European Journal of Echocardiography

European Journal of Echocardiography 2006 7(5):348-355; doi:10.1016/j.euje.2005.07.007

This Article Abstract FREE Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to My Personal Archive Download to citation manager Request Permissions Disclaimer Google Scholar Articles by Palmieri, V. Articles by Celentano, A. Search for Related Content PubMed PubMed Citation Articles by Palmieri, V. Articles by Celentano, A. Social Bookmarking          What's this?

Copyright © 2005, The European Society of Cardiology

Relations of longitudinal left ventricular systolic function to left ventricular mass, load, and Doppler stroke volume^*

Vittorio Palmieri^a,*, Cesare Russo^a, Emma Arezzi^a, Salvatore Pezzullo^a, Maria Sabatella^a, Stefana Minichiello^a and Aldo Celentano^a,b

^aDepartment of Clinical and Experimental Medicine, Federico II University School of Medicine, 80131 Naples, Italy
^b"CTO" Hospital, ASL Napoli 1, Italy

Received 14 February 2005; received in revised form 12 July 2005; accepted after revision 27 July 2005.

^* Corresponding author. Department of Internal Medicine, Federico II University School of Medicine, via Pansini 5, Edifico 1/A, Room 421, 80131 Naples, Italy. Tel.: +39 81 7464323; fax: +39 81 5466152. vpalmier{at}med.cornell.edu

	Abstract

Top Notes Abstract Methods Results Discussion Conclusions References

 
Aims To evaluate whether the peak systolic velocities of the displacement of the lateral mitral anulus (S_a) and of the mid-portion of the interventricular septal wall (S_m) correlate with measures of left ventricular load, left ventricular mass, and Doppler stroke volume in normotensive and hypertensive subjects without clinically overt cardiovascular disease.

Methods and results Tissue Doppler imaging was used to evaluate S_a and S_m in apical 4-chamber view; standard echocardiographic procedures were used to assess left ventricular structure and traditional parameters of systolic function (ejection fraction, stress-corrected midwall shortening, meridional and circumferential end-systolic stress); pulsed Doppler was employed to evaluate stroke volume. In 87 subjects meeting inclusion criteria, S_a and S_m were not significantly correlated either with left ventricular end-diastolic volume and end-systolic stress, or with stroke volume; in contrast, endocardial and midwall fractional shortening were lower with higher afterload, as expected. Fractional shortening at endocardium and midwall, and S_m were lower with higher left ventricular mass. Mean S_a and S_m values were lower in subjects with low vs. those with normal stress-corrected midwall shortening, but low S_a was not associated with lower stress-corrected midwall shortening in our study sample.

Conclusions While S_a and S_m might be indices of longitudinal left ventricular systolic mechanics, they should not be considered as measures of left ventricular contractility alternative to well-established parameters of systolic function, such as stress-corrected midwall shortening, in subjects at rest without overt heart disease.

Keywords: Left ventricular; Systole; Function; Tissue Doppler imaging; Echocardiography

---

Supported in part by Educational Grant, PhD. Program 2000–2004 "XVI Ciclo", Department of Clinical and Experimental Medicine, Federico II University School of Medicine, Recipient Dr. Vittorio Palmieri; Educational Grant, GE Medical Systems Ultrasound, Italy, Recipient Dr. Aldo Celentano.

Although precise assessment of left ventricular contractility requires simultaneous measurement of intracavitary pressure, chamber dimension, and wall thickness over a range of loading conditions, in chronic stable hemodynamic conditions, left ventricular chamber function and myocardial contractility can be estimated by examining the relations of left ventricular fractional shortening to afterload.¹ Meridional² and circumferential midwall¹ end-systolic stress are indirect and validated measures of LV afterload; in particular, the circumferential end-systolic stress-corrected midwall fractional shortening has been extensively used to characterize myocardial contractility in chronic and stable hemodynamic conditions,¹ allowing identification of subnormal myocardial systolic function even in subjects with normal ejection fraction.³ Circumferential fiber shortening is the main contributor to left ventricular cavity reduction during ejection phase.⁴ However, computation of stress-corrected midwall fractional shortening requires offline analysis, mathematical processing and is time consuming.

