Skip Navigation

European Journal of Echocardiography 2005 6(2):127-133; doi:10.1016/j.euje.2004.07.008
This Article
Right arrow Abstract Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Quintana, M.
Right arrow Articles by Langanger, J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Quintana, M.
Right arrow Articles by Langanger, J.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Copyright © 2005, The European Society of Cardiology

The effects of heart rate on myocardial velocity and atrio-ventricular displacement during exercise with and without beta-blockade: a tissue Doppler echocardiographic study

Miguel Quintanaa,*, Thomas Gustafssonb, Patrick Sundbladb and Jenny Langangerc

aDepartments of Clinical Physiology and Cardiology, Huddinge University Hospital, Karolinska Institute, 141 86 Stockholm, Sweden
bDepartment of Clinical Physiology, Huddinge University Hospital, Karolinska Institute, 141 86 Stockholm, Sweden
cCardiovascular Research Laboratory, Danderyd Hospital, Karolinska Institute, 141 86 Stockholm, Sweden

Received 19 May 2004; received in revised form 30 July 2004; accepted after revision 30 July 2004.

* Corresponding author. Tel.: +46 8 585 86777; fax: +46 8 774 8082. miguel.quintana{at}labmed.ki.se


   Abstract
Top
 Abstract
Introduction
 Material and methods
 Results
 Discussion
 Limitations of the study
 References
 
Background Colour tissue Doppler echocardiography (TDE) allows an objective assessment of regional myocardial function. Peak systolic velocity (PSV) and A-V plane displacement (AVPD) obtained from colour TDE correlate well with changes in cardiac wall motion and can discriminate ischemic areas during stress echocardiography. During exercise, the relationship between PSV and AVPD depends on several factors besides ischemia and should be considered when performing exercise stress echocardiography.

Aims To investigate the relation between PSV, AVPD and heart rate (HR) during semi-upright exercise with and without beta-blockade.

Subjects and methods Twelve healthy men underwent semi-upright exercise stress echocardiography with and without beta-blockade on two separate occasions. Standard echocardiographic projections were used for the stress echocardiography. Grey-scale echocardiographic pictures containing colour TDE information were obtained at rest and during a two-stage exercise test, and the images were analyzed off-line. The PSV and AVPD were measured at four points at the base of the left ventricle at the septum and lateral, inferior and anterior walls.

Results PSV, AVPD and HR gradually increased during exercise. The increases in PSV and AVPD were linearly correlated with the increase in HR. The increases in PSV were significantly lower during exercise with beta-blockade than without beta-blockade (P<0.05). This was not observed in AVPD, as increments were not affected by beta-blockade.

Conclusion These data showing a relationship between HR and PSV, and a significantly lower PSV with beta-blockade at a given HR, suggest that PSV is influenced by HR and myocardial contractility, both of which are augmented by physical exercise-induced sympathetic stimulation.

Keywords: Tissue Doppler echocardiography; Left ventricular function; Exercise; Beta-blockade


   Introduction
Top
 Abstract
 Introduction
Material and methods
 Results
 Discussion
 Limitations of the study
 References
 
Assessment of left ventricular (LV) longitudinal function has become an essential tool to evaluate global LV function.1,2 Its importance has been studied extensively by M-mode echocardiography in patients with coronary artery disease3–5 and congestive heart failure.6,7 The introduction of pulsed-wave and colour tissue Doppler echocardiography (TDE) has further improved the analysis of the LV longitudinal function and the accuracy of diagnosis of coronary artery disease and detection of acute myocardial ischemia.8–13 In clinical practice, exercise stress echocardiography is used to detect myocardial ischemia in patients treated with beta-blockers for systemic hypertension, compensated heart failure, or suspected or known coronary artery disease.14–17 Animal studies have shown that beta-adrenergic blocking agents decrease the myocardial peak systolic velocity (PSV) and other colour TDE-derived variables.18–21 TDE has been proposed recently as a valuable method to detect coronary artery disease9,10 without considering the possible effects of beta-blockade on colour TDE-derived variables. Our objective was to investigate the effects of alterations in the inotropic and chronotropic state induced by physical exercise and intravenous beta-blockade on colour TDE-derived variables.


