Estimation of left ventricular end-diastolic pressure from Doppler transmitral flow velocity in cardiac patients independent of systolic performance.

In patients with heart disease, changes in left ventricular filling pressures produce alterations in the Doppler transmitral flow velocity and isovolumetric relaxation time. This investigation explored the hypothesis that combining isovolumetric relaxation time with measurements derived from the transmitral flow velocity can be used to estimate left ventricular end-diastolic pressure. Simultaneous Doppler and left ventricular pressure recordings were obtained in 33 patients (24 men with a mean age of 58 +/- 11 years) and an ejection fraction ranging from 15% to 74% (mean 55 +/- 15%). The following Doppler measurements correlated significantly with left ventricular end-diastolic pressure (range 4 to 36 mm Hg): isovolumetric relaxation time (IVRT; r = -0.73), atrial filling fraction (AFF; r = -0.66), deceleration time (DT; r = -0.59), ratio of early transmitral flow velocity to atrial flow velocity (E/A ratio; r = -0.53) and time from termination of mitral flow to the electrocardiographic R wave (MAR; r = 0.37). Combining these measurements into a multilinear regression equation provided a more accurate estimate of end-diastolic pressure (LVEDP; r = 0.80; SEE = 7.4). The equation LVEDP = 46 -0.22 IVRT -0.10 AFF -0.03 DT -(2 divided by E/A) + 0.05 MAR was tested prospectively in 26 additional patients (mean age 55 +/- 11 years; ejection fraction 41 +/- 23%) with simultaneous Doppler and hemodynamic recordings but with the two measurements made independently, in blinded fashion, by additional observers. Estimated and measured end-diastolic pressures correlated well with each other (r = 0.86).(ABSTRACT TRUNCATED AT 250 WORDS)     

Evaluation of left ventricular filling dynamics by pulsed Doppler echocardiography during afterload stress in ischemic heart disease using angiotensin II infusion

To evaluate cardiac reserve in ischemic heart disease, we simultaneously investigated left ventricular filling parameters using pulsed Doppler echocardiography (PDE) and catheter-obtained hemodynamics before and during afterload stress (angiotensin II test) in 14 patients with ischemic heart disease. The patients were divided into two groups according to their left ventricular function, i.e., mean left ventricular ejection fraction (mLVEF): Group I (n = 7, mLVEF = 65%) and Group II (n = 7, mLVEF = 43%). The peak velocity of rapid filling (R), the peak velocity of atrial contraction (A), the ratio of the two peak velocities (A/R), flow velocity integrals of the rapid filling phase (IR) and atrial contraction phase (IA) were obtained by PDE. Results were as follows: 1. During afterload stress, blood pressure, pulmonary artery wedge pressure, and left ventricular end-diastolic pressures (LVEDP) were elevated in both groups (p less than 0.01). The stroke work index (SWI) increased (p less than 0.01) and the time constant of left ventricular isovolumic pressure decay (T) was unchanged in Group I. SWI did not increase and T was prolonged in Group II (p less than 0.05). delta SWI/delta LVEDP, the ratio of the SWI change to the LVEDP change, during afterload stress was larger in Group I than in Group II (p less than 0.02). 2. Before the infusion of angiotensin II, R and IR were larger in Group I than in Group II. The A/R in Group I was less than that in Group II (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)     

Determinants of left ventricular inflow: the relation of the transmitral velocity profile to loading conditions]