In recent years, advance in technology in echocardiography provided new tools for evaluation of left ventricular systolic function based on tissue Doppler imaging (TDI), which can be used to measure the systolic velocity of the longitudinal displacement of the mitral anulus (S_a) and of the myocardium at the level of the interventricular septal wall (S_m) in apical 4-chamber view. S_a and S_m are proposed as indicators of left ventricular systolic function.^5–10 However, while the inverse relation between shortening and afterload is well described and used to estimate myocardial contractility,¹ the relationship of S_a and S_m to afterload remains elusive. Therefore, in a group of clinically healthy normotensive and hypertensive subjects with chronically stable hemodynamics, we aimed at evaluating the relations of TDI-based indices of left ventricular systolic function, S_a and S_m, to wall stress in comparison with the relations of traditional indices of left ventricular systolic function (fractional shortening at endocardial and midwall levels) to end-systolic stress; in addition, we evaluated the relations of S_a and S_m to left ventricular end-diastolic volume as indicator of preload to left ventricular mass and to Doppler stroke volume.

	Methods

Top Notes Abstract Methods Results Discussion Conclusions References

 
Study sample
The study sample comprised 87 consecutive subjects who underwent cardiovascular evaluation for arterial hypertension or obesity between April 2002 and December 2004 and met inclusion criteria. All subjects gave written informed consent to the study and the study protocol was compliant with the Declaration of Helsinki. Personal history of disease and cardiovascular risk factors were evaluated, and those who referred previous myocardial infarction or acute coronary syndrome or procedures of coronary revascularization, stroke or transient cerebral ischaemic attack, kidney disease, peripheral vascular disease, endocrinal disease including diabetes, or were under physical training programs were excluded from the present study. Subjects underwent a standardized assessment of clinical and anthropometrical data, a 24-h ambulatory blood pressure monitoring, and a stress test to exclude subclinical coronary artery disease. Subsequently, subjects underwent echocardiographic evaluation of heart structure and function. Arterial hypertension was defined as supine clinical blood pressure (mean of 3 measurements in 2 different visits)140 or 90mmHg.¹¹ Among subjects classified as hypertensive, 88% was new discovered, whereas those who were taking antihypertensive drugs were included if treated for less than 3 months with a single drug and if blood pressure was >140 or 90mmHg during treatment; those hypertensive patients were studied after a 3-week wash-out period.

Echocardiography
All echocardiographic exams were performed and recorded on sVHS videotapes using one single echocardiographic machine (VIVID 7, General Electric, Horten, Norway, equipped with a matrix-array probe M3S), by trained medical doctors (EA, CR, MS, VP), following a standardized echocardiographic protocol allowing reproducible assessment of left ventricular structure and function.^11–14 All studies were read by a single reader (VP) using an in-house developed multimedia software (EchoReviewSystem©). Inter-study reproducibility of the assessments of S_a and S_m was between good and fair (in a series of 31 pair studies performed 24h apart, intraclass correlation coefficients and 95% confidence intervals: S_a=0.78, 0.58–0.88; S_m=0.51, 0.23–0.77). Left ventricular internal dimension and wall thickness were evaluated according to the recommendations of the American Society of Echocardiography.¹⁵ However, linear measurements of left ventricles were obtained from bi-dimensional left parasternal views when the parasternal long-axis view did not yield anatomically-correct visualization of left ventricles, according to recommendations of the American Society of Echocardiography.¹⁶ Left ventricular end-diastolic and end-systolic volumes were derived from left ventricular internal dimensions using the Teichholz et al.'s formula.¹⁷ Left ventricular mass was calculated using left ventricular linear dimension and wall thickness.¹⁸ Stroke volume was calculated by Doppler method using the time–velocity integral of the transaortic flow sampled at level of a virtual anulus identified by the hinging points of the aortic cusps in apical 5-chamber view; the time–velocity integral was multiplied by the cross-sectional area of a virtual anulus identified by the trailing edge to leading edge at the hinging points of the aortic cusps in left parasternal long-axis view.¹⁹ Meridional end-systolic stress and circumferential end-systolic stress were calculated by validated formulae,^1,2,20 and used as validated measures of afterload. As in previous studies,^1,11 fractional shortening at endocardial level was calculated as 100x(left ventricular diastolic diameter–left ventricular systolic diameter)/(left ventricular diastolic diameter); and used as a measure of left ventricular chamber function. In addition, ejection fraction was calculated as 100x(end diastolic volume–end systolic volume)/(end diastolic volume); left ventricular shortening was also assessed at midwall level according to the previously described methods¹: midwall fractional shortening=100x(left ventricular diastolic diameter+Hd–left ventricular systolic diameter+Hs)/(left ventricular diastolic diameter+Hd); where Hd and Hs represent the left ventricular inner shell in diastole and systole, respectively, and were calculated under the assumption that left ventricular mass does not change during the cardiac cycle.¹ Circumferential end-systolic stress was used to predict midwall fractional shortening according a standard equation¹; the ratio between measured and predicted midwall fractional shortening, expressed in percent and termed stress-corrected midwall fractional shortening, was used as indicator of contractility of the circumferentially-oriented myocardial fibers.^1,21