   Material and methods
Top
 Abstract
 Introduction
 Material and methods
Results
 Discussion
 Limitations of the study
 References
 
Subjects
Twelve young, healthy males between 25 and 33 years of age were studied. They had no symptoms or history of cardiac disease and none of them had a high level of physical fitness. All subjects had a normal resting 12-lead ECG and normal findings on a 2D, colour Doppler echocardiogram. They were studied at rest and during exercise in the basal state and during intravenous administration of beta-blockade. All subjects gave informed consent. The Ethic Committee at Karolinska University Hospital, Huddinge approved the protocol.

Exercise protocol
A 12-lead ECG, blood pressure and HR were recorded with subjects in a supine position in the basal state, after which the subjects adopted a semi-sitting (60 degrees) and light left lateral position on a bicycle ergometer designed for that purpose. Subjects then performed exercise with a starting load of 100W. After 6min exercising at 100W, the workload was increased to 150W and the subjects continued to exercise for a further 6min. The protocol allowed the acquisition of adequate echocardiographic images at steady state during sub-maximal and near-maximal work, minimizing the respiratory artefacts that usually occur during maximal exercise making it difficult to perform the TDE analysis. Systolic blood pressure and HR were registered every third minute and at the end of exercise. After 30min of rest, selective beta-blockade was induced by the intravenous administration of metoprolol at a dose of 0.175mgkg–1 22,23 and the exercise test was repeated. All subjects successfully completed the exercise protocol.

Rest and stress echocardiography
A standard 2D and Doppler echocardiographic examination was performed on all subjects lying in the left lateral supine position using a 2.5MHz probe on the Vingmed System-FiveTM ultrasound equipment (General Electric, Horten, Norway) and data were stored digitally as cineloops on magnet optical discs. Conventional projections were obtained to assess atrial and ventricular dimensions and function according to standard procedures.24 LV volumes and ejection fraction at rest and during exercise were calculated according to Simpson's method.24 Colour, continuous and pulsed Doppler echocardiography was performed according to standard techniques to assess valvular and overall cardiac function.25 For the purposes of stress echocardiography, images from apical four- and two-chamber views were acquired in the semi-sitting left lateral position at rest and at the end of each of the two exercise stages (100 and 150W) at a frame rate greater than 100 frames/s. The registered images contained both grey-scale and colour TDE information and the pulse repetition frequency was adjusted to avoid aliasing. Three heartbeats were collected from each view and analyzed off-line with an EchoPACTM 6.3.6 system (General Electric, Horten, Norway).

Tissue Doppler echocardiography
The velocity profiles were obtained at the basal segment of the septal, lateral, inferior and anterior walls from cineloops containing four- and two-chamber views. The following variables were measured, as shown in Fig. 1: peak systolic velocity (PSV), the ejection time (ET) measured from the beginning to the end of the systolic velocity curve profile and the RR interval. The atrio-ventricular plane displacement (AVPD) was derived by time integration of the velocity curve profile. The integration of the velocity curve profile started at the beginning of the QRS complex (including the isovolumic contraction time or pre-ejection period) until the end of the ejection time. The TDE analysis was performed by one observer (JL) in a random manner, although the observer was not blinded to the condition (i.e. with or without beta-blockade). The average values obtained from the four basal segments are presented.


Figure 1
View larger version (67K):
[in this window]
[in a new window]
[Download PowerPoint slide]
  		Figure 1 (A) On the left side, a four-chamber view obtained with colour tissue Doppler echocardiography. On the right, a typical velocity profile showing time intervals and systolic and diastolic velocities. The yellow arrow shows the area of interest at the basal portion of the septum. ET, ejection time; IVCT, isovolumic contraction time; IVRT, isovolumic relaxation time. (B) The derived A-V plane displacement obtained by time integration of the velocity curve profile.

 
Statistical analysis
Values are presented as means±S.D. Student's paired two-tailed t-tests were performed to compare the mean values for each parameter between the conditions with and without beta-blockade. Two-way analysis of variance (ANOVA) with repeated measures was used to assess the changes in PSV and AVPD at different workloads in the two exercise conditions. Unpaired t-tests were performed on the average slope coefficients to compare the correlations between the changes in HR and the changes in PSV or AVPD. The slope coefficients were obtained from the equation line corresponding to the values from the three stages for each subject during both conditions (with and without beta-blockade). The level of significance was set at P<0.05.


