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This article compares the wall motion of the left heart ventricle during diastolic filling in trained athletes and sedentary adults. Findings indicate that increases in left ventricular mass and volume associated with physical training do not significantly affect regional wall motion during the diastolic filling phase of the left ventricle.

It appears that the extent and rate of left ventricular (LV) isovolumic relaxation is improved by exercise training. The relationship between aerobic fitness and isovolumic LV relaxation was studied using human and rat models in two series of experiments. Two groups of college men, numbering 18, with variable peak run times were studied. Sedentary and exercise-trained rats were also studied. Morphological assessment was carried out afterward in rats.

* Objective: To test whether a substantial proportion of measured resting left ventricular diastolic pressure stems from forces external to the left ventricle (such as right-heart filling) in normal and chronically diseased hearts. * Design: Nonrandomized study with single intervention. * Setting: University hospital. * Patients: 29 patients referred for cardiac catheterization who had normal left ventricles and ejection fractions (n = 12); chronic heart disease due to idiopathic dilated cardiomyopathy (n = 6); ischemic heart disease (n = 6); or left ventricular hypertrophy (n = 5). * Intervention: Acute reduction of external forces imposed on the left ventricle using balloon obstruction of inferior vena caval inflow to the right heart. * Measurements: Continuous catheter-derived left ventricular pressure-volume data before and after abrupt obstruction of inferior vena caval inflow. Diastolic pressures were measured at the same volume just before atrial systole before and after sudden decrease of external right-heart and pericardial) forces. The resulting decline in pressure was a measure of the contribution of these external forces to resting left ventricular diastolic pressure. * Results: The decline in pressure when external forces were released averaged -19% [+ or -] 13% with minimal change in left ventricular end-diastolic volume (-3.66% [+ or -] 6.7%) and cardiac output (-5% [+ or -] 8%). In all patients combined, the decline in pressure when external forces ([delta][P.sub.d]) were released correlated with resting left ventricular diastolic pressure ([LVP.sub.d]) given by: [delta][P.sub.d] = 0.38 x ([LVP.sub.d] - 6) [r = 0.86, P < 0.0001]. This indicates that when resting diastolic pressure was more than 6 mm Hg, almost 38% of the pressure was due to external factors. This percentage was similar among all subgroups. Furthermore, the left ventricular diastolic pressure could be reduced by this percentage with only minimal compromise to ventricular filling and cardiac output. * Conclusions: A substantial proportion of measured resting left ventricular diastolic pressure stems from forces extrinsic to the left ventricle rather than from diastolic stiffness in the left ventricle itself. This markedly influences the dependence of cardiac output on filling pressure and has important implications for clinical application of the Starling law., Part of the diastolic pressure measured in the resting left ventricle of the heart appears to be due to forces outside the left ventricle. Of 29 patients who had heart catheterization, 12 had normal left ventricles and 12 had heart disease affecting the left ventricle. Researchers tested the effect of external forces on the left ventricle by blocking blood flow through the inferior vena cava for a brief period with a balloon catheter. This markedly reduced forces on the left ventricle from the right heart and the pericardium. Pressures within the ventricle were measured continuously before, during, and after blocking the inferior vena cava. Pressure declined an average of 19%, but cardiac output remained stable. Thirty to forty percent of the pressure inside the left ventricle was a result of external factors. The presence of heart disease had little effect on this.

To assess the immediate effects of aortic valve replacement (AVR) for valvular aortic stenosis (AS) on left ventricular (LV) systolic and diastolic function and global hemodynamics, 17 patients with AS underwent transesophageal echocardiography combined with high-fidelity LV pressure recording and thermodilution cardiac output measurements before cardiopulmonary bypass and 0.5, 6, 12, and 20 hours after AVR. Compared with results before bypass, LV systolic function had already changed 30 minutes after AVR, and remained constant thereafter: peak LV systolic wall stress decreased (from 210 [+ or -] 60 to 130 [+ or -] 40 g-[cm.sup.-2]), peak rate of dimension shortening increased (from 7.3 [+ or -] 2.2 to 9.7 [+ or -] 2.1 cm-[s.sup.-1]), both p (Am J Cardiol 1994; 74:1142--1146)

Left ventricular (LV) diastolic filling is impaired in hearts with healed myocardial infarction. Possible hemodynamic parameters related to impaired LV filling include left atrial pressure, time constant of isovolumic relaxation, chamber stiffness and wall motion asynchrony. Previous studies demonstrated univariate correlations between each of these parameters and LV filling, The current study was designed to compare relative importance of these parameters in patients with a myocardial infarction. Left ventriculograms with simultaneous LV pressure measurement were analyzed in 15 patients with a myocardial infarction and in 10 control subjects. Every frame of the left ventriculogram was divided into 8 segments and the volume of each segment was obtained frame-by-frame by planimetry and area-length method. Asynchrony was quantitated as the sum of areas of discrepancy between each segmental and global volume. time curve. Patients with myocardial infarction had greater asynchrony (20 [+ or -] 2 vs 10 [+ or -] 1%, p