Pulsed TDI was used to evaluate S_a and S_m in apical 4-chamber view using a sample volume size of 4mm. Views were optimized to have best axial alignment with the cursor beam, and no angle correction was used. The first peak from the QRS within the Doppler-tissue systolic wave was used as peak velocity.¹¹ Because S_a and S_m occur on the left ventricular long axis, S_a and S_m were related to meridional end-systolic stress.²²

Statistical analysis
Data in Table 1 are mean±standard deviation, minimum and maximum in parenthesis, and percent. Continuous variables were log-transformed before their use in parametric tests. In Table 3, data are mean±standard deviation, or percent. Independent samples t-test was used to compare between-group differences for continuous variables, using log-transformation to approximate normal distribution when needed. Between-group differences in proportions were tested using the ² analysis corrected for 2x2 cross-tabulation. Data in Table 2 are age- and gender-adjusted standardized correlation coefficients obtained by multiple linear regression analysis, in overall and in normotensive and hypertensive populations separately. Low stress-corrected midwall shortening and low S_a were identified based on values<1 standard deviation from the mean, respectively. Patients with low stress-corrected midwall shortening were compared to those with normal stress-corrected midwall shortening; similarly, patients with low S_a were compared to those with normal S_a. In all statistical tests a 2-tailed p<0.05 was used to indicate the statistical significance.

View this table: [in this window] [in a new window]   Table 1 Demographics, clinical and echocardiographic characteristics of the study sample

 

View this table: [in this window] [in a new window]   Table 2 Age- and gender-adjusted relations of traditional and TDI-based indices of left ventricular systolic function to pre-load, afterload, left ventricular mass and stroke volume

 

View this table: [in this window] [in a new window]   Table 3 Longitudinal systolic function in subjects with normal vs. low stress-corrected midwall fractional shortening

 

	Results

Top Notes Abstract Methods Results Discussion Conclusions References

 
Characteristics of the study sample
The study sample comprised 87 subjects of both genders, 48 hypertensive and 39 normotensive (Table 1). In our study sample, ejection fraction ranged between 48 and 72%, whereas S_a values ranged between 5.3 and 15.3cm/s (Fig. 1). Compared to normotensives, on average hypertensive patients were slightly older and more often of male gender, had higher BMI and BP at the time of echocardiogram, whereas heart rate did not differ between the two groups. Hypertensive patients had higher LV end-diastolic volume, LV mass index, stroke volume and end-systolic stress, both circumferential and meridional than normotensive subjects; fractional shortening did not differ between the two groups, but midwall fractional shortening was lower in hypertensive patients than normotensive subjects. Relative wall thickness, indicator of left ventricular geometry, was higher in hypertensive than normotensive subjects (0.30±0.03 vs. 0.27±0.03, p<0.03), but no subjects had concentric left ventricular geometry (relative wall thickness >0.430). S_a was lower in hypertensive than normotensive subjects, whereas S_m did not differ between the two groups.

