Hypothesis of the compression of morbidity: an example of theoretical development in epidemiology]

To assess the usefulness of the tissue Doppler imaging variables for the evaluation of left ventricular (LV) systolic function, we compared variables obtained by the pulsed Doppler method with the LV ejection fraction (%EF) and the maximum value for the first derivative of LV pressure (peak dP/dt). We examined 65 patients, including 15 patients with noncardiac chest pain, 15 with ischemic heart disease, 15 with dilated cardiomyopathy, 10 with hypertensive heart disease, and 10 with asymmetric septal hypertrophic cardiomyopathy. The subendocardial systolic wall motion velocity patterns were recorded for LV posterior wall and ventricular septum in the parasternal LV long-axis view. The peak dP/dt was significantly lower in the hypertensive heart disease, hypertrophic cardiomyopathy, and dilated cardiomyopathy groups. The peak systolic velocity was lower and the time from the electrocardiographic Q wave to the peak of the systolic wave for the posterior wall was longer in the hypertensive heart disease (5.9 +/- 0.5 cm/sec and 215 +/- 21 msec, respectively), hypertrophic cardiomyopathy (6.2 +/- 0.9 cm/sec and 217 +/- 17 msec, respectively), and dilated cardiomyopathy (5.2 +/- 0.8 cm/sec and 235 +/- 26 msec, respectively) groups than in the noncardiac chest pain (7.7 +/- 0.9 cm/sec and 187 +/- 24 msec, respectively) and the ischemic heart disease (7.6 +/- 0.8 cm/sec and 184 +/- 22 msec, respectively) groups. In all groups, the peak systolic velocity and the time from the electrocardiographic Q wave to the peak of the systolic wave for the posterior wall correlated directly and inversely, respectively, with the %EF (r = 0.59, p < 0.0001; r = -0.59, p < 0.0001) and the peak dP/dt (r = 0.75, p < 0.0001; r = -0.68, p < 0.0001). Both tissue Doppler variables for the ventricular septum did not correlate with the %EF but roughly correlated with peak dP/dt. We conclude that the systolic LV wall motion velocity parameters obtained by pulsed tissue Doppler imaging may be useful for noninvasive evaluation of global LV systolic function in patients with no regional asynergy.     

Hemodynamic determinants of the time-course of fall in canine left ventricular pressure

The hemodynamic determinants of the time-course of fall in isovolumic left ventricular pressure were assessed in isolated canine left ventricular preparations. Pressure fall was studied in isovolumic beats or during prolonged isovolumic diastole after ejection. Pressure fall was studied in isovolumic relaxation for isovolumic and ejecting beats (r less than or equal to 0.98) and was therefore characterized by a time constant, T. Higher heart rates shortened T slightly from 52.6 +/- 4.5 ms at 110/min to 48.2 +/- 6.0 ms at 160/min (P less than 0.01, n = 8). Higher ventricular volumes under isovolumic conditions resulted in higher peak left ventricular pressure but no significant change in T. T did shorten from 67.1 +/- 5.0 ms in isovolumic beats to 45.8 +/- 2.9 ms in the ejecting beats (P less than 0.001, n = 14). In the ejecting beats, peak systolic pressure was lower, and end-systolic volume smaller. To differentiate the effects of systolic shortening during ejection from those of lower systolic pressure and smaller end-systolic volume, beats with large end-diastolic volumes were compared to beats with smaller end-diastolic volumes. The beats with smaller end-diastolic volumes exhibited less shortening but similar end-systolic volumes and peak systolic pressure. T again shortened to a greater extent in the beats with greater systolic shortening. Calcium chloride and acetylstrophanthidin resulted in no significant change in T, but norepinephrine, which accelerates active relaxation, resulted in a significant shortening of T (65.6 +/- 13.4 vs. 46.3 +/- 7.0 ms, P less than 0.02). During recovery from ischemia, T increased significantly from 59.3 +/- 9.6 to 76.8 +/- 13.1 ms when compared with the preischemic control beat (P less than 0.05). Thus, the present studies show that the time-course of isovolumic pressure fall subsequent to maximum negative dP/dt is exponential, independent of systolic stress and end-systolic fiber length, and minimally dependent on heart rate. T may be an index of the activity of the active cardiac relaxing system and appears dependent on systolic fiber shortening.     

