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Introduction
The increased left ventricular diastolic filling pressure evolves in left ventricular (LV) diastolic dysfunction.1)2) This haemodynamic condition usually is demonstrated by the impairment of E/A mitral inflow ratio (E/A < 1) or by the change of normal pattern of pulmonary veins' flow. The combination of early inflow velocity curve and tissue Doppler imaging of the mitral annulus (E/E' ratio) better estimates this condition. But, in the absence of any mitral valve derangement, LV diastolic dysfunction directly affects Left Atrial Volume (LAV). This parameter can be easily measured by two-dimensional echocardiography and indexed to the body surface area (BSA) as left atrial volume index (LAVI).3)4) Therefore, LAVI also may be used as faithful indicator of LV diastolic dysfunction.5) On the other hand, LV function can be adequately evaluated by myocardial performance index (MPI).6)7) This (also called Tei index) can be measured either with conventional Doppler method or tissue Doppler echocardiography (TDE).8) This last method has the advantage to directly assess transmural myocardial velocities.9) In addition, TDE-MPI is more sensitive than the conventional Doppler MPI in to define LV function, especially in the presence of regional wall motion abnormality.9)
In this study, we evaluated the relationship between LAVI and diastolic LV function defined with TDE-MPI in a group of hypertensive patients with LV diastolic dysfunction and ejection fraction% (EF%) > 50%.
Methods
Since October 2009 to February 2011, 62 hypertensive patients (43 males and 29 females) aged from 45 to 61 years (mean age = 55 ± 6 years) and without any valvular heart diseases were examined. The leading epidemiological, metabolic and echocardiographic characteristics of controls and hypertensive patients (group II) were shown in Table 1. These were in sinus rhythm and have an echocardiographic finding of left ventricular hypertrophy (LVH).10) Coronary artery disease was excluded by coronary angiography in 24 of these, and by rest and effort myocardial SPECT in the remaining 38. Cumulative anti-hypertensive treatments given in patients of group II were shown in Table 2. In accordance with the recommendations for the evaluation of LV function by echocardiography,11) the patients were diagnosed as affected by LV diastolic dysfunction, with EF% > 50% (group II).12)
Fifteen (8 males and 7 females) healthy subjects (M and F; mean age = 54 ± 3 years) was also enrolled, as controls. In these, echocardiographic left ventricular function was defined too (group I).
Conventional and tissue Doppler echocardiography
Two groups were echocardiographically examined in the left-lateral position by using a iE33 machine (Philips, Amsterdam, the Netherlands). According to the biplane Simpson's rule, LV end-diastolic volume (LVEDV) and LV end-systolic volume (LVESV) in mL and EF% were defined.13) Inter ventricular septum (IVS) thickness was measured (in mm) during systole. LV wall thickness was also measured (in mm). Left ventricular mass and its indexed value was assessed by the method proposed by Devereux et al.10) Left atrial (LA) volume in systole was also measured just before the mitral valve opening, using the biplane Simpson's method, as a mean between the values recorded in apical four- and two-chamber approaches. Subsequently, LAV was indexed for BSA, such as LAVI in mL/m2.14) Finally, MPI was evaluated by using TDE method. Pulsed-wave TDE was performed by activating the tissue Doppler function. Sample volume was placed at the lateral annular mitral site in apical four chamber view, in order to record the following cardiac time intervals: iso-volumetric contraction time (IVCT) in ms; iso-volumetric relaxation time (IVRT) in ms; and ejection time (ET) in ms. Images were acquired with a variable frequency phased-array transducer. The filter settings were kept low, and gains were adjusted to the minimal optimal level to minimize noise and eliminate the signals produced by the transmitral flow. Three consecutive beats were measured and averaged for each parameter at a sweep speed of 100 mm/s. MPI was defined as the sum of IVCT and IVRT divided by ET.15) LAVI; MPI; IVCT; IVRT; and ET were defined in controls (group I) too, as reference values (Table 3).
Statistical analysis
Echocardiographic data are presented as a mean values ± SD. Statistical analyses were performed with SPSS statistical software (SPSS, Chicago, IL, USA). Differences between two groups were examined by an unpaired t test. A p value < 0.05 was considered significant. Finally, LAVI was compared to MPI, IVCT, IVRT and ET between controls (group I) and hypertensive patients (group II) by unpaired t-test.