   Results
Top
 Abstract
 Introduction
 Material and methods
 Results
Discussion
 Limitations of the study
 References
 
Measurements obtained from the standard echocardiographic examination values were within the normal ranges for age and body mass index (Table 1).24 Heart rate and systolic blood pressure increased with incremental exercise workload both with and without beta-blockade (P<0.05). The increase in HR and systolic blood pressure from rest to 150W was significantly greater without beta-blockade than with beta-blockade (P<0.001) (Table 2, Fig. 2GoA).


Figure 2
View larger version (13K):
[in this window]
[in a new window]
[Download PowerPoint slide]
  		Figure 2 The relationship between heart rate (A), peak systolic velocity (B) and A-V plane displacement (C) during exercise with and without beta-blockade. *P<0.05, **P<0.001, with vs without beta-blockade.

 


View this table:
[in this window]
[in a new window]

  		Table 1 Echocardiographic data obtained by standard 2D echocardiography performed in the lying left lateral position

 


View this table:
[in this window]
[in a new window]

  		Table 2 Colour tissue Doppler echocardiographic variables and haemodynamic responses to exercise with and without beta-blockade

 
The PSV increased linearly from rest to maximal workload in both conditions; however, the increase in PSV was significantly lower during exercise with beta-blockade than without beta-blockade (P<0.01) (Table 2, Fig. 2GoB). This pattern was observed in 11 of the 12 subjects. In the 12th subject, the increase in PSV did not differ between the two conditions. The increase in PSV was linearly correlated with the increase in HR regardless of the exercise condition (i.e. with or without beta-blockade). For any given increase in HR, there was a significantly smaller increase in PSV during exercise with beta-blockade than without beta-blockade (P<0.01, Fig. 3A).


Figure 3
View larger version (13K):
[in this window]
[in a new window]
[Download PowerPoint slide]
  		Figure 3 The correlation between the increases in heart rate and PSV or A-V plane displacement was tested by comparing the slope coefficients obtained from the equation lines corresponding to the values from the three stages for each subject and during both conditions (with and without beta-blockade). P values reflect the significance of the difference between the two slope coefficients.

 
The AVPD increased during the first stage of exercise, but this pattern did not differ between exercise with and without beta-blockade (Table 2, Fig. 2GoC). The increase in AVPD was linearly correlated with the increase in HR in both conditions (Fig. 3B). The ejection time continuously decreased from rest to 100W and from 100 to 150W; the decrease was less pronounced during exercise with beta-blockade (Table 2).

The LV end-diastolic volume showed a biphasic response, increasing in the first phase of exercise and decreasing in the second phase. The LV end-systolic volume progressively decreased and the LV ejection fraction progressively increased during exercise. Beta-blockade did not affect LV volume or ejection fraction at rest and during exercise (Table 2).


   Discussion
Top
 Abstract
 Introduction
 Material and methods
 Results
 Discussion
Limitations of the study
 References
 
Our main findings were that PSV and AVPD increased progressively during exercise in parallel with increasing HR. At any given increase in HR, the increase in PSV was smaller during exercise with beta-blockade than without beta-blockade. However, the increase in AVPD during exercise was not affected by beta-blockade and was accompanied by a significantly smaller decrease in the ejection time. These findings have not been reported previously in humans.

At a given HR, the PSV was lower during exercise with beta-blockade than without beta-blockade, i.e. a given change in HR resulted in a smaller change in PSV. This observation cannot only be explained by the differences in HR between the two conditions, which indicate the influence of the inotropic state in addition to the relationship between HR and PSV. Moreover, the significant reduction in systolic blood pressure indicates that afterload decreased during exercise with beta-blockade. This suggests that the effect of beta-blockade on PSV could have been underestimated in our study. The mechanism responsible for the effect of inotropy on the achieved PSV has been described in animal studies in which beta-blockade of pacemaker-instrumented animals induced a decrease in PSV at rest.18,19

Exercise caused sympathetic activation of both HR and contractility. However, this parallel increase in HR and contractility cannot fully explain the observed increase in PSV at higher heart rates during exercise without beta-blockade. Other mechanisms may be involved, such as the treppe effect where an increased HR leads to enhanced force of contractility because of enhanced calcium myocardial influx.