To clarify the factors controlling left ventricular inflow, hemodynamics and Doppler-derived indices were analyzed in six anesthetized open-chest dogs with intact pericardia. Low molecular dextran was intravenously infused at 1 L/hr. During rapid infusion, an electrocardiographic lead, left ventricular pressure curve, and a transmitral Doppler signal were recorded at various heart rates produced by right atrial pacing. In five of the six dogs, the relationship of the ratio of peak velocity during atrial contraction to that during rapid filling (A/R) and left ventricular end-diastolic pressure (LVEDP) showed a non-linear quadratic curve concave to the LVEDP axis. Data from the ascending and descending limbs of the A/R-LVEDP relationship were subjected to stepwise multiple linear regression analysis (criterion variables: A/R; explanatory variables: peak dP/dt, maximum left ventricular pressure, time constant T, minimum left ventricular pressure, LVEDP, and heart rate). In both limbs, the A/R correlated positively with maximum left ventricular pressure (left ventricular afterload) and negatively with LVEDP (left ventricular preload). The time constant T was selected as a positive correlate only in the ascending limb. The transmitral flow velocity profile is determined in a complex manner by multiple factors, including left ventricular loading conditions and heart rate, as well as the left ventricular diastolic property. It was suggested that the A/R is not altered unidirectionally by the changes in cardiac function and loading conditions, but that it returns to the initial value accompanied by systolic and diastolic cardiac dysfunction.     

Noninvasive prediction of left ventricular end-diastolic pressure in patients with coronary artery disease and preserved ejection fraction

Background

The aim of this study was to compare 3 different available methods for estimating left ventricular end-diastolic pressure (LVEDP) noninvasively in patients with coronary artery disease and preserved left ventricular ejection fraction (EF).

Methods

We used 3 equations for noninvasive estimation of LVEDP: The equation of Mulvagh et al., LVEDP₁ = 46 − 0.22 (IVRT) − 0.10 (AFF) − 0.03 (DT) − (2 ÷ E/A) + 0.05 MAR; the equation of Stork et al., LVEDP₂ = 1.06 + 15.15 × Ai/Ei; and the equation of Abd-El-Aziz, LVEDP₃ = [0.54 (MABP) × (1 − EF)] − 2.23. (Abbreviations: A, A-wave velocity; AFF, atrial filling fraction; Ai, time velocity integral of A wave; DT, deceleration time; E, E-wave velocity; Ei, time velocity integral of E wave; IVRT, isovolumic relaxation time; MABP, mean arterial blood pressure; MAR, time from termination of mitral flow to the electrocardiographic R wave; Ti, time velocity integral of total wave.)

Results

LVEDP measured by catheterization was correlated with LVEDP₁ (r = 0.52, P < 0.001), LVEDP₂ (r = 0.31, P < 0.05), and LVEDP₃ (r = 0.81, P < 0.001).

Conclusions

The equation described by Abd-El-Aziz, LVEDP = [0.54 MABP × (1 − EF)] − 2.23, appears to be the most accurate, reliable, and easily applied method for estimating LVEDP noninvasively in patients with preserved left ventricular ejection fraction and an LVEDP < 20 mm Hg.     

Validity of estimating left ventricular relaxation and filling dynamics by Doppler trans-mitral flow

To evaluate the validity of estimating left ventricular (LV) diastolic function using the Doppler transmitral flow profile, the relationship of transmitral flow to LV relaxation and LV filling dynamics was observed. A total of 54 subjects, including patients with ischemic heart disease, idiopathic cardiomyopathy, and normal persons were examined. LV filling dynamics were assessed in 20 of them who had no regional wall motion abnormality or irregular LV geometry. Peak velocity of rapid filling (R) and acceleration of rapid filling (AR) at the mitral annular level were measured as indices of transmitral flow during the rapid filling period. LV relaxation was evaluated according to the time constant of LV isovolumic pressure decline (T) using the method of Weiss et al. The correlation coefficient between R and T was -0.27 and that between AR and T was -0.16, indicating lack of correlations. The v-wave of pulmonary wedge pressure (PWPv) was measured as an index for left atrial driving pressure during the rapid LV filling period. Multiple regression analyses of R or AR as dependent variables and T and PWPv as independent variables revealed significant correlations (r = 0.66 and r = 0.59). The peak transit rate (PTR = R/TVI) and atrial transit fraction (ATF = TVIa/TVI) were determined from the time integral of the transmitral flow velocity (TVI = time velocity integral during diastole, TVIa = time velocity integral during the atrial contraction phase). Also, the peak filling rate (PFR) during the rapid filling and atrial filling fraction (AFF) were determined by left ventriculography.(ABSTRACT TRUNCATED AT 250 WORDS)     

