Systolic Pulmonary Venous Flow Velocity Research Articles

The relationship of interleukin-6 and C-reactive protein with left ventricular geometry and function in patients with obstructive sleep apnea syndrome and pre-hypertension.

To assess the relationship of interleukin-6 (IL-6) and C-reactive protein (CRP) levels with left ventricular geometry (LVG) and function in patients with obstructive sleep apnea syndrome (OSAS) and pre-hypertension. A total of 458 patients were assigned into four groups: normal geometry (NG), concentric remodeling (CR), eccentric hypertrophy (EH), and concentric hypertrophy (CH). Pearson correlation and multivariate logistic regression analyses were used to determine the correlation between IL-6, CRP, and clinical, polysomnographic, and biochemical parameters with LVG and function. IL-6 and CRP levels were higher in the EH and CH groups than those in the NG and CR groups. The results of the Pearson correlation analysis showed that IL-6 level was positively correlated with the E/e' ratio and peak systolic pulmonary venous reverse velocity (PVa) duration time (PVaD), while negatively correlated with the E/A ratio, s', and left ventricular ejection fraction (LVEF). CRP level was positively correlated with A-wave duration time (AD), peak systolic pulmonary venous flow velocity (PVs), PVa and PVaD, while negatively correlated with the E/A ratio. The results of the multivariate logistic regression analysis revealed that IL-6 and CRP levels were correlated with EH (β=1.213, odds ratio [OR]=3.363, p<0.001; β=1.258, OR=3.518, p<0.001) and CH (β=.938, OR=2.555, p=0.008; β=1.239, OR=3.454, p<0.001). IL-6 and CRP levels are associated with LVG and function, suggesting that IL-6 and CRP levels are involved in OSAS and pre-hypertension, leading to abnormal left ventricular structure and function.

Relation Between Pulmonary Venous Flow and Left Atrial Pressure During Percutaneous Mitral Valve Repair With the MitraClip

Pulmonary venous (PV) flow may provide valuable information in terms of the severity of mitral regurgitation and left atrial (LA) pressure. We sought to find PV flow determinants of LA pressure during MitraClip procedure. We analyzed 575 PV flows in 290 patients using transesophageal echocardiography before and after MitraClip procedure. We measured peak systolic velocity (Sv), diastolic velocity (Dv), systolic velocity time integral (Svti), diastolic velocity time integral (Dvti), and those systolic to diastolic ratio as PV flow parameters. Systolic PV flow velocity was lower than diastolic PV flow velocity before the procedure, but systolic PV flow velocity markedly increased after the procedure. Peak Sv/Dv ratio and Svti/Dvti ratio after the procedure were significantly higher than those before the procedure (peak Sv/Dv; 1.06 [inter-quartile range (IQR) 0.73 to 1.34] vs 0.32 [IQR 0.03 to 0.55], p <0.001, Svti/Dvti; 1.06 [IQR 0.76 to 1.61] vs 0.26 [IQR 0.02 to 0.51], p <0.001). Peak Sv/Dv ratio and Svti/Dvti ratio were negatively correlated with mean LA pressure and LA pressure V wave, respectively (peak Sv/Dv ratio; r = -0.50 and r = -0.59, Svti/Dvti ratio; r = -0.47 and r = -0.58, p <0.001). In receiver operating characteristics curve assessing the ability of PV flow to predict mean LA pressure ≥20 mm Hg after the successful procedure, the area under the curve of peak Sv/Dv ratio was 0.76 (p <0.001). Peak Sv/Dv ratio <0.98 best predicted LA pressure ≥20 mm Hg with 77% sensitivity and 71% specificity. In conclusion, systolic PV flow velocity immediately increased in response to mitral regurgitation reduction during MitraClip procedure. PV flow velocity, specifically systolic to diastolic ratio, was useful to evaluate invasively determined LA pressure.

Echocardiographic Parameters Associated With Asymmetrical Structural Remodeling In Patients With Or Without Atrial Fibrillation.