View larger version (11K): [in this window] [in a new window] [Download PowerPoint slide]   Figure 1 Scatter-plot of peak systolic velocity of the lateral mitral anulus detected by tissue Doppler (Sa, vertical axis) over ejection fraction (horizontal axis), in patients with (black circles) or without (white triangles) arterial hypertension. Continuous line represents the bivariate relationship between EF and Sa within hypertensives (r=0.24, p=0.1); dashed-line represents the bivariate relationship between EF and Sa within normotensives (r=0.14, p=0.4).

 
Relations of indices of left ventricular systolic function to afterload, left ventricular structure and stroke volume
After systematic adjustment for age and gender, endocardial fractional shortening showed a negative relationship to end-diastolic volume, more strongly so within normotensives; midwall fractional shortening, S_a and S_m showed no significant correlations with end-diastolic volume (Table 2). As expected, endocardial and midwall fractional shortenings were inversely correlated with circumferential end-systolic stress, independent of age and gender. Contrariwise, S_a and S_m did not show significant covariates-adjusted correlations with end-systolic stress. Both endocardial and midwall fractional shortenings, and S_m were lower with higher LV mass, whereas S_a showed only a trend toward lower values with higher LV mass without reaching the statistical significance. Endocardial fractional shortening, midwall fractional shortening, S_a and S_m showed no relevant correlation with stroke volume.

Low circumferential myocardial contractility and left ventricular longitudinal systolic function
Approximately 17% of the study sample had values of stress-corrected midwall fractional shortening 1 standard deviation below the mean value in the population (105%). Compared to subjects with normal stress-corrected midwall fractional shortening, those with low-normal stress-corrected midwall fractional shortening had lower endocardial fractional shortening, lower S_a and S_m (Table 3). In a subsequent subanalysis comparing subjects with low S_a (i.e., 7.8cm/s, which is 1 standard deviation below the mean in the population, 15 subjects) vs. those with normal S_a (>7.8cm/s), those with low S_a had values of endocardial fractional shortening and stress-corrected midwall fractional shortening comparable to those shown by subjects with normal S_a, whereas S_m was lower in subjects with low S_a than in subjects with normal S_a.

	Discussion

Top Notes Abstract Methods Results Discussion Conclusions References

 
In our study we found that S_a and S_m did not show significant relationships with myocardial afterload, either with end-diastolic volume, a measure of preload, or with Doppler stroke volume. Contrariwise, in our study sample, the inverse relationship between shortening and stress was consistent with established literature.^1,20,21,23 Subjects with low S_a did not show significantly lower endocardial fractional shortening and stress-corrected midwall fractional shortening compared to subjects with normal S_a. In contrast, S_a and S_m were significantly lower in subjects with relatively low vs. those with normal myocardial contractility. It was suggested that longitudinal left ventricular systolic function may be impaired in subjects with normal fractional shortening at endocardium.²⁴ Our findings may suggest that lower circumferential myocardial contractility identified lower longitudinal systolic function, whereas lower S_a may not be a reliable indicator of impaired contractility of the circumferentially oriented fibers in relatively normal hearts.

Longitudinal systolic function and afterload
The lack of significant relationships of longitudinal systolic velocities with systolic wall stress may suggest that longitudinal peak systolic velocities are not reliable measures of myocardial contractility, at least in stable hemodynamic conditions at rest. Interestingly, our findings resemble the lack of relationship between longitudinal shortening evaluated by bi-dimensional echocardiography and end-systolic stress previously shown in normal hearts.⁴ Notwithstanding, the lack of correlations between S_a and S_m with myocardial afterload may suggest that S_a and S_m are afterload-independent measure of left ventricular systolic function. However, in a previous study in healthy volunteers, acute infusion of angiotensin II to increase afterload also induced a reduction of the left ventricular peak systolic longitudinal velocities,²² proving that longitudinal left ventricular systolic velocities are indeed affected by acute hemodynamic manipulation. In our study, S_a showed a trend toward lower values with higher end-systolic stress, which did not reach the statistical significance.