A primary intervention program (pilot study) for Mexican American children at risk for type 2 diabetes

Diastolic dysfunction is common in hypertrophic cardiomyopathy (HC). Previous studies suggest that Doppler transmitral flow velocity profiles, and the left atrial (LA) M-mode echogram can be used noninvasively to evaluate left ventricular (LV) diastolic function. However, this has not been proved in HC. In this study we determined the relation of Doppler transmitral flow velocity profiles and the LA M-mode echograms to invasive indexes of LV diastolic function in patients with HC. We studied 25 patients with HC, while off drugs, and calculated LA global and active fractional shortening and the slope of both early and late displacement of the posterior aortic wall during LA emptying by M-mode echocardiography. We calculated peak velocity of early (E) and atrial (A) filling, E to A ratio, and E-wave deceleration time by pulsed Doppler echocardiography, and simultaneous radionuclide angiography, LV pressures, time constant of isovolumic relaxation tau, and the constant of chamber stiffness k by cardiac catheterization. The time constant of isovolumic relaxation tau correlated with the slope of early posterior aortic wall displacement (r = 0.59; p <0.01). LV end-diastolic pressure correlated with global LA fractional shortening (r = -0.75; p <0.001); the constant of chamber stiffness k correlated with active LA fractional shortening (r = -0.53; p <0.02). In a subset of 13 patients, in whom echocardiography and cardiac catheterization were performed simultaneously, similar results were found. LA M-mode recordings provide a more reliable noninvasive assessment of diastolic function in HC than mitral Doppler indexes.     

A comparison of cathepsin B processing and distribution during neuronal death in rats following global ischemia or decapitation necrosis

OBJECTIVE: The relationship between the left ventricular (LV) relaxation time constant and early diastolic filling is not fully defined. This study provides additional evidence that LV isovolumic pressure fall in the normal intact heart in response to certain interventions is not adequately described by a model of monoexponential decay and that its relationship to filling is complex. METHODS AND RESULTS: To gain further insight into the relationship between LV relaxation and early rapid filling we measured LV isovolumic relaxation rate, peak early filling velocity (E), LV volumes, and transmitral pressures at baseline and in the first postextrasystolic beat after a short-coupled extrasystole in 9 anesthetized dogs. Postextrasystolic isovolumic relaxation rate was slowed as measured by 3 commonly used time constants, while E was increased 32%. LV contractility and peak pressure were also increased, while LV end-systolic volume was decreased. LV minimum pressure was deceased, while the early diastolic transmitral pressure gradient was increased. Although all relaxation time constants measured over the entire isovolumic relaxation phase indicated slowed relaxation, direct measurement of isovolumic relaxation time indicated no change in relaxation rate. Calculation of the time constants and direct measurement of isovolumic relaxation time during early isovolumic pressure decay indicated slowed postextrasystolic pressure decay rate compared with baseline, while calculation of time constants and direct measurement of isovolumic relaxation time during late isovolumic relaxation indicated augmented postextrasystolic pressure decay rate versus baseline. CONCLUSIONS: This non-exponential behavior of LV isovolumic pressure decay in postextrasystolic beats after short-coupled extrasystoles provides further evidence that the relationship that exists between ventricular relaxation and early filling is not simple. The results are interpreted in terms of current theoretical formulations that attribute control of myocardial relaxation to the interaction between inactivation-dependent and load-dependent mechanisms.     

Angiotensin-converting enzyme (ACE) inhibitors revert abnormal right ventricular filling in patients with restrictive left ventricular disease

OBJECTIVES: Our aim was to determine mechanisms underlying abnormalities of right ventricular (RV) diastolic function seen in heart failure. BACKGROUND: It is not clear whether these right-sided abnormalities are due to primary RV disease or are secondary to restrictive physiology on the left side of the heart. The latter regresses with angiotensin-converting enzyme inhibition (ACE-I). METHODS: Transthoracic echo-Doppler measurements of left- and right-ventricular function in 17 patients with systolic left ventricular (LV) disease and restrictive filling before and 3 weeks after the institution of ACE-I were compared with those in 21 controls. RESULTS: Before ACE-I, LV filling was restrictive, with isovolumic relaxation time short and transmitral E wave acceleration and deceleration rates increased (p < 0.001). Right ventricular long axis amplitude and rates of change were all reduced (p < 0.001), the onset of transtricuspid Doppler was delayed by 160 ms after the pulmonary second sound versus 40 ms in normals (p < 0.001) and overall RV filling time reduced to 59% of total diastole. Right ventricular relaxation was very incoordinate and peak E wave velocity was reduced. Peak RV to right atrial (RA) pressure drop, estimated from tricuspid regurgitation, was 45+/-6 mm Hg, and peak pulmonary stroke distance was 40% lower than normal (p < 0.001). With ACE-I, LV isovolumic relaxation time lengthened, E wave acceleration and deceleration rates decreased and RV to RA pressure drop fell to 30+/-5 mm Hg (p < 0.001) versus pre-ACE-I. Right ventricular long axis dynamics did not change, but tricuspid flow started 85 ms earlier to occupy 85% of total diastole; E wave amplitude increased but acceleration and deceleration rates were unaltered. Values of long axis systolic and diastolic measurements did not change. Peak pulmonary artery velocity increased (p < 0.01). CONCLUSIONS: Abnormalities of RV filling in patients with heart failure normalize with ACE-I as restrictive filling regresses on the left. This was not due to altered right ventricular relaxation or to a fall in pulmonary artery pressure or tricuspid pressure gradient, but appears to reflect direct ventricular interaction during early diastole.     

