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European Journal of Heart Failure 2001 3(4):429-436; doi:10.1016/S1388-9842(01)00143-X
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© 2001 European Society of Cardiology

Abnormal contractile responses during dobutamine stress echocardiography in patients with idiopathic dilated cardiomyopathy

Richard M. de Jonga, Jan H. Cornelb, Harry J.G.M. Crijnsa and Dirk J. van Veldhuisen*,a,1

a Department of Cardiology/Thorax Centre, University Hospital Groningen P.O. Box 30001, 9700 RB Groningen, The Netherlands
b Medical Centre Alkmaar Alkmaar, The Netherlands

* Corresponding author. Tel.: +31-50-361-2355; fax: +31-50-361-4391. E-mail address: d.j.van.veldhuisen{at}thorax.azg.nl (D.J. van Velduisen).


   Abstract
Top
 Notes
 Abstract
1. Introduction
 2. Methods
 3. Results
 4. Discussion
 References
 
Background: In chronic heart failure augmented wall stress leads to increased energy demand. Supply, however, may be reduced due to coronary vasoconstriction and endothelial dysfunction. This might lead to a mismatch between demand and supply. In the present study we further explored the effect of increased demand during dobutamine stress echocardiography.

Methods and results: Sixteen patients with idiopathic dilated cardiomyopathy (mean age 44±13 years, New York Heart Association class II–III, mean left ventricular ejection fraction 0.27±0.10) underwent dobutamine stress echocardiography (5–40 µg/min per kg bodyweight+atropine if required). Wall motion and thickening was assessed in 16 segments using a four-point scale. Eleven patients (69%) showed regions with worsening of wall motion or a biphasic response during dobutamine infusion. Of the remaining five patients one patient did not show any wall motion changes and one patient showed a partial improvement while only in three patients wall motion improvement in the whole heart was found.

Conclusion: A majority of patients with idiopathic dilated cardiomyopathy showed decreased wall motion during increased demand, i.e. ischemia-like myocardial contractile responses during dobutamine stress echocardiography. These findings further support the concept that an energy mismatch between demand and supply might play a pathophysiological role in idiopathic dilated cardiomyopathy.

Key Words: Idiopathic dilated cardiomyopathy • Dobutamine stress echocardiography

Received November 3, 2000; Revised January 11, 2001; Accepted February 12, 2001


   1. Introduction
Top
 Notes
 Abstract
 1. Introduction
2. Methods
 3. Results
 4. Discussion
 References
 
Idiopathic dilated cardiomyopathy (IDC) is a disease of cardiac muscle of unknown etiology and is characterized by an enlargement of cardiac chambers, particularly the left ventricle, systolic dysfunction and a normal coronary angiogram [1]. It leads to symptomatic chronic heart failure in the majority of patients [2] and carries a high morbidity and mortality [3].

Several mechanisms have been assumed to play a role in the progression of IDC to end-stage heart failure [4]. Progression of heart failure might be caused by a vicious circle in which ischemia may lead to heart failure and heart failure itself may induce ischemia [5]. A combination of increased energy demand due to augmented wall stress and decreased supply (i.e. coronary vasoconstriction and endothelial dysfunction) may lead to an energy mismatch. This is supported by a recent study using positron emission tomography in patients with IDC [6]. A reduced myocardial perfusion reserve and regional mismatches between myocardial perfusion and metabolism were observed. These mismatches are known to indicate regional ischemia in patients with coronary artery disease and might be a presentation of the imbalance between supply and demand in patients with IDC.

In general, IDC is supposed to be a disease concerning the whole left and/or right ventricle. However, regional differences in myocardial perfusion and metabolism as well as regional wall motion abnormalities have been reported [7–10]. Thallium scintigraphy showed regional differences in patients with IDC comparable with those observed in patients with ischemic heart disease [7,11–14]. However, while abnormalities in patients with coronary artery disease are generally limited to coronary areas this in not necessarily so in patients with IDC. Furthermore, patients with IDC may present with irreversible patchy defects [11]. With positron emission tomography, in patients with IDC a heterogeneous uptake of palmitate [15] and glucose [16] were found as well as regional differences in the sympatho-adrenergic system [17].

Dobutamine stress echocardiography is a widely used and safe technique [18] with good sensitivity and specificity to evaluate wall thickening abnormalities reflecting an ischemic response in patients with coronary artery disease [19]. Ischemic responses in these patients are defined as worsening of wall motion or a biphasic response on infusion of higher dobutamine dose [20–22].

The aim of this study was to investigate whether there is an imbalance between energy demand and supply in patients with IDC. Therefore, dobutamine stress echocardiography was used to detect possible abnormal contractile responses during increased demand.