Our observation of parallel increases in PSV and HR contrasts with those of previous studies. For example, only a weak correlation was observed between maximal dobutamine-induced HR and PSV.10,26,27 However, those results probably reflected the individual differences in maximal tolerated dose of dobutamine or differences in maximal HR rather than the actual relationship between stress-induced changes in HR and PSV. Nonetheless, using a multiple regression analysis, Pasquet et al. found that HR was one of the most important independent determinants of PSV. Moreover, multiple logistic regression analysis showed that the peak HR achieved during exercise was an independent predictor of abnormal regional myocardial function in a group of patients with known or suspected coronary artery disease.28,29 The recently published MYDISE study further emphasized the importance of the achieved HR when selecting diagnostic cutoff values for the PSV response during maximal dose dobutamine infusion.10

In contrast to the PSV, the AVPD response was similar with and without beta-blockade. One explanation for this discrepancy is that the decreased afterload produced by beta-blockade maintained the LV stroke volume and consequently the AVPD. This is supported by the observed lower decrements in LV ejection time during exercise with beta-blockade, which would allow the LV to contract to a similar degree but at a slower rate of contraction (i.e. decreased PSV). Gorcsan et al. showed the interdependency of the PSV and pressure–volume relationships in animal experiments.18 Other clinical studies have shown that LV volumes and haemodynamics26,28,29 may not be the most important predictors of PSV in peak stress induced by dobutamine or physical exercise. However, the unreliability of LV volumes and ejection fraction assessed by echocardiography3 may preclude interpretation of the observed changes in LV volumes and ejection fraction.

If chronic beta-blockade impairs both the inotropic and chronotropic responses to exercise, we might expect that PSV and other TDE-derived variables would also be affected during exercise stress. This could be important when defining the ischemic response and the diagnosis of coronary artery disease during quantitative stress echocardiography using colour TDE.9,28,30 Two studies have shown the importance of selecting appropriate diagnostic criteria;9,10 the possible effects of chronic beta-blockade on these diagnostic criteria have yet to be established.


   Limitations of the study
Top
 Abstract
 Introduction
 Material and methods
 Results
 Discussion
 Limitations of the study
References
 
The methodology of colour TDE has inherent limitations. Our study assessed the regional response of normal myocardium to physical exercise with and without beta-blockade only in the longitudinal direction, and we did not assess the circumferential myocardial function. Because of the known physiological differences between dobutamine-induced and physical exercise-induced stress, our results do not necessarily apply to dobutamine stress echocardiography. It is unclear whether our results can be generalized to healthy individuals of other ages. In addition, our data apply only to the acute beta-blockade condition because the effects of chronic beta-blockade on the PSV and AVPD in segments with normal and abnormal wall motion at rest have yet to be determined.

In conclusion, the attenuation of sympathetic stimulation by intravenous selective beta-blockade influenced both the myocardial contractility and the HR, each of which affect PSV. These data suggest that during the increased sympathetic state induced by physical exercise, a parallel increase in heart rate and contractility induce continuous increments in PSV and other TDE-assessed variables.


   References
Top
 Abstract
 Introduction
 Material and methods
 Results
 Discussion
 Limitations of the study
 References
 

