Skip Navigation



European Journal of Echocardiography Advance Access published online on August 23, 2007
European Journal of Echocardiography, doi:10.1016/j.euje.2007.06.007
This Article
Right arrow Abstract Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow All Versions of this Article:
9/4/458    most recent
j.euje.2007.06.007v1
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 Streb, W.
Right arrow Articles by Sutherland, G. R.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Streb, W.
Right arrow Articles by Sutherland, G. R.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2008. For permissions please email: journals.permissions@oxfordjournals.org

Full or pressure limited reperfusion of an acute myocardial infarct results in a different wall thickness and deformation of the distal myocardium – implications for clinical reperfusion strategies

Witold Streb, Maciej Marciniak, Piet Claus, Anna Marciniak, Myles McLaughlin, Jan D'hooge, Frank E. Rademakers, Bart Bijnens* and George R. Sutherland

Department of Cardiology, K.U.Leuven, Herestraat 49, B-3000 Leuven, Belgium

Received 18 January 2007; accepted after revision 20 June 2007.

* Corresponding author. Tel: +32 16 343472; fax: +32 16 343467; E-mail address: bart.bijnens{at}med.kuleuven.be (B. Bijnens).


   Abstract
Top
 Abstract
Introduction
 Methods
 Results
 Discussion
 References
 
Aim: The study aim was to determine the sequence of changes in both wall thickness and function in ‘at risk’ myocardium (using M-mode and radial strain/strain-rate imaging) induced by reperfusion of an acute transmural infarction, and to relate these changes to the presence or absence of a pressure-limiting stenosis in the infarct related epicardial vessel.

Methods: Eighteen closed-chest pigs were randomized into two groups (each with nine animals). In Group I, 4 weeks prior to induction of an acute transmural infarct, a copper coated stent was implanted in the proximal circumflex artery (Cx) to create a coronary artery stenosis of between 30 and 95% lumen diameter. At 4 weeks, the stenotic Cx vessel was occluded for 90 min by inflation of a PTCA balloon placed proximal to the stenosis to produce an acute transmural infarction. In Group II (the control group), 90 min Cx occlusion was performed in a normal vessel. In both groups the resulting acute transmural infarction was reperfused after 90 min by removing the PTCA balloon. For both groups, cardiac ultrasound data, including strain/strain-rate imaging, were collected at all stages of the investigation for subsequent offline analysis.

Results: In both groups, acute reperfusion (TIMI flow 3 or 2), immediately increased infarct zone end-diastolic wall thickness due to the development of oedema. The acute increase in wall thickness was significantly higher in the non-stenotic animals as compared to the ones with a residual stenosis. Neither of the groups showed any tendency to normalize deformation (strain) during the reperfusion period.

Conclusion: In this experimental study, the measurement of end-diastolic wall thickness was a simple and non-invasive tool to monitor acute infarct reperfusion. It also provided information on the presence of a flow limiting stenosis in the infarct related artery after restoration of the flow. The deformation of the myocardium remained impaired during early reperfusion, whether reflow was at full pressure or low pressure due to a residual stenosis in the infarct related artery.

Keywords: Reperfusion injury; Reperfusion oedema; Thrombolysis; Coronary angioplasty (PCI); Strain/strain-rate imaging


   Introduction
Top
 Abstract
 Introduction
Methods
 Results
 Discussion
 References
 
In current clinical practice, it is accepted that acutely ischaemic myocardium should be reperfused as early as possible. The efficacy of such a strategy has been proven in many experimental as well as clinical studies. However, the benefit of early reopening of an infarct related artery may be obviated by the so-called ‘reperfusion injury’. Such reperfusion injury has been defined as the subsequent loss of potentially viable myocytes, alive at the time of reperfusion, which occurs as a direct result of one or more phenomena initiated by the reperfusion itself.1 Differing causative mechanisms have been proposed among which are the following: the production of oxygen free radicals, alterations in calcium homeostasis, activation of complement system, microvascular injury and neutrofil-induced cellular injury.2,3 However, few authors have invoked extra-cellular oedema with increased tissue turgor as being a major determinant of outcome in the chain of events which follow acute infarct reperfusion.