Doppler estimation of left ventricular filling pressure in sinus tachycardia. A new application of tissue doppler imaging

BACKGROUND: Doppler echocardiography is frequently used to predict filling pressures in normal sinus rhythm, but it is unknown whether it can be applied in sinus tachycardia, with merging of E and A velocities. Tissue Doppler imaging (TDI) can record the mitral annular velocity. The early diastolic velocity (Ea) behaves as a relative load-independent index of left ventricular relaxation, which corrects the influence of relaxation on the transmitral E velocity. METHODS AND RESULTS: We evaluated 100 patients 64+/-12 years old with simultaneous Doppler and invasive hemodynamics. Mitral inflow was classified into 3 patterns: complete merging of E and A velocities (pattern A), discernible velocities with A dominance (B), or E dominance (C). The Doppler data were analyzed at the mitral valve tips for E, acceleration and deceleration times of E, and isovolumic relaxation time. In patterns B and C, the A velocity, E/A ratio, and atrial filling fraction were derived. Pulmonary venous flow velocities were also measured, and TDI was used to acquire Ea and Aa. Weak significant relations were observed between pulmonary capillary wedge pressure (PCWP) and sole parameters of mitral flow, pulmonary venous flow, and annular measurements. These were better for patterns A and C. E/Ea ratio had the strongest relation to PCWP [r=0.86, PCWP=1.55+1.47(E/Ea)], irrespective of the pattern and ejection fraction. This equation was tested prospectively in 20 patients with sinus tachycardia. A strong relation was observed between catheter and Doppler PCWP (r=0.91), with a mean difference of 0.4+/-2.8 mm Hg. CONCLUSIONS: The ratio of transmitral E velocity to Ea can be used to estimate PCWP with reasonable accuracy in sinus tachycardia, even with complete merging of E and A velocities.     

A new approach for evaluation of left ventricular diastolic function: spatial and temporal analysis of left ventricular filling flow propagation by color M-mode Doppler echocardiography

OBJECTIVES: To evaluate left ventricular diastolic function and differentiate the pseudonormalized transmitral flow pattern from the normal pattern, the propagation of left ventricular early filling flow was assessed quantitatively using color M-mode Doppler echocardiography. BACKGROUND: Because the propagation of left ventricular early filling flow is disturbed in the left ventricle with impaired relaxation, quantification of such alterations should provide useful indexes for the evaluation of left ventricular diastolic function. METHODS: Study subjects were classified into three groups according to the ratio of early to late transmitral flow velocity (E/A ratio) and left ventricular ejection fraction: 29 subjects with an ejection fraction > or = 60% (control group); 34 with an ejection fraction < 60% and E/A ratio < 1 (group I); and 25 with ejection fraction < 60% and E/A ratio > or = 1 (group II). The propagation of peak early filling flow was visualized by changing the first aliasing limit of the color Doppler signals. The rate of propagation of peak early filling flow velocity was defined as the distance/time ratio between two sampling points: the point of the maximal velocity around the mitral orifice and the point in the mid-left ventricle at which the velocity decreased to 70% of its initial value. High fidelity manometer-tipped measurement was performed in 40 randomly selected subjects. RESULTS: The rate of propagation decreased in groups I and II compared with that in the control group (33.8 +/- 13.8 [mean +/- SD] and 30.0 +/- 8.6 vs. 74.3 +/- 17.4 cm/s, p < 0.001, respectively) and correlated inversely with the time constant of left ventricular isovolumetric relaxation and the minimal first derivative of left ventricular pressure (peak negative dP/dt) (r = 0.82 and r = 0.72, respectively). CONCLUSIONS: Spatial and temporal analysis of filling flow propagation by color M-mode Doppler echocardiography was free of pseudonormalization and correlated well with the invasive variables of left ventricular relaxation.     