Transmitral flow velocity patterns as influenced by preload, afterload and heart rate alterations: pulsed Doppler echocardiographic study]

The influences of preload, afterload and heart rate alterations on the pattern of left ventricular filling were investigated using pulsed Doppler echocardiography (PDE) in humans. Transmitral flow at the level of the valvular tip was recorded during dextran infusion, lower body negative pressure, angiotensin II infusion, and atrial and atrioventricular sequential pacings. Peak velocity of rapid filling (R), peak velocity of atrial contraction (A), the ratio of peak velocities (A/R), flow velocity integrals of the rapid filling phase (IR) and atrial contraction (IA) were obtained. PDE and the measurement of hemodynamics during lower body negative pressure (0, -10 mmHg, -20 mmHg) and dextran infusion (100 ml, 200 ml) were studied in 22 patients with ischemic heart disease. R decreased significantly after lower body negative pressure, and increased significantly during dextran infusion. Before and during angiotensin II infusion, PDE and the measurement of hemodynamics were studied in 14 patients with ischemic heart disease. The patients were categorized into 2 subgroups according to left ventricular function. During afterload stress, the A/R and IA increased in patients with normal left ventricular function; whereas, the A/R decreased in patients with poor left ventricular function. PDE was recorded during right atrial and atrioventricular sequential pacings at the heart rates of 60 to 100 beats/min in 29 patients with ischemic heart disease. When the heart rates increased, R decreased during atrial and atrioventricular sequential pacings. The A increased after the occurrence of the summation between the rapid and atrial filling waves. The A/R gradually increased with incremental heart rate. These results indicate that changes in the preload alter the peak velocity of left ventricular filling pattern of transmitral flow. The effects of the increasing afterload depend on the basal left ventricular function, with an increase in the peak velocity of atrial contraction being observed in the presence of normal left ventricular function. Both the peak velocity of rapid filling and atrial contraction were related to the heart rate and atrioventricular conduction delay. In assessing left ventricular filling dynamics using PDE, the influence of the preload, afterload and heart rate must be considered.     

Determinants of left ventricular filling dynamics: alteration in the Doppler-derived transmitral filling profile with progressive impairment of cardiac function in a dog preparation.

To clarify the factors determining transmitral filling, left ventricular and atrial pressures (LVP and LAP) and Doppler-derived diastolic indices were analysed in six anaesthetized dogs at various right atrial pacing rates during dextran infusion. The relationship of the late to early diastolic peak velocity ratio (A/E ratio) to end-diastolic LVP (LVEDP) showed a quadratic curve concave to the LVEDP axis in five animals (r2 = 0.320-0.588). An elevation in LVEDP up to 25 mmHg accompanied an increase in A/E ratio (ascending limb), and further LVEDP elevation caused its inverse decline (descending limb). Multiple regression analysis indicated that A/E ratio correlated positively with maximal LVP, a-wave LAP and heart rate, and negatively with v-wave LAP in both limbs. The time constant of isovolumic LVP decline, which was prolonged as LVEDP was elevated, was a positive correlate of A/E ratio in the ascending limb, but lost its influence on A/E ratio in the descending limb. An elevation in v-wave LAP must have masked the expected effect of left ventricular relaxation abnormality on A/E ratio in this limb. Thus, the transmitral filling profile did not alter unidirectionally, but returned to that seen before volume loading, with a simultaneous progressive impairment of cardiac function.     

