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European Journal of Heart Failure 2005 7(1):63-68; doi:10.1016/j.ejheart.2004.03.019
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© 2004 European Society of Cardiology

Assessment of left atrial input impedance in normal subjects and in hypertensive patients

John Dernellis* and Maria Panaretou

Department of Cardiology Vostanion Hospital, 1 Kathigitou Karakatsani St., 811 00 Mytilini, Greece

* Corresponding author. Tel./fax: +30 2510 26 588. E-mail address: dernellis{at}yahoo.gr


   Abstract
Top
 Abstract
1. Introduction
 2. Methods
 3. Results
 4. Discussion
 Appendix A
 References
 
Background: To assess left atrial (LA) input impedance in patients with signs and/or symptoms of heart failure and normal left ventricular ejection fraction, transesophageal Doppler pulmonary venous (PV) flow velocity and pulmonary capillary wedge pressure (PCWP) were studied in 20 patients and compared to 20 matched normal controls.

Methods: LA impedance was calculated as the ratio of harmonic terms of the PCWP (measured by right heart catheterization) to the corresponding harmonic terms of PV flow (measured by transesophageal Doppler echocardiography). Eight harmonics were analyzed.

Results: Left ventricular mass index (LVMI, p<0.001), heart rate (p<0.05), systolic and diastolic blood pressure (p<0.001), isovolumic relaxation time (IVRT, p<0.001), peak A transmitral flow velocity (p<0.001), peak reversal atrial PV flow velocity (p<0.001) and LA diameter (p<0.001) were increased in patients compared to controls. Spectra of impedance moduli were displaced upwards and to the right. The increase in the impedance moduli was observed at all frequencies of the first to seventh harmonic components (p<0.001). In multivariate tests LVMI (p=0.003), IVRT (p=0.001), and LA diameter (p=0.007) had a significant effect on all harmonic components of the impedance moduli (adjusted R2=0.970 to 0.999, p<0.001).

Conclusions: LA input impedance derived from data obtained invasively and semi-invasively represents left ventricular diastolic function. Resistance to left ventricular filling is increased in hypertensive patients.

Key Words: Left atrial input impedance • Left ventricular filling • Hypertension • Diastolic heart failure

Received November 24, 2003; Revised March 17, 2004; Accepted March 23, 2004


   1. Introduction
Top
 Abstract
 1. Introduction
2. Methods
 3. Results
 4. Discussion
 Appendix A
 References
 
Left atrial (LA) impedance is the measure of the opposition to blood flow from the pulmonary veins to the left atrium presented by the heart [1,2]. The input impedance of any region of the circulatory system is the ratio of harmonic terms of pressure at the input to the corresponding harmonic terms of flow [3]. Thus, the ratio of pulsatile pressure and pulsatile flow in a pulmonary vein determines the input impedance of the left atrium. The atrium has three functional phases: a reservoir phase (the capability to accept blood), a conduit phase (when the atrio-ventricular valve is open the atrium becomes a pipe in which blood flows from veins to the ventricle) and a pump phase (the contraction following the P wave). LA impedance measures the resistance of the left atrium during the three phases. LA input impedance depicts resistance to the heart filling. Consequently, it may be a sensitive diastolic index of the heart, which expresses both left ventricular and LA diastolic function. Thus, the aim of this study was to calculate LA input impedance based on the more general concept of frequency spectrum analysis, which expresses results in the frequency domain [4].


   2. Methods
Top
 Abstract
 1. Introduction
 2. Methods
3. Results
 4. Discussion
 Appendix A
 References
 
2.1. Study population
The primary objective was to assess LA input impedance in normal subjects and in hypertensive patients with left ventricular diastolic dysfunction. The most important step in including eligible patients was echocardiographic evaluation of left ventricular performance with preserved systolic function in hypertensive symptomatic patients.