Left atrial (LA) dilation can evolve into asymmetrical remodeling. The aim of this study was to determine the echocardiographic parameters associated with LA asymmetric structural remodeling (ASR) in patients with and without nonvalvular atrial fibrillation (AF). A total of 170 patients with a dilated LA were prospectively enrolled. ASR was defined as an atrium shape that is no longer ellipsoidal (LA basal dimension measured at the junction between the pulmonary vein and atrium greater than the mitral annular dimension). Symmetric structural remodeling (SSR) was defined as all other cases. Echocardiographic parameters of LA function and left ventricular diastolic function, measured by pulsed-wave Doppler and Tissue Doppler Imaging, were analyzed to identify the parameters associated with ASR. The mean age of the patients was 67 ± 11 years. Forty-one percent had a stable sinus rhythm (SR), and 59% had AF. LA-ASR was detected in 66% of the patients: 55% with AF and 45% with SR (p=0.002). The mean LA-ASR and LA-SSR volume indexes were 49 ± 14 ml/m² and 29 ± 13 ml/m², respectively (p<0.001). LA systolic myocardial velocity (p=0.036) and peak systolic pulmonary venous flow velocity (p=0.033) were the parameters best associated with ASR. The sensitivity and specificity of both parameters, based on ROC curve analysis, were 77 and 70%, respectively. The AUC was 0.765 (95% CI: 0.662-0.849, p=0.0001). LA dilation is associated with a great number of asymmetrical structural remodeling. Echocardiographic parameters that reflect LA reservoir function are best associated with asymmetrical remodeling.

Effects of Preemptive Enoximone on Left Ventricular Diastolic Function After Valve Replacement for Aortic Stenosis

Left ventricular (LV) hypertrophy is associated with increased diastolic chamber stiffness early after aortic valve replacement for valve stenosis. Enoximone, a phosphodiesterase III inhibitor, has been shown to improve myocardial contractility and relaxation when administered as a single dose after cardiac surgery. The present study investigated, by analysis of transmitral flow velocity patterns and end-diastolic pressure-area relations, whether enoximone administered before aortic valve surgery has an effect on LV diastolic properties. Prospective, randomized study. Referral center for cardiothoracic surgery at a university hospital. Thirty-four patients undergoing aortic valve replacement for aortic stenosis. Patients in the enoximone group (n = 17) received a bolus dose of 0.35 mg/kg (0.15 mg/kg before aortic cross-clamping and 0.2 mg/kg added to the cardioplegic solution). Individual pressure-area relations (pulmonary capillary wedge pressure v left ventricular end-diastolic area) were obtained by using volume loading by leg elevation before and after surgery with closed chest. The pressure-area relation on the pressure-area plot was shifted to the left after surgery, indicating decreased LV diastolic distensibility in the enoximone and control groups and providing evidence of decreased LV diastolic function. Indices of LV diastolic chamber stiffness, LV operating stiffness (K(LV)) derived from the deceleration time of early ventricular filling, and the constant of chamber stiffness (beta) derived from pressure-area relations were not different after enoximone treatment. Systolic LV function was unaltered after cardiac surgery in both groups. Analysis of changes in transmitral flow patterns identified an increased atrial filling fraction in enoximone-treated patients, suggesting increased atrial systolic function. The unaltered systolic pulmonary venous flow velocity compared with the decrease in the control group after volume loading further supports preservation of left atrial reservoir function with enoximone in the absence of evidence for decreased LV stiffness. Preemptive enoximone did not change LV diastolic function based on diastolic filling patterns or LV stiffness indices (K(LV) and beta) derived from Doppler early filling deceleration time and pressure-area relations. Doppler data suggested improvement of left atrial systolic function and preservation of left atrial reservoir function with enoximone.

Pulmonary venous systolic flow: Influence of gravity on pulmonary venous flow velocities assessed in patients with atrial fibrillation

