|Year : 2007 | Volume
| Issue : 2 | Page : 34-39
Left ventricular function in the successive phases of systemic hypertension evaluated with pulsed doppler echocardiography
Federico Cacciapuoti1, Eleonora Manfredi1, Raffaele Marfella1, Fulvio Cacciapuoti1, Giuseppe Caruso2, Giovanna Nittolo1
1 Echocardiography laboratory and Cardiovascular Research Center -IInd University of Naples, Italy
2 XII Medical Division A.O.R.N. “A. Cardarelli”, Naples, Italy
|Date of Web Publication||17-Jun-2010|
Cattedra di Medicina Interna, Facolta di Medicina e Chirurgia, Seconda Universita di Napoli, Piazza L. Miraglia, 2, 80138-Napoli
Source of Support: None, Conflict of Interest: None
| Abstract|| |
Background: Systolic and diastolic function is impaired in patients with hypertensive heart disease. Systolic hypertension induces a succession of LV hemodynamic changes and can be regarded as a spectrum from maladaptive hypertophy to heart failure. The left ventricular hemdynamic changes that occur can be measured non-invasively by Doppler echocardiography.
Objective: The aim of the study was to hemodynamically characterize the different phases of left ventricular (LV) function in patients affected by systemic hypertension (SH).
Method: 95 normotensive healthy controls (group I) and 94 hypertensives (group II) were enrolled. Hypertensive patients were divided in two sub-groups according to echocardiographic signs of left ventricular hypertrophy (LVH). Other echocardiographic parameters measured using tissue Doppler were Isovolumic Relaxation Time (IRT), isovolumic contraction time (ICT), and systolic motion (Sm). Myocardial Performance Index (MPI) using Tissue Doppler Echocardiography (TDE) was defined in both the control group and the two hypertensive subgroups. Ejection fraction (EF) was also calculated in all participants.
Results: An increased MPI derived from the rise of isovolumetric relaxation time (IRT) was found in hypertensives without LVH (sub-group II-a), whereas isovolumetric contraction time (ICT) and Systolic motion (Sm) were unchanged. Hypertensive patients with LVH demonstrated more prominent increase of MPI, increase in IRT-prolongation, ICT-increase and Sm-decrease. The results obtained indicate impaired relaxation in sub-group II-a. On the contrary, a systolo-diastolic LV dysfunction was found in sub-group II-b. E.F decreased in this same sub-group of hypertensives in comparison with controls and sub-group II-a, as a sign of maladaptive LVH evolving towards heart failure.
Conclusion: Doppler echocardiography appears able to distinguish the different forms and degrees of LV dysfunction in SH in relation to the different phases of the hypertensive disease process.
Keywords: Systemic hypertension, tissue Doppler echocardiography, left ventricular function
|How to cite this article:|
Cacciapuoti F, Manfredi E, Marfella R, Cacciapuoti F, Caruso G, Nittolo G. Left ventricular function in the successive phases of systemic hypertension evaluated with pulsed doppler echocardiography. Heart Views 2007;8:34-9
|How to cite this URL:|
Cacciapuoti F, Manfredi E, Marfella R, Cacciapuoti F, Caruso G, Nittolo G. Left ventricular function in the successive phases of systemic hypertension evaluated with pulsed doppler echocardiography. Heart Views [serial online] 2007 [cited 2019 May 21];8:34-9. Available from: http://www.heartviews.org/text.asp?2007/8/2/34/63719
| Introduction|| |
Systemic Hypertension (SH) induces a progressive increase of left ventricular mass with consequent left ventricular hypertrophy (LVH). The morphologic changes that occur in the left ventricular walls with resulting hypertrophy causes derangement of left ventricular function. A recent metanalysis has shown that LVH increases the risk of cardiovascular morbidity and mortality  . LV function can be evaluated non-invasively by Myocardial Performance Index (MPI) obtained from time-intervals of the cardiac cycle  . MPI can be non-invasively evaluated by Doppler echocardiography and many studies have demonstrated that MPI is significantly related to cardiac hemodynamics in both healthy subjects  and in patients with various cardiovascular diseases ,,,, . Tissue Doppler Echocardiography (TDE) is a relatively new ultrasound technique that measures MPI and cardiac time-intervals from the Doppler shifts induced by the motion of the cardiac walls rather than the systolo-diastolic blood displacements. The values obtained are closely related to LV regional function  and also reflects global LV function .