Specifically, eligible patients were those admitted to hospital with untreated hypertension with clinical evidence of limitation of exercise tolerance (18 patients), pulmonary congestion (10 patients), or fluid retention (8 patients). The clinical symptomatology was disproportionately severe compared to the objective assessment of systolic cardiac function. Patients had to have echocardiographic left ventricular ejection fraction >55% measured at admission to the hospital, [5] concentric left ventricular hypertrophy defined as the presence of ≤12.6 mm wall thickness by two-dimensional or M-Mode criteria, and transmitral filling showing an early (E) filling wave less than late filling (A) wave.

Exclusion criteria were: Non-cardiac etiologies for the presenting symptoms and signs, valvular heart disease and chest pain at the time of randomization; atrioventricular or intraventricular conduction disturbances; heart rate more than 100 beats/min at rest; severe renal or hepatic failure. Twenty patients (12 men and 8 women; mean [±SD] age, 64±8 years) were selected. Patients were treated with diuretics, ACE inhibitors, β-blockers and calcium channel blockers to eliminate symptoms before entering the study.

Twenty healthy matched subjects with normal physical examination, normal two dimensional and Doppler echocardiographic studies, who underwent transesophageal echocardiography for evaluation of suspected endocarditis (n=9), aortic dissection (n=5) or compensate for a poor acoustic window (n=6) and who proved to have normal transesophageal echocardiogram, were used as controls. The criteria for matching were age and sex. The Institutional Ethics Committee approved the study. Informed consent was obtained before the study in all subjects.

2.2. Echocardiographic and Doppler studies
Patients were receiving pharmacological treatment at the time the studies were performed. The protocol required clinical recompensation before data collection. Diuretics were used in 18 patients, ACE inhibitors in 17 patients, β-blockers in 8 patients and calcium channel blockers in 12 patients. The studies were performed with the patient in the supine position, using a Hewlett-Packard, Image point echocardiographic instrument equipped with 2.5 MHz transducer. Two-dimensional images were obtained in the standard parasternal and apical views. LA M-mode echocardiography was carried out by directing the M-Mode echo beam to the aortic root where the LA dimension was obtained. All Doppler and M-mode recordings were obtained at a sweep speed of 50 mm/s.

A pulsed Doppler sample volume was placed at the tips of the mitral valve and the transmitral velocity recorded during five cardiac cycles. The Doppler cursor was then positioned between the mitral valve and the left ventricular outflow, and a continuous wave Doppler recording was obtained to allow measurement of the isovolumic relaxation time (IVRT) [6–8].

After induction of topical anesthesia a Hewlett-Packard 5-MHz transesophageal echocardiographic probe was inserted into the esophagus. The transducer was manipulated to obtain a clear view of the left upper pulmonary vein as it emptied into the left atrium. A sample volume was then placed 1–2 cm into the pulmonary vein from its junction with the left atrium. Color flow imaging was used to obtain a beam direction as parallel as possible to pulmonary vein flow [9,10].

2.3. Pressure measurements
Diazepam (5 mg, I.M.) was given to all subjects 1 h before the study to minimise the stress of the procedure. A Swan-Ganz catheter 7F was placed in the pulmonary artery through the right subclavian vein. All pressures were referenced to 50% of the transthoracic diameter and were obtained at end tidal volume apnea in the supine position. Pressures were recorded on a physiologic recorder (Nihon Kohden, Life Scope 9) and the pressure signals were electronically transmitted to the auxiliary input of a Hewlett-Packard, Image point echocardiographic device so that simultaneous recordings of pressure, Doppler transesophageal echocardiogram and electrocardiogram were obtained (Fig. 1). The pulmonary capillary wedge pressure (PCWP) tracing was adjusted for the time delay of transmitting pressure in the fluid filled catheter. All data were recorded on a videocassette recorder for later playback and analysis.


Figure 1
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  		Fig. 1 Simultaneous recordings of Doppler pulmonary venous flow, pulmonary capillary wedge pressure and electrocardiogram. Sixteen equally spaced intervals separate one RR period.

 
Occlusive pressure was verified by comparing the pressure tracing waveforms to the waveforms observed in the pulmonary artery position and by looking for the expected rise in oxygen saturation. The pressures reported represented an average of five cardiac cycles. Recordings were obtained when all homodynamic parameters were stable.