  1. Zaky A., Grabhorn L., Feigenbaum H. Movement of the mitral ring: a study in ultrasoundcardiography. Cardiovasc Res (1967) 1:121–131.[Abstract/Free Full Text]
  2. Isaaz K., Munoz del Romeral L., Lee E., Schiller N.B. Quantitation of the motion of the cardiac base in normal subjects by Doppler echocardiography. J Am Soc Echocardiogr (1993) 6:166–176.[Medline]
  3. Jensen-Urstad K., Bouvier F., Hojer J., Ruiz H., Hulting J., Samad B., et al. Comparison of different echocardiographic methods with radionuclide imaging for measuring left ventricular ejection fraction during acute myocardial infarction treated by thrombolytic therapy. Am J Cardiol (1998) 81:538–544.[CrossRef][Web of Science][Medline]
  4. Alam M., Hoglund C., Thorstrand C., Hellekant C. Haemodynamic significance of the atrioventricular plane displacement in patients with coronary artery disease. Eur Heart J (1992) 13:194–200.[Abstract/Free Full Text]
  5. Henein M.Y., Anagnostopoulos C., Das S.K., O'Sullivan C., Underwood S.R., Gibson D.G. Left ventricular long axis disturbances as predictors for thallium perfusion defects in patients with known peripheral vascular disease. Heart (1998) 79:295–300.[Abstract/Free Full Text]
  6. Alam M., Hoglund C., Thorstrand C., Philip A. Atrioventricular plane displacement in severe congestive heart failure following dilated cardiomyopathy or myocardial infarction. J Intern Med (1990) 228:569–575.[Web of Science][Medline]
  7. Willenheimer R., Cline C., Erhardt L., Israelsson B. Left ventricular atrioventricular plane displacement: an echocardiographic technique for rapid assessment of prognosis in heart failure. Heart (1997) 78:230–236.[Abstract/Free Full Text]
  8. von Bibra H., Tuchnitz A., Klein A., Schneider-Eicke J., Schomig A., Schwaiger M. Regional diastolic function by pulsed Doppler myocardial mapping for the detection of left ventricular ischemia during pharmacologic stress testing: a comparison with stress echocardiography and perfusion scintigraphy. J Am Coll Cardiol (2000) 36:444–452.[Abstract/Free Full Text]
  9. 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]
  10. Madler C.F., Payne N., Wilkenshoff U., Cohen A., Derumeaux G.A., Pierard L.A., et al. Non-invasive diagnosis of coronary artery disease by quantitative stress echocardiography: optimal diagnostic models using off-line tissue Doppler in the MYDISE study. Eur Heart J (2003) 24:1584–1594.[Abstract/Free Full Text]
  11. Edvardsen T., Skulstad H., Aakhus S., Urheim S., Ihlen H. Regional myocardial systolic function during acute myocardial ischemia assessed by strain Doppler echocardiography. J Am Coll Cardiol (2001) 37:726–730.[Abstract/Free Full Text]
  12. Kukulski T., Jamal F., D'Hooge J., Bijnens B., De Scheerder I., Sutherland G.R. Acute changes in systolic and diastolic events during clinical coronary angioplasty: a comparison of regional velocity, strain rate, and strain measurement. J Am Soc Echocardiogr (2002) 15:1–12.[CrossRef][Web of Science][Medline]
  13. Kukulski T., Jamal F., Herbots L., D'Hooge J., Bijnens B., Hatle L., et al. Identification of acutely ischemic myocardium using ultrasonic strain measurements. A clinical study in patients undergoing coronary angioplasty. J Am Coll Cardiol (2003) 41:810–819.[Abstract/Free Full Text]
  14. Wikstrand J., Warnold I., Olsson G., Tuomilehto J., Elmfeldt D., Berglund G. Primary prevention with metoprolol in patients with hypertension. Mortality results from the MAPHY study. JAMA (1988) 259:1976–1982.[Abstract/Free Full Text]
  15. Packer M., Bristow M.R., Cohn J.N., Colucci W.S., Fowler M.B., Gilbert E.M., et al. The effect of carvedilol on morbidity and mortality in patients with chronic heart failure. U.S. Carvedilol Heart Failure Study Group. N Engl J Med (1996) 334:1349–1355.[Abstract/Free Full Text]
  16. Freemantle N., Cleland J., Young P., Mason J., Harrison J. beta Blockade after myocardial infarction: systematic review and meta regression analysis. BMJ (1999) 318:1730–1737.[Abstract/Free Full Text]
  17. von Arnim T. Medical treatment to reduce total ischemic burden: total ischemic burden bisoprolol study (TIBBS), a multicenter trial comparing bisoprolol and nifedipine. The TIBBS Investigators. J Am Coll Cardiol (1995) 25:231–238.[Abstract]