In the present study, we calculated MPI and time-intervals of the cardiac cycle by TDE method in a hypertensive population with and without LVH and compared the values obtained to the normotensive controls in order to define the changes that occur in LV function in hypertensive subjects in the successive phases of SH.
| Method|| |
Between January 2004 and November 2006, 95 normotensive volunteers ranging in age from 37 to 65 years were enrolled (Group I); 94 hypertensive patients, with ages ranging from 38 to 70 years and without metabolic, cardiovascular and lung disease were also evaluated (Group II). Both controls and hypertensives were in sinus rhythm with heart rate <100 beats/min. All were free of signs or clinical symptoms for cardiovascular disease and pulmonary disease. BMI was calculated as weight in kilograms divided by square of height in meters.
The hypertensive patients were divided in two sub-groups according to the echocardiographic criteria for LVH11: sub-group II-a included 46 hypertensives without echocardiographic signs of LVH and sub-group II-b constituted the remaining 48 hypertensives with LVH by echocardiography. Any anti-hypertensive drug was stopped three days before the echocardiographic examination. Two-dimensional and Doppler examinations were performed in healthy subjects of group I and in patients of subgroup II-a and II-b respectively. LV end-diastolic and end-systolic volumes and Ejection Fraction % (EF%) were measured according to the Simpson's biplane disc method  .
Pulsed-wave TDE was performed by activating the tissue Doppler function. Images were acquired using a variable frequency phased-array transducer (2.0 to 4.0 MHz). Sample volume was placed at 1cm sidelong at the mitral annulus, in the apical four-chamber view. The pulsed-wave TDE tracings were recorded over 5 cardiac cycles, at paper speed of 100mm/sec and a mean value was calculated. In controls and in hypertensive patients of subgroup II-a and subgroup II-b, Myocardial Performance Index (MPI) was defined. Its value was obtained from: Isovolumetric Contraction Time (ICT) in ms; Isovolumetric Relaxation Time (IRT) in ms; and Systolic motion (Sm) in ms. 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. A 1.7 mm. sample volume was used  . The mean of TDE parameters were calculated over 5 cardiac cycles, at paper speed of 100mm/sec [Figure 1].
Mean values ± SD of LVEDV, LVESV, EF% and LV mass were measured in Group I and in both hypertensive sub-groups and were compared using the Mann-Whitney U test for unpaired data. Means ± SD of Systolic Blood Pressure (SBP), Diastolic Blood Pressure (DBP) in mmHg and Heart Rate (HR)/min were also measured in controls and the two hypertensive sub-groups and compared by the same statistical method. Mean values of the TDE parameters obtained in group I were compared with those recorded in hypertensives without (sub-group II-a) and with LVH (sub-group II-b) by means table ANOVA with Fisher's post-hoc test. The difference was considered significant at p < 0.05.
| Results|| |
Body Mass Index was in the normal range in both groups. The mean values of S.B.P. and D.B.P. were higher in hypertensives than in controls. The LVEDV and LVESV were within normal values in both groups. LV mass index was significantly greater in patients with SH. Blood glucose serum levels were normal both in controls and in hypertensives. Total cholesterol and triglyceride serum values were almost similar in the two groups. The EF% was significantly lower in the hypertensive group(56 ± 3) than in controls (61 ± 5). The mean values ± SD of TDE-parameters and EF% recorded in healthy controls and in all hypertensives are reported in [Table 2].
