Importance of Strain Imaging in Cardiac Rehabilitation
Philip Claessens, MD,
Jan Meulendijks,
Christophe Claessens, MD,
Marc Claessens, MD,
Maria Claessens,
Jan Claessens, MD
Hospital Sint Jozef, Malle, Antwerp, Belgium
Jan Claessens, MD, Tel: + 32 3 232 2803, Fax: + 32 3 233 3651, Email: jan.claessens{at}village.uunet.be, Rubenslei 35, B-2018, Antwerp, Belgium.
ABSTRACT
Cardiac rehabilitation improves the subjective condition of the patient; but are there associated structural and functional cardiac adaptations? The study group consisted of 39 patients with an inferior infarction and 21 patients with an anterior infarction, treated by surgical revascularization followed by 4 months of cardiac rehabilitation. Maximal exercise testing and Doppler echocardiography were performed before and after the rehabilitation program. Performance capacity was significantly improved after cardiac rehabilitation, but left ventricular function remained unchanged on Doppler imaging. Only by analyzing the subgroups using strain imaging significant differences were noted after cardiac rehabilitation: patients with an inferior infarction exhibited improved strain values in the anterior wall; those with an anterior infarction had improved strain values in the inferior wall. Strain values in the infarcted regions were worse after cardiac rehabilitation. Strain imaging indicated that cardiac rehabilitation could bring about improvements in cardiac function exclusively in the healthy non-infarcted myocardium, while there were signs of further deterioration of myocardial function in the highly ischemic zones.
Key Words: Echocardiography • Doppler • Myocardial Infarction • Rehabilitation
INTRODUCTION
Cardiac rehabilitation significantly reduces cardiac morbidity and mortality in patients with documented atherosclerotic heart disease. The main aim of cardiac rehabilitation is undoubtedly to improve subjective well-being and exercise capacity.1 Cardiac rehabilitation programs are intended to improve cardiovascular risk factors, cardiac function and work capacity, as well as to stabilize the patient psychologically to accelerate social integration.2 Such programs support the recovery process after acute myocardial infarction (MI) and coronary artery bypass grafting.3,4 Rehabilitation and exercise training may reduce the subsequent risks of malign ventricular arrhythmias and sudden cardiac death.5,6 Without such programs, cardiac morphology and function might undergo changes during the first months after surgical revascularization. By analogy with the training effect in athletes, attempts are made to optimize the exercise capacity of cardiac patients through personalized exercises and endurance training. Endurance training in athletes not only raises performance but also causes clear structural and functional changes in the heart: a larger left ventricle (LV), thicker walls, and improved LV diastolic function, with signs of improved myocardial distensibility and elasticity.7,8 Thus it may be speculated that structural and functional myocardial adjustments might also be observed in cardiac patients after a rehabilitation program.9 Strain imaging is a new tool to study regional myocardial function by assessing intrinsic LV contractility.10,11 The aim of this study was to investigate using strain imaging whether changes in cardiac function and structure concern the global LV or a more localized area, depending on the location of the preceding MI.
PATIENTS AND METHODS
Between January 2007 and July 2007, 60 male patients with a first-time transmural MI were studied: 39 had an inferior wall MI, and 21 had an anterior wall MI. Their medical histories were otherwise unremarkable. All patients had critical 3-vessel coronary disease and underwent surgical myocardial revascularization 2–6 weeks after suffering MI. In all patients, left internal mammary artery anastomosis was performed as well as multiple vein grafting. Each patient underwent a cardiac rehabilitation program starting at 1 month postoperatively. All patients were in sinus rhythm without signs of important valvular heart disease or evidence of LV aneurysm. The surgical reports of all patients indicated a scar at either the inferior or anterior wall, surrounded by ischemic myocardial tissue. We did not use a control group because the structural and functional heart adaptations due to increased training by healthy persons or athletes are well known.7,8
Just before starting the rehabilitation program, all patients underwent a clinical assessment to determine anthropometric data, a resting electrocardiogram, 2-dimensional Doppler echocardiography with tissue Doppler and strain imaging, and an incremental maximal exercise test on a bicycle ergometer to determine maximal oxygen consumption (VO2). Measurement of peak VO2 remains the best available index of exercise capacity. Peak VO2 represents the maximal achievable level of dynamic exercise involving large muscle groups. Cardiac structure and LV systolic and diastolic function were explored by 2-dimensional Doppler echocardiography. To eliminate the influence of preload on the evaluation of LV function, measurements of the motion velocities of the LV inferior wall and interventricular septum were obtained by tissue Doppler imaging. Strain echocardiography permits quantification of the intrinsic deformation of the myocardium, especially lengthening and shortening, irrespective of the global motion of the heart.12–14 Negative strain in the longitudinal axis means that the tissue segment is becoming shorter, whereas positive strain means that the tissue segment is lengthening.15,16 Strain measurements were performed in the longitudinal axis at the basal sites of the septum and inferior wall. Strain values at these sites were determined at aortic valve closure and at the end of the A wave.