The origin of the pulmonary venous (PV) systolic flow wave is still unclear and could be the atrial relaxation and systolic descent of the atrioventricular plane, which decrease atrial pressure (suction) or raised PV pressure. In atrial fibrillation (AF), loss of atrial contraction and relaxation significantly modifies the systolic PV flow wave. The effect of recumbent positional changes on PV, however, has not yet been characterized in AF. The purpose of this study was to evaluate the effect of positional changes on systolic PV flow in patients with AF studied by transesophageal echocardiography. The study group consisted of 45 patients with AF (34 patients with AF, alone, and 11 patients with mitral stenosis [MS]). To assess the influence of left atrial pressure, we included patients with MS and AF. Pulsed wave Doppler transesophageal echocardiography of the left and right upper PV were performed in the left lateral recumbent position in all patients and repeated records were obtained with the subject in the supine position in 25 (AF alone: n = 20, MS: n = 5) of 45 patients. In the left lateral recumbent position, the systolic PV flow velocity and systolic fraction of the left PV, which were recorded on the recumbent subject's lower side, were significantly increased compared with those of the right PV in both AF alone and MS with AF (33.9 ± 10.8 vs 13.8 ± 6.4 cm/s, 0.45 ± 0.09 vs 0.20 ± 0.10 in AF alone; 30.2 ± 11.7 vs 14.6 ± 6.0 cm/s, 0.43 ± 0.12 vs 0.20 ± 0.07 in MS, respectively, P < .01). By changing the position from the left lateral to the supine position, systolic PV flow velocity and systolic fraction of the left and right PV became the same (29.3 ± 8.4 vs 27.9 ± 8.4 cm/s, 0.39 ± 0.09 vs 0.36 ± 0.06 in AF alone, 23.5 ± 8.8 vs 27.5 ± 5.0 cm/s, 0.35 ± 0.08 vs 0.35 ± 0.09 in MS, respectively). These findings show that the PV volume (hydrostatic pressure) significantly modifies systolic PV flow wave in patients without atrial contraction and relaxation. We should take into consideration the body position on which PV flow is studied. (J Am Soc Echocardiogr 2002;15:1087-93.)

Assessment of left atrial appendage function and its relationship to pulmonary venous flow pattern by transesophageal echocardiography

We evaluated left atrial appendage function and its relationship to pulmonary venous flow in 53 patients divided into four groups. Group 1 consisted of 10 normal subjects. Group 2 included 15 patients with significant pure mitral stenosis in sinus rhythm. In group 3, there were 13 patients with pure significant mitral stenosis and atrial fibrillation. Group 4 consisted of 15 patients with normal mitral valve and atrial fibrilltion. We found significant decrease in left atrial appendage ejection fraction and maximum emptying flow velocity, velocity time integral of systolic pulmonary venous flow in Groups 2, 3 and 4 in comparison with normal subjects. Systolic pulmonary venous flow velocity was significantly decreased in Groups 3 and 4. There was significant correlation between left atrial appendage ejection fraction and peak emptying flow velocity ( r=0.62, P<0,001). Systolic peak pulmonary venous flow velocity was significantly correlated with left atrial appendage ejection fraction and maximum emptying flow velocity ( r=0.67, P=0,01; r=0.58, P<0,001, respectively). There was also significant correlation between systolic pulmonary venous flow velocity time integral and left atrial appendage ejection fraction ( r=0.66, P=0.001). When normals were excluded from analysis, all the correlations were still significant. We concluded that left atrial appendage is a contractile structure, and that systolic pulmonary venous flow velocity is influenced by left atrial appendage dysfunction. Therefore left atrial appendage function needs to be considered when interpreting Doppler transmitral and systolic pulmonary venous flow patterns.

Determinants of pulmonary venous flow reversal in mitral regurgitation and its usefulness in determining the severity of regurgitation

Pulmonary venous flow (PVF) reversal is observed in mitral regurgitation (MR) and can be detected by Doppler echocardiography. However, the determinants of PVF alterations in MR have not been analyzed with simultaneous quantitative methods, and the diagnostic accuracy of flow reversal is uncertain. Prospectively, in 128 patients with isolated MR of various degrees (regurgitant fraction 4% to 81%), Doppler echocardiography was used to measure PVF velocity simultaneously to quantify MR by 2 methods and to perform a comprehensive hemodynamic assessment. Systolic PVF velocity was 4 ± 56 cm/s (systolic flow reversal in 39 patients) and showed the strongest correlations with mitral effective regurgitant orifice (r = −0.56, p <0.0001). In multivariate analysis, larger effective regurgitant orifice (p <0.0001), eccentric jets (p = 0.0023), longer jets (p = 0.0033), and lower mitral regurgitant velocity (p = 0.0015) were independent determinants of decreased systolic PVF velocity. In organic MR, increased filling pressures were associated with systolic PVF reversal. Blunted systolic flow was associated with shorter mitral deceleration time (p <0.0001) and enlarged left atrium (p = 0.0007). For the diagnosis of severe MR (regurgitant orifice ≥35 mm 2, regurgitant fraction ≥50%), systolic flow reversal sensitivity was 61% and 60%, and specificity was 92% and 85%, respectively. Among 29 patients in whom surgery demonstrated severe mitral lesions, 12 (41%) had no systolic flow reversal preoperatively. In patients with MR, the determinants of systolic PVF are complex and, in addition to the degree of MR, include the hemodynamic consequences of MR, jet characteristics, left ventricular filling, and left atrial volume alterations. Consequently, systolic PVF reversal is a useful sign of severe MR but of relatively low sensitivity, emphasizing the importance of quantifying MR.