   2. Methods
Top
 Notes
 Abstract
 1. Introduction
 2. Methods
3. Results
 4. Discussion
 References
 
2.1. Characteristics of the patients
Clinically stable patients with IDC and mild to moderate heart failure, with an eligible echocardiogram for wall motion analysis, were included in the study. Patients had left ventricular dysfunction (left ventricular ejection fraction ≤0.45) and underwent coronary angiography to exclude coronary artery disease. No patient showed any degree of stenosis. The diagnosis of IDC was supported by endomyocardial biopsy. In all patients, microscopical features included hypertrophy as well as degeneration of myocytes and varying degrees of interstitial fibrosis. Patients with other underlying etiologies were excluded, i.e. hypertension (systolic blood pressure >150 mmHg, diastolic blood pressure>95 mmHg), valvular disease, diabetes mellitus, hypercholesterolemia, or any other systemic illness. Furthermore, patients with frequent ectopic activity at rest were not included.

All patients were on optimal medication for chronic heart failure, including diuretics, angiotensin converting enzyme inhibitor or angiotensin-2 antagonist, and digoxin, while beta-blockers were discontinued for the test. The severity of heart failure was assessed scoring functional class according to the New York Heart Association (NYHA) classification, measuring left ventricular ejection fraction using radionuclide ventriculography and determining peak oxygen consumption on a treadmill with respiratory gas exchange measurements as previously described [23].

This study conforms with the principles outlined in the Declaration of Helsinki, patients gave written informed consent and the Institutional Review Board approved the protocol.

2.2. Dobutamine stress echocardiography
Before the test, patients were asked to discontinue beta-blockers for 36 h. All other cardiac medications were continued. The dobutamine stress test was performed as previously described by Cornel et al. [24]. In short, a two-dimensional transthoracic echocardiogram in standard views and a 12-lead electrocardiogram (ECG) were recorded with the patient at rest (baseline). Dobutamine was then infused through an antecubital vein at dosages of 5 and 10 µg/kg body weight per min for 5 min at each dose (these two steps were considered as ‘low dose’). Subsequently, three other steps from 20 to 40 µg/kg per min (3 min each) were added. Finally, atropine (up to 1 mg) was injected when 85% of the predicted maximal (men [220–age]x85%, women [200–age]x85%) heart rate had not been reached [25]. A three-lead ECG was monitored continuously, and a 12-lead ECG was recorded every minute. Cuff blood pressure was measured at each stage. The test was terminated prematurely if 85% of the predicted maximal heart rate was reached, at the occurrence of severe chest pain, ST segment deviation >2 mm, significant ventricular or supraventricular arrhythmia, or a fall in systolic blood pressure of >40 mmHg, or if any other intolerable side effect occurred during the test.

The echocardiogram was monitored throughout the test, and the last minute of each stage, including recovery, was recorded on videotape. The echocardiographic images were also digitized on optical disk (Vingmed CFM 800) and displayed side by side in quad screen format to facilitate the comparison of images at rest and at various stages of the test.

2.3. Analysis of echocardiograms
The interpretation of echocardiograms was done by two experienced observers who had no knowledge of the clinical, radionuclide, angiographic and previous echocardiographic results of the individual patients. In case of disagreement, a third observer reviewed the study and a majority decision was attained. The assessment was based on both the digitized images displayed in a quad screen format and a review of the images recorded on the videotape. For analysis of wall motion, the left ventricle was divided into 16 segments, as recommended by the American Society of Echocardiography [26]. The wall motion, including wall thickening, of each segment was semiquantitated using a four-point scoring system: 1=normal wall motion and thickening; 2=mildly hypokinetic; 3=severely hypokinetic; 4=akinetic or dyskinetic. We defined a segment as severely hypokinetic in the presence of minimal wall thickening with very limited inward motion (during the first half of systole); as akinetic in the absence of systolic wall motion and thickening, confirmed by M-mode echocardiographic tracing whenever possible; and as dyskinetic in the presence of systolic outward motion with thinning. Wall thickening was primarily utilized for the classification of wall motion. To reduce the confounding effect of tethering from adjacent segments, segmental wall thickening was analyzed only during the first half of systole.

During dobutamine infusion, abnormally contracting segments at rest were classified into four different patterns of contractile response: biphasic, defined as improvement at low dose and worsening at peak stress; sustained improvement, defined as improvement at low dose without further deterioration at peak stress; worsening, defined as direct worsening with no improvement at any stage; and no change, defined as unchanged wall motion abnormality throughout the test.

An ischemic response was judged to be present when there was worsening of the segmental score by 1 (in normally contracting segments or dyssynergic segments showing worsening or a biphasic response). As previously reported, ischemic responses were not considered when akinetic segments at baseline became dyskinetic at stress without improvement during low-dose dobutamine infusion [27].


