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European Journal of Echocardiography 2004 5(2):149-155; doi:10.1016/S1525-2167(03)00074-X
© 2004 by European Society of Cardiology
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Copyright © 2003, The European Society of Cardiology

The incremental value of myocardial contrast echocardiography (MCE) as a bedside decision-making tool in the coronary care unit

R Winter* and R Willenheimer

Department of Cardiology, University Hospital Malmö, Lund University, Malmö, Sweden

Received 4 March 2003; received in revised form 1 July 2003; accepted after revision 1 July 2003.

* Corresponding author. Department of Cardiology, Malmö University Hospital, S-205 02 Malmö, Sweden. Tel.: +46-40-33-10-00; fax: +46-40-33-62-09. reidar.winter{at}skane.se


    1 Background
 Top
 1 Background
 2 Case report
 3 Discussion
 References
 
Patients with a developing acute myocardial infarction (MI) and ST elevation or bundle branch block should be treated with percutaneous coronary intervention (PCI) or thrombolytic therapy, according to current guidelines. However, there are several problems in this context. In smaller hospitals, especially outside office hours, there is still a commonly limited access to PCI. Thrombolysis, on the other hand, should be used only according to strict criteria since it is associated with some risk.1,2 The choice of treatment is crucially important in this patient category, and can be challenging in some cases. One particular area of concern is the lack of consensus in the interpretation of ST elevations. This is illustrated by the considerable variability in assessment of ST elevation, demonstrated in a recent study by Carley et al.3 Moreover, the degree of ST elevation is not a very accurate measurement of the extent of the area at risk: there is some degree of mismatch between ST elevation and perfusion defects,4 and there seems to be considerable mismatch between wall motion abnormality using echocardiography, and the presence or absence of ST elevations.5 One possible explanation for this is the phenomena of hyperacute T waves without J point elevation, that can occur in the early phases of an acute MI. Hyperacute T waves are often associated with proximal LAD occlusion, and are therefore often associated with a relatively large area at risk.6–9

In other words, some of the patients with myocardial ischemia without ST elevations could have a relatively large area at risk of MI.

Myocardial contrast echocardiography (MCE) is a promising tool for estimating the area at risk, and can also accurately predict an open LAD in an anterior MI. This has been shown both in the experimental setting and in clinical studies.3,10–16 However, MCE has yet to prove its incremental value as a bedside tool in the clinical setting of the acute coronary syndrome.


    2 Case report
 Top
 1 Background
 2 Case report
 3 Discussion
 References
 
A 47-year-old male presented with severe chest pain and elevated anterior T waves, without J point elevation (Fig. 1). The patient had been admitted only 6 weeks earlier due to an anterior MI. At this point of time he had similar T waves but clear anterior ST elevation, where the J point was elevated in leads V1 through V4 (Fig. 2). At this occasion the patient was given thrombolytic treatment with Metalyse®. He had a clinical reperfusion with clear ST segment regression and cessation of the chest pain. Echocardiography 3 days after the admission showed normal global systolic left ventricular (LV) function with an LV ejection fraction EF of 60%, and without any regional contractility defects. The patient was mobilised in an uncomplicated way, without recurrent angina and underwent submaximal exercise testing that did not show any signs of myocardial ischemia or other markers of risk. The patient was discharged and referred to coronary angiography, which due to the patient's low risk profile was planned for a later time point. He received secondary prophylactic medication with aspirin, beta-blockade and a statin. He had no recurrent angina at home during the following weeks.


Figure 1
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Figure 1 ECG at admission, showing a pathological R wave progression and high T-waves, but no J-point elevation.

 


Figure 2
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Figure 2 ECG 6 weeks earlier at admission. Prominent anterior ST elevations are seen in the ECG.

 
Six weeks after discharge he suddenly woke up while sleeping, once again experiencing severe chest pain, similar to what he had felt 6 weeks earlier. He arrived at the emergency department at 02.30 a.m. Upon arrival, the chest pain had substantially diminished in response to treatment with nitroglycerine and morphine in the ambulance. The ECG showed elevated T waves but no J point elevation (Fig. 1). Due to the clinical picture with a non-conclusive ECG and considerable clinical improvement after primary treatment, the patient was given low molecular heparin, clopidogrel and nitroglycerine infusion at the coronary care unit. He was however still feeling some chest discomfort and pain in his left arm. The ECG monitoring system did not show any significant ECG abnormalities and the patient was hemodynamically stable.

A bedside echocardiography examination was now performed, using a combination of three modalities: 2D echocardiography, contrast-enhanced real time perfusion imaging and high frequency colour Doppler examination. Bolus injection of the contrast medium Sonovue® was used for echo-enhancement. This allowed for an analysis of myocardial contractility based on the 2D echocardiogram, an assessment of the area at risk based on the real time perfusion imaging, and a search for blood flow in the apical perforators using high frequency colour Doppler technique.