  18. Gorcsan J. 3rd, Strum D.P., Mandarino W.A., Gulati V.K., Pinsky M.R. Quantitative assessment of alterations in regional left ventricular contractility with color-coded tissue Doppler echocardiography. Comparison with sonomicrometry and pressure–volume relations. Circulation (1997) 95:2423–2433.[Abstract/Free Full Text]
  19. Strotmann J.M., Janerot-Sjoberg B., Kimme P., Frohlich B., Voigt J.U., Schreckenberger A.B., et al. The effect of pacing-induced heart rate variation on longitudinal and circumferential regional myocardial function after acute beta-blockade—a cardiac ultrasound study. Eur J Echocardiogr (2000) 1:184–195.[Abstract/Free Full Text]
  20. Weidemann F., Jamal F., Kowalski M., Kukulski T., D'Hooge J., Bijnens B., et al. Can strain rate and strain quantify changes in regional systolic function during dobutamine infusion, B-blockade, and atrial pacing—implications for quantitative stress echocardiography. J Am Soc Echocardiogr (2002) 15:416–424.[CrossRef][Web of Science][Medline]
  21. Weidemann F., Jamal F., Sutherland G.R., Claus P., Kowalski M., Hatle L., et al. Myocardial function defined by strain rate and strain during alterations in inotropic states and heart rate. Am J Physiol Heart Circ Physiol (2002) 283:H792–H799.[Abstract/Free Full Text]
  22. Abraham T.A., Hasan F.M., Fenster P.E., Marcus F.I. Effect of intravenous metoprolol on reversible obstructive airways disease. Clin Pharmacol Ther (1981) 29:582–587.[Web of Science][Medline]
  23. Camm A.J., Ward D.E., Whitmarsh V.B. The acute electrophysiological effects of intravenous metoprolol. Clin Cardiol (1982) 5:327–331.[Web of Science][Medline]
  24. 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]
  25. Quinones M.A., Otto C.M., Stoddard M., Waggoner A., Zoghbi W.A. Recommendations for quantification of Doppler echocardiography: a report from the Doppler Quantification Task Force of the Nomenclature and Standards Committee of the American Society of Echocardiography. J Am Soc Echocardiogr (2002) 15:167–184.[CrossRef][Web of Science][Medline]
  26. Cain P., Napier S., Haluska B., Short L., Marwick T.H. Influence of left ventricular size and hemodynamics on the systolic longitudinal myocardial Doppler velocity response to stress. Am Heart J (2002) 143:169–175.[CrossRef][Web of Science][Medline]
  27. Pasquet A., Yamada E., Armstrong G., Beachler L., Marwick T.H. Influence of dobutamine or exercise stress on the results of pulsed-wave Doppler assessment of myocardial velocity. Am Heart J (1999) 138:753–758.[CrossRef][Web of Science][Medline]
  28. Pasquet A., Armstrong G., Beachler L., Lauer M.S., Marwick T.H. Use of segmental tissue Doppler velocity to quantitate exercise echocardiography. J Am Soc Echocardiogr (1999) 12:901–912.[CrossRef][Web of Science][Medline]
  29. Pasquet A., Armstrong G., Rimmerman C., Marwick T.H. Correlation of myocardial Doppler velocity response to exercise with independent evidence of myocardial ischemia by dual-isotope single-photon emission computed tomography. Am J Cardiol (2000) 85:536–542.[CrossRef][Web of Science][Medline]
  30. Katz W.E., Gulati V.K., Mahler C.M., Gorcsan J. 3rd. Quantitative evaluation of the segmental left ventricular response to dobutamine stress by tissue Doppler echocardiography. Am J Cardiol (1997) 79:1036–1042.[CrossRef][Web of Science][Medline]

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


This article has been cited by other articles:


Home page
 Eur J EchocardiogrHome page
P. Ballo, A. Bocelli, A. Motto, and S. Mondillo
Concordance between M-mode, pulsed Tissue Doppler, and colour Tissue Doppler in the assessment of mitral annulus systolic excursion in normal subjects
Eur J Echocardiogr, November 1, 2008; 9(6): 748 - 753.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Heart Circ. Physiol.Home page
M. Carlsson, M. Ugander, E. Heiberg, and H. Arheden
The quantitative relationship between longitudinal and radial function in left, right, and total heart pumping in humans
Am J Physiol Heart Circ Physiol, July 1, 2007; 293(1): H636 - H644.
[Abstract] [Full Text] [PDF]

This Article
Right arrow Abstract Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Quintana, M.
Right arrow Articles by Langanger, J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Quintana, M.
Right arrow Articles by Langanger, J.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?