Left ventricular diastolic filling alterations in subjects with mitral valve prolapse: a Doppler echocardiographic study

To assess left ventricular diastolic filling in mitral valve prolapse (MVP), we studied 22 patients with idiopathic MVP and 22 healthy controls matched for sex, age, body surface area and heart rate. A two-dimensional, M-mode and Doppler echocardiographic examination was performed to exclude any cardiac abnormalities. The two groups had similar diastolic and systolic left ventricular volumes, left ventricle mass and ejection fraction. Doppler measurements of mitral inflow were: E and A areas (the components of the total flow velocity-time integral in the early passive period of ventricular filling, E; and the late active period of atrial emptying, A), the peak E and A velocities (cm.s-1), acceleration and deceleration half-times (ms) of early diastolic rapid inflow, acceleration time of early diastolic flow (AT), total diastolic filling time (DFT) (ms), and the deceleration of early diastolic flow (cm.s-2). From these measurements were calculate: peak A/E ratio (A/E), E area/A area, the early filling fraction, the atrial filling fraction, AT/DFT ratio. All the Doppler measurements reported are the average of three cardiac cycles selected at end expiration. The mean peak A velocity, A/E velocity ratio, deceleration half time and atrial filling fraction were each significantly higher for subjects presenting a MVP (60 +/- 12 cm.s-1 vs 49 +/- 14, P < 0.008; 98 +/- 13% vs 64 +/- 12%, P < 0.0001; 120 +/- 36 ms vs 92 +/- 11, P < 0.002; 0.45 +/- 0.14 vs 0.36 +/- 0.08, P < 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)     

Use of pulsed Doppler tissue imaging to assess regional left ventricular diastolic dysfunction in hypertrophic cardiomyopathy

In this study, regional diastolic patterns and their relations with transmitral Doppler inflow were investigated in hypertrophic cardiomyopathy (HC) by pulsed Doppler tissue imaging (DTI). Doppler echocardiography and DTI of basal septum and lateral wall (apical 4-chamber view) were performed in 20 patients (15 men and 5 women) with HC and in 10 healthy subjects (7 men and 3 women). Diabetes, hypertension, coronary artery and valvular disease, mitral regurgitation, New York Heart Association functional classes III to IV, sinus tachycardia, atrial fibrillation, and inadequate echocardiograms were exclusion criteria. Peak velocity and time-velocity integral of early and late waves and their ratios, and deceleration and isovolumic relaxation times were determined by standard Doppler and by DTI at the septal and lateral wall levels. The 2 groups were comparable for age, heart rate, blood pressure, and ejection fraction. Transmitral peak velocity and time-velocity integral E/A ratios were reduced (both p <0.05) and deceleration and isovolumic relaxation times prolonged (both p <0.00001) in HC. Septal DTI showed lower peak velocity and time-velocity integral e/a ratios (p <0.00001 and p <0.001, respectively) and lengthened regional deceleration (p <0.01) and isovolumic (p <0.001) relaxation times. DTI of the lateral wall showed a prolongation of deceleration and isovolumic relaxation times (both p <0.01). By dividing HC according to transmitral E/A, 8 patients with E/A <1 had lower DTI septal e/a ratio (p <0.01) and prolonged septal deceleration and isovolumic relaxation times (both p <0.01) but no changes in DTI pattern of lateral wall than 12 patients with E/A > 1. In conclusion, DTI is useful and complementary to standard Doppler imaging to characterize diastolic properties in HC, reflecting a typical pattern of intramyocardial impaired relaxation at the level of hypertrophied septum and also providing information about the degree of this regional impairment. The lateral wall presents minor changes in diastolic times, which indicate how diastolic asynchrony is not confined to the hypertrophied segment in HC.     

Acute illnesses in children. A description and analysis of the cumulative incidence proportion

In order to evaluate left ventricular diastolic function by means of Doppler echocardiography in borderline and established hypertension, identified by office and ABPM, compared with normotensives, 54 subjects: 15 normotensives, 11 borderlines and 28 nontreated mild to moderate essential hypertensives were studied. Age and weight were similar among groups. Established hypertensives showed higher left ventricular mass index (p < 0.05), peak velocity of late left ventricular filling (peak A; p < 0.01), ratio peak A/peak velocity of early ventricular filling, peak E (p < 0.01), velocity time integral of systolic atrial volume (p < 0.001), deceleration half time of peak early diastolic inflow velocity (p < 0.05), left ventricular isovolumic relaxation period (IRP; p < 0.01) than normotensives and lower Doppler indexes of early diastolic left ventricular filling (p < 0.01), peak filling rat normalized to mitral stroke volume (PFRn; p < 0.01) than normotensives. Although borderline hypertensives showed intermediate LVM and Doppler indexes between hypertensives and normotensives only IRP (p < 0.05) and PFRn (p < 0.05) were significant different to normotensives. In conclusion, established hypertension leads to abnormalities in left ventricular diastolic function which can be detected by Doppler echocardiography. In borderline hypertension, the left ventricular diastolic abnormalities are predominantly related to the active process of early diastole. Therefore, these indexes may be early markers of left ventricular dysfunction in hypertension.     