Echocardiographic evaluation of left ventricular filling pressures validated against an implantable left ventricular pressure monitoring system

Background: Aim of this study was to assess the ability of different echocardiographic indices to evaluate left ventricular (LV) filling pressures in patients with reduced LV function. Methods: In 5 patients scheduled for aortocoronary bypass surgery, a telemetric intraventricular pressure sensor was implanted. Over 6 months, these patients underwent a total of 21 echocardiographic examinations with a simultaneous recording of left ventricular mean (LVMDP) and end‐diastolic pressure (LVEDP). The following echocardiographic parameters were extracted from the transmitral flow profile: early (E) and late (A) diastolic flow velocity, deceleration time of the E‐wave (DT) and the isovolumic relaxation time (IVRT). Early diastolic velocity of the mitral ring (E’) was recorded using pulsed‐wave tissue Doppler echocardiography. Results: All patients were in NYHA class III and mean ejection fraction was 30%. E correlated only moderately with LVMDP (r =–0.60, P = 0.003), but revealed the highest area under the receiver operating characteristic curve for the prediction of an elevated LVMDP > 12 mmHg (AUC = 0.94, sensitivity of 92% and specificity of 86%, cut‐off value 7.5 cm/s). E/A > 1 predicted LVEDP > 15 mmHg with a sensitivity of 87% and a specificity of 80%. E/E’ was not correlated with LVMDP or LVEDP. Conclusion: Although linear correlation between echocardiographic parameters and diastolic LV pressures reached statistical significance, the correlation coefficients were low. However, in these patients with severely reduced LV function due to ischemic heart disease conventional echocardiographic parameters of transmitral flow showed higher predictive values for elevated LV filling pressures than E/E’. (Echocardiography 2011;28:619‐625)     

Comparison of usefulness of echocardiographic Doppler variables to left ventricular end-diastolic pressure in predicting future heart failure events

We sought to determine whether the echocardiographic Doppler parameters of left ventricular diastolic dysfunction predict future heart failure (HF) events and, if so, which parameters best predict HF. We also examined whether the predictive ability of echocardiographic Doppler parameters was related to their prediction of left ventricular end-diastolic pressure (LVEDP). We studied patients who underwent cardiac catheterization and echocardiography performed within a 30-day period. The end point was HF, defined as new-onset or recurrent HF diagnosed by a physician and requiring the initiation or modification of treatment of HF. We identified 289 patients (mean age 63.5 +/- 12.6 years) with a mean follow-up of 10.9 +/- 10.2 months. A total of 24 HF events occurred. LVEDP was a significant predictor of HF univariately and independently in multiple regression models after adjustment for ejection fraction. In Cox models adjusted for age, gender, LVEDP, and ejection fraction, only the left atrial volume index and early mitral inflow to early diastolic tissue velocity (E/e') ratio remained predictive of HF. A multiple regression model, including all echocardiographic variables, showed a persistent, although attenuated, relation of early to late mitral inflow velocity (E/A) ratio and E/e' with LVEDP (p = 0.06 and p = 0.002, respectively). The addition of E/e' or the left atrial volume indexed to body surface area, but not E/A, to the clinical history and left ventricular ejection fraction provided incremental prognostic information. A LVEDP of > or =20 mm Hg, E/e' ratio of > or =15, and left atrial volume index of > or =23 ml/m(2) identified those with a higher risk of HF. In conclusion, invasively determined LVEDP is an independent predictor of future HF events. E/e' and the left atrial volume indexed to body surface area are the best independent predictors of future HF and provide prognostic information incremental to the clinical history and left ventricular ejection fraction.     