Experiments with acute manipulation of loading conditions have shown that elevated left ventricular meridional shortening in relation to end-systolic stress reflects an increased inotropic state,²⁵ while shortening is low in relation to end-systolic stress in patients with heart failure.²¹ Fractional shortening at endocardium and midwall explore the function of myocardial fibers where the majority of them are oriented circumferentially, and shorten in a curvilinear way. In contrast, at level of left ventricles where linear measurements are conventionally obtained to assess left ventricular systolic function,¹⁵ longitudinal fibers are located in the sub-epicardium and sub-endocardium, and represent less than 40% of the normal myocardium²⁶; in normal hearts, their contraction contributes to left ventricular chamber systolic function by generating a fulcrum for the contracting myocardium more than by participating in the reduction of the left ventricular chamber volume during the ejection-phase.^4,26,27 Therefore, due to the nature of the function of the longitudinal fibers, S_a and S_m may be both not related to circumferential shortening and not reliable indicators of myocardial contractility, but representative of the function of the sub-endocardial and sub-epicardial myocardial areas. Our findings do not imply, however, that S_a and S_m are not useful in assessing segmental systolic function, especially in patients with myocardial disease due to coronary heart disease and or diabetes before and after myocardial pharmacological stimulation.^10,28–30

Systolic function and left ventricular mass
In our study, lower S_m correlated with higher LV mass, which was in turn associated also with lower fractional shortening at endocardium and midwall. The association of lower S_m with higher left ventricular mass is partially new in comparison with a previous study including athletes, patients with arterial hypertension and in those with hypertrophic cardiomyopathy,³¹ and reinforces the possible association of increased left ventricular mass with subclinical left ventricular systolic dysfunction.¹¹

Left ventricular output and systolic function
In our study, we also found that stroke volume was not related to the longitudinal systolic velocities, which was not previously shown. Moreover, the stroke volume showed no significant correlations with circumferential fiber contractility (i.e., fractional shortening at endocardium and midwall). The use of Doppler stroke volume in our analyses avoided any mathematical bias. These findings are important since they demonstrate that in resting steady-state hemodynamic conditions, in substantially normal hearts left ventricular pump function is accommodated at a variable range of myocardial contractility, which may reflect in part an inheritable pattern.³²

Study limitations
In our study sample, subjects with moderately to severely impaired left ventricular systolic function are not represented, which may be seen as a limitation. Nevertheless, our study sample showed a wide range of ejection fraction, limiting the impact of narrow distributions on correlations. In studies including subjects with depressed left ventricular ejection fraction, S_a was related to the global left ventricular chamber systolic performance assessed by the peak dP/dt³³ or by ejection fraction.⁹ We found a non-statistically significant trend toward lower S_a with lower ejection fraction (Fig. 1). However, in healthy volunteers peak longitudinal systolic velocity of the excursion of the posterior mitral anulus showed no significant relationship with left ventricular chamber systolic function.³⁴ Moreover, in our study sample, no subjects had concentric left ventricular geometry, potentially due to low mean age and short duration of hypertension in our study sample. Therefore, the impact of left ventricular geometry on the relations between longitudinal systolic velocities and wall stress remains to be further investigated.

	Conclusions

Top Notes Abstract Methods Results Discussion Conclusions References

 
In a group of clinically healthy subjects comprising normotensives and hypertensive patients in chronically stable hemodynamic conditions, peak velocities of the systolic longitudinal displacement of lateral mitral anulus and of the myocardium at mid-posterior interventricular septal wall were not related to left ventricular myocardial afterload, either to indirect indices of preload, or to stroke volume. Therefore, while S_a and S_m might be indices of longitudinal left ventricular systolic mechanics, they should not be considered as measures of left ventricular contractility alternative to well-established parameters of systolic function, such as stress-corrected midwall shortening, in subjects at rest without overt heart disease.

	Notes

Top Notes Abstract Methods Results Discussion Conclusions References

 
Supported in part by Educational Grant, PhD. Program 2000–2004 "XVI Ciclo", Department of Clinical and Experimental Medicine, Federico II University School of Medicine, Recipient Dr. Vittorio Palmieri; Educational Grant, GE Medical Systems Ultrasound, Italy, Recipient Dr. Aldo Celentano.