Finally, the mean values ± SD of TDE-parameters and EF% obtained in the two sub-groups of hypertensives are reported in [Table 3]. In those without LVH, ICT (38 ± 5 ms) and Sm (298 ± 17 ms) were unchanged but IRT (98 ± 7 ms) and MPI (0.44 ± 0.02) were significantly increased. In hypertensive patients with LVH, ICT increased (44 ± 9 ms), IRT further increased (123 ± 6 ms) in respect to the hypertensives of sub-group II-a, whereas Sm decreased (282 ± 11 ms), and therefore, MPI was further increased (0.53 ± 0.05). On the contrary, in hypertensives of sub-group II-b, EF.% was lower (51 ± 6) than in patients of subgroup II-a (54 ± 4).
| Discussion|| |
The advantage of TDE in defining the value of MPI is its ability to simultaneously record systolic and diastolic flows from the systolic-diastolic displacements of ventricular wall recorded at the level of the lateral mitral annulus  . This site appears to be more reliable than others, according to Harada and coworkers . In relation to this place of record, Tekten et al. comparing the results obtained by pulsed Doppler and those recorded by TDE from the lateral site of the posterior mitral annulus concluded that this same site is the best place to measure MPI and time-intervals with TDE  .
We found that left ventricular volumes did not differ both in controls (Group I) and in hypertensive patients (Group II). EF% decreased in patients of Group II in comparison with the controls (Group I). On the contrary, left ventricular mass was significantly higher in hypertensives (Group II) than in normotensives (Group I).
In patients suffering from SH without LVH (sub-group II-a), ICT and Sm were unchanged in comparison to the healthy controls but IRT significantly increased. These patterns indicate that in hypertensives not yet affected by LVH, left ventricular diastolic dysfunction is already present as an early indicator of the increased after-load  . The specific effects of chronic high blood pressure readings on diastolic function are not precisely identified but a good correlation between diastolic left ventricular dysfunction and SH without LVH were previously reported by Galderisi  and Verdecchia  . Recently Aeschbacher  also noted LV diastolic dysfunction in patients with SH, before the development of LVH. These results are in accordance with other studies .
As result of increased hemodynamic demand, the heart becomes able to augment the cardiac output by means of growth of cardiomyocytes. It is known that LVH is in part the result of this morphological adaptation to the chronic pressure-overload and is characterized by thickening of the myocardial walls  . The adaptation further increases LV diastolic dysfunction  , because growth of cardiomyocytes causes increased stiffness of muscular fibers. However, LVH is not a completely adaptive mechanism because it is associated with activation of the molecular program that involves persistent activation of unfavourable signalling pathways. In addition, LVH increases the rate of cardiomyocyte apoptosis and extracellular matrix-deposition, processes that further reduce diastolic compliance and LV systolic impairment (for an aberrant intracellular Ca2+ handling) .
In our hypertensive subjects with LVH group (sub-group II-b), the lengthening of some time-intervals indicative of LV systolic dysfunction combine with deranged measures of diastolic function to manifest as "global" LV dysfunction. In these patients, we found a slight increase in ICT, moderate decrease of Sm and significantly increased IRT. In addition, EF% was further reduced in hypertensives with echocardiographic signs of LVH. These findings provide evidence that LVH is a pathological condition and constitutes a major risk factor for subsequent heart decompensation and chronic heart failure. The transition from hypertrophy to failure is easily dependent from the intracellular calcium milieu, although the detailed molecular processes of Ca++ derangement are yet uncertain ,,.
Myocyte apoptosis plays also a role in the pathophysiology of maladaptive cardiac hypertrophy and heart failure ,, . Initiation of apoptosis is associated with the activation of different cascades, including the release of cytochrome c and of proteolytic caspases  . An adverse accumulation of extracellular matrix structural protein also happens in LVH, adversely affecting myocardial viscoelasticity  . In fact, it is known that the accumulation of fibrillar collagen leads to diastolic and systolic ventricular dysfunction.