Results
Mean values of LVEDV and LVESV were 95 ± 18 mL and 39 ± 17 mL respectively in controls (group I). These resulted 125 ± 15 mL (LVEDV), and 48 ± 11 mL (LVESV) in hypertensive patients (group II). Differences were significant (p < 0.05). IVS thickness was = 10 ± 0.4 mm in controls, it resulted 135 ± 0.5 mm in hypertensive-patients. Mean value of E/A waves ratio was 1.21 ± 0.38 in normal and 0.85 ± 0.27 in hypertensives (p < 0.01). Mitral deceleration time (DT) resulted = 135 ± 3.4 ms in healthy adults and 245 ± 31 in hypertensive patients (p < 0.01). On the other hand, LV walls' thickness was 9 ± 0.3 mm in controls (group I) and 17 ± 0.2 mm in hypertensives (group II). Differences were significant (p < 0.001). The mean value of LV mass index was 90 ± 21 g/m2 in control group. It increased to 178 ± 29 g/m2 in hypertensive group (p < 0.001). EF% resulted of 61 ± 0.8% in controls (group I) and of 57 ± 0.9% in hypertrophic patients (group II). Differences between two groups weren't significant (NS) (Table 1).
With reference to LAVI, a mean of 47 ± 5 mL/m2 was found in hypertensive-hypertrophic patients (group II). This value was significantly higher (p < 0.001) than that recorded in controls (group I) (23 ± 4 mL/m2). Normal values of TDE-MPI (0.34 ± 0.05) obtained in control-group significantly increased (p < 0.01) in patients with LV hypertrophy (0.46 ± 0.09). Particularly, IVCT resulted 28 ± 7 ms in healthy individuals, almost similar to that obtained in hypertensive patients (30 ± 8 ms), without significant differences (NS). On the contrary, IVRT was significantly (p < 0.001) prolonged (107 ± 9 ms) in hypertensives in comparison to healthy subjects (79 ± 6 ms). ET was within the limits both in normals (315 ± 10 ms) and in hypertensive patients (312 ± 10 ms) (NS) (Table 3).
Discussion
LAV may be calculated by three different methods: the biplane area lengh; the biplane modified Simpson's, and the prolate ellipse method.16) Significant differences among three diverse methods exist, even through all three shown highly satisfactory reproducibility. In this study, we used biplane Simpson's method indexed for BSA, to obtain LAVI mesaured in mL/m2. Mean value of LAVI reported by several AA is 22 ± 6 mL/m2.17-21) In our healthy controls, a mean value of 23 ± 4 mL/m2 was found. This was reported as reference value for our laboratory.
It is known that mechanical function of LA has described in three phases: reservoir; conduit, and contractile phase. The "reservoir" corresponds to the difference between maximal and minimum LA volumes occurring in the interval-just before the opening mitral valve and just before the aortic valve opening. "Conduit" is the early phase of ventricular diastole. The blood is passively transferred to left ventricle just after mitral valve opening. "Contractile" phase or "booster pump" is calculated as the difference between minimum and pre-atrial contraction. It serves to augment the stroke volume. The contribution of three phases of LA function changes according to the diastolic properties of LV. In normal conditions, the contribution of reservoir, conduit and contractile function of the LA to the LV filling is 40%, 35%, and 25% respectively. As LV relaxation worsens, the contribution of different LA phases gradually increases,22) in accordance with recent experiences performed in patients with LV diastolic dysfunction.23)24)
In the present study, we evaluated the relationship between LAVI and LV diastolic dysfunction due to LV hypertrophy. LV diastolic impairment was demonstrated by the increase of IVRT and TDE-MPI. Achieved results indicate that LAVI significantly raised in comparison to the contol values in hypertensives with LV hypertrophy. This faithfullly certainly reflects LV diastolic dyfunction consequent to LVH. The increase of IVRT and TDE-MPI (with normal values of IVCT) can be considered as an useful and reliable tool to identify LV diastolic LV dysfunction.25)26) Several research groups previously have shown that MPI and IVRT reflect LV diastolic dysfunction, independently of arterial pressure,27) heart failure28) or heart rate,29) in presence of preserved systolic function especially.30) A previous study has also demonstrated an association between LVH induced by systemic hypertension and left atrial dimension.31) Successively, Pritchett et al.32) evidenced that LAVI is a highly sensitive and specific tool for the detection of severe LV diastolic dysfunction (III degree of diastolic dysfunction). These AAs. = Authors also demonstrated that LAVI may better reflect the cumulative effect of increased LV filling pressures over time in comparison to the Doppler indexes, as E/A ratio, DT and E/E' ratio (that reflect increased LV filling pressures at one point in time). The incremental value of LAVI measurement is its prognostic implications towards cardiovascular death and/or adverse cardiovascular outcomes in hypertensive patients with LV diastolic dysfunction, as recently demonstrated by Leung et al.33)
In the present report, we firstly identified LV diastolic dysfunction using TDE-MPI. LAVI (in the absence of any mitral disease) appeared also expressive of LV diastolic dysfunction, further confirming the relationship between LAV and LV diastolic dysfunction. But, other studies performed in a wide range are requested to definitively demonstrate the relationship among LAVI, TDE-MPI and LV diastolic dysfunction.
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