	References

Top Notes Abstract Methods Results Discussion Conclusions References

 

1. de Simone G., Devereux R.B., Roman M.J., Ganau A., Saba P.S., Alderman M.H., et al. Assessment of left ventricular function by the midwall fractional shortening/end-systolic stress relation in human hypertension. J Am Coll Cardiol (1994) 23:1444–1451. [erratum in J Am Coll Cardiol 1994 Sep;24(3):844].[Abstract]
2. Grossman W., Jones D., McLaurin L.P. Wall stress and patterns of hypertrophy in the human left ventricle. J Clin Invest (1975) 56:56–64.[Web of Science][Medline]
3. Palmieri V., Bella J.N., Arnett D.K., Liu J.E., Oberman A., Schuck M.Y., et al. Effect of type 2 diabetes mellitus on left ventricular geometry and systolic function in hypertensive subjects: Hypertension Genetic Epidemiology Network (HyperGEN) Study. Circulation (2001) 103:102–107.[Abstract/Free Full Text]
4. de Simone G., Ganau A., Roman M.J., Devereux R.B. Relation of left ventricular longitudinal and circumferential shortening to ejection fraction in the presence or in the absence of mild hypertension. J Hypertens (1997) 15:1011–1017.[CrossRef][Web of Science][Medline]
5. Oki T., Tabata T., Mishiro Y., Yamada H., Abe M., Onose Y., et al. Pulsed tissue Doppler imaging of left ventricular systolic and diastolic wall motion velocities to evaluate differences between long and short axes in healthy subjects. J Am Soc Echocardiogr (1999) 12:308–313.[CrossRef][Web of Science][Medline]
6. Alam M., Wardell J., Andersson E., Samad B.A., Nordlander R. Characteristics of mitral and tricuspid annular velocities determined by pulsed wave Doppler tissue imaging in healthy subjects. J Am Soc Echocardiogr (1999) 12:618–628.[CrossRef][Web of Science][Medline]
7. Waggoner A.D., Bierig S.M. Tissue Doppler imaging: a useful echocardiographic method for the cardiac sonographer to assess systolic and diastolic ventricular function. J Am Soc Echocardiogr (2001) 14:1143–1152.[CrossRef][Web of Science][Medline]
8. Vinereanu D., Ionescu A.A., Fraser A.G. Assessment of left ventricular long axis contraction can detect early myocardial dysfunction in asymptomatic patients with severe aortic regurgitation. Heart (2001) 85:30–36.[Abstract/Free Full Text]
9. Vinereanu D., Khokhar A., Tweddel A.C., Cinteza M., Fraser A.G. Estimation of global left ventricular function from the velocity of longitudinal shortening. Echocardiography (2002) 19:177–185.[CrossRef][Web of Science][Medline]
10. Vinereanu D., Nicolaides E., Tweddel A.C., Madler C.F., Holst B., Boden L.E., et al. Subclinical left ventricular dysfunction in asymptomatic patients with Type II diabetes mellitus, related to serum lipids and glycated haemoglobin. Clin Sci (Lond) (2003) 105:591–599.[Medline]
11. Celentano A., Palmieri V., Arezzi E., Mureddu G.F., Sabatella M., Di Minno G., et al. Gender differences in left ventricular chamber and midwall systolic function in normotensive and hypertensive adults. J Hypertens (2003) 21:1415–1423.[CrossRef][Web of Science][Medline]
12. Devereux R.B., Roman J.M. Evaluation of cardiac and vascular structure by echocardiography and other noninvasive techniques. In: Hypertension: pathophysiology, diagnosis, treatment—Laragh J.H., Brenner B.M., eds. (1995) New York (NY): Raven Press. 1969–1985.
13. Palmieri V., Dahlöf B., DeQuattro V., Sharpe N., Bella J.N., de Simone G., et al. Reliability of echocardiographic assessment of left ventricular structure and function: the PRESERVE study. J Am Coll Cardiol (1999) 34:1625–1632.[Abstract/Free Full Text]
14. Palmieri V., Arezzi E., Sabatella M., Celentano A. Interstudy reproducibility of parameters of left ventricular diastolic function: a Doppler echocardiography study. J Am Soc Echocardiogr (2003) 16:1128–1135.[CrossRef][Web of Science][Medline]
15. Sahn D.J., DeMaria A., Kisslo J., Weyman A. Recommendations regarding quantitation in M-mode echocardiography: results of a survey of echocardiographic measurements. Circulation (1978) 58:1072–1083.[Abstract/Free Full Text]
16. Schiller N.B., Shah P.M., Crawford M., DeMaria A., Devereux R., Feigenbaum H., et al. Recommendations for quantitation of the left ventricle by two-dimensional echocardiography. American Society of Echocardiography Committee on Standards, Subcommittee on Quantitation of Two-Dimensional Echocardiograms. J Am Soc Echocardiogr (1989) 2:358–367.[Medline]