Effects of aging on left ventricular relaxation in humans. Analysis of left ventricular isovolumic pressure decay

BACKGROUND: Some experimental studies in animals have shown that myocardial relaxation is prolonged with aging. However, it is not known whether aging alters ventricular isovolumic relaxation in human subjects. METHODS AND RESULTS: We analyzed high-fidelity left ventricular pressures, measured by use of a catheter-tipped manometer, and biplane left ventriculograms in 55 normal subjects who underwent diagnostic cardiac catheterization but who were found to have normal cardiac anatomy and function. There were 38 men and 17 women, ranging in age from 20 to 77 years. Left ventricular isovolumic relaxation was assessed by the exponential time constants of isovolumic pressure decay with (Tb) and without (Tw) an asymptote pressure. Left ventricular volume, ejection fraction, and wall thickness or mass were calculated from left ventricular angiograms. Neither of the time constants of left ventricular relaxation correlated with age (Tb: r = .001 to .10, P = NS: Tw: r = .02 to .05, P = NS). Left ventricular systolic function (ie, ejection fraction and end-systolic volume index), heart rate, and left ventricular wall thickness or mass, which are major hemodynamic determinants of left ventricular relaxation, were not significantly affected by aging. The multivariate analysis of age and hemodynamic variables against the time constants of left ventricular relaxation also indicated that no significant relation was found between age and left ventricular relaxation. CONCLUSIONS: In the absence of coronary artery disease, systemic hypertension, left ventricular systolic dysfunction, or hypertrophy, left ventricular relaxation assessed by the time constant of isovolumic pressure decay remains essentially unchanged with normal adult aging, at least until the eighth decade.     

Early effects of coronary artery bypass surgery and cold cardioplegic ischemia on left ventricular diastolic function: evaluation by computer-assisted transesophageal echocardiography

OBJECTIVE: Although left ventricular (LV) systolic function undergoes a temporary decrease after cardiopulmonary bypass (CPB) in patients undergoing coronary artery bypass grafting (CABG), data on the effects of CABG and cardioplegic arrest on LV diastolic function are contradictory. The objective of the present study was to further evaluate the effects of CABG and CPB on LV diastolic function. DESIGN: A prospective study. SETTING: A multi-institutional investigation at a university hospital. PARTICIPANTS: 20 patients on beta-receptor antagonists, scheduled for CABG and with a preoperative ejection fraction over 0.5. INTERVENTIONS: Central hemodynamic measurements, transesophageal LV short-axis images, and mitral Doppler flow profiles were obtained before and after volume loading that in turn was performed both before surgical incision and after weaning from CPB. MEASUREMENTS AND MAIN RESULTS: Heart rate, cardiac output, and peak atrial filling velocity increased; systemic vascular resistance decreased; whereas stroke volume, LV area ejection fraction, deceleration rate and slope of early diastolic filling, time-velocity integral of early diastolic filling, and the ratio between early and atrial peak filling velocity were unchanged post-CPB compared with pre-CPB. LV end-diastolic stiffness that was calculated for each patient pre-CPB and post-CPB using the formula: P = B*eS*A), where P is the LV filling pressure and A is the end-diastolic short-axis area, was unchanged post-CPB compared with pre-CPB. CONCLUSIONS: Both the active and passive components of LV diastolic function are well maintained shortly after CABG and cardioplegic arrest in patients with a good preoperative systolic LV function.     

