Skip Navigation

European Journal of Heart Failure 2004 6(6):715-722; doi:10.1016/j.ejheart.2003.12.018
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 Fuchs, E.
Right arrow Articles by Hess, O. M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Fuchs, E.
Right arrow Articles by Hess, O. M.
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© 2004 European Society of Cardiology

Cardiac rotation and relaxation in patients with chronic heart failure

Esther Fuchs, Markus F. Müller, Helmut Oswald, Harriet Thöny, Paul Mohacsi and Otto M. Hess*

Swiss Cardiovascular Center and Institute of Diagnostic Radiology, Debis Systemhaus Health Care Services, University Hospital Freiburgstrasse, Bern CH-3010, Switzerland

* Corresponding author. Tel.: +41-31-632-96-53; fax: +41-31-632-47-71. E-mail address: otto.martin.hess{at}insel.ch


    Abstract
 Top
 Abstract
 1. Introduction
 2. MR myocardial tagging
 3. Methods
 4. Results
 5. Discussion
 References
 
Background: The normal left ventricle shows a systolic wringing motion with clockwise rotation at the base and counterclockwise rotation at the apex.

Purpose: The aim of the present study was (1) to assess left ventricular (LV) contraction and relaxation in patients with chronic heart failure (CHF), and (2) to evaluate the effect of medical therapy on LV contraction–relaxation behavior.

Methods: Magnetic resonance was used to examine LV motion by labeling specific LV regions in three planes (myocardial tagging). Twenty-three subjects were included, nine healthy controls and 14 CHF patients. Cardiac motion was determined from the deformation of a rectangular grid in a basal and apical plane. CHF patients were put on triple therapy with ACE-inhibitors, β-blockers and spironolactone. Follow-up examination (n=9) was performed after 6 months.

Results: In controls, systolic rotation was –9.5±2° at the base and +3.3±1° at the apex. In CHF patients, rotation was reduced both at the base (–3.4±2°, P<0.01) and the apex (+0.9±3°, P<0.05). Similarly, regional ejection fraction (REF) was reduced in CHF patients both at the base and the apex. Medical therapy was associated with an improvement in REF, but systolic rotation improved only at the base (–4.6±2°, P<0.05).

Conclusions: Systolic wringing motion with clockwise rotation at the base and counterclockwise rotation at the apex is maintained in CHF although reduced. Heart failure treatment is associated with an improvement in REF, whereas rotation improved only at the base, but not at the apex. Thus, there is an uncoupling between regional shortening and rotation in CHF patients.

Key Words: Abbreviations • CHF, chronic heart failure • LV, left ventricular • MR, magnetic resonance • C, controls • NS, not significant • ACE, angiotensin-converting enzyme

Received June 5, 2003; Revised September 13, 2003; Accepted December 23, 2003


    1. Introduction
 Top
 Abstract
 1. Introduction
 2. MR myocardial tagging
 3. Methods
 4. Results
 5. Discussion
 References
 
Cardiac three-dimensional-motion can be described by three components, i.e. radial displacement (=inward motion during systole and outward motion during diastole), rotation and translation of the left ventricle.

Early attempts to determine cardiac motion have been based on echodense or radiopaque intramyocardial markers [13] which may induce myocardial scarring and have an ill-defined position within the myocardium. These early invasive studies have shown a twisting motion of the left ventricle [46].

Myocardial tagging is a non-invasive technique based on magnetic resonance which allows to label specific myocardial regions with a rectangular or radial grid by spatial modulation of magnetization (SPAMM) [7,8]. These tags are fixed on the myocardium during systolic contraction and diastolic relaxation. The distortion of the grid with displacement of the grid-crossing points can be used for assessment of cardiac motion.

This technique has been used to assess cardiac three-dimensional-motion in normals and patients with LV hypertrophy. Alterations in three-dimensional-motion have been described in hypertrophic [9,10] and dilated cardiomyopathy [11], aortic stenosis [12,13], myocardial ischemia, and acute infarction [1423]. A prolonged systolic rotation with an enhanced torsional motion has been reported in patients with severe aortic stenosis. In these patients, a prolongation of diastolic untwisting was observed which was related to the occurrence of diastolic dysfunction [13].

However, only limited data are available on systolic contraction and diastolic relaxation in patients with CHF.