17. Teichholz L.E., Kreulen T., Herman M.V., Gorlin R. Problems in echocardiographic volume determinations: echocardiographic–angiographic correlations in the presence or absence of asynergy. Am J Cardiol (1976) 37:7–11.[CrossRef][Web of Science][Medline]
18. Devereux R.B., Alonso D.R., Lutas E.M., Gottlieb G.J., Campo E., Sachs I., et al. Echocardiographic assessment of left ventricular hypertrophy: comparison to necropsy findings. Am J Cardiol (1986) 57:450–458.[CrossRef][Web of Science][Medline]
19. Devereux R.B., Roman M.J., Paranicas M., O'Grady M.J., Wood E.A., Howard B.V., et al. Relations of Doppler stroke volume and its components to left ventricular stroke volume in normotensive and hypertensive American Indians: the Strong Heart Study. Am J Hypertens (1997) 10:619–628.[CrossRef][Web of Science][Medline]
20. Shimizu G., Hirota Y., Kita Y., Kawamura K., Saito T., Gaasch W.H. Left ventricular midwall mechanics in systemic arterial hypertension. Myocardial function is depressed in pressure-overload hypertrophy. Circulation (1991) 83:1676–1684.[Abstract/Free Full Text]
21. Roman M.J., Devereux R.B., Cody R.J. Ability of left ventricular stress-shortening relations, end-systolic stress/volume ratio and indirect indexes to detect severe contractile failure in ischemic or idiopathic dilated cardiomyopathy. Am J Cardiol (1989) 64:1338–1343.[CrossRef][Web of Science][Medline]
22. Oki T., Fukuda K., Tabata T., Mishiro Y., Yamada H., Abe M., et al. Effect of an acute increase in afterload on left ventricular regional wall motion velocity in healthy subjects. J Am Soc Echocardiogr (1999) 12:476–483.[CrossRef][Web of Science][Medline]
23. Devereux R.B., Savage D.D., Sachs I., Laragh J.H. Relation of hemodynamic load to left ventricular hypertrophy and performance in hypertension. Am J Cardiol (1983) 51:171–176.[CrossRef][Web of Science][Medline]
24. Jones C.J., Raposo L., Gibson D.G. Functional importance of the long axis dynamics of the human left ventricle. Br Heart J (1990) 63:215–220.[Abstract/Free Full Text]
25. Borow K.M., Neumann A., Wynne J. Sensitivity of end-systolic pressure–dimension and pressure–volume relations to the inotropic state in humans. Circulation (1982) 65:988–997.[Abstract/Free Full Text]
26. Robb J.S., Robb R.C. The normal heart. Anatomy and physiology of the structural units. Am Heart J (1942) 23:455–467.[CrossRef][Web of Science]
27. Dumesnil J.G., Shoucri R.M., Laurenceau J.L., Turcot J. A mathematical model of the dynamic geometry of the intact left ventricle and its application to clinical data. Circulation (1979) 59:1024–1034.[Abstract/Free Full Text]
28. Cain P., Baglin T., Case C., Spicer D., Short L., Marwick T.H. Application of tissue Doppler to interpretation of dobutamine echocardiography and comparison with quantitative coronary angiography. Am J Cardiol (2001) 87:525–531.[CrossRef][Web of Science][Medline]
29. Bountioukos M., Schinkel A.F., Bax J.J., Rizzello V., Valkema R., Krenning B.J., et al. Pulsed wave tissue Doppler imaging for the quantification of contractile reserve in stunned, hibernating, and scarred myocardium. Heart (2004) 90:506–510.[Abstract/Free Full Text]
30. Kozakova M., Fraser A.G., Buralli S., Magagna A., Salvetti A., Ferrannini E., et al. Reduced left ventricular functional reserve in hypertensive patients with preserved function at rest. Hypertension (2005) 45:619–624.[Abstract/Free Full Text]
31. Vinereanu D., Florescu N., Sculthorpe N., Tweddel A.C., Stephens M.R., Fraser A.G. Differentiation between pathologic and physiologic left ventricular hypertrophy by tissue Doppler assessment of long-axis function in patients with hypertrophic cardiomyopathy or systemic hypertension and in athletes. Am J Cardiol (2001) 88:53–58.[CrossRef][Web of Science][Medline]
32. Tang W., Arnett D.K., Devereux R.B., Province M.A., Atwood L.D., Oberman A., et al. Sibling resemblance for left ventricular structure, contractility, and diastolic filling. Hypertension (2002) 40:233–238.[Abstract/Free Full Text]
33. Sohn D.W., Chung W.Y., Chai I.H., Zo J.H., Lee M.M., Park Y.B., et al. Mitral annulus velocity in the noninvasive estimation of left ventricular peak dP/dt. Am J Cardiol (2001) 87:933–936.[CrossRef][Web of Science][Medline]
34. Onose Y., Oki T., Mishiro Y., Yamada H., Abe M., Manabe K., et al. Influence of aging on systolic left ventricular wall motion velocities along the long and short axes in clinically normal patients determined by pulsed tissue Doppler imaging. J Am Soc Echocardiogr (1999) 12:921–926.[CrossRef][Web of Science][Medline]