SH induces a succession of LV hemodynamic changes and can be regarded as a spectrum from maladaptive hypertophy to heart failure. These hemodynamic changes that occur during the different phases of hypertensive heart disease can be non-invasively measured by TDE. The factors that favor the transition from LVH to heart failure seems to be changes in cellular signaling of molecules, myocyte apoptosis, interstitial deposition of collagen, and the alterations in intracellular calcium handling. [Table 1]
| Conclusion|| |
| References|| |
|1.||Vakili BA; Okin PM; Devereux RB. Prognostic implications of left ventricular hypertrophy. Am Heart J. 2001;141:334-341. |
|2.||Tei C. New non-invasive index for combined systolic and diastolic ventricular function. J. Cardiol. 1995;26:135-136. |
|3.||Dagdelen S; Eren N; Karaburut H; Caglar N. Importance of the index of myocardial performance in evaluation of left ventricular function. Echocardiography. 2002; 19:273-278. |
|4.||Dujardin K; Tei C.; Yeo TC; Hodge DO; Rossi A; Seward JB. Prognostic value of a Doppler index combining systolic and diastolic performance in dilated cardiomyopathy. Am. J. Cardiol. 1998; 82:1071-1076. |
|5.||Pfeffer MA; Pfeffer JM; Lamas GA. Development and prevention of congestive heart failure following myocardial infarction. Circulation 1993; 87 (suppl. IV), 120-IV-125. |
|6.||Chenzebraun A; Keren A; Stern S. Doppler echocardiograpic patterns of left ventricular filling in patients early after acute myocardial infarction. Am. J. Cardiol. 1992; 70:711-714. |
|7.||Cacciapuoti F; Arciello A; Fiandra M; Manfredi E; Cacciapuoti F; Lama D. Index of myocardial performance after early phase of myocardial infarction in relation to its location. J. Am. Soc Echocardiogr. 2004; 17:345-349. |
|8.||Kang SM; Ha JW; Rim SJ; Chung N. Index of myocardial performance using Doppler-derived parameters in the evaluation of left ventricular function in patients with essential hypertension. Yansei Med. J. 1998; 39:446-452. |
|9.||Fukuda K; Oki T; Tabata T; Iuchi A; Ito S. Regional left ventricular wall motion abnormalities in myocardial infarction and mitral annular descent velocities studied with pulsed tissue Doppler imaging. J. Am. Soc. Echocardiogr. 1998;11: 841-848. |
|10.||Gulati VK; Katz WE; Follansbee WP; Gorcsan J. III. Mitral annular descent velocity by tissue Doppler echocardiography as an index of global left ventricular function. Am. J. Cardiol. 1996; 77:979-984. |
|11.||Devereux RB; Alonso DR; Lutas EM; Gorrlieb GJ; Campo E; Sachs I; Reichek N. Echocardiographic assessment of left ventricular hypertrophy: comparison to necropsy findings. Am J. Cardiol. 1986; 57: 450-458. |
|12.||Schiller N B; Shah PM; Crawford M; De Maria A; Devereux R; Feigenbaum H; Gutgesell H; Reichek N; Sahn D; Schnittger I; Silverman WH.; Tajik AJ. Recommendations for quantification of the left ventricle by two-dimensional echocardiography. J. Am. Soc. Echocardiogr. 1989; 2, 358-367. |
|13.||Galiuto L; Ignone G; De Maria AN. Contraction and relaxation velocities of the normal left ventricle using pulsed-wave tissue Doppler echocardiography. Am. J. Cardiol. 1998; 81:609-614. |
|14.||Yamazaki N; Mine Y; Sano A. Analysis of ventricular wall motion using color-coded using tissue doppler imaging system. Jpn. Appl. Physiol. 1994; 33:3141-3146. |