Thus, the purpose of our study was to assess systolic contraction and diastolic relaxation pattern in patients with chronic heart failure and to evaluate the effect of medical therapy on cardiac motion in these patients.


    2. MR myocardial tagging
 Top
 Abstract
 1. Introduction
 2. MR myocardial tagging
 3. Methods
 4. Results
 5. Discussion
 References
 
Labeling of specific myocardial regions can be achieved by SPAtial Modulation of Magnetization (SPAMM-technique) [7,8] using magnetic resonance imaging. This technique enables us to label specific myocardial regions in different views and projections with a rectangular grid (Fig. 1). A grid of magnetically altered lines is physically placed on the heart at end-diastole. From the distortion of the grid and the displacement of the grid-crossing points during systolic contraction and diastolic filling regional motion of the myocardium can be assessed in different projections or locations, e.g. basal, equatorial and apical short-axis plane.


Figure 1
View larger version (91K):
[in this window]
[in a new window]
[Download PowerPoint slide]
 
Fig. 1 End diastolic image (basal plane) in a normal volunteer (left) and a patient with CHF (right). The tagged image is overlaid with corresponding local trajectories (contraction–relaxation-loops). Arrows start at the beginning of systole (orange) and end in late diastole (green).

 

    3. Methods
 Top
 Abstract
 1. Introduction
 2. MR myocardial tagging
 3. Methods
 4. Results
 5. Discussion
 References
 
3.1. Patients
A total of 23 subjects were included in the present analysis: nine healthy volunteers (four females and five males, age 26±3, heart rate 72±11 bpm), and 14 patients with chronic heart failure (four females and 10 males, age 53±9, heart rate 67±9 bpm). Contraindications involved severe shortness of breath, implanted pacemakers or defibrillators, claustrophobia, decompensation or tachycardia (heart rate >100 bpm). Of the 14 CHF-patients, three had a history of prior myocardial infarction and one had a history of angina pectoris (Table 1). One of the three patients with myocardial infarction had no follow-up examination (drop out). In the remaining two cases, both infarcts could not be localized in the ECG. One was treated by thrombolysis (no intervention) and the other one received medical therapy. The other 11 patients had either hypertensive heart disease or dilated cardiomyopathy. Nine CHF-patients had to be hospitalized because of severe dyspnea, while seven of the nine patients suffered from pulmonary edema. At clinical examination, six had a positive hepato-jugular reflux and three peripheral edema at the time of hospitalization. In the ECG, 12 of the 14 patients showed arrhythmias at a certain time, seven patients had ventricular extrasystoles, four patients showed non-sustained ventricular tachycardias, and four intermittent atrial fibrillation. At the time of examination, all patients were in sinus rhythm. Patients with left bundle-branch block were excluded from the present study, but in two cases, there was a right bundle-branch block. Echocardiographically, ejection fraction was 26±8% and LV end-diastolic chamber diameter (LVEDD) was 74±13 mm (norm ≤56 mm).


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

 
Table 1 Patient characteristics

 
Nine CHF-patients underwent follow-up examination after 6 months under triple therapy with ACE-inhibitors, betablockers and spironolactone (Table 2) [2426]. Follow-up examination was not possible in all 14 CHF patients either due to transplantation (n=1), defibrillator implantation (n=1), claustrophobia (n=1), premature sudden death (n=1) or non-compliance (n=1).


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

 
Table 2 Medication

 
3.2. Image acquisition
The study was approved by the local ethics committee, within a framework for clinical studies involving MRI examinations. Written informed consent was obtained from all participants. MRI was performed on a 1.5-T whole-body imaging system (Vision, Siemens Medical Systems, Erlangen, Germany). A circularly polarized body coil was used with the subject in supine position. Three ECG leads were attached to the anterior chest wall over the heart. Cardiac motion was determined in the short axis plane of the left ventricle at the base (1 cm below the mitral valve), equatorial (middistance between the basal and apical plane), and apical (1 cm above the apical endocardium). The pulse sequence was an R-wave-triggered, segmented (9 lines/segment with echo sharing) gradient echo (fast low angle shot) cine sequence with grid tagging to visualize regional and global wall motion alterations. The grid lines were 1–2-mm thick, 8 mm spaced and applied during the first 13 ms following the R-wave. They were oriented at a 45° angle relative to the imaging plane. A total number of 13–19 images were acquired at each position starting at end-diastole of the first and ending at late-diastole of the next cycle. Temporal resolution was 35–45 ms. Since small variations in heart rate occurred during acquisition, a safety margin had to be included at the end of diastole, and thus, not the total numbers of images for a given RR-interval could be recorded. Scan parameters were TR/TE=90 ms/4.0 ms, flip angle=15°. An acquisition matrix of 128x256 data points and a rectangular field of view, typically 320 mm, was used giving a spatial resolution of 1.9x1.25x8 mm. Number of acquisitions was 1. The acquisition time was 15–20 s per section depending on the heart rate on the subject.

