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European Journal of Echocardiography 2007 8(5):352-359; doi:10.1016/j.euje.2006.07.006
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Copyright © 2006, The European Society of Cardiology

Post-systolic motion in patients with heart failure – A marker of left ventricular dyssynchrony?

Margareta Ringb,*, Hans Perssona, Märit Mejhertc and Magnus Ednera

aDepartment of Clinical Sciences, Division of Internal Medicine, Karolinska Institutet Danderyd Hospital, Stockholm, Sweden
bSection of Clinical Physiology N2:01, Department of Molecular Medicine and Surgery, Karolinska Institutet, Karolinska University Hospital, Solna, Stockholm, Sweden
cDivision of Internal Medicicine, Ersta Hospital, Stockholm, Sweden

Received 18 April 2006; received in revised form 7 July 2006; accepted after revision 15 July 2006.

margareta.ring{at}karolinska.se

* Corresponding author. Tel.: +46 8 5177 4427; fax: +46 8 5177 3800.


   Abstract
Top
 Abstract
Introduction
 Methods
 Results
 Discussion
 References
 
Aims The pathophysiology of post- systolic motion (PSM) is not yet fully resolved. Our aim was to study PSM in patients with heart failure (HF) and its relation to left ventricular (LV) function, brain natriuretic peptide (BNP) and to mortality.

Method and results Forty- seven HF patients, mean-age 75±8years with LV ejection fraction (EF) 31±11% were studied prospectively and compared with 10 age-matched healthy controls. Doppler Tissue Imaging data were obtained in the basal 4-chamber segments of the septal wall and PSM were measured as the ratio between velocity time integral (vti) of the positive post-systolic and systolic motion. Mean septal wall PSM was increased 0.52±0.41 vs controls 0.05±0.07 (p<0.001) and abnormal PSM (>0.18) was detected in 79% of all HF patients (92% if QRS >130ms).

Septal wall PSM correlated with QRS-duration, LV volume indices, myocardial isovolumic relaxation time (IVRTm) and inversely with heart rate and diastolic blood pressure, but not with BNP levels or LVEF. Only IVRTm correlated independently with the PSM (R2=0.55, p<0.001). Seventeen patients died during a mean follow-up time of 30±18months. The PSM value was similar in non-survivors and survivors, 0.53±0.45 vs 0.52±0.45 (ns).

Conclusions PSM is a common phenomenon in patients with HF especially in patients with wide QRS and long IVRTm suggesting that PSM is a manifestation of LV intra-ventricular dyssynchrony. In this study PSM did not predict mortality.

Keywords: Heart failure; Post-systolic motion; Doppler tissue imaging

Abbreviations: LBBB, left bundle branch block • RBBB, right bundle branch block • LAH, left bundle anterolateral hemi block • ACE, angiotensin converting enzyme • E/E', early E transmitral maximal blood flow velocity/mitral e-wave measured by DTI • QRS, time of QRS duration, ms, on the electrocardiogram • PQ, time of PQ duration, ms, on the electrocardiogram • LVEDV, left ventricle end diastolic volume • LVESV, left ventricle end systolic volume • BSA, body surface area • BMI, body mass index • LVEDVi, • LVEDV/BSA, • LVESVi, • LVESV/BSA, • CRT, cardiac resynchronization therapy


   Introduction
Top
 Abstract
 Introduction
Methods
 Results
 Discussion
 References
 
Heart failure is the most common diagnoses in departments of Internal medicine and is associated with high morbidity, mortality and health care expenditure.1–3 Modern medical therapy with angiotensin converting enzyme-inhibitors, beta-blockers, aldosteron-antagonists and angiotensin receptor-antagonists reduce morbidity and mortality,4–9 still the prevalence of heart failure is increasing, partly due to an ageing population.

Echocardiography is an important tool for evaluation of heart failure aetiology, for measurement of the left ventricular volumes and function and as a guidance of therapy.