Change in filling pattern with preload reduction reflects left ventricular relaxation

BACKGROUND: The early diastolic mitral valve pressure gradient and the rate of left ventricular filling are determined by the rate of left ventricular relaxation and left atrial pressure at the time of mitral valve opening. Accordingly, we hypothesized that the left ventricular filling pattern with preload reduction can be used to estimate left ventricular relaxation in patients with preserved systolic function. METHODS: We evaluated the relationship between the logistic time constant of left ventricular relaxation and left ventricular filling pattern calculated from the time derivative of left ventricular volume using a microtipmanometer and a conductance catheter in 26 consecutive patients with preserved left ventricular ejection fraction (>45%). Left ventricular filling patterns were determined from the maximal rates of early diastolic left ventricular filling (E velocity) and atrial filling (A velocity) before and after preload reduction by inferior venal caval occlusion. RESULTS AND CONCLUSIONS: There was no significant relationship between the logistic time constant of left ventricular relaxation and the E/A velocity ratio at baseline. However, the time constant was correlated with the E/A velocity ratio after venal caval occlusion (r=-0.47, p=0.02). Furthermore, the time constant was correlated with %E/A velocity change, which was defined as the rate of change of E/A before and after caval occlusion divided by E/A after caval occlusion, more significantly (r=-0.67, p<0.01) than with the E/A velocity ratio after caval occlusion. Thus, the left ventricular filling pattern with preload reduction can be used to estimate left ventricular relaxation in patients with preserved left ventricular ejection fraction.     

Effect of increasing heart rate on Doppler indices of left ventricular performance in healthy men.

OBJECTIVE--To investigate the effects of heart rate on the Doppler measurements of left ventricular function and to determine the normal pattern of rate dependency. SETTING--University hospital specialising in internal medicine. PARTICIPANTS--14 healthy male volunteers 10 of whom were studied. INTERVENTION--Transoesophageal atrial pacing. MAIN OUTCOME MEASURES--At paced rates of 70, 80, and 90 ppm the ratio of early to late peak transmitral flow velocity (E/A) was 1.97 (0.28), 1.49 (0.21), and 0.95 (0.11) respectively; the ratio of early to late time-velocity integrals of transmitral flow (Ei/Ai) was 3.03 (0.51), 2.11 (0.24), and 1.14 (0.30) respectively; and the atrial filling fraction (AFF) was 0.17 (0.03), 0.21, (0.04), and 0.24 (0.04) (mean (SD)). RESULTS--Heart rate showed a linear correlation with E/A (r2 = 0.806), Ei/Ai (r2 = 0.838), and AFF (r2 = 0.343). Neither the peak aortic flow velocity or the mean aortic flow acceleration showed significant changes during pacing at rates of 70, 80, 90, and 100 ppm. CONCLUSIONS--E/A and Ei/Ai can be expected to decrease by 0.5 and 0.9 for each increase of 10 beats/min in heart rate. Knowledge of this relation may be useful for the development of algorithms to correct for heart rate when diastolic function is assessed.     

Noninvasive assessment of left ventricular end-diastolic pressure by the response of the transmitral a-wave velocity to a standardized Valsalva maneuver

Impaired relaxation is frequently masked by elevated filling pressures, resulting in a pseudonormal flow pattern (E/A >1.0). Because the E/A wave ratio increases as filling pressures rise, it is generally assumed that patients with an E/A ratio of <1.0 (impaired relaxation pattern) have relatively low filling pressures. Nevertheless, patients with an E/A ratio of <1.0 can have as profoundly elevated filling pressures as patients with a pseudonormal or restrictive filling pattern. Because left ventricular (LV) pressure during end-diastole essentially determines atrial afterload, the response of the A-wave velocity to a reduction of atrial afterload by a standardized Valsalva maneuver should allow estimation of LV end-diastolic pressure (LVEDP) regardless of the baseline Doppler flow pattern. This was tested in 20 consecutive patients who were studied by pulse-wave Doppler echocardiography during cardiac catheterization. There was a close correlation between LVEDP and the change in A-wave velocity during the Valsalva maneuver (r = 0.85, SEE 6.7 mm Hg) regardless of the baseline E/A ratio. In patients with a LVEDP of <15 mm Hg the A wave decreased by 21 +/- 15 cm/s. In patients with a LVEDP of >25 mm Hg the A wave increased by 18 +/- 13 cm/s. The change in the E/A ratio during Valsalva correlated fairly with LVEDP (r = -0.72, SEE 8.8 mm Hg), the baseline E/A ratio correlated poorly, and scatter was substantial (r = 0.46, SEE 11.2 mm Hg). Just as elevated filling pressures can mask impaired relaxation, the impaired relaxation pattern can mask the presence of elevated filling pressures. This can be revealed by testing the response of the A wave to the Valsalva maneuver, allowing estimation of LVEDP independent of the baseline E/A ratio.     