3.3. Image analysis
The intersection points of the tagging lines were marked and tracked from end-diastole to late diastole of the following cardiac cycle. Midmyocardial points (n=6) were calculated for each heart phase, resulting in trajectories, which are visualized in Fig. 1. Cardiac rotation was assessed from the rotation of these points with respect to their initial position using an intraventricular reference point from the crossing points of the end-diastolic reference lines (Fig. 1). Rotating angles were averaged for each short axis plane. End-diastole was defined as the first image after the R-wave, end-systole as the image with the smallest cavity volume. Isovolumic contraction was considered to occur within the first two frames after end-diastole (80–90 ms duration). Clockwise rotation or negative angle change, and counterclockwise rotation or positive angle change, were defined as viewed from the apex. LV shortening was calculated from the difference of the end-diastolic and end-systolic diameter divided by the end-diastolic diameter multiplied by 100 (%). Regional ejection fraction was determined from the difference of end-diastolic and end-systolic LV area divided by the end-diastolic area multiplied by 100 (%). Both shortening and regional ejection fraction were assessed at the base and the apex.

Intra- and inter-observer variability were calculated in nine controls as the difference between the two observations divided by the mean and expressed as percentage. For cardiac rotation we calculated 4% for intra-observer and 6% for inter-observer variability.

3.4. Calculations

  1. Systolic rotation (°) was defined as systolic circular motion of a given region with respect to the intraventricular reference point (Fig. 1). Clockwise rotation was described as negative and counterclockwise rotation as positive values.
  2. Diastolic untwisting (°) was defined as the diastolic circular motion component of a given region with respect to the intraventricular reference point.
  3. Systolic shortening (%) was defined as the change in length of the distance between two myocardial regions (defined by two grid-crossing points) during systolic contraction.
  4. Regional ejection fraction (%) was defined as the change in end-diastolic and end-systolic area of the left ventricle during systolic contraction.

3.5. Statistical analysis
All values are given as mean±S.D. Comparison between the two groups (controls vs. CHF patients) are performed with a Mann–Whitney rank sum test and between CHF patients at baseline and 6 month follow-up with a Wilcoxon signed rank test. These tests have been used because of the small patient number (no assumption of normal distribution). Boxplots (median, first and third quartiles and max./min. values) are used for representation of cardiac rotation and shortening data. A value of P<0.05 is considered to be statistically significant.


    4. Results
 Top
 Abstract
 1. Introduction
 2. MR myocardial tagging
 3. Methods
 4. Results
 5. Discussion
 References
 
Original recordings of a control patient and a patient with chronic heart failure are shown in Fig. 1. Tagged images at end-diastole are depicted with the motion of six midmyocardial regions during systolic contraction and diastolic lengthening. The rotational motion is given by arrows indicating the direction of rotation. The patient with CHF shows clearly a reduced contraction–relaxation pattern.

4.1. Left ventricular motion in control subjects
When viewed from the apex, the normal left ventricle performs a systolic wringing motion with a clockwise rotation at the base and a counterclockwise rotation at the apex (Figs. 2 and 3). Systolic rotation can be divided into two components: At the base, there is a counterrotation of +6.7±2° during isovolumic contraction, visible in the first two images (45 ms; 90 ms), followed by a clockwise rotation of –9.5±2° (Fig. 2).


Figure 2
View larger version (12K):
[in this window]
[in a new window]
[Download PowerPoint slide]
 
Fig. 2 Systolic and diastolic rotation (basal plane) in controls (C; black boxes), and patients with CHF at baseline (hatched boxes) and at 6 months follow-up (open boxes). There is a short counterclockwise rotation during isovolumic contraction followed by a clockwise rotation during systolic contraction and counterclockwise rotation during diastole. In CHF patients, systolic rotation is reduced compared to controls, but not during diastole. BL=baseline, FU=follow-up.