Doppler Tissue Imaging (DTI) is an echocardiographic technique most often used for studies of regional diastolic and systolic myocardial function.10,11 Also, DTI has turned out to be a suitable technique for studying left ventricular (LV) dyssynchrony in patients with advanced HF requiring cardiac resynchronisation therapy (CRT) and also for predicting response to such therapy.12–15 A post-systolic motion (PSM) occurring after normal contraction and during a prolonged isovolumic relaxation time (IVRT) has been described in coronary heart disease16,17 and in LV hypertrophy with normal pump function.18 In healthy subjects, it was found in approximately one-third of myocardial segments but it occurred significantly more often, approximately in 80% and with a greater magnitude, in patients with chronic ischemic heart disease or acute myocardial infarction.19 It has been suggested that PSM is either an active phenomenon or a passive motion due to wall dyskinesia.20 PSM has been described in left bundle branch block (LBBB) and might be a sign of myocardial wall dyssynchrony.21

The pathophysiology of post- systolic motion (PSM) is not yet fully resolved. Our aim was to study PSM in patients with heart failure and its relation to LV function, brain natriuretic peptide (BNP) and to mortality.


   Methods
Top
 Abstract
 Introduction
 Methods
Results
 Discussion
 References
 
Study population
The study involved 47 patients participating in the OPTIMAL study (optimising congestive heart failure outpatient clinic project) in which 208 patients were included.22

The inclusion criterias were patients hospitalized with congestive heart failure, New York Heart Association functional class (NYHA class) II–IV, left ventricular systolic dysfunction by echocardiography and age ≥60years. Exclusion criterias were acute myocardial infarction or unstable angina within the last three months, valvular stenosis, dementia, severe concomitant disease or unwillingness to participate. The additional inclusion criteria for this substudy were sinus rhythm with a complete echocardiogram including DTI. Sixty-four percent of the patients were men, mean-age 75±8years for all patients. Demographic data are presented in Tables 1 and 2Go. A control group including ten age-matched healthy subjects with normal ECG and a normal echocardiography was compared with the study group. None of the controls had a history of previous or current cardiovascular disease or were on medication. All healthy subjects had a normal physical examination. PQ and QRS duration time were analysed from a 12-lead ECG (Megacart, Siemens-Elema AB) in conjunction with the echocardiography examination.


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  		Table 1 Demographic data

 


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  		Table 2 Clinical, echocardiographic and electrocardiographic characteristics

 
The study was approved by the Committee of Ethics, Karolinska Institutet. All subjects gave informed consent to participate.

Conventional echocardiography
All examinations were performed with an Acuson 128 XP/10 (Mountain View, CA, U.S.A.) with a 2.5–4.0MHz probe. The recordings were performed from parasternal long axis, (PLAX) and apical four chamber position with the subjects in the left semilateral position. All recordings were stored on videotapes and analysed at the end of the study. Left ventricular dimensions in systole and diastole were measured by the M-mode technique in PLAX. Early (E) and atrial (A) transmitral maximal flow velocities and E-deceleration time were measured by conventional Pulsed Wave (PW) doppler flow, placing the 3mm sampling volume between the tips of the open mitral leaflets in apical four chamber view. Isovolumic relaxation time (IVRT) was obtained by placing the sampling volume between left ventricular outflow tract and mitral leaflets. The LV volume and the ejection fraction were calculated according to the recommendations of the American Society of Echocardiography.23 Biplane volumes were calculated from area tracings using the disc summation method (modified Simpson's rule) using dedicated computer equipment and software (TomTec Imaging Systems Inc., CO, U.S.A.)

Doppler tissue imaging
DTI was performed with PW doppler in apical four-chamber view. The sampling volume of 4mm was placed in the basal septal and lateral wall, 5–10mm below and on the apical side of the mitral annulus, with the sampling volume placed in the LV myocardium during systole. We measured maximal velocities (max vel), duration time (dur) and velocity time integral (vti) in systolic myocardial motion (S2) and post-systolic motion (S3). The relative size of PSM was defined as the ratio of S3 vti/S2 vti. Isovolumic relaxation time (IVRTm) is the time interval, including both the positive and the negative wave, occurring between the end of S2 and the onset of early diastolic myocardial wall motion (E'), Fig 1. The Isovolumic contraction time (IVCTm) is from end of late diastolic myocardial wall motion to the onset of S2, Fig 1. The E/E' was calculated as an estimate of filling pressure, as it corrects for the influence of left atrial pressure and LV relaxation rate on transmitral E velocity.24


Figure 1
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  		Figure 1 Doppler tissue imaging in a healthy subject (left) and in a heart failure patient (right). The systolic contraction (S2) has a shorter duration time and the velocity is decreased in the HF patient. A post systolic motion (S3) appears in the HF patient and IVCTm and IVRTm are prolonged. See abbreviations for list of explanations.