Evaluation of the hemodynamic relationship between the left atrium and left ventricle during atrial systole by pulsed tissue Doppler imaging in patients with left heart failure.

The objective of the present study was to evaluate the hemodynamic relationship between the left atrium (LA) and left ventricle (LV) during atrial systole in the presence of an elevated left ventricular end-diastolic pressure (LVEDP) and LV failure using pulsed tissue Doppler imaging (TDI). Fifty-three patients with LV systolic dysfunction and no regional LV asynergy were divided into 3 groups: relaxation failure group (RF, n=20) with a ratio of peak early diastolic to atrial systolic velocity of the transmitral flow (E/A) < or = 1; pseudonormalization group (PN, n=19) with 1 <E/A<2; and restrictive group (RS, n=14) with E/A> or =2. In addition, 20 normal patients (E/A > or = 1) were studied as a control group. The transmitral and pulmonary venous flow velocities were recorded by transesophageal pulsed Doppler echocardiography. The wall motion velocity patterns were recorded at the middle portion of the LV posterior wall (LVPW) and at the mitral annulus (MA) of the LVPW site in the apical LV long-axis view by transthoracic pulsed TDI. The LVEDP was significantly greater in the PN and RS groups than in the RF and control groups. The moan pulmonary capillary wedge pressure was greatest in the RS group. The percent fractional change of the LA area during atrial systole determined by 2-dimensional echocardiography was significantly lower in the RS group than in the PN group. The peak atrial systolic pulmonary venous flow velocity was significantly greater in the PN group than in the RS group. The peak atrial systolic motion velocity (Aw) at the LVPW was significantly lower in the PN and RS groups than in the RF and control groups. The Aw at the MA was significantly lower in the RS group than in the other groups. There was no significant difference in Aw between the LVPW and MA in the RS group, whereas Aw at the MA was significantly greater than that at the LVPW in the PN group. In conclusion, the measurements of Aw at the LVPW and MA can be used to noninvasively evaluate the hemodynamic relationship between the LA and LV during atrial systole in patients with LV failure.

Evaluation of left atrial filling using systolic pulmonary venous flow velocity measurements in patients with atrial fibrillation.

The pattern of pulmonary venous flow velocity is useful for understanding the hemodynamic relationship between the left atrium and left ventricle in patients with a variety of diseases, and the systolic flow wave, in particular, is considered a clinically important parameter that reflects left atrial filling. The study was undertaken to determine whether systolic pulmonary venous flow velocity patterns can be used to evaluate left atrial filling in patients with atrial fibrillation. We performed transesophageal pulsed Doppler echocardiography and cardiac catheterization in 34 patients with chronic atrial fibrillation (10 with hypertrophic cardiomyopathy, 5 with dilated cardiomyopathy, 7 with previous myocardial infarction, and 12 with isolated atrial fibrillation) and 15 normal controls in sinus rhythm. Mean pulmonary capillary wedge pressure, V-wave height in the pulmonary capillary wedge pressure curve, and left ventricular end-diastolic pressure were significantly higher in the hypertrophic cardiomyopathy and dilated failing heart (previous myocardial infarction and dilated cardiomyopathy) groups than in the isolated atrial fibrillation and normal groups. The peak velocity and time-velocity integral of the systolic pulmonary venous flow velocity, and percent left atrial emptying fraction were significantly lower in the dilated failing heart group than in the isolated atrial fibrillation, hypertrophic cardiomyopathy, and normal groups. The peak velocity and time-velocity integral of the systolic pulmonary venous flow velocity, percent left atrial emptying fraction, and V-wave height were comparatively constant when the preceding R-R intervals were relatively stable in the isolated atrial fibrillation group and in 4 of the 10 patients with hypertrophic cardiomyopathy. However, changes in these variables correlated with the preceding R-R interval in all patients with dilated failing hearts and in 6 of the 10 patients with hypertrophic cardiomyopathy. Transesophageal pulsed Doppler echocardiographic measurements of systolic pulmonary venous flow velocity are valid indicators of left atrial filling in patients with atrial fibrillation.