 


Figure 3
View larger version (11K):
[in this window]
[in a new window]
[Download PowerPoint slide]
 
Fig. 3 Systolic and diastolic rotation (apical plane) in controls (C; black boxes), and in patients with CHF at baseline (hatched boxes) and at 6 months follow-up (open boxes). There is a counterclockwise rotation during isovolumic contraction as in the basal plane followed by a further counterclockwise rotation during systolic contraction and clockwise rotation during diastole. In CHF patients, systolic and diastolic rotation is reduced. BL=baseline, FU=follow-up.

 
The apex is first rotating +9.1±4° in counterclockwise direction during isovolumic contraction and then followed by a rotation of +3.3±1° until the smallest cavity lumen is reached at end-systole (Fig. 3). Systolic rotation mainly occurs during isovolumic contraction with minimal cardiac rotation during ejection (Fig. 4).


Figure 4
View larger version (11K):
[in this window]
[in a new window]
[Download PowerPoint slide]
 
Fig. 4 LV rotation during systole and diastole in controls (hatched line) and patients with CHF (solid line). The rotation pattern is similar in both groups but reduced in CHF patients. There is a rapid counterclockwise (CCW) rotation during isovolumic contraction in both controls and CHF patients, which is followed by a clockwise (CW) rotation at the base and a slight counterclockwise rotation at the apex. Untwisting occurs during isovolumic relaxation followed by diastolic backrotation, counterclockwise at the base and clockwise at the apex. ED=end-diastole, AVO=aortic valve opening, ES=end-systole, MVO=mitral valve opening.

 
An ‘untwisting’ motion can be observed during isovolumic relaxation [5,9] which precedes diastolic filling (Fig. 4). Diastolic relaxation results in a counterclockwise rotation of +3±3° at the base and clockwise rotation of –12.4±4° at the apex (Figs. 2 and 3).

Systolic shortening was 24±5% at the base and 29±8% at the apex (Fig. 5).


Figure 5
View larger version (11K):
[in this window]
[in a new window]
[Download PowerPoint slide]
 
Fig. 5 Systolic shortening in controls (C), CHF patients at baseline (BL) and during follow-up (FU). Systolic shortening (%) is significantly reduced in CHF patients when compared to controls, and improves in CHF during 6 months follow-up only at the apex.

 
4.2. Left ventricular motion in CHF patients
In CHF patients, both systolic components of LV rotation are significantly reduced at the base, namely +2.9±2° (counterclockwise) (P<0.01 vs. C) during isovolumic contraction and –3.4±2° (clockwise) (P<0.001 vs. C) during systolic ejection.

After 6 months of medical treatment, rotation at the base was +2.2±1° (NS) during isovolumic contraction and –4.6±2° (P<0.05 vs. CHF baseline) during systolic ejection, respectively.

Diastolic rotation at the base was +0.7±2° (NS vs. C), and increased to +2.4±2° (P<0.01 vs. CHF baseline) after 6 months of treatment (Fig. 2).

Both components of systolic rotation were reduced at the apex, namely +3.5±2° (P<0.01 vs. C) during isovolumic contraction and +0.9±3° (P<0.05 vs. C) during systolic ejection.

After 6 months of therapy, cardiac rotation at the apex was +4.1±2° (NS) during isovolumic contraction and +1.7±2° (NS) during systolic ejection.

Diastolic relaxation at the apex was significantly reduced to –4.8±4° (P<0.01 vs. C), and did not change (–5.8±4°) after 6 months of therapy (Fig. 3).

Systolic shortening (Fig. 5) was significantly reduced in CHF patients at the base (9±3%; P<0.001 vs. C) as well as at the apex (9±4%; P<0.001 vs. C).

After 6 months of treatment, systolic shortening changed not significantly at the base (11±4%; P=0.08 vs. CHF baseline) but improved significantly at the apex (13±4%; P<0.05 vs. CHF baseline).

Regional ejection fraction was significantly diminished in CHF patients at the base and the apex (Table 3) when compared to controls. During follow-up, regional ejection fraction improved significantly both at the base and the apex by approximately 30–40%.


