement in diastolic passive properties of myocardium. The higher early diastolic velocity of the inferior wall and its relation to increased preload may represent an indicator of aerobic training, allowing quantification of the degree of LV adaptation to endurance exercise.

Involvement of Right Ventricle in Left Ventricular Hypertrophic Cardiomyopathy: Analysis by Pulsed Doppler Tissue Imaging

Abstract: Aims: This study uses pulsed Doppler tissue imaging to analyse right ventricular myocardial function and its interaction with left ventricle in hypertrophic cardiomyopathy involving ventricular septum. Methods and Results: Thirty-four patients with septal hypertrophic cardiomyopathy and 30 normal subjects, comparable for sex, age, body mass index and heart rate, underwent complete standard Doppler echocardiography and pulsed Doppler tissue imaging of both posterior septum and right ventricular free wall, calculating myocardial velocities and both systolic and diastolic time intervals. Except for peak velocity A, the other Doppler tricuspid inflow measurements were significantly impaired in hypertrophic cardiomyopathy, without changes of tricuspid annular systolic excursion. Right ventricular Doppler tissue imaging showed longer right ventricular myocardial relaxation time in hypertrophic cardiomyopathy than in controls ( P <0·00001), without a significant difference from other myocardial diastolic and systolic measurements. In the overall population, Doppler measurements of right and left ventricular inflow were not significantly associated, while (with the exception of myocardial deceleration time) all the other myocardial systolic and diastolic measurements derived by tissue imaging were directly related to the homologous septal myocardial indexes. In addition, a significant inverse relation was found between septal wall thickness and myocardial relaxation index (right–left myocardial relaxation time/right ventricular relaxation time×100). Conclusions: This study shows the usefulness of pulsed Doppler tissue imaging to detect impairment of right ventricular myocardial function and to provide evidence about ventricular interaction in forms of hypertrophic cardiomyopathy which involve interventricular septum.

Cardiac toxicity after anthracycline chemotherapy in childhood.

Abstract: The clinical use of anthracyclines, a family of chemotherapeutic agents with efficacy against many solid tumors and leukemias is limited by unique cumulative dose-limiting cardiotoxicity Overt heart failure occurs in 45% to 7% of patients treated with anthracyclines and the incidence of cardiac function abnormalities increases with the time Anthracycline-induced congestive heart failure is usually due to permanent changes in the myocardium, changes most consistent with the contractile failure of cardiomyopathy Although the causes of anthracycline-induced cardiotoxicity are probably many, a large body of evidence points to free-radical-mediated myocyte damage The risk of developing cardiac heart failure is modified by the presence of certain risk factors that reduce cardiac tolerance to anthracyclines Age and female gender seem to have an important role in the anthracycline cardiotoxicity This cardiotoxicity can be divided, on the base of when it started, into acute, subacute and progressive late, chronic form Various invasive and non-invasive methods have been used to measure the extent of cardiac damage done Depending on the sensitivity of the method employed, the proportion of hearts found to be damaged has varied widely Attempts to ameliorate anthracycline cardiotoxicity have been directed toward: 1 decreasing myocardial concentrations of anthracyclines and their metabolites, 2 developing less cardiotoxic analogous, and 3 concurrently administering cardioprotectants to attenuate the effects of anthracyclines on the heart Much progress has been made in terms of monitoring of clinical and subclinical anthracycline cardiotoxicity, finding alternative schedules, introducing special carriers of anthracyclines and using cardioprotecting agents It is hoped that with all these effects and with results of ongoing and future trials, we will be able to reduce further or even eliminate anthracycline cardiotoxicity