 
Mean values were calculated from three to five RR intervals.

Brain natriuretic peptide
Blood samples for neurohormone measurements were drawn after 30min of supine rest, immediately centrifuged at +4°C and plasma was thereafter frozen at –70°C until analyses. Brain natriuretic peptide (BNP) was measured by immunoradiometric assay.25 (Shionoria Cis Bio International, Osaka, Japan).

Mortality
Cause of mortality was determined from death certificates.

Statistical analysis
All values are given as mean±SD unless otherwise stated. Group differences were analysed by Student's t-test and chi-square test for differences of proportion. Pearson correlation coefficient was performed to determine linear relationships. A multiple stepwise regression analysis was used to determine the most powerful determinants for PSM. All factors with a univariate correlation p<0.05 to PSM were entered in the multivariate analysis using a forward stepwise selection procedure.

A probability of <0.05 was considered statistically significant. Statistica 6.0 (StatSoft Inc, Tulsa, USA) was used for the statistical analysis.


   Results
Top
 Abstract
 Introduction
 Methods
 Results
Discussion
 References
 
Echocardiography, electrocardiography and BNP
Clinical and echocardiographic characteristics in HF patients and controls are given in Table 2. In HF patients QRS duration time was prolonged and left ventricular end diastolic diameter (LVEDD), left ventricular end systolic diameter (LVESD) as well as LVEDVi (LVEDD/BSA) and LVESVi (LVESD/BSA) were increased in comparison to the control group.

BNP blood samples were obtained only in HF patients, the median values was 191 (9–1290) pg/ml.

Doppler tissue imaging
Table 3 presents S2 max velocity, S2 duration time, S2 vti from septal wall and shows decreasing values in patients with HF compared to the controls. S3 max velocity, S3 duration time, S3 vti and E/E' were increased and IVCTm and IVRTm were prolonged in HF patients. Mean septal PSM (S3 vti/S2 vti) was significantly increased 0.52±0.41 vs controls 0.05±0.07 (p<0.001). PSM values calculated from the control group show a normal range 0.05±0.07 (±2SD) i.e. <0.18. Abnormal PSM (>0.18) was detected in 79% of all HF patients and in 92% if QRS >130ms.


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  		Table 3 DTI values from septal and lateral wall

 
In the HF group PSM (S3 vti/S2 vti) correlated with QRS duration time, r=0.40 (p<0.01), LVEDVi, r=0.34 (p<0.05), LVESVi, r=0.31 (p<0.05), IVRTm, r=0.68 (p<0.001) and was inversely correlated with heart rate, r=–0.52 (p<0.001) and diastolic blood pressure r=–0.37 (p<0.001). There was no correlation with E/E' septal, E/E' lateral, or BNP plasma levels.

Table 3 describes measurements of the lateral wall. There was a correlation between lateral wall PSM and lateral wall IVRTm, r=0.50 (p<0.01) and with septal wall PSM, r=0.50 (p<0.01).

Mortality
The mean follow up in the heart failure group was 30±18months. Seventeen of 47 patients died, the mean follow up time for the non-survivors was 15±11months and 39±15months for the survivors. BNP, PQ duration time, LVESD, LVESVi, E/E' septal was significantly increased, while EF% and diastolic blood pressure was significantly decreased in the non-survival group. There was no association between PSM and survival at 18months follow up, and no association between PSM and all cause or cardiac readmission rates (Table 4).


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  		Table 4 Clinical, electrocardiographic and echocardiographic data in surviving and non-surviving in HF patients

 
Presence of PSM in patients with readmission by cardiac events vs patients with no readmission was 0.54±0.42 and 0.49±0.40 (p=0.66) respectively. In the non-surviving group septal wall PSM correlated with septal IVRTm, r=0.71 (p<0.01) and was inversely correlated with diastolic blood pressure, r=–0.58 (p<0.05).

Furthermore, there were no correlations between septal wall PSM and BNP, QRS duration time, E/E' septal, E/E' lateral, readmission rate or readmissions caused by cardiac events.

Multiple regression analysis
Septal wall PSM was tested in a multiple linear regression analysis model. Heart rate, QRS duration time, LVEDVi, diastolic blood pressure and IVRTm were included in the model as well as age and gender. PSM was independently correlated with IVRTm, p=0.0009, beta 0.47, std. error of beta 0.13, R2=0.55.