|15.||Harada K; Tamura M; Toyono M. Comparison of the right ventricular Tei index y tissue doppler imaging to that obtained by pulsed Doppler in children without heart disease. Am. J. Cardiol. 2002; 90:566-569. |
|16.||Tekten T; Onabasili AO; Ceyhan C; Unal S; Discigil B. Novel approach to measure myocardial performance index: pulsed-wave tissue Doppler echocardiography. Echocardiography 2003; 20:503-510. |
|17.||Philips RA; Goldman ME; Ardeljan M.;Arora R; Eison HB; Buyan Y; Krakoff LR. Determinant of abnormal left ventricular filling in early hypertension. J. Am. Coll. Cardiol. 1989;14:979-985. |
|18.||Galderisi M; Petrocelli A; Alfieri A; Garofano M. de Divitiis O. Impact of ambulatory blood pressure on left ventricular diastolic dysfunction in uncomplicated arterial systemic hypertension. Am. J. Cardiol. 1996; 77:597-601. |
|19.||Verdecchia P; Schillaci G; Guerrieri M. Prevalence and determinants of left ventricular diastolic filling abnormalities in an unselected hypertensive population. Eur. Heart J. 1990;11:679-691. |
|20.||Aeschbacher BC; Hutter D; Fuhrer J; Weidmann P; Delecretaz E; Allemann Y; Diastolic dysfunction precedes mypocardial hypertrophy in the development of hypertension. Am. J. Hypertension 2001;14 (2):106-113. |
|21.||Inouye I.; Massie B.; Loge D.; Topic N.; Silverstein D.; Simpson P. ; Tubau JF. : Abnormal LV filling : an early finding in mild to moderate systemic hypertension. Am. J. Cardiol. 1984: 53, 120-126. |
|22.||Lorell H; Carabello A. Left ventricular hypertrophy: pathogenesis, detection, and prognosis. Circulation 2000;102: 470-479. |
|23.||Molinero E; Murga N; Sastagoitia JD; Fernandez R; Garrido J. Treatment of diastolic dysfunction in hypertensive patients without left ventricular hypertrophy. J. Human Hypert. 1998;12:21-27. |
|24.||Lips DJ; de Windt LJ; van Kraaij DJW; Doevedans PA. Molecular determinants of myocardial hypertrophy and failure: alternative pathways for beneficial and maladaptive hypertrophy. Eur. Heart J. 2003; 24:883-896. |
|25.||Bailey BA; Houser SR. Sarcoplasmic reticulum-related changes in cytosolic calcium in pressure overload-induced feline LV hypertrophy. Am. J. Physiol. 1993;265:H2009-H2016. |
|26.||Arai M; Matsui H; Periasamy M. Sarcoplasmic reticulum gene expression in cardiac hypertrophy and heart failure. Circ. Res. 1994; 74:555-564. |
|27.||Movesian MA; Schwinger RH. Calcium sequestration by the sarcoplasmic reticulum in heart failure. Cardiovasc. Res. 1998;37:352-359. |
|28.||Narula J; Kolodgie FD; Virmani R. Apoptosis and cardiomyopathy. Curr. Opin. Cardiol. 2000; 15:183-188. |
|29.||Narula J; Pandey P; Arbustini E; et al. Apoptosis in heart failure: release of cytochrome c from mitochondria and activation of caspase-3 in human cardiomyopathy. Proc. Natl. Sci. USA 1999;96:8144-8149. |
|30.||Narula J; Hajjar RJ;Dec GW. Apoptosis in the failing heart. Cardiol. Clin. 1998; 16:691-710. |
|31.||Hisatomi T; Sakamoto T; Murata T; et al. Relocalization of apoptosis-inducing factor in photoreceptor apoptosis induced by retinal detachment in vivo. Am. J. Pathol. 2001;158:1271-1278. |
|32.||Burlew BS; Weber KT. Connective tissue and the heart. Functional significance and regulatory mechanisms. Cardiol. Clin. 2000; 18:435-442. |
[Table 2], [Table 3], [Table 1]