Reversibility of changes in left and right ventricular geometry and hemodynamics in pulmonary hypertension. Echocardiographic characteristics before and after pulmonary thromboendarterectomy

Pulmonary thromboendarterectomy (PTE) leads to an acute decrease of right ventricular (RV) afterload in patients with chronic thromboembolic pulmonary hypertension. We investigated the changes in right and left ventricular (LV) geometry and hemodynamics by means of transthoracic echocardiography. The prospective study was performed in 14 patients (8 female, 6 male; age 55 +/- 20 years) before and 18 +/- 12 days after PTE. Total pulmonary vascular resistance and systolic pulmonary artery pressure were significantly decreased (PVR: preoperative 986 +/- 318, postoperative 323 +/- 280 dyn x s/cm5, p < 0.05; PAP preoperative 71 +/- 40, postoperative 41 +/- 40 mm Hg + right atrial pressure, p < 0.05). End diastolic and end systolic RV area decreased from 33 +/- 12 to 23 +/- 8 cm2, respectively, from 26 +/- 10 to 16 +/- 6 cm2, p < 0.05. There was an increase in systolic RV fractional area change from 20 +/- 12 to 30 +/- 16%, p < 0.05. RV systolic pressure rise remained unchanged (516 +/- 166 vs. 556 +/- 128 mm Hg/sec). LV ejection fraction remained within normal ranges (64 +/- 16 vs. 62 +/- 12%). Echocardiographically determined cardiac index increased from 2.8 +/- 0.74 to 4.1 +/- 1.74 l/min/m2. A decrease in LV excentricity indices (end diastolic: 1.9 +/- 1 vs. 1.1 +/- 0.3, end systolic: 1.7 +/- 0.6 vs. 1.1 +/- 0.4, p < 0.05) proved a normalization of preoperatively altered septum motion. LV diastolic filling returned to normal limits: (E/A ratio: 0.62 +/- 0.34 vs. 1.3 +/- 0.8; p < 0.05); Peak E velocity: 0.51 +/- 0.34 vs. 0.88 +/- 0.28 m/sec, p < 0.05; Peak A velocity: 0.81 +/- 0.36 vs. 0.72 +/- 0.42 m/sec, ns; E deceleration velocity: 299 +/- 328 vs. 582 +/- 294 cm/sec2, p < 0.05; Isovolumic relaxation time: 134 +/- 40 vs. 83 +/- 38 m/sec, p < 0.05). We could show a marked decrease in RV afterload shortly after PTE with a profound recovery of right ventricular systolic function--even in case of severe pulmonary hypertension. A decrease in paradoxic motion of the interventricular septum and normalization of LV diastolic filling pattern resulted in a significant increase of cardiac index.     

Presurgical profile preferences of patients and clinicians

BACKGROUND: Aortic regurgitation results from a pressure gradient across the aortic valve during left ventricular (LV) isovolumic relaxation, LV filling, and isovolumic contraction periods. Assuming the applicability of the simplified Bernoulli equation to this pressure-flow relation and constancy of aortic pressure during LV isovolumic relaxation and contraction periods, one can theoretically obtain estimates of the rates of LV isovolumic pressure fall and rise (deltaP/delta t) from the aortic regurgitation (AR) velocity signal. METHODS AND RESULTS: Mitral regurgitation (MR) and AR signals were recorded by using the continuous wave Doppler technique in 26 patients with combined mitral and aortic regurgitant lesions. The LV negative deltaP/delta t was obtained by dividing the time taken for the AR velocity to rise from 1 m/sec to 2.5 m/sec into 21 mm Hg, which is the estimated LV pressure drop between these points. In a similar fashion, the LV positive deltaP/delta t was obtained between 2.5 m/sec and 1 m/sec of the fast decelerating portion of the AR signal. The LV negative deltaP/delta t by the AR method ranged from 420 to 3500 mm Hg/sec and correlated well with that obtained by the MR method obtained in a blinded fashion (r = 0.95, p < 0.0001). The mean (SD) difference between the two methods was 30 (129) mm Hg/sec. Similarly, the LV positive deltaP/delta t by the AR method (range 420 to 2625 mm Hg/sec) correlated closely with that obtained by the MR method (r = 0.93, p < 0.0001), with the mean (SD) difference between the two methods being 38 (138) mm Hg/sec. CONCLUSIONS: Preliminary data presented in this study indicate the feasibility of obtaining a reliable estimate of LV positive and negative deltaP/delta t from the AR velocity profile. Thus the examination of the AR signal may give valuable insights into both LV systolic and diastolic functions.     