Reproducibility
Reproducibility measurements of the analyses were obtained in 20 subjects. The coefficients of variance in intra- observer differences in DTI were: S2 max 3%, S2 dur 3%, S2 vti 3%, S3 max 11%, S3 dur 12% and S3 vti 13%, IVCTm 5% and finally IVRTm 4%.


   Discussion
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
References
 
This study shows that PSM is a common phenomenon in patients with HF especially in patients with wide QRS and long IVRTm suggesting that PSM is a manifestation of LV intra-ventricular dyssynchrony. In this study PSM did not predict mortality. Post-systolic motions occurring in healthy subjects have been described to have smaller amplitudes and to take place earlier during the isovolumic relaxation phase compared to PSM in patients with ischemic heart disease.19 Pathologic PSM might be caused by regional disturbances in the myocardial wall due to prolonged contraction, delayed relaxation or elastic recoil after systolic bulging. Experimental animal studies using strain and strain rate have shown that PSM is an active, energy-consuming contraction immediately after induced ischemia, but later during ongoing ischemia it changes into elastic recoil as a passive consequence of systolic bulging.26 Citro et al. examined patients with left bundle branch block (LBBB) and normal pump function and found that PSM was evident in 42 of 53 (79%) of the patients with LBBB.27 Thus, small PSM <0.18 as described in our study can be found in normal myocardium. However if PSM is greater than 0.18 it seems to be related to structural myocardial changes. In our study the length of the IVRTm was the most important factor associated with PSM.

Tissue synchronisation imaging (TSI) is a recently developed tissue doppler technique in which regional tissue peak-velocities in the myocardium are colour-coded. If the maximal velocity occurs during the time-period, from 60ms from the start of the QRS and within 150ms the myocardial wall is given a green colour. If the maximal velocity appears after 150–300ms it becomes yellow-orange, and if the maximal velocity occurs after 300ms it becomes red. This new method can be used for measuring PSM if its velocity is higher than during the S2-contraction (Fig. 1). It has recently been shown that heart failure patients with LV intra-ventricular dyssynchrony at the TSI examination seem to respond to cardiac resynchronisation therapy.28,29 In the study by Gorcsan et al., it was demonstrated that differences in time-to-peak velocities of opposing ventricular walls measured by TSI were greater in patients who responded to biventricular pacing. A difference exceeding 64ms between the anterior septum and the posterior wall using the apical long-axis view had 87% sensitivity and 100% specificity for predicting an acute response to CRT. In the study by Yu et al. it was confirmed that TSI could be used for a quick evaluation of regional wall motion delay making it possible to predict reverse remodelling after CRT.

Thus, the results of these studies support that PSM in heart failure patients is a manifestation of LV intra-ventricular dyssynchrony. In our study seven of 13 (54%) of the patients with QRS >130ms and 12 of 34 (35%) of the patients with QRS <130ms could have been potential CRT responders if these criterias were applied.

Activation of the neuro-endocrine system is of great importance in heart failure and BNP is a marker of this. Indeed, similar to others reports, elevated BNP levels were associated with a poor prognosis in our study.30,31 The lack of relationship between PSM and BNP in our study can be explained by the difference between localised segmental disturbance and global chamber wall stress. Secondly, segmental PSM showed no correlation with E/E' as a marker of left atrial pressure which itself is the consequence of increased left ventricular diastolic pressures and concomitant decrease in global systolic or diastolic function. Global dysfunction, as described by increased LV volumes and a low LV ejection fraction are important factors for prognosis in heart failure, as has been shown previously.32,33

The lack of prognostic value of PSM thus probably depends on that septal systolic motion only represent local segmental abnormality. Therefore PSM is unlikely to predict life events, although this needs confirmation in a larger study.

In conclusion our results demonstrate that PSM is a common phenomenon in patients with heart failure and in particular in patients with wide QRS and long IVRTm, suggesting that PSM is a manifestation of left ventricular intra-ventricular dyssynchrony. However, in this small study PSM was not correlated with an increased readmission rate or with higher mortality.


   Acknowledgements
 
The authors thank Ann-Catrin Kjerr, Elisabeth Johansson and Inger Bergbom for skilful technical assistance. This study was supported by Swedish Heart-Lung Foundation and Karolinska Institutet, Stockholm, Sweden


   References
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 References
 

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