Left ventricular function and the relationship between left atrial pressure and peak early diastolic filling velocity in dog.

OBJECTIVE: The aim was to clarify the roles of left atrial pressure and ventricular function in the determination of early diastolic filling. METHODS: Various grades of ventricular dysfunction were made in 12 mongrel dogs by coronary microembolization under pentobarbitone anaesthesia. Left atrial pressure was altered by volume loading. Peak early diastolic filling velocity was measured using pulsed Doppler echocardiography. Ventricular fractional shortening was measured using M mode echocardiography. RESULTS: Peak early filling velocity increased as left atrial pressure increased. There was a direct relationship between mean left atrial pressure and the velocity before and after induction of ventricular dysfunction. The slope of the regression line between mean left atrial pressure and peak early filling velocity decreased as the grade of the dysfunction increased. There was a significant correlation between the slope of the regression line and mean left ventricular fractional shortening (r = 0.65, n = 31, p less than 0.01). CONCLUSIONS: Early diastolic filling was affected by both left atrial pressure and left ventricular function. These facts are useful in interpreting the various transmitral flow patterns observed clinically.     

Left atrial systolic time intervals: their relations to left atrial preload, afterload and acute left ventricular pressure loading

Using pulsed Doppler echocardiography, the left atrial pre-ejection period (LAPEP) and left atrial ejection time (LAET) were studied in relation to left atrial loading and acute left ventricular pressure loading conditions in 17 patients with various heart diseases. LAPEP was defined as the time interval from the onset of a right atrial pacing pulse to the upstroke in the atrial contraction phase on the mitral flow velocity pattern; LAET was defined as the duration of left ventricular filling due to atrial contraction. 1. LAPEP did not correlate significantly with mean pulmonary capillary wedge pressure (mPCWP) indicating preload for the left atrium, nor with left ventricular end-diastolic pressure (LVEDP) indicating afterload for the left atrium. There were significant inverse correlations of LAET with mPCWP (r = -0.72) and with LVEDP (r = -0.75). 2. LAPEP, LAET and LAPEP/LAET correlated significantly with the ratio of the peak velocity in the atrial contraction phase and to that in the rapid filling phase (r = -0.62, -0.50 and -0.59, respectively). There was a significant inverse correlation of LAPEP/LAET with the left ventricular ejection fraction (r = -0.62). 3. When left ventricular systolic pressure became elevated by 25% of its basal value at a constant right atrial pacing rate, LAPEP decreased from 110 +/- 21 msec to 103 +/- 22 msec (p less than 0.05), LAET increased from 123 +/- 33 msec to 129 +/- 24 msec and LAPEP/LAET decreased from 0.95 +/- 0.37 to 0.84 +/- 0.32 (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)     

Left atrial systolic force in hypertensive patients with left ventricular hypertrophy: the LIFE study