Differences in Transmitral Flow Velocity Pattern during Increase in Preload in Patients with Abnormal Left Ventricular Relaxation

Changes in transmitral flow (TMF) and pulmonary venous flow (PVF) velocities during increases in preload were compared in patients with a higher peak atrial systolic velocity than peak early diastolic velocity (A/E > 1) for the TMF velocity to determine differences in hemodynamic response. Fifteen patients with dilated hearts, 22 with hypertrophied hearts and 15 control patients were studied. TMF and PVF velocities were recorded by transesophageal pulsed Doppler echocardiography before and during application of lower body positive pressure. The value for peak early diastolic velocity increased, while the isovolumic relaxation time decreased with increases in preload in all groups. The value for peak atrial systolic velocity decreased in the dilated-heart group, but increased in the hypertrophied-heart and control groups. The peak second systolic and early diastolic PVF velocities increased in the dilated- and hypertrophied-heart groups, but did not change in the control group. The peak atrial systolic PVF velocity and the difference in duration of the atrial systolic PVF and TMF velocities increased in the dilated- and hypertrophied-heart groups, and its changing rate was highest in the group with dilated hearts. These results suggest that both peak early diastolic and atrial systolic TMF velocities increase during increases in preload through the Frank-Starling mechanism in hypertrophied hearts. Furthermore, the left ventricular functional reserve was lower in the dilated-heart group. Thus, TMF and PVF velocities respond differently during increases in preload, depending on the underlying heart disease.

Left Atrial Systolic Performance in the Presence of Elevated Left Ventricular End-Diastolic Pressure: Evaluation by Transesophageal Pulsed Doppler Echocardiography of Left Ventricular Inflow and Pulmonary Venous Flow Velocities.

We recorded left ventricular inflow (LVIF) and pulmonary venous flow (PVF) velocities by transesophageal pulsed Doppler echocardiography in 25 patients with a ratio of peak atrial systolic to early diastolic LVIF velocity of <1 and a left ventricular end-diastolic pressure (LVEDP) of 15 mmHg or greater, as well as in 30 normal subjects. The group consisted of 14 patients with prior myocardial infarction, 7 with dilated cardiomyopathy, and 4 with cardiac amyloidosis, and were divided into: (1) group A (n = 7): peak atrial systolic LVIF velocity of 40 cm/sec or greater; (2) group B (n = 7): peak atrial systolic LVIF velocity of <40 cm/sec and peak atrial systolic PVF velocity of 30 cm/sec or greater; and (3) group C (n = 11): peak atrial systolic LVIF velocity of <40 cm/sec and peak atrial systolic PVF velocity of <30 cm/sec. Although LVEDPs in groups B and C were significantly greater than in group A, there was no difference between groups B and C. The mean pulmonary capillary wedge pressure (mPCWP) in group C was significantly greater than in groups A and B, but there was no difference between groups A and B. The difference between LVEDP and mPCWP (LVEDP - mPCWP) in group B was significantly higher than in groups A and C. Dilatation of the left atrium (LA) was seen in all three groups, particularly in groups B and C. There were no differences in peak atrial systolic LVIF velocity and LA volume change during atrial contraction between group A and the control group, and there were no differences in LA volume change and peak second systolic PVF velocity between groups A and B. LA volume change and peak second systolic PVF velocity were significantly less in group C than in groups A and B. Among the four patients whose courses could be observed after medical treatment with diuretic and vasodilator, one changed from group B to A, one from group B to C, one from group C to A, and one remained in group C. Thus, recording of peak atrial systolic LVIF and PVF by transesophageal pulsed Doppler echocardiography permits detailed evaluation of LA systolic performance in the presence of elevated LVEDP. These two variables provide important information for less invasive differentiation of LA afterload mismatch from LA myocardial failure.