   3. Results
Top
 Notes
 Abstract
 1. Introduction
 2. Methods
 3. Results
4. Discussion
 References
 
We studied 16 patients at rest and during dobutamine infusion. The patient characteristics are presented in Table 1. Three patients used low dose β-blockers (no. 8, 13 and 14). In 14 patients the maximal dobutamine dose or 85% of the maximal predicted heart rate was reached. In two patients (no. 1 and 2) dobutamine stress echocardiography was prematurely stopped because of dyspnea.


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  		Table 1 Patient characteristics

 
The hemodynamic and wall motion responses during dobutamine stress are presented in Tables 2 and 3. Thirteen patients (81%) showed abnormal contractile responses in >2 segments, i.e. no response, worsening wall motion or a biphasic response. Three patients showed improved contractility in the whole left ventricle. Six patients had regions in which wall motion worsened. Seven patients showed regions that improved on low dose dobutamine and worsened on higher dosage. All patients but one showed >2 segments with improving wall motion during the test.


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  		Table 2 Hemodynamic response during dobutamine infusion

 


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  		Table 3 Wall motion response during dobutamine infusion

 
Analysis per segment: in total 239 segments were eligible for wall motion evaluation. During baseline measurements 49 akinetic, 119 severely hypokinetic and 71 mildly hypokinetic segments were found. Fig. 1 shows the distribution of dobutamine induced wall motion responses for all segments. One hundred forty-two segments (59.4%) showed a normal response, i.e. improved wall motion during dobutamine infusion, 47 segments (19.7%) showed an ischemic contractile response and 50 segments (20.9%) showed no response of which eight were hypokinetic and 42 akinetic at rest.


Figure 1
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  		Fig. 1 Wall motion response in all 239 segments during dobutamine infusion. In 40.6% of the segments an abnormal response is seen of which 19.7% show an ischemic response (worsening wall motion or biphasic response).

 
Fig. 2 shows the wall motion response during dobutamine infusion of segments which are hypokinetic (mildly and severely) and akinetic at baseline. Of the 71 mildly hypokinetic segments four worsened, five showed a biphasic response and 62 improved in wall motion. Thus, 13% of the mildly hypokinetic segments showed an abnormal response. Of the 119 severely hypokinetic segments 21 worsened, 16 showed a biphasic response, 8 segments showed no response and 74 an improved wall motion during dobutamine infusion. This means that an abnormal response was observed in 38% of the severely hypokinetic segments. Of the 49 akinetic segments six improved in wall motion and one showed a biphasic response and 42 did not show any reaction on dobutamine. Thus, 88% of the akinetic segments showed an abnormal response.


Figure 2
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  		Fig. 2 Relation between baseline wall motion and response during dobutamine infusion in patients with idiopathic dilated cardiomyopathy. Percentage of segments with different wall motion responses.

 

   4. Discussion
Top
 Notes
 Abstract
 1. Introduction
 2. Methods
 3. Results
 4. Discussion
References
 
This study demonstrates regional differences in myocardial contractile response in 81% of the patients with IDC using dobutamine stress echocardiography. Thirteen out of 16 patients in this study showed regional worsening of wall motion, a biphasic or no response during dobutamine stress.

Non-ischemic cardiomyopathy has been presumed to involve the myocardium diffusely with homogeneous effects on ventricular function. Regional wall motion differences in rest, however, have been described before [7,8,10,28–31] in these patients as in this study, while abnormal contractile responses during dobutamine infusion have been mainly described in patients with coronary artery disease [21]. Several hypotheses have been proposed to explain the heterogeneous wall motion in rest in patients with non-ischemic cardiomyopathy. Asynergy in wall motion may be accompanied by worse thallium-201 uptake and it has been suggested that regional asynergy may be related to localized fibrosis within the left ventricle in IDC [32]. Furthermore, regional differences in wall stress [30,33] and oxidative metabolism [31] have been found that might explain the heterogeneous wall motion in rest.

Besides regional wall motion abnormalities in rest, this study shows abnormal contractile responses during dobutamine stress echocardiography in patients with IDC. It is generally accepted that these responses indicate ischemia or hibernation in patients with coronary artery disease and abnormalities during dobutamine stress echocardiography have been shown to be in agreement with measurements of perfusion [20]. In these patients the number of segments with abnormal contractile function are a measure of myocardial jeopardy [34]. Although this study investigates patients with IDC which have by definition normal epicardial coronary arteries, we found the same patterns in wall thickening as have been observed in patients with ischemic heart disease. We suggest that these wall-thickening abnormalities are a representation of an imbalance between energy demand and supply. Although dobutamine infusion causes an increased energy demand wall motion worsens regionally. The imbalance between demand and supply represented by abnormal wall thickening responses might be a pathophysiological factor in the etiology or progression of IDC to heart failure. Notably, abnormal wall motion responses (i.e. ischemic or no response) were more present in segments with a worse wall motion at rest. Furthermore, 14% of the akinetic segments showed inducible wall motion, which could be compatible with local hibernating myocardium. Non-responding akinetic segments might be interpreted as regions with replacement of myocardial tissue by fibrotic tissue. As in patients with ischemic heart disease the number of regions with abnormal myocardial contractions might be a representation of the myocardial jeopardy. This could be a predictor of improvement of ventricular function or survival after therapeutic interventions in patients with IDC. This, however, has to be investigated in a larger prospective study.