In hypertensive patients without prevalent cardiovascular disease, enhanced left atrial systolic force is associated with left ventricular hypertrophy and increased preload. It also predicts cardiovascular events in a population with high prevalence of obesity. Relations between left atrial systolic force and left ventricular geometry and function have not been investigated in high-risk hypertrophic hypertensive patients. Participants in the Losartan Intervention For Endpoint reduction in hypertension echocardiography substudy without prevalent cardiovascular disease or atrial fibrillation (n = 567) underwent standard Doppler echocardiography. Left atrial systolic force was obtained from the mitral orifice area and Doppler mitral peak A velocity. Patients were divided into groups with normal or increased left atrial systolic force (>14.33 kdyn). Left atrial systolic force was high in 297 patients (52.3%), who were older and had higher body mass index and heart rate (all P < 0.01) but similar systolic and diastolic blood pressure, in comparison with patients with normal left atrial systolic force. After controlling for confounders, increased left atrial systolic force was associated with larger left ventricular diameter and higher left ventricular mass index (both P < 0.01). Prevalence of left ventricular hypertrophy was greater (84 vs. 64%; P < 0.001). Participants with increased left atrial systolic force exhibited normal ejection fraction; higher stroke volume, cardiac output, transmitral peak E velocities and peak A velocities; and lower E/A ratio (all P < 0.01). Enhanced left atrial systolic force identifies hypertensive patients with greater left ventricular mass and prevalence of left ventricular hypertrophy, but normal left ventricular chamber systolic function with increased transmitral flow gradient occurring during early filling, consistent with increased preload.     

Assessment of global and regional left ventricular diastolic function in hypertensive heart disease using automated border detection techniques

Acoustic quantification (AQ) and color kinesis (CK) are techniques that involve automated detection and tracking of endocardial borders. These methods are useful for the evaluation of global and regional left ventricular (LV) systolic function and more recently have been applied to evaluating LV diastolic performance. Assessment of diastolic dysfunction in hypertensive heart disease is a relevant clinical issue in which these techniques have proven useful. The diastolic portion of left atrium and LV AQ area waveforms are frequently abnormal in patients with left ventricular hypertrophy (LVH). Left ventricular AQ curves consistently demonstrate reduced rapid filling fraction (RFF) and peak rapid filling rate (PRFR), elevated atrial filling fraction (AFF), peak atrial filling rate (PAFR), and reductions in the ratio PRFR/PAFR. Acoustic quantification complements traditional Doppler echocardiographic evaluation of global diastolic function. Many patients with significant LVH and normal Doppler diastolic parameters can be identified as having diastolic dysfunction with AQ. In addition, CK has allowed the evaluation of regional diastolic performance in hypertensive patients. Regional filling curves obtained from CK have demonstrated that endocardial diastolic motion is commonly delayed and heterogeneous in patients with LVH.     

Effect of elevated left ventricular diastolic filling pressure on the frequency of left atrial appendage thrombus in patients with nonvalvular atrial fibrillation

We investigated the relation between left ventricular diastolic dysfunction and left atrial appendage (LAA) thrombus in patients with atrial fibrillation (AF). We performed transesophageal echocardiography to examine LAA thrombus or spontaneous echo contrast (SEC) and to measure LAA emptying flow velocity in consecutive 376 patients with AF. We estimated diastolic filling pressure as the ratio of early transmitral flow velocity (E) to mitral annular velocity (e') on transthoracic echocardiogram. E/e' ratio in 28 patients (7.4%) with LAA thrombi was higher than that in patients without thrombus (18.3 ± 9.3 vs 11.4 ± 5.9, p <0.0001). The fourth quartile of E/e' (>13.6) consisted of 19 patients with thrombi and had a higher prevalence of thrombi than the others (p <0.0001). Multivariate regression analysis selected E/e' ≥13 as an independent predictor of LAA thrombus with an odds ratio of 3.50 (1.22 to 10.61) in addition to LA dimension and ejection fraction. Increased quartile of E/e' was negatively associated with LAA flow velocity and positively with rate of SEC. In conclusion, increased diastolic filling pressure is associated with a higher rate of LAA thrombus in AF, partly through blood stasis or impaired LAA function.     