Transesophageal pulsed Doppler echocardiographic evaluation of left atrial systolic performance in hypertrophic cardiomyopathy: combined analysis of transmitral and pulmonary venous flow velocities.

Hypertrophic cardiomyopathy (HC) is characterized by impaired left ventricular (LV) diastolic function due to an increase in LV wall thickness. The severity of this disease varies depending on the localization and extent of the hypertrophied myocardium and the presence and extent of myocardial disarray or fibrosis. The purpose of this study was to examine the background of hemodynamic abnormalities between the left atrium and the left ventricle during atrial systole in patients with HC using pulsed Doppler echocardiography. Hemodynamic abnormalities between the left atrium and left ventricle during atrial systole were evaluated in patients with HC using transmitral flow (TMF) and pulmonary venous flow (PVF) velocities obtained by transesophageal pulsed Doppler echocardiography. The study population included 50 patients with HC, including 39 with asymmetric septal hypertrophy and 11 with apical hypertrophy, and showing fractional shortening of the left ventricle > or = 30%. They were classified into three groups: (1) Group A (n = 11): the ratio of the late to early TMF velocity < 1, and peak atrial systolic PVF velocity (PVA) < 25 mm/s; (2) Group B (n = 13): their ratio < 1, and PVA > or = 25 mm/s; and (3) Group C (n = 26): their ratio > or = 1. The mean age of patients in Group A was lower than that in Groups B and C. Left atrial dimension in Group B was significantly greater than that in the other HC groups and the control group. Furthermore, left atrial volume changes during atrial systole in Group B were significantly smaller than those in the other HC groups and the control group. Peak atrial systolic PVF velocity in Group B was significantly higher than that in the control group and in Group C. The duration of the atrial systolic waves of the TMF and PVF in Group B was significantly shorter and longer, respectively, than that in Group A. Left ventricular end-diastolic pressure (LVEDP) decreased in descending order with Group B > Group C > Group A. In all patients there was a significant positive correlation between the LVEDP and peak atrial systolic PVF velocity or the difference in duration between the atrial systolic waves of PVF and TMF. Plots of these values shifted toward the left and inferiorly in Group A, and toward the right and superiorly in Group B. Peak velocity and duration of TMF and PVF during atrial systole by transesophageal pulsed Doppler echocardiography are useful indices of hemodynamic abnormalities between the left atrium and the left ventricle during atrial systole, particularly a forceful atrial contraction mismatched to the left atrial afterload and severity of LV diastolic dysfunction, in HC.

Relationship between pulmonary capillary wedge V wave and transmitral and pulmonary venous flow velocity patterns in various heart diseases

Background: A large V wave in a pulmonary capillary wedge pressure (PCWP) tracing is characteristic of mitral regurgitation. However, the V wave is often increased in patients without or with no significant mitral regurgitaion. Methods and Results: The V wave was in the PCWP tracing investigated in 65 patientsusing transmitral flow (TMF) and pulmonary venous flow (PVF) velocity patterns obtained by transesophageal pulsed Doppler echocardiography. A large V wave was defined if the peak V wave minus the mean PCWP (V - mPCWP) was greater than 7 mmHg. Three study groups were formed: 15 patients with large V waves and significant mitral regurgitation, 15 patients with large V waves with no significant mitral regurgitation, and 35 patients with small V waves. The mPCWP and left ventricular end-diastolic pressure were greatest in the group with large V waves and no significant mitral regurgitation. Peak early diastolic TMF and PVF velocities were significantly greater in the two groups with large V waves. The peak second systolic PVF velocity was lowest in the group with large V waves and significant mitral regurgitation, followed by the group with large V waves and no significant mitral regurgitation. The V - mPCWP was positively correlated with the peak early diastolic TMF and PVF velocities and negatively correlated with the peak second systolic PVF velocities. Additionally, mitral regurgitation severity in patients with large V waves and significant mitral regurgitation was positively correlated with the peak early diastolic TMF and PVF velocities and negatively correlated with the peak second systolic PVF velocity. Conclusions: These results suggest that large V waves in PCWP tracings appear not only insevere mitral regurgitation, but also in any condition with markedly elevated left ventricular end-diastolic pressure. Combined analysis of the TMF and PVF velocity patterns is helpful in determining the etiology of these hemodynamic abnormalities.