Although cardiac involvement in the form of conduction abnormalities or aortic regurgitation occurs in 5 to 10% of patients with ankylosing spondylitis, few studies have assessed left ventricular (LV) function. This study assesses the prevalence of both systolic and diastolic LV dysfunction and other cardiac abnormalities in patients with ankylosing spondylitis who have no clinical cardiac manifestations. Fifty-nine patients (49 men and 10 women, mean age 42 [plus or minus] 10 years) underwent full clinical examination, electrocardiography, 24-hour Hoiter monitoring and 2-dimensional, IM-mode and Doppler echocardiography. Mean disease duration was 17 [plus or minus] 9 years (range 1 to 42). Seventeen patients had evidence of noncardiac extraarticular manifestations. Precordial examination was normal in all. An age- and sex-matched control group of 44 healthy subjects was also studied. On ochocardiography, abnormal LV diastolic function was detected in 12 patients (20%). Prolonged isevolumic relaxation time, prolonged deceleration time, reduced rate of descent of flow velocity in early diastole (EF slope) and reversal of the early and late peak transmitral diastolic flow velocities (E/A ratio) were noted in 9 patients. In 3 patients there was an increased E/A ratio, reduced deceleration time and increased EF slope. Mild aortic regurgitation and mitral regurgitation was seen in 1 and 3 patients, respectively. No abnormalities of left atrial size, LV systolic or diastolic dimensions or wall thicknesses were noted. There was no conelation between the presence of LV diastolic dysfunction and age, disease severity, disease duration, or the presence of extraarticalar manifestations. It is concluded that LV diastolic dysfunction occurs frequently in patients with ankylosing spondylitis, even in the absence of clinical cardiac involvement. (Am J Cardiol 1993;71:1337-1340)

The impedance diastolic waveforms, early O wave (zO) and late A wave (zA), were evaluated their relation to diastolic mitral flow pattern under changes in loading conditions was Eight normal subjects and 9 patients with Doppler evidence of delayed ventricular relaxation were studied with simultaneous transmitral Doppler flow and computerized, ensemble-averaged, impedance. cardiography in the supine position. Thirty-degree, head-down and head-up tilt were performed to alter preload. Peak Doppler early diastolic volocity (E) and E intogral were preload-dependent in both normal and abnormal groups (p cO.003), but were not significantly between patients and normal subjects. Peak Doppler late diastolic volocity (A) and A integral, although signiticantly different between groups (p < 0.001), did not vary significantly with tilt. E/A ratio was significantly different between groups in all positions (p < 0.006). impedance zA was pendent (p < 0.001) in both groups and significantly different between groups (p < 0.05). Impedance zO was also preload-dependent (p < 0.003), but not significantly different between groups. Impedance zO correlated with Doppler peak E (r = 0.64; P = 0.001). Impedance zA did not correlate with Doppler A. Impedance cardiography diastolic waveforms can be altered by position and may reflect changes in vena caval or pulmonary vein volume flow, or both. This technique, in combination with Doppler mitral flow patterns, may be useful in evaluating diastolic function. (Am J Cardiol 1993;71:1099-1103)

To characterize the early (1 week) and late (6 weeks) changes in left ventricular (LV) filling pattern associated with acute myocardial infarction (AMI) 45 patients (mean age 65[+ or -]2 years) were studied by Dotspier echocardiegraphy. Based on clinical criteria, patients were divided into those with large (group L; n = 12) and those with small (group S; n = 33) infarcts and then compared with 16 age-matched control subjects. The following parameters were calculated from the mitral velocity waveform: (1) peak early and peak atrial velocities and their integrals; (2) peak early to atrial velocity ratio and velodty integral ratio; and (3) the pressure half-time of the early wave. One week after AMI, group L showed a decreased atrial and increased early velocity, velocity ratio and integral ratio, whereas the pressure half-time of the early wave was shorter than that in group S and in control subjects. At 6 weeks group L showed a reduction in early velocity, early to atrial velocity ratio and integral ratio, whereas pressure half-time increased. When groups S and L were combined there was a good inverse correlation between prossure half-time and infarct size as measured by peak enzyme release (r = -0.64, p (Am J Cardiol 1992;70:1397-1401)

The reproducibility of a variety of Doppler indexes of diastolic function in an epidemiologic setting and in atrial fibrillation have not been reported. This study examined the reproducibility of left ventricular inflow in subjects in sinus rhythm (n = 80) and atrial fibrillation (n = 12), randomly selected from the original cohort of the Framingham Heart Study. The following Doppler indexes were assessed for all subjects: peak and integral of early (E) diastolic inflow velocity, acceleration slope and time, deceleration slope and time, and pressure half-time. For subjects in sinus rhythm, the following parameters also were measured: the peak and integral of late (A) diastolic inflow velocity, ratios of peak velocities and integrals E/A, and atrial filling fraction. Intraobserver and interobserver variability were evaluated by statistical methods including Student's t test of the systematic differences 9bias), percent bias, correlation co-efficients, measurement precision, and percent precision. In subjects in sinus rhythm, although the interobserver bias was statistically significant for most of the parameters, it was