Estimation of left ventricular filling pressures using two-dimensional and Doppler echocardiography in adult patients with cardiac disease. Additional value of analyzing left atrial size, left atrial ejection fraction and the difference in duration of pulmonary venous and mitral flow velocity at atrial contraction

OBJECTIVES: The purpose of this study was to determine whether left atrial size and ejection fraction are related to left ventricular filling pressures in patients with coronary artery disease. BACKGROUND: In patients with coronary artery disease, left ventricular filling pressures can be estimated by using Doppler mitral and pulmonary venous flow velocity variables. However, because these flow velocities are age dependent, additional variables that indicate elevated left ventricular filling pressures are needed to increase diagnostic accuracy. METHODS: Echocardiographic left atrial and Doppler mitral and pulmonary venous flow velocity variables were correlated with left ventricular filling pressures in 70 patients undergoing cardiac catheterization. RESULTS: Left atrial size and volumes were larger and left atrial ejection fractions were lower in patients with elevated left ventricular filling pressures. Mean pulmonary wedge pressure was related to mitral E/A wave velocity ratio (r = 0.72), left atrial minimal volume (r = 0.70), left atrial ejection fraction (r = -0.66) and atrial filling fraction (r = -0.66). Left ventricular end-diastolic and A wave pressures were related to the difference in pulmonary venous and mitral A wave duration (both r = 0.77). By stepwise multilinear regression analysis, the ratio of mitral E to A wave velocity was the most important determinant of pulmonary wedge (r = 0.63) and left ventricular pre-A wave (r = 0.75) pressures, whereas the difference in pulmonary venous and mitral A wave duration was the most important variable for both left ventricular A wave (r = 0.75) and left ventricular end-diastolic (r = 0.80) pressures. The sensitivity of a left atrial minimal volume > 40 cm3 for identifying a mean pulmonary wedge pressure > 12 mm Hg was 82%, with a specificity of 98%. CONCLUSIONS: Left atrial size, left atrial ejection fraction and the difference between mitral and pulmonary venous flow duration at atrial contraction are independent determinants of left ventricular filling pressures in patients with coronary artery disease. The additive value of left atrial size and Doppler variables in estimating filling pressures and the possibility that left atrial size may be less age dependent than other mitral and pulmonary venous flow velocity variables merit further investigation.     

Aortic blood momentum--the more the better for the ejecting heart in vivo?

OBJECTIVES: The aim of the present study was to test two hypotheses: (1) the momentum of the blood flowing out of the left ventricle toward the aorta (inertia force) plays an important role in the initiation of decay and the maximum rate of decay (peak (-dP/dt)) of left ventricular pressure (P); (2) a normal heart itself generates the inertia force which enhances its function. METHODS: The contribution of the inertia force to (-dP/dt) was theoretically given as rho c alpha, where rho is the blood density, c the pulse wave velocity, and alpha the deceleration rate of aortic blood flow. The correlations of peak (-dP/dt) with rho c alpha and with the time constant (tau) of the pressure decay during isovolumic relaxation, which was considered to represent myocardial relaxation characteristics, were compared in seven dogs. We developed a method of grading the strength of the inertia force, using the phase loop of left ventricular pressure (dP/dt vs. P relation). The method was applied to the records of 25 patients with ischemic heart disease, from which high fidelity left ventricular pressure recordings were available. RESULTS: The correlation of peak (-dP/dt) with rho c alpha was much higher than with tau (0.75 vs. -0.46). 16 of the 25 patients showed evidence of the inertia force. However, other patients showed no inertia force. The strength of the inertia force showed a significant (P < 0.05) correlation with left ventricular end-diastolic pressure (r = -0.46), cardiac index (r = 0.62), stroke volume index (r = 0.69), ejection fraction (r = 0.46), and peak (-dP/dt) (r = 0.56). CONCLUSION: The inertia force of late systolic aortic flow contributed to ventricular relaxation in the normal heart.     

The age-associated alterations in late diastolic function in mice are improved by caloric restriction

Caloric restriction reduces the magnitude of many age-related changes in rodents. Cardiac function is altered with senescence in mice, rats, and healthy humans. We examined the effects of life-long caloric restriction on diastolic and systolic cardiac function in situ using Doppler techniques in ad libitum-fed 30- to 32-month-old (AL) and calorically restricted (CR) 32- to 35-month-old female B6D2-F1 hybrid mice. The heart weight to body weight ratio was similar in AL (5.74 +/- .24 mg/g) and CR (5.68 +/- .20 mg/g) mice. Two systolic functional parameters known to decrease with age in both humans and mice, peak aortic velocity and aortic acceleration, were unchanged by CR compared to AL. In contrast, diastolic function was altered by caloric restriction. Although left ventricular peak early filling velocity (E) was not different between CR and AL, peak atrial filling velocity (A) was 50% lower in CR compared to AL (p < .001). The ratio of early diastolic filling to atrial filling (E/A ratio) was 64% higher in the CR (2.74 +/- .31) than the AL (1.55 +/- .07; p = .004). The fraction of ventricular filling due to atrial systole, the atrial filling fraction, was also reduced in CR (.21 +/- .04) compared to AL (.36 +/- .02; p = .007). These changes occurred in CR without alteration in E deceleration time, which is consistent with improved diastolic function in CR. Through mechanisms that remain unknown, lifelong caloric restriction may prevent the age-related impairments in late diastolic function but does not alter the impairments in systolic or early diastolic cardiac function.     