The cardiac rehabilitation program was maintained for 4 months with three 90-min sessions per week during the first 2 months, and 2 per week during the last 2 months. A warm-up period was followed by exercises on an bicycle ergometer, gymnastics, and running on a treadmill, ending with relaxation exercises. The load and duration were both gradually increased on the bicycle ergometer, the frequency of the gymnastic exercises was systematically increased, and the speed and slope of the treadmill and duration of running exercises were adjusted. At the end of the rehabilitation exercises, all patients underwent the same noninvasive cardiac examinations. Results before and after the cardiac rehabilitation program were compared in each patient, using each subject as his own control. The patients were also divided into 2 groups depending on whether they had an inferior or anterior MI.
To acknowledge the dependence of the observations in the samples, paired statistical tests were performed. As the tests are considered directional, a one-tailed alpha level of 0.05 was used. All calculations were performed using SPSS version 12.0 software (SPSS, Inc., Chicago, IL, USA). An essential step in the process of statistical hypothesis testing involves evaluating the extent to which the analyzed parameters meet the assumptions of the tests being considered. The first important characteristic is the normality of distribution. Comparisons of the histograms with the normal bell-shaped curve showed that most parameters were distributed normally. These observations were supported by evaluating the skewness and kurtosis of the distributions, and by performing the Kolmogorov-Smirnov test for normality (alpha = 0.05). Although our data met the assumptions for the parametric paired t test, the nonparametric alternative for testing differences between paired samples, the Wilcoxon signed-ranks test was also performed. This test has the advantage of being fairly robust against violations of its assumptions, and it quickly approaches the power of the t test, which was confirmed by the results obtained by both approaches. Outliners and extreme values were identified by creating box plots. In view of our choice of nonparametric rank-ordered statistics, which tend to be insensitive to these atypical data points, no attempt was made to remedy them. Another important assumption of several statistical tests that compare differences between 2 or more groups is that the variance among the subgroups must be similar, especially when groups of unequal size are being compared. In our study, the homogeneity of variance among different groups was tested using Levene’s test (alpha = 0.05) which is fairly independent of the assumption of normality. We concluded from these tests that not all variances could be assumed equal.
RESULTS
Anthropometric data were identical for both groups of patients, and remained almost unchanged after the cardiac rehabilitation program (Table 1
). There were no statistically significant differences in weight, body mass index, mean blood pressure, or cholesterol levels after the rehabilitation program. There were significant differences in spiroergometric data after cardiac rehabilitation: mean peak VO2 and maximal watts attained during exercise on the bicycle, and the difference between maximal and resting heart rate were considerably higher (Table 2). Two-dimensional Doppler echocardiography showed that the mean maximal end-diastolic diameters of both ventricles were unchanged after the rehabilitation program, while we were unable to observe any differences in the thickness of the interventricular septum or LV posterior wall. No measurable changes in the functional characteristics of the heart could be found after cardiac rehabilitation (Table 3). Systolic and diastolic LV function was explored by tissue Doppler imaging. In the apical long axis at the basal site of the septum and the basal site of the LV inferior wall, the mean peak systolic velocity of the study group of 60 patients was almost unchanged by cardiac rehabilitation. The ratio early to late peak diastolic LV velocity at the basal site of the septum and the basal site of the inferior wall were slightly but not significantly higher; these improved ratios were noted in the whole group and in each subgroup (Table 4). In the study group, post-rehabilitation strain values were unchanged; however, significant differences were noted when we analyzed the subgroups. After cardiac rehabilitation, patients with an inferior MI exhibited improved strain values in the anterior myocardial wall region at both end-systole and end-diastole, whereas those with an anterior wall MI exhibited improved strain values in the inferior myocardium. Even more striking was the fact that strain values in the infarcted region were clearly worse after cardiac rehabilitation (Table 5).
DISCUSSION
The anthropometric data of the 2 subgroups showed no significant differences, which led us to conclude that they were comparable groups, and the data after cardiac rehabilitation remained unchanged. As expected, both the basic endurance capacity and maximal exercise capacity improved significantly after cardiac rehabilitation. In these circumstances, clear structural and functional heart adjustments have been noted in athletes, but we could not ascertain these by traditional 2-dimensional Doppler echocardiography or tissue Doppler imaging in our patients with ischemic heart disease.
Until now, it has been uncertain whether cardiac rehabilitation could ameliorate LV function in suitable candidates with MI. On the other hand, there is good evidence that post-MI patients may benefit from long-term physical training, without any additional negative effect on ventricular size and geometry.17 Furthermore, it was absolutely out of the question that exercise training early after acute MI in patients with moderate to severe LV dysfunction could cause a deterioration in LV remodeling.18,19 Myocardial velocities measured by tissue Doppler echocardiography vary throughout the LV because of the tethering effect of adjacent tissue. Strain Doppler echocardiography is a new tool for measuring myocardial deformation, which excludes the effect of adjacent myocardial tissue. The more negative the strain value, the better the contractility. A positive end-diastolic strain value indicates that the tissue segment elongates further as a result of atrial contraction. Our observations at the basal site of the septum in the longitudinal axis showed significant differences in the strain curves of cardiac patients, normal healthy controls, and endurance-trained athletes.9 In patients with important ischemic heart disease, we noted significantly decreased contractility at end-systole and a positive end-diastolic strain value, probably due to a substantial contribution from atrial contraction to produce supplementary elongation of the myocardium, which is still characterized by decreased contractile force and reduced capacity to maintain muscular tone (Figure 1). The strain values for the whole group did not differ after cardiac rehabilitation, either in systole or diastole (Figure 2). However, in both subgroups, strain values were clearly improved in non-infarcted myocardium after cardiac rehabilitation.