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

 
Table 3 Hemodynamics

 

    5. Discussion
 Top
 Abstract
 1. Introduction
 2. MR myocardial tagging
 3. Methods
 4. Results
 5. Discussion
 References
 
Characterization of LV dysfunction in chronic heart failure has mainly been based on clinical examination, i.e. forward output failure with cerebral hypoperfusion, exercise intolerance and fatigue, diastolic backward failure with pulmonary congestion, hepatomegaly and peripheral edema. New diagnostic techniques such as two-dimensional or Doppler echocardiography allow to differentiate between systolic contraction and diastolic filling abnormalities. However, determination of three-dimensional-motion—we calculated two-dimensional-motion in three planes—can be achieved only with the use of new imaging techniques such as myocardial tagging based on magnetic resonance imaging [2729]. This method allows to determine systolic shortening and diastolic lengthening, as well as cardiac rotation and translation. From the motion of the tagged myocardium, true cardiac motion can be determined which is not possible with other tomographic methods such as two-dimensional echocardiography or computer tomography.

From the present study, the following conclusions can be drawn:

  1. The normal left ventricle performs a systolic wringing motion with clockwise rotation at the base and counterclockwise rotation at the apex, which is maintained although reduced in CHF patients.
  2. Heart failure treatment with triple therapy leads to an improvement in systolic rotation at the base, whereas shortening improved only at the apex.
  3. There is an uncoupling of systolic shortening and rotation between base and apex in CHF patients.

5.1. Pathophysiology of cardiac motion in CHF patients
LV systolic dysfunction is the major cause of heart failure and is associated with a reduction in myocardial contractility and an increase in pre- and afterload [30]. Neurohumeral adaptation leads to an increase in heart rate with elevated oxygen consumption contributing to subendocardial ischemia and an enhanced risk of cardiac arrhythmias.

LV diastolic dysfunction is mainly seen in elderly patients with hypertensive heart disease and maintained LV pump function. In the present study, all patients had LV systolic dysfunction with reduced ejection fraction, mean 26±8% (normal >57%). Not only systolic but also diastolic function was abnormal in our patients with a reduced lengthening rate and a diminished diastolic rotation (Fig. 3). In patients with advanced heart failure, a reduction in both, systolic and diastolic function is common and often represents the end-stage of either dilated or ischemic cardiomyopathy. Brutsaert et al. [31] proposed a three phase model of heart failure with an initial phase of systolic compensation, followed by diastolic dysfunction and a late phase of systolic and diastolic dysfunction. This classification suggests that our patients are in phase III, when systolic and diastolic dysfunction are present. Myocardial tagging allows differentiation between these two disorders. Not only systolic and diastolic dysfunction can be differentiated, but also regional differences, such as seen in pressure overload hypertrophy [12], myocardial infarction [19] or chronic heart failure. Follow-up examinations with myocardial tagging allow to document changes in the different motion components rendering myocardial tagging as a useful tool for assessing ventricular function in heart failure.

In previous studies, regional heterogeneity of LV rotation was reported [11]. The present study showed a rather large heterogeneity between different CHF-patients. However, rotation was best preserved at the lateral portion of the left ventricle, as reported previously [11].

5.2. Limitations
Following limitations have to be considered as potential shortcomings of the present study:

  1. Breath-holds of up to 20 s are difficult in patients with chronic heart failure and was one of the exclusion criteria.
  2. Quantification of grid-motion may be limited in patients with insufficient cooperation or motion artifacts. Temporal resolution varied between 35 and 45 ms depending on heart rate and may be a limiting factor for assessing rapid changes, such as during isovolumic contraction and relaxation. Since grid-contrast was usually excellent during the first images in cardiac cycle, it deteriorated during late systole and early diastole, rendering isovolumic relaxation and filling more difficult to evaluate.
  3. CHF patients were on triple therapy with ACE-inhibitors, β-blockers and diuretics. Triple therapy was optimized during follow-up by titrating β-blockers and ACE-inhibitors up and reducing diuretics. As a result, heart rate decreased during follow-up by approximately 10% (Table 3).
  4. The comparison between normals (=controls) and CHF patients from different age groups may be problematic with regard to age-dependent changes in systolic and diastolic function [32]. However, changes in LV function are minimal up to 50 or 60 years of age, and thus, age-effects within the study can be expected to be of minor importance [33]. At least, blood pressure and heart rate were similar in the two groups (Table 3). Decompensated patients or those with tachycardia (heart rates >100 bpm) were excluded from the study for technical reasons.
  5. Study population is rather small, but the high reproducibility of cardiac MR, also demonstrated in patients with heart failure [34,35], results in a considerable reduction in sample size, when compared with echocardiography. According to Bellenger et al. [34] a 10-ml difference in EDV and ESV, and a 10-g difference in mass, with a power of 90% and a P-value of 0.05, only 12, 10 and nine patients, respectively, would be needed for each of these parameters by cardiac MR vs. 97, 53, 190 patients by two-dimensional echocardiography [34,35].