CiteULike    Connotea    Del.icio.us    What's this?

This article has been cited by other articles:

				V. Palmieri, C. Russo, E. A. Palmieri, S. Pezzullo, and A. Celentano Changes in components of left ventricular mechanics under selective beta-1 blockade: insight from traditional and new technologies in echocardiography Eur J Echocardiogr, August 1, 2009; 10(6): 745 - 752. [Abstract] [Full Text] [PDF]

				H. Pavlopoulos and P. Nihoyannopoulos Pulse pressure/stroke volume: a surrogate index of arterial stiffness and the relation to segmental relaxation and longitudinal systolic deformation in hypertensive disease Eur J Echocardiogr, June 1, 2009; 10(4): 519 - 526. [Abstract] [Full Text] [PDF]

				P. Innelli, R. Sanchez, F. Marra, R. Esposito, and M. Galderisi The impact of aging on left ventricular longitudinal function in healthy subjects: a pulsed tissue Doppler study Eur J Echocardiogr, March 1, 2008; 9(2): 241 - 249. [Abstract] [Full Text] [PDF]

This Article Abstract FREE Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to My Personal Archive Download to citation manager Request Permissions Disclaimer Google Scholar Articles by Palmieri, V. Articles by Celentano, A. Search for Related Content PubMed PubMed Citation Articles by Palmieri, V. Articles by Celentano, A. Social Bookmarking          What's this?

Online ISSN 1532-2114 - Print ISSN 1525-2167

Copyright © 2010 European Society of Cardiology

Oxford Journals Oxford University Press

• Site Map
• Privacy Policy
• Frequently Asked Questions

Other Oxford University Press sites: Oxford University Press Oxford Journals China Oxford Journals Japan American National Biography Booksellers' Information Service Children's Fiction and Poetry Children's Reference Corporate & Special Sales Dictionaries Dictionary of National Biography Digital Reference English Language Teaching Higher Education Textbooks Humanities International Education Unit Law Medicine Music Online Products Oxford English Dictionary Reference Rights and Permissions Science School Books Social Sciences Very Short Introductions World's Classics