A potential method of correcting intracavitary left ventricular filling pressures for the effects of positive end-expiratory airway pressure

Based on the observation that positive end-expiratory airway pressure (PEEP) causes comparable increments in intrapericardial and right-sided intracardiac pressures, we hypothesized that intracavitary left ventricular filling pressures measured in the presence of PEEP can be corrected for increased intrathoracic pressure by subtracting the effects of PEEP on intracavitary right ventricular filling pressures. Ventricular function curves (aortic blood flow vs intracavitary left ventricular end-diastolic pressure [LVEDP]) were generated with and without 15 cm of water of PEEP in eight dogs. All curves were shifted to the right by PEEP (i.e., intracavitary LVEDP was higher for any submaximal level of aortic blood flow). However, when pressures measured in the presence of PEEP were "corrected" by subtracting the corresponding increment in intracavitary right ventricular end-diastolic pressure caused by PEEP at each level of ventricular filling, control and corrected PEEP data points appeared to fall on the same curve in five dogs, and differed only slightly in three dogs. Mean control and corrected PEEP curves derived by averaging polynomial regression coefficients for each condition differed significantly from uncorrected PEEP curves (p less than .05), but not from each other. Analogous curves based on mean left atrial pressure were corrected equally well by subtracting the effects of PEEP on mean right atrial pressure. We conclude that the increments in intracavitary right heart filling pressures caused by PEEP can be used to correct intracavitary left heart filling pressures for the effects of PEEP on intrathoracic pressure.     

Prevalence and significance of left ventricular filling abnormalities determined by Doppler echocardiography in young type I (insulin-dependent) diabetic patients

In 16 insulin-dependent diabetic patients, 36 +/- 8 years old with no microangiopathy, hypertension or coronary artery disease, and 16 healthy control subjects matched for sex, age and body surface area, the following parameters were obtained by Doppler-echocardiography: (1) end-diastolic left ventricular thickness and radius; (2) aortic pulse wave velocity; (3) mitral flow with measurement of early and late (atrial) peak velocities (E and A), pressure half-time and the velocity time integrals of the entire mitral curve and of the atrial wave; and (4) isovolumic relaxation time (i.e., the time between aortic closure and the mitral opening signals recorded simultaneously by continuous-wave Doppler). Heart rate and systolic blood pressure were not different in the 2 groups. Aortic pulse wave velocity and the wall thickness to radius ratio were significantly increased in the diabetic patients compared to the controls. E was significantly reduced whereas A/E, pressure half-time, the atrial contribution to the left ventricular filling (i.e., the ratio of the atrial velocity time integral to the mitral velocity time integral) and the isovolumic relaxation time were significantly increased in the diabetic group versus the control subjects. Lastly, 11 of 16 diabetic patients (69%) had at least 2 of the following abnormalities: A/E greater than 0.71, an atrial contribution to the left ventricular filling greater than 0.25, a pressure half-time greater than 50 ms and an isovolumic relaxation time greater than 88 ms. No correlations were found between the wall thickness to radius ratio, aortic pulse wave velocity and the filling indexes.(ABSTRACT TRUNCATED AT 250 WORDS)     

A comparison of two exponential models of the time constant during left ventricular isovolumic pressure decay in coronary artery disease

To make a comparison of two exponential models of the time constant (Tw: Weiss's method, Tc: exponential analysis with a variable asymptote) during left ventricular (LV) isovolumic relaxation, we assessed LV pressure decay in 104 patients with coronary artery disease (CADpts) and 21 normal subjects at rest and after pacing, and investigated the hemodynamic determinants of these two models using forward-backward stepwise multiple regression analysis. At rest, Tw was prolonged as the left ventricular minimal pressure (LVPmin), the left ventricular end-diastolic pressure (LVEDP) and the end-systolic volume (ESV) increased (multiple regression coefficient: R = 0.87), whereas Tc was prolonged as ESV and regional wall motion abnormality (RWMA) increased (R = 0.72). Pacing-induced changes in Tw were augmented as LVPmin and RWMA increased (R = 0.75), whereas changes in Tc were augmented as RWMA increased (R = 0.63). Thus, the changes in Tw may be due to an increase in LVPmin rather than to any direct effect of ischemia on the relaxation rate. The relaxation rate can be evaluated more reliably by Tc than by Tw, irrespective of associated pressure changes during ischemia in CADpts.