2.4. Data analysis
Five consecutive cardiac cycles were selected for measurements, and the results were averaged. The following parameters were derived from the transmitral velocity: peak early (E) velocity (cm/s), peak late (A) velocity (cm/s), and deceleration time of the E wave (ms). IVRT (ms) was measured from the end of the aortic flow to the onset of mitral inflow by use of continuous wave Doppler. The following variables were measured from the transesophageal Doppler pulmonary venous flow: peak systolic (S) velocity (cm/s), peak diastolic velocity (D, cm/s), peak reverse flow velocity at atrial contraction (peak AR, cm/s) and the ratios of peak systolic to peak diastolic velocity.

LA volumes were measured in the apical four and two-chamber view by the area-length method, using the formula V=8/3{pi}LxA1xA2, where {pi}=3.14, A1=the LA area in the frontal plane, A2=the LA area in the lateral plane and L=the shorter of the long diameters in both planes [11]. The maximal LA volume (Vmax) was obtained before mitral valve opening, the minimal volume before valve closure (Vmin) and Va at the onset of the electrocardiographic P wave. LA ejection fraction was derived as the difference between Va–Vmin divided by the Va. Volume measurements were averaged over five cycles.

Fourier series were used to analyze the pressure and flow waves. One beat was selected for analysis and its period was divided into 16 equally spaced intervals (Fig. 1). An easily recognizable feature of the electrocardiogram, such as the peak of the QRS complex was chosen as the first point to be measured; the same point was used to stop the digital sampling. The pressure and flow value of each ordinate was measured by electronic analog-to-digital conversion, and the Fourier harmonics were calculated using Microsoft Excel for Windows computer program. The impedance is the ratio of harmonic terms of pressure to the corresponding harmonic terms of flow [4,12]. Expressing each complex harmonic term in modulus and phase form gives the impedance as a set of terms versus frequency (see Appendix A). The results of Fourier series were displayed as a graphic spectrum plotting the moduli and the phase angles as functions of frequency and are called line spectra (Fig. 2). If N intervals are taken in one cycle, the number of harmonics that can be determined is N/2. All higher harmonics are indeterminate. Thus, eight harmonics were valid in this analysis because 16 points were taken. Measurements were averaged over five cardiac cycles [4].


Figure 2
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  		Fig. 2 Left atrial input impedance modulus (A) and phase (B) in a group of normal subjects (circles) and in a group of hypertensive patients (squares). In (A) Y error bars are referred to standard errors of the modulus, and X error bars are referred to frequency. Similarly, in (B) Y error bars are referred to standard errors of the phase and X error bars are referred to frequency. Spectra of impedance moduli were displaced upwards and to the right in hypertensive patients.

 
2.5. Statistical analysis
The SPSS 8.0 for Windows statistical-program software was used. The Independent-Samples T Test procedure was used to compare means for the two groups of cases (Table 1). For comparison of sex between the two groups Chi-square was selected. The General Linear Model (GLM) Multivariate procedure provided regression analysis and analysis of variance for multiple dependent variables by a factor variable and covariates. The eight harmonics of the LA impedance spectrum were used as dependent variables. The group (normal subjects: 1, hypertensive patients: 2) was used as factor variable. The following variables were used as covariates: age, intraventricular septum thickness (IST), left ventricular mass index (LVMI), heart rate, systolic blood pressure, diastolic blood pressure, mean blood pressure, left ventricular ejection fraction, PCWP, deceleration time, IVRT, peak E, peak A, E/A, peak S, peak D, S/D, peak AR, LA diameter, LA ejection fraction. Using this general linear model procedure, we tested null hypothesis about the effects of the above variables on the means of various groupings of a joint distribution of the eight harmonics. The level of significance was p<0.05.


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  		Table 1 Comparisons between hypertensive patients and controls

 
2.6. Reproducibility
Ten studies were chosen at random for analysis of mitral and pulmonary venous profile and derivation of PCWP. The same observer analyzed the studies at a later date. Reproducibility was assessed as the mean±1 SD difference between the two sets of observations. In addition, mean percent error was calculated as the absolute difference divided by the average of the two observations.