Transoesophageal echocardiographic evaluation of ventricular function during transvenous defibrillator implantation.

Intraoperative testing and defibrillation threshold determination may jeopardise patients, scheduled for implantation of a cardioverter-defibrillator (ICD). The purpose of this study was the assessment of the influence of consecutive defibrillation attempts on left ventricular systolic and diastolic function by means of transoesophageal echocardiography (TEE). Eighteen patients with malignant ventricular arrhythmias that were resistant to antiarrhythmic drugs were monitored with TEE before, during and after implantation of a cardioverter-defibrillator. Left ventricular fractional area contraction as a measure of ejection fraction was assessed before and after each defibrillation attempt. Transmitral and right upper pulmonary venous flow parameters were evaluated before and after the whole implantation procedure. Adequate data were available in 14 patients during 4 consecutive attempts. No major alterations were observed in heart rate or fractional area contraction, measured at 30 s and 3 min after defibrillation. Overall, the ratio of early-to-late transmitral filling decreased significantly after the implantation procedure (from 0.91 +/- 0.12 to 0.82 +/- 0.14; P < 0.05). Systolic pulmonary venous flow velocity decreased from 0.49 +/- 0.11 to 0.41 +/- 0.10 m/s (P = 0.04); this decrease was observed in both groups. A significant increase of the atrial contraction wave (from 0.25 +/- 0.06 to 0.34 +/- 0.07 m/s; P < 0.03) was seen. Subdividing patients related to their precperative ejection fraction, a significant decrease of the early-to-late transmitral filling of the LV was revealed in patients with ejection fraction less than 35% (group 1). Also, a significantly lower systolic fraction of the pulmonary venous flow after ICD implantation in conjunction with a significantly longer diastolic flow time was shown in this patient group in comparison with patients with a preoperative ejection fraction of more than 35% (group 2). Defibrillation threshold testing of the ICD system changes LV inflow characteristics and impedes diastolic function of the left ventricle and may thus precipitate heart failure by this mechanism. No deleterious effects of threshold testing were observed with respect to fractional area contraction nor any deterioration of LV function was found in a clinically significant amount due to consecutive defibrillation attempts.

Assessment of left atrial pressure and volume changes during atrial systole with transesophageal pulsed Doppler echocardiography of transmitral and pulmonary venous flow velocities.

To determine whether transmitral and pulmonary venous flow velocity patterns can be used to evaluate left atrial pressure and volume changes during atrial systole, we performed transesophageal pulsed Doppler echocardiography and right heart catheterization in 85 patients (20 with hypertrophic cardiomyopathy, 20 with dilated cardiomyopathy, 30 with prior myocardial infarction, and 15 with mitral regurgitation), and 35 normal subjects. Pulsed Doppler variables from transmitral and pulmonary venous flow velocities during atrial systole were compared with mean pulmonary capillary wedge pressure (mean PCWP), pressure rise during atrial systole (PCWP-A), and left atrial volume change during atrial systole (delta LAV). The mean PCWP correlated significantly with the peak atrial systolic transmitral flow (r = -0.38, p < 0.05) and pulmonary venous flow (r = 0.40, p < 0.05) velocities in all patients. The PCWP-A correlated significantly with the peak atrial systolic transmitral flow (r = -0.39, p < 0.05) and pulmonary venous flow (r = 0.68, p < 0.0001) velocities in all patients. There was a particularly close correlation between the PCWP-A and the peak atrial systolic pulmonary venous flow velocities. The sum of the time-velocity integral of the atrial systolic transmitral and pulmonary venous flow velocities (TAI) correlated closely with the delta LAV (r = 0.70, p < 0.0001) in all patients. Thus, the peak atrial systolic pulmonary venous flow velocity correlated well with left atrial pressure changes during atrial systole. Furthermore, the sum of the time-velocity integral of the atrial systolic transmitral and pulmonary venous flow velocities correlated well with left atrial volume changes during atrial systole. Therefore, transesophageal echocardiographic measurements of atrial systolic transmitral and pulmonary venous flow velocities are reasonable indicators of left atrial pressure and volume changes during atrial systole.