The abnormal contractile responses observed in our study are compatible with the concept of a pathophysiological role of ischemia in IDC. This concept has previously been proposed by Unverferth et al. suggesting a role for subendocardial ischemia [35]. Although this is not directly proven by the present study, the role of ischemia in IDC has been supported by previous studies, as mentioned in the introduction. A study of our group using positron emission tomography showed regional differences in myocardial perfusion and glucose metabolism suggesting ischemia [6]. Although dobutamine stress echocardiography is mainly used in patients with coronary artery disease, some recent studies have used this technique in patients with dilated cardiomyopathy [22,36–41]. Few of these studies focussed on wall motion abnormalities. Some dobutamine stress echocardiography studies compared heart failure patients with coronary artery disease and patients with non-ischemic cardiomyopathy. Contractile responses reflecting ischemia were more often observed in the ischemic group, as expected. Although patients without coronary artery disease showed these responses too [39,40] these observations were interpreted as false positive test results. However, in the light of the present and previous data these results can also be interpreted as a sign of ischemia in ‘non-ischemic’ heart failure [5]. The association between the frequency of ischemic responses and the severity of wall motion abnormalities at rest supports this and suggests that ischemia is most active in segments with severe wall motion abnormalities at rest. In patients with IDC endothelial dysfunction [42], changes in the microvasculature [43] have been described that might lead to ischemia. Furthermore, a cardiodepressant effect on myocardial contractile performance mediated by beta-adrenergic stimulation and factors released from the coronary endothelium have been described. These changes together with an increased wall stress may lead to a reduced myocardial perfusion reserve [6,44] resulting in wall motion abnormalities during dobutamine stimulation. Regional differences in myocardial perfusion and metabolism as mentioned in the introduction could be interpreted as a result of ischemia. A combination of myocardial perfusion measurements and the assessment of contractile responses during stress protocols in patients with IDC might add further insight in this relation.

The observation of abnormal contractile responses during dobutamine stress in patients with IDC in this study emphasizes the importance of performing a coronary angiogram in patients with dilated cardiomyopathy and an abnormal dobutamine stress echocardiogram to exclude the presence of coronary artery disease. Dobutamine stress echocardiography might be a good tool to assess the effects of aggressive therapy. However, nowadays the use of β-adrenoceptor blocking agents makes interpretation of the test more difficult. Tests might be performed before patients start therapy with β-blockers or after temporarily ceasing or alternative techniques have to be used to detect ischemia. The clinical significance of dobutamine stress testing in patients with heart failure and IDC has to be evaluated in larger studies.

In conclusion, patients with IDC show abnormalities in contractile response during dobutamine stimulation. This supports the hypothesis that an imbalance between energy demand and supply presenting as ischemia might play a pathophysiological role in IDC. Further investigations, however, are needed to elucidate the pathophysiological mechanism leading to these regional wall motion abnormalities.


   Acknowledgements
 
Richard M. de Jong is supported by the Netherlands Organisation for Scientific Research (NWO). We want to thank Rutger L. Anthonio M.D., and Arie Breekland M.D., for their help in the conduction of these studies.


   Notes
Top
 Notes
Abstract
 1. Introduction
 2. Methods
 3. Results
 4. Discussion
 References
 
1 Dirk J. van Veldhuisen is an Established Investigator of the Netherlands Heart Foundation (Grant D97.017). Back


   References
Top
 Notes
 Abstract
 1. Introduction
 2. Methods
 3. Results
 4. Discussion
 References
 

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A. F.M van den Heuvel, J. J Bax, P. K Blanksma, W. Vaalburg, H. J.G.M Crijns, and D. J van Veldhuisen
Abnormalities in myocardial contractility, metabolism and perfusion reserve in non-stenotic coronary segments in heart failure patients
Cardiovasc Res, July 1, 2002; 55(1): 97 - 103.
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 Eur J Heart FailHome page
S. Thackray, A. Coletta, P. Jones, A. Dunn, A. L. Clark, and J. G.F. Cleland
Clinical trials update: Highlights of the Scientific Sessions of Heart Failure 2001, a meeting of the Working Group on Heart Failure of the European Society of Cardiology. CONTAK-CD, CHRISTMAS, OPTIME-CHF
Eur J Heart Fail, August 1, 2001; 3(4): 491 - 494.
[Abstract] [Full Text] [PDF]

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