   3. Results
Top
 Abstract
 1. Introduction
 2. Methods
 3. Results
4. Discussion
 Appendix A
 References
 
3.1. Comparison between patients and controls
The results of the comparisons between normal subjects and hypertensive patients are shown in Table 1. There was no difference between patients and controls concerning age and sex (p=NS). As expected, heart rate (p<0.05), LVMI, IST, systolic and diastolic blood pressure, IVRT, peak A transmitral flow velocity, peak reversal atrial PV flow velocity and LA diameter (p<0.001 for all comparisons) were increased in patients compared to controls. E/A ratio was decreased in patients compared to controls (p<0.001). Left ventricular and LA ejection fraction, PCWP and peak S and D Doppler PV flow velocities were similar in the two groups (p=NS).

The first to seventh harmonics of the LA impedance moduli were increased in hypertensive patients compared to normal subjects (p<0.001, Table 1). The eighth harmonic of the LA impedance was decreased in hypertensive patients compared to normal subjects (p<0.001, Table 1). Furthermore, line spectra of impedance moduli were displaced upwards and to the right in hypertensive patients (Fig. 2).

3.2. Determinants of LA impedance
We found that LA diameter (p=0.007), LVMI (p=0.003) and IVRT (p=0.001), were significantly associated with LA impedance using the GLM multivariate analysis. All other covariates did not have a significant effect on the joint distribution of dependent variables. The values of adjusted R2 were between 0.970 and 0.999 for the eight harmonics, p<0.001.

3.3. Reproducibility
The intra-observer reproducibility for the parameters listed in Table 1 ranged from 6% to 12%. Little variability was observed for individual measurements, with a mean percent error ranging from 5% to 12% for the same observer. Although in terms of percent error, the variability of estimated LA pressure was similar to that of the individual measurements, in terms of absolute values, the variability ranged from 0 to 3 mm Hg for the same observer.


   4. Discussion
Top
 Abstract
 1. Introduction
 2. Methods
 3. Results
 4. Discussion
Appendix A
 References
 
The main findings of this study were that the harmonics of LA input impedance moduli can be calculated using Fourier analysis, which expresses the resistance presented by the heart to the filling of the left atrium from the pulmonary veins. LA impedance is increased in patients with signs and/or symptoms of heart failure and normal left ventricular ejection fraction compared to normal subjects. Impedance modulus is determined by LA size and left ventricular mass and relaxation and may be a valuable index of diastolic heart function.

4.1. Methodological considerations
Fourier analysis is used to describe LA impedance, as at any one time, pressure depends not only on flow at the same instant but also on flow at previous instants [13]. This is a consequence of blood inertia and LA distensibility. Impedance cannot be instantaneous because it is a frequency-dependent quantity, rather than a time-dependent quantity. A simple ratio of mean pressure to mean flow will represent only the modulus of the first harmonic while Fourier analysis provides the whole spectrum of all frequencies. Thus, LA impedance includes information of the whole wave of the pulsatile pressure and flow [4,14].

In the theoretical development of the concept of LA impedance, no consideration was given to the important practical problem that LA pressure was derived from PCWP. Although PCWP is widely used to evaluate LA pressure it may not be as precise as has been assumed [15].

4.2. Left atrial input impedance
LA input impedance is the relationship between pulsatile pressure and pulsatile flow at a pulmonary vein, which may be regarded as the input to all the heart beyond pulmonary vein. It depends not only on the local vessel properties, but also on the properties of the heart beyond, down to the point where pulsations are generated. Thus, the findings of this study are reasonable. Left ventricular (LVMI and IVRT) and LA (LA diameter) structural and functional parameters had a significant effect on all harmonic components of the impedance moduli.

We also found that left ventricular hypertrophy, as expressed by the LVMI opposes left ventricular filling and increases LA input impedance. The more LVMI increases the more LA impedance increases. This relationship seems to be independent from left ventricular relaxation, as IVRT was significantly related to LA impedance spectrum, independently from LVMI. Increased LVMI probably affects not only relaxation, the first component of diastolic function, but also the sequential phases of diastole expressed by left ventricular stiffness [16].