The examination showed a relatively large apical anteroseptal akinetic area, an accompanying perfusion defect and no detectable apical perforator flow (Figs. 3–5GoGo). The area at risk was determined using the standard 16-segment model. It constituted five segments of 16, i.e. approximately 1/3 of the LV. On the basis of a strong suspicion of ongoing ischemia and a large area at risk, the patient was given thrombolytic therapy with Metalyse®. The patient had a good clinical effect of the thrombolytic treatment with relief of the pain. There were no signs of acute heart failure.


Figure 3
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Figure 3 End-systolic still frame in the four-chamber view; there is a clear anteroseptal apical akinesia, with preserved myocardial thickness which is typical for an acute infarction.

 


Figure 4
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Figure 4 A relatively large apical perfusion defect is seen in this end systolic frame of power modulation, realtime perfusion study.

 


Figure 5
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Figure 5 No left ventricular apical perforators can be seen using contrast-enhanced high frequency colour Doppler.

 
Two hours after the thrombolytic treatment the echocardiography examination was repeated. It showed a considerably better contractility, as demonstrated by the end systolic frame of the four-chamber view in Fig. 6. Furthermore, there was a restored perfusion in the area at risk, and flow in the apical perforators could be clearly seen (Figs. 7 and 8Go).


Figure 6
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Figure 6 End-systolic frame in four-chamber view showing improved wall motion in the apical region of the left ventricle.

 


Figure 7
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Figure 7 Perfusion is clearly restored in this end-systolic still frame of a power modulation real time study.

 


Figure 8
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Figure 8 Apical perforators are clearly demonstrated in this diastolic frame of a contrast-enhanced high frequency colour Doppler study of the apical region of the left ventricle.

 
The patient was stable for the rest of the night, but again experienced chest pain the following day. Dynamic ECG changes were registered on the automated ST monitor. An acute coronary angiogram was performed, showing an occluded left anterior descending coronary artery (LAD), directly after the first diagonal branch (D1). The LAD was opened using balloon angioplasty and a stent was implanted with satisfactory final result. There was also significant stenosis in D1, the right coronary artery and distally in the circumflex artery. The patient was mobilised without further complications 2 days after the procedure.


    3 Discussion
 Top
 1 Background
 2 Case report
 3 Discussion
 References
 
This patient undoubtedly had good reperfusion in response to the thrombolytic therapy given the second time he was admitted to hospital. On the basis of the initial relatively large non-reperfused area, i.e. the myocardium at risk, there was a high likelihood that the patient would have developed significant heart failure, had he not received thrombolytic therapy. Instead, echocardiography showed good myocardial contractility following thrombolysis and clinically the patient showed no signs of acute heart failure. Since there was no indication for thrombolytic treatment based on standard criteria, this case report illustrates that there is a ‘grey-zone’ where new echocardiographic technique, using a combination of different modalities bedside, can be of incremental value for decision-making in the individual case. In this case the patient had a relatively short duration of symptoms, which at least partly can explain the lack of clear ST elevation, having instead what could be interpreted as hyperacute T waves.

One might argue that there was a clear clinical suspicion of an ongoing myocardial infarction and that there was reason to treat this patient with reperfusion therapy anyway. However, using strict indications for reperfusion therapy there was no basis for such treatment. It may also be claimed that the patient should have been transported to the catheterisation laboratory for an acute coronary angiogram. In many hospitals this is, however, not possible, at least not outside office hours. This is also the case at our hospital.

Earlier studies have shown MCE to be a valuable instrument for assessing the area at risk.3,10–16 However, to our knowledge, MCE has not been shown to have an incremental decision-making value in the setting of the acute coronary syndrome. This case report suggests that, in such an acute scenario, bedside MCE is feasible and provides valuable help in choosing between treatment with reperfusion therapy and plaque stabilising therapy, in uncertain cases. The use of a combination of different imaging modalities—2D echocardiography, contrast-enhanced real time perfusion imaging and high frequency colour Doppler examination—clearly played a decisive role in this particular case. Without it, the patient would not have received thrombolytic therapy.

One important limitation of the technique is that it does not separate previous from acute infarctions. In this particular case this was apparent from comparing the echocardiography from the earlier admission to compare with, thus confirming that the wall motion defect was indeed a new one.

Another limitation of MCE is artefacts in the basal anterior and basal lateral wall. This is often presented as the disadvantage of MCE compared to radionuclide techniques. On the other hand, radionuclide technique is not applicable bedside in the coronary care unit. Furthermore, MCE almost always provides high quality perfusion assessment in the anteroseptal parts of the left ventricle. Anterior wall ischemia is more likely to result in a large MI compared to ischemia in other regions of the myocardium. Indeed, cardiogenic shock is most often caused by an anterior MI. When the mortality is the highest the potential gain is the greatest. Therefore MCE is likely to be most useful in cases of threatening anterior MI.

In conclusion, this case report clearly illustrates the potential incremental value of MCE as a feasible bedside decision-making tool in the clinical setting of the acute coronary syndrome.

Prospective clinical studies are required to determine the precise value of MCE in this regard.


    References
 Top
 1 Background
 2 Case report
 3 Discussion
 References
 

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