    References
 Top
 Abstract
 1. Introduction
 2. MR myocardial tagging
 3. Methods
 4. Results
 5. Discussion
 References
 

  1. Carlsson E., Milne E.N. Permanent implantation of endocardial tantalum screws: a new technique for functional studies of the heart in the experimental animal. J Can Assoc Radiol (1967) 18:304–309.[Medline]
  2. Ingels N.B., Daughters G.T., Stinson E.B., Alderman E.L. Measurement of midwall myocardial dynamics in intact man by radiography of surgically implanted markers. Circulation (1975) 52:859–867.[Abstract/Free Full Text]
  3. Myers J.H., Stirling M.C., Choy M., Buda A.J., Gallgher K.P. Direct measurement of inner and outer wall thickening dynamics with epicardial echocardiography. Circulation (1986) 74:164–172.[Abstract/Free Full Text]
  4. Arts T., Meerbaum S., Reneman R.S., Corday E. Torsion of the left ventricle during the ejection phase in the intact dog. Cardiovasc Res (1984) 18:183–193.[Abstract/Free Full Text]
  5. Beyar R., Yin F.C., Hausknecht M., Weisfeldt M.L., Kass D.A. Dependence of left ventricular twist-radial shortening relations on cardiac cycle phase. Am J Physiol (1989) 257:H1119–H1126.[Web of Science][Medline]
  6. Hansen D.E., Daughters Gd., Alderman E.L., Ingels N.J., Miller D.C. Torsional deformation of the left ventricular midwall in human hearts with intramyocardial markers: regional heterogeneity and sensitivity to the inotropic effects of abrupt rate changes. Circ Res (1988) 62:941–952.[Abstract/Free Full Text]
  7. Young A.A., Imai H., Chang C.N., Axel L. Two-dimensional left ventricular deformation during systole using magnetic resonance imaging with spatial modulation of magnetization. Circulation (1994) 89:740–752.[Abstract/Free Full Text]
  8. Park J., Metaxas D., Axel. Analysis of left ventricular motion based on volumetric deformable models and MRI-SPAMM. Med Image Anal (1996) 1:53–71.[CrossRef][Medline]
  9. Maier S.E., Fischer S.E., McKinnon G.C., Hess O.M., Krayenbuehl H.P., Boesiger P. Evaluation of left ventricular segmental motion in hypertrophic cardiomyopathy with myocardial tagging. Circulation (1992) 86:1919–1928.[Abstract/Free Full Text]
  10. Young A.A., Kramer C.M., Ferrari V.A., Axel L., Reichek N. Three-dimensional left ventricular deformation in hypertrophic cardiomyopathy. Circulation (1994) 90:854–867.[Abstract/Free Full Text]
  11. Young A.A., Dokos S., Powell K.A., et al. Regional heterogeneity of function in non-ischemic dilated cardiomyopathy. Cardiovasc Res (2001) 49:308–318.[Abstract/Free Full Text]
  12. Stuber M., Scheidegger M.B., Fischer S.E., et al. Alterations in the local myocardial motion pattern in patients suffering from pressure overload due to aortic stenosis. Circulation (1999) 100:361–368.[Abstract/Free Full Text]
  13. Nagel E., Stuber M., Burkhard B., et al. Cardiac rotation and relaxation in patients with aortic valve stenosis. Eur Heart J (2000) 21:582–589.[Abstract/Free Full Text]
  14. Knudtson M., Galbraith P., Hildebrand K., Tyberg J., Beyar R. Dynamics of left ventricular apex rotation during angioplasty: a sensitive index of ischemic dysfunction. Circulation (1997) 96:801–808.[Abstract/Free Full Text]
  15. Buchalter M.B., Rademakers F.E., Weiss J.L., Rogers W.J., Weisfeldt M.L., Shapiro E.P. Rotational deformation of the canine left ventricle measured by magnetic resonance tagging: effects of catecholamines, ischaemia, and pacing. Cardiovasc Res (1994) 28:629–635.[Abstract/Free Full Text]
  16. Kroeker C.A., Tyberg J.V., Beyar R. Effects of ischemia on left ventricular apex rotation. An experimental study in anesthetized dogs. Circulation (1995) 92(12):3539–3548.[Abstract/Free Full Text]
  17. Lima J.A., Ferrar V.A., Reichek N., et al. Segmental motion and deformation of transmurally infarcted myocardium in acute postinfarct period. Am J Physiol (1995) 268:H1304–H1312.[Web of Science][Medline]