Doppler echocardiographic study of left ventricular function in patients with systemic lupus erythematosus

This study was aimed at investigating abnormalities in left ventricular size and function in patients with systemic lupus erythematosus without overt cardiovascular manifestations, in order to detect a very early impairment in myocardial function. Seventeen females and 1 male with systemic lupus erythematosus of 4 to 20 year duration and without clinical evidence of heart disease were studied. Twelve healthy volunteers, matched for age, sex and quatelet index, were utilized as controls. Each patient had a two-dimensional M-mode echocardiographic and Doppler examination. In patients with systemic lupus erythematosus there was an increase in left ventricular ejection fraction (p < 0.001), a slight reduction of end-diastolic volume index and a significant decrease of end-systolic volume index (p < 0.001). In the same patients we also found prolongation of the isovolumic relaxation time (p < 0.02), a clear impairment of diastolic filling parameters. Peak E velocity was lower (p < 0.01), peak A velocity was higher (p < 0.01), with a clear lowering, of the corresponding E/A ratio (p < 0.001) in patients with systemic lupus erythematosus.     

Adverse effects and recovery after total intravenous anesthesia in children

INTRODUCTION: The asynchrony of the left ventricle--i.e., its nonuniform contraction and relaxation--is an important factor for left ventricular function. Heart failure is often related to abnormal systolic function, sometimes associated with a diastolic dysfunction. We studied the relationship of left ventricular asynchrony to left ventricular function in patients with nonischemic heart failure. MATERIAL AND METHODS: Radionuclide angiography at rest was performed in 25 patients with nonischemic heart failure and in 26 age and sex matched normal subjects. In addition to ejection fraction and peak filling rate, two indices of left ventricular asynchrony were calculated: the coefficient of variation of regional time to end systole and the coefficient of variation of regional time to peak filling rate. These factors indicate how disperse are the regional values of time to end systole and of time to peak filling rate. In fact, the higher the value, the greater the asynchrony. RESULTS: A significant (r = .46, p < .05) inverse correlation was found between the ejection fraction and the coefficient of variation of regional time to end systole in both the normal subjects and the heart failure patients, while the ejection fraction correlated significantly (r = .46, p < .05) with the coefficient of variation of regional time to peak filling rate only in the patients. Moreover, the peak filling rate was inversely correlated (r = .57, p < .05) with the coefficient of variation of regional time to peak filling rate in the heart failure patients but not in the normal subjects. CONCLUSIONS: These results suggest that left ventricular systolic and diastolic asynchrony may contribute to impair left ventricular systolic and diastolic function in patients with nonischemic heart failure.     

Beta-adrenergic stimulation enhances left ventricular diastolic performance in normal subjects

To determine the effects of beta-adrenergic stimulation on transmitral Doppler echocardiography flow characteristics of left ventricular diastolic filling, we studied 10 healthy volunteers aged 23-31 years (mean age, 26.6 years) during intravenous infusion of isoprenaline in consecutive steps of 0.1, 0.2, 0.4, 0.75, and 1.5 micrograms/min (each for 15 min). Saline control infusion was given in the same manner in a crossover and blinded protocol. Compared with the infusion of placebo, stepwise increasing doses of isoprenaline caused a dose-related increase in early and late diastolic filling velocities and velocity-time integrals, a lengthening of the acceleration time, and a shortening of the deceleration and filling time. The chosen method proved highly sensitive, as statistically significant changes were detectable at the lowest dose of 0.1 microgram/min for all variables except velocity-time integral of late filling and deceleration time (> or = 0.2 microgram/min). The effects related to dose in a log-linear fashion except for the lengthening of the acceleration time (early ceiling), the increase of peak early filling velocity (increased steepness at higher doses), and the shortening of the filling time. Inclusion of the associated increases in heart rate and systolic blood pressure and the decrease in diastolic blood pressure blunted all treatment contrasts except for the increase of peak early filling velocity. In addition, the hemodynamics with respect to heart rate and loading conditions were not altered at low dosages of drug (< 0.4 microgram/min). Effects of at least the peak early filling velocity must be interpreted as an active adrenergically mediated myocardial relaxation process. These findings have potentially important clinical implications for this noninvasive, readily available, and convenient technique in clinical pharmacology, stress testing, and possibly therapeutic interventions in diastolic dysfunction in humans.