Normative Doppler values and determinants of left ventricular (LV) diastolic function in healthy subjects have not been fully elucidated. Subjects from the Framingham Heart Study were examined to describe reference values and determinants of echocardiographic Doppler indexes of diastolic function. One hundred twenty-seven randomly selected, rigorously defined, normal subjects, approximately evenly distributed by sex and age from the third through the eighth decades were studied by Doppler echocardiography. Normative values for 7 frequently used Doppler indexes of LV diastolic function are presented. Doppler indexes of LV diastolic function change dramatically with age; the peak velocity of early filling divided by late filling (peak velocity E/A) ranges from a mean of 2.08 [+ or -] 0.55 for subjects in their third decade to 0.84 [+ or -] 0.29 for those in their eighth decade. A peak velocity E/A ratio Age is the predominant determinant of Doppler indexes of LV diastolic function in normal subjects, whereas heart rate, PR interval, sex, systolic blood pressure and LV systolic function have a lesser impact. The independence of the age-diastolic function relation from changes in physiology and LV geometry is consistent with an intrinsic reduction in LV distensibility with advancing age. These findings indicate that Doppler diastolic function should be assessed with reference to age-specific normative values. (Am J Cardiol 1992;70:508-515)

In secondary hypertrophy from chronic pressure or volume overload, or both, systolic as well as diastolic abnormalities of left ventricular (LV) function have been described, but their relation has not been defined. In 58 patients with aortic valve disease (28 with aortic valve stenosis, and 30 with aortic regurgitation) and in 11 control subjects, LV biplane cineangiography was performed simultaneously with LV high-fidelity pressure measurements. LV ejection performance was assessed by ejection fraction, and diastolic function by the time constant of LV pressure decay, the early and late peak filling rates, and the constants of chamber (pressure-volume relation) and myocardial stiffness (stress-strain relation). In the entire cohort (n=69), ejection fraction was inversely related to the time constant of LV relaxation (r = -0.58, p Thus, it appears that abnormalities of relaxation and passive diastolic myocardial stiffness precede alterations in myocardial contractility. Assessment of peak filling rates is not helpful to detect diastolic dysfunction in patients with aortic valve disease.

Myasthenia gravis is an autoimmune disorder with autoantibodies to acetylcholine receptors of skeletal muscle. Left ventricular diastolic function was studied with M-mode and Doppler echocardiography in 25 patients with myasthenia and in a group of age- and heart rate-matched control subjects. In the patients, diastolic peak filling rate was reduced by 37%, and Doppler peak early filling velocity (E) was reduced by 12% compared with the control subject (2.7 [+ or -] 0.7 vs 4.2 [+ or -] 1.0 [s.sup.1], and 76 [+ or -] 8 vs 85 [+ or -] 15 cm/s, respectively; p

The time course of left ventricular (LV) filling and LV diastolic performance were examined in 27 consecutive patients in sinus rhythm before and acutely after balloon mitral valvotomy (BMV). The mitral valve area acutely increased from 1.1 [+ or -] 0.3 to 2.1 [+ or -] 0.8 [cm.sup.2]. Simultaneous pressure-volume data were obtained using digital subtraction left ventriculography and LV micromanometer pressure before and 10 minutes after BMV. The time constant of LV isovolumic relaxation was unchanged after BMV (50 [+ or -] 10 ms before BMV vs 47 [+ or -] 13 ms after BMV). In addition, values before and after BMV for LV end-diastolic volume (123 [+ or -] 29 vs 125 [+ or -] 36 ml), end-diastolic pressure (11 [+ or -] 4 vs 12 [+ or -] 4 mm Hg) and diastolic filling time (337 [+ or -] 126 vs 338 [+ or -] 152 ms) were not altered by the procedure. After BMV the peak diastolic filling rate (403 [+ or -]143 vs 469 [+ or -] 302 ml/s) maintain despite a 36% reduction in left atrial filling pressure. There was a trend toward earlier occurrence of the peak filling rate (196 [+ or -] 127 vs 146 [+ or -] 148 ms, p = 0.08). The percentage of diastolic filling in the first third of diastole, however, was similar (42 [+ or -] 9 vs 48 [+ or -] 16%) before and after the procedure. Thus, the time course of LV filling is not significantly altered acutely after BMV, but is maintained at reduced left atrial filling pressure. Neither LV relaxation or LV chamber compliance are altered acutely after BMV. Changes in LV diastolic performance, which have recently been shown to alter Doppler mitral valve half-time measurements independent of changes in valve area, do not contribute to the decreased correlation between Doppler and invasive data observed acutely after BMV. In addition, the lack of impairment of LV isovolumic relaxation suggests that LV ischemia or papillary muscle injury are unlikely to contribute to increased mitral regurgitation after BMV.

Results indicate that exercise may protect against 'diastolic dysfunction' condition and subsequent pulmonary edema after myocardial infarction. This occurs by heart filling at a lower end-diastolic pressure per end-diastolic volume. Furthermore, moderate-intensity treadmill running induces a rightward shift in the left ventricularend-diastolic pressure-volume relatinship.