  18. Nagel E., Stuber M., Matter C., Lakatos M., Boesiger P., Hess O.M. Rotational and translational motion post myocardial infarction. J Cardiovasc Pharmacol (1996) 28:31–35.
  19. Nagel E., Stuber M., Lakatos M., Scheidegger M.B., Boesiger P., Hess O.M. Cardiac rotation and relaxation after anterolateral myocardial infarction. Coron Artery Dis (2000) 11:261–267.[CrossRef][Web of Science][Medline]
  20. Kramer C.M., Rogers W.J., Theobald T.M., Power R.P., Petruolo S., Reichek N. Remote non-infarcted region dysfunction soon after first anterior myocardial infarction. Circulation (1996) 94:660–666.[Abstract/Free Full Text]
  21. Marcus J.T., Gotte M.J., van Rossum A.C., et al. Myocardial function in infarcted and remote regions early after infarction in man: assessment by magnetic resonance tagging and strain analysis. Magn Reson Med (1997) 38:803–810.[Web of Science][Medline]
  22. Kramer C.M., Ferrari V.A., Rogers W.J., et al. Angiotensin-converting enzyme inhibition limits dysfunction in adjacent non-infarcted regions during left ventricular remodeling. J Am Coll Cardiol (1996) 27(1):211–217.[Abstract]
  23. Geskin G., Kramer C.M., Rogers W.J., et al. Quantitative assessment of myocardial viability after infarction by dobutamine magnetic resonance tagging. Circulation (1998) 98:217–223.[Abstract/Free Full Text]
  24. Packer M. Current role of beta-adrenergic blockers in the management of chronic heart failure. Am J Med (2001) 110(Suppl_7A):81S–94.[Medline]
  25. Eichhorn E.J., Bristow M.R. Medical therapy can improve the biological properties of the chronically failing heart. A new era of treatment of heart failure. Circulation (1996) 94:2285–2296.[Abstract/Free Full Text]
  26. Cleland J.G., Dewhurst N.G., Murphy R.L., Struijker Boudier H.A., Tan L.B., Visser C.A. The concept of cardioreparation: Part 2. Medical implications of cardioreparation. J Cardiovasc Risk (1996) 3:287–293.[CrossRef][Medline]
  27. Rajappan K., Bellenger N.G., Anderson L., Pennell D.J. The role of cardiovascular magnetic resonance in heart failure. Eur J Heart Fail (2000) 2:241–252.[Abstract/Free Full Text]
  28. Moore C.C., Lugo-Olivieri C.H., McVeigh E.R., Zerhouni E.A. Three-dimensional systolic strain patterns in the normal human left ventricle: characterization with tagged MR imaging. Radiology (2000) 214:453–466.[Abstract/Free Full Text]
  29. Reichek N. MRI myocardial tagging. J Magn Reson Imaging (1999) 10:609–616.[CrossRef][Web of Science][Medline]
  30. de Tombe P.P. Altered contractile function in heart failure. Cardiovasc Res (1998) 37:367–380.[Abstract/Free Full Text]
  31. Brutsaert D.L., Sys S.U., Gillebert T.C. Diastolic Failure: pathophysiology and therapeutic implications. J Am Coll Cardiol (1993) 22:318–325.[Abstract]
  32. Hughes C.V., Wong M., Johnson G., Cohn J.N. Influence of age on mechanisms and prognosis of heart failure. The V-HeFT VA Cooperative Studies Group. Circulation (1993) 87:VI111, VI117.
  33. Fleg J.L., O'Connor F., Gerstenblith G., et al. Impact of age on the cardiovascular response to dynamic upright exercise in healthy men and women. J. Appl. Physiol (1995) 78:890–900.[Abstract/Free Full Text]
  34. Bellenger N.G., Davies L.C., Francis J.M., Coats A.J., Pennell D.J. Reduction in sample size for studies of remodeling in heart failure by the use of cardiovascular magnetic resonance. J Cardiovasc Magn Reson (2000) 2(4):271–278.[Web of Science][Medline]
  35. Grothues F., Smith G.C., Moon J.C., et al. Comparison of interstudy reproducibility of cardiovascular magnetic resonance with two-dimensional echocardiography in normal subjects and in patient with heart failure or left ventricular hypertrophy. Am J Cardiol (1 July 2002) 90(1):29–34.[CrossRef]