LA diameter, independent of left ventricular indexes, determines LA input impedance. As LA diameter increases LA impedance increases. It is known that LA dimension expresses LA properties and LA dilatation expresses LA dysfunction [17,18]. First LA dysfunction appears as disturbed LA distensibility and later as reduced LA ejection fraction. In our study only LA diameter and LA ejection fraction were measured. LA ejection fraction did not significantly correlate with LA impedance, while LA diameter did. This may be explained by the fact that patients with disturbed LA ejection fraction were not included in this study. Thus, LA impedance may be more dependent on diastolic LA properties rather than on systolic properties. These findings enforce the concept of LA impedance as an index of left ventricular filling induced by the major determinants of diastolic function.

4.3. Left atrial impedance in hypertensive patients
Spectra of impedance moduli in hypertensive patients are displaced upwards and to the right, as a consequence of left ventricular hypertrophy, impaired left ventricular relaxation and LA dilatation. This shift shows increased LA impedance, which results in impaired left ventricular filling. Diastolic dysfunction is a well known manifestation of essential hypertension [18,19]. We specifically selected a study population consisting of patients with diastolic dysfunction. This new index, LA input impedance, was able to discriminate these patients from controls. It is important to notice that the diastolic indexes often used in diastolic dysfunction like transmitral E and A Doppler blood flow velocities, IVRT and reversal atrial pulmonary venous flow were significantly different between the patients and controls in our study.

In view of the difficulties in diagnosing diastolic dysfunction, especially for patients with pseudo-normalized pattern of transmitral Doppler flow velocities, it needs to be demonstrated that LA impedance can detect left ventricular diastolic dysfunction [20]. No patient had a such pattern in this study. Certainly more studies are needed to evaluate the usefulness of this new index. In this first study of LA impedance, we selected hypertensive patients with signs and/or symptoms of heart failure and normal left ventricular ejection fraction.

4.4. Clinical implications
LA impedance is of particular significance, because it describes the relationship between pressure and flow at the pulmonary vein, and so characterizes the filling properties of the heart, it can also be taken to represent the resistance to venous return of the blood to the left ventricle. It describes the properties of the heart downstream. Hence, LA impedance is regarded, quite properly, as an expression of resistance to left ventricular filling. Several definitions of diastolic function have been proposed [21,22]. These definitions have in common an abnormal resistance to filling. Diastolic function affects filling of the ventricle by inducing relaxation (early diastole), compliance (early to late diastole) or by external constraint from the pericardium. In our study LA impedance moduli was significantly affected by LVMI, IVRT and LA diameter. All of these variables are determinants of diastolic function. Each variable can be affected by different physiologic states and organic heart diseases [15,21].

LA impedance may help give a more accurate understanding of diastolic function. It would be helpful to distinguish subgroups of patients with suspected diastolic heart failure who should have measurements of LA impedance.

4.5. Conclusion
LA input impedance can have a role during clinical interpretation of the filling properties of the heart.


   Appendix A
Top
 Abstract
 1. Introduction
 2. Methods
 3. Results
 4. Discussion
 Appendix A
References
 
In complex notation, an harmonic component of pressure is p=|P|ei({omega}–{varphi}) and flow is Q=|Q|ei({omega}–β). The impedance for this particular harmonic term is Zi=P/Q=|P|ei({omega}–{varphi})/|Q|ei({omega}–β)=|P|ei(β–{varphi})/|Q|. Where |Z|=|P|/|Q|. |Z| is the modulus and {theta}=(β–{varphi}) is the phase of the impedance. The units of impedance modulus is dyne s cm–3 because this is the modulus of pressure divided by the modulus of flow; flow is measured in terms of linear velocity, as cm/s [4,13,23].


   References
Top
 Abstract
 1. Introduction
 2. Methods
 3. Results
 4. Discussion
 Appendix A
 References
 

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