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Figure 1. Longitudinal strain curves (in basal septum longitudinal axis) during the cardiac cycle in 3 groups: normal healthy controls (dotted line), patients with ischemic heart disease (dashed line), and triathletes (solid line). End-systolic strain at aortic valve closure is marked by a triangle, end-diastolic strain at end A wave is marked by a circle.
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Figure 2. Longitudinal strain curves during the cardiac cycle for the whole study group of 60 patients before (solid line) and after cardiac rehabilitation (dotted line): (A) in basal septum longitudinal axis, (B) in basal inferior longitudinal axis. Strain measurements at the basal septal wall and basal inferior wall were not significantly different when examining all the subjects as one group. End-systolic strain at aortic valve closure is marked by a triangle, end-diastolic strain at end A wave is marked by a circle.
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A thorough training program appears to have a positive effect on healthy myocardium, with signs of improved systolic and diastolic myocardial function. On the other hand, the post-cardiac rehabilitation strain values in the infarcted myocardial region were noticeably worse, indicating an adverse effect of the rehabilitation sessions. At end-systole, we noted clearly improved contractility of non-infarcted myocardium after rehabilitation, while there was a negative inotropic effect in the infarcted segment (Figures 3 and 4). Before rehabilitation, atrial contraction at end-diastole caused passive elongation of non-infarcted myocardium, while after rehabilitation, a slight shortening of the same myocardial region was observed, indicating improved contractility. Elongation of the infarcted myocardial segment was noted at end-diastole after cardiac rehabilitation. This means that after progressively increased training, the infarcted myocardial segment cannot compensate for the stress imposed at end-diastole with active atrial contraction. Strain imaging obliged us to consider that continued cardiac rehabilitation might cause further functional deterioration of the infarcted myocardium. Whether this could facilitate LV aneurysm development remains unanswered. Cardiac rehabilitation appears to improve the function of healthy myocardium, while the damaged myocardial segment undergoes further end-diastolic elongation with end-systolic evidence of reduced contractility.
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Figure 3. Longitudinal strain curves during the cardiac cycle in patients with anterior myocardial infarction before (solid line) and after cardiac rehabilitation (dotted line): (A) in basal septum wall longitudinal axis, (B) in basal inferior wall longitudinal axis, showing improved (more negative) end-systolic strain values at the non-infarcted inferior wall and less negative values at the infarcted anteroseptal wall. End-systolic strain at aortic valve closure is marked by a triangle, end-diastolic strain at end A wave is marked by a circle.
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Figure 4. Longitudinal strain curves during the cardiac cycle in patients with an inferior myocardial infarction before (solid line) and after cardiac rehabilitation (dotted line): (A) in basal septum wall longitudinal axis, (B) in basal inferior wall longitudinal axis, showingimproved (more negative) end-systolic strain values and slightly negative end-diastolic strain values at the non-infarcted anteroseptal wall of the left ventricle. The opposite effects were noted at the infarcted and damaged inferior wall. End-systolic strain at aortic valve closure is marked by a triangle, end-diastolic strain at end A wave is marked by a circle.
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This study demonstrates that cardiac rehabilitation cannot induce structural or functional heart adaptations in patients with MI. There were no signs of improved blood supply or muscular hypertrophy in healthy myocardial segments. Only by strain imaging improved contractility, confined to unaffected myocardial segments only, could be demonstrated. These results focus attention on the role of left atrial function, principally active atrial contraction, with a consistent relationship between presystolic left atrial pressure and LV systolic performance, at least in unaffected myocardium. In scarred myocardial tissue, active left atrial contraction provokes the opposite effect of passive, possibly aneurysmatic, elongation of the involved myocardial segment. Besides left atrial function, the contractile machinery composed of myosin and actin filaments could also play an important role. From the standpoint of myocardial performance, the major effect of coronary disease is to render segments of myocardium nonfunctional, because of either scar formation or severe ischemia, which prevents myocardial cells from functioning normally even though they are still viable despite altered function of the actin-myosin crossbridge cycle. Studies have consistently indicated altered actin-myosin crossbridge function in the failing human heart, with decreased myosin and myofibrillar adenosine triphosphatase activity, a decreased crossbridge cycling rate, and increased crossbridge force-time integral.20 Under increasing load, only healthy myocardium can improve contractility by activation and up-regulation of the contractile actin-myosin complex. More recently, there has been increasing evidence to implicate cytokines as a potentially important component in functional and structural heart adaptations. Further investigations are required to confirm our findings and suggestions.
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Asian Cardiovasc Thorac Ann 2009;
17:240-247
© 2009 by SAGE Publications
DOI: 10.1177/0218492309104768