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
J Am Coll CardiolHome page
M. Bertini, N. A. Marsan, V. Delgado, R. J. van Bommel, G. Nucifora, C. J. W. Borleffs, G. Boriani, M. Biffi, E. R. Holman, E. E. van der Wall, et al.
Effects of cardiac resynchronization therapy on left ventricular twist.
J. Am. Coll. Cardiol., September 29, 2009; 54(14): 1317 - 1325.
[Abstract] [Full Text] [PDF]


Home page
Circ Arrhythm ElectrophysiolHome page
V. Delgado, L. F. Tops, S. A. Trines, K. Zeppenfeld, N. Ajmone Marsan, M. Bertini, E. R. Holman, M. J. Schalij, and J. J. Bax
Acute Effects of Right Ventricular Apical Pacing on Left Ventricular Synchrony and Mechanics
Circ Arrhythm Electrophysiol, April 1, 2009; 2(2): 135 - 145.
[Abstract] [Full Text] [PDF]


Home page
CirculationHome page
J. Wang and S. F. Nagueh
Current Perspectives on Cardiac Function in Patients With Diastolic Heart Failure
Circulation, March 3, 2009; 119(8): 1146 - 1157.
[Full Text] [PDF]


Home page
Eur J EchocardiogrHome page
S. F. Nagueh, C. P. Appleton, T. C. Gillebert, P. N. Marino, J. K. Oh, O. A. Smiseth, A. D. Waggoner, F. A. Flachskampf, P. A. Pellikka, and A. Evangelisa
Recommendations for the Evaluation of Left Ventricular Diastolic Function by Echocardiography
Eur J Echocardiogr, March 1, 2009; 10(2): 165 - 193.
[Full Text] [PDF]


Home page
J. Appl. Physiol.Home page
B. T. Esch and D. E. R. Warburton
Left ventricular torsion and recoil: implications for exercise performance and cardiovascular disease
J Appl Physiol, February 1, 2009; 106(2): 362 - 369.
[Abstract] [Full Text] [PDF]


Home page
RadiologyHome page
P. G. Masci, S. Dymarkowski, F. E. Rademakers, and J. Bogaert
Determination of Regional Ejection Fraction in Patients with Myocardial Infarction by Using Merged Late Gadolinium Enhancement and Cine MR: Feasibility Study
Radiology, January 1, 2009; 250(1): 50 - 60.
[Abstract] [Full Text] [PDF]


Home page
HeartHome page
A T Burns, I G McDonald, J D Thomas, A MacIsaac, and D Prior
Doin' the twist: new tools for an old concept of myocardial function
Heart, August 1, 2008; 94(8): 978 - 983.
[Abstract] [Full Text] [PDF]


Home page
J Am Coll CardiolHome page
J. N. Kirkpatrick, M. A. Vannan, J. Narula, and R. M. Lang
Echocardiography in Heart Failure: Applications, Utility, and New Horizons
J. Am. Coll. Cardiol., July 31, 2007; 50(5): 381 - 396.
[Abstract] [Full Text] [PDF]


Home page
CirculationHome page
T. Helle-Valle, J. Crosby, T. Edvardsen, E. Lyseggen, B. H. Amundsen, H.-J. Smith, B. D. Rosen, J. A.C. Lima, H. Torp, H. Ihlen, et al.
New Noninvasive Method for Assessment of Left Ventricular Rotation: Speckle Tracking Echocardiography
Circulation, November 15, 2005; 112(20): 3149 - 3156.
[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 Fuchs, E.
Right arrow Articles by Hess, O. M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Fuchs, E.
Right arrow Articles by Hess, O. M.
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?