In an experimental study Turschner et al.4 had previously reported on the series of morphological changes which occur when an acute transmural infarct is reperfused at full pressure with unobstructed flow in the epicardial vessel. They showed that acute reperfusion resulted in an immediate large increase in late end-diastolic and end-systolic wall thickness.4 Similar findings have been reported by Pislaru et al.5 Histological studies showed that this was due to the development of acute, massive, extra-cellular oedema.4 Currently, there is little known regarding the mechanisms leading to the development of oedema after infarct reperfusion or its physiologic consequences. Both biochemical and mechanical factors may contribute to the occurrence of the swelling of the wall. Reperfusion-induced microvascular dysfunction leads to fluid filtration, leukocyte plugging in capillaries and increased protein extravasation.6,7 On the other hand, reactive hyperaemia after the opening of an occluded artery has also been observed.8,9

The oedema caused by acute infarct reperfusion will result in a stiffer and thicker infarct segment, which subsequently will become the substrate on which scar is formed.10 This may positively increase wall stress and improve the remodelling of the left ventricle. However, the increased oedema and tissue turgor may cause compression of the residual capillary bed in both the infarcted segment itself and the adjacent myocardium, resulting in a decrease in flow, further jeopardizing any surviving viable cardiomyocytes. Therefore, the oedema itself could potentially worsen reperfusion injury and extend ultimate infarct size.

The changes in deformation of the myocardium during the development of acute ischaemia have been well documented in experimental and clinical studies.11–14 However, surprisingly little information is available regarding the changes in regional deformation during reperfusion, especially in the presence of pre-existing (chronic) coronary artery disease.

The aims of this study were to quantify myocardial wall thickness and deformation during reperfusion, which simulated two current clinical substrates: unrestricted flow in the epicardial vessel (as should occur in successful primary PCI) and restricted epicardial flow (as frequently occurs following thrombolytic therapy). The main aim was to determine whether they differed in the distal myocardial substrate produced.


   Methods
Top
 Abstract
 Introduction
 Methods
Results
 Discussion
 References
 
Experimental protocol
The animals were divided into two groups (nine pigs each). In Group I, a copper coated stent was implanted into the proximal segment of the left circumflex coronary artery (LCx), resulting in a severe coronary stenosis due to reactive intima hyperplasia, without the development of significant collaterals.13,15,16 These animals were followed for 4 weeks, during which they daily received aspirin (300 mg) and clopidogrel (150 mg). Group II consisted of normal animals, without any pre-existing stenosis. Next, in both groups a 90 min occlusion followed by reperfusion was induced. The study protocol is summarized in Figure 1.


Figure 1
View larger version (15K):
[in this window]
[in a new window]
[Download PowerPoint slide]
  		Figure 1 A schematic illustration of the time course of the experimental protocol.

 
Animal instrumentation
Eighteen pigs (25–30 kg) were included in the study. All were pre-medicated with ketamine (10–20 mg/kg IM). Anaesthesia was maintained with an IV infusion of propofol (10–20 mg/kg/h). The animals were intubated and mechanically ventilated with a mixture of air and oxygen using a Titus respirator pump (Dräger, Germany) set at a tidal volume of 250–400 ml and a respiratory rate 15–20/min. Care was taken to maintain arterial blood gases within a physiologic range. To get access to the coronary arteries and left ventricle, two 8F sheaths were inserted into the right and left carotid arteries. The left coronary artery was catheterized using a Judkins left catheter. Via the second sheath, a micro-manometer-tipped catheter (Millar Instruments, Houston, TX) was introduced into the left ventricle.

In Group I animals, a copper coated stent had been implanted 4 weeks previously in the proximal segment of the circumflex artery. For this purpose standard stents (Freedom Force, Global Therapeutics, Broomfield, USA) were electrolytically covered with copper.

At baseline, before the induction of the infarction, echocardiographic, haemodynamic and angiographic data were acquired. Occlusion of the LCx (proximal to the stenosis, if present) was induced by inflating an angioplasty balloon for 90 min. During the occlusion, all measurements were performed after 1 and 90 min of balloon inflation. Reperfusion was initiated by deflation of the balloon.

Ultrasound and haemodynamic data were acquired at 1, 5, 10, 30, 60 and 90 min after the onset of the reperfusion. The success of the reperfusion was confirmed angiographically. Finally the heart was arrested using an intravenous injection of saturated potassium chloride and excised for further evaluation of the infarct. The LV was cut into 8-mm-thick slices perpendicular to the long axis and immersed for 20 min at 37°C in a 2,3,4-triphenyltetrazolium chloride 1% solution for macroscopic evaluation of the extent of the infarction.

All animals were treated according to the National Institutes of Health Guide for the Care and Use of Laboratory Animals.

Data acquisition
A continuous 3-lead electrocardiogram was recorded. Left ventricular (LV) pressure and its first derivative (dP/dt) were measured by the micro-manometer-tipped catheter after adequate calibration. The haemodynamic recordings were digitized on-line and transferred to an external PC-workstation using a commercially available software package (Powerlab/Chart, ADInstruments, Mountain View, California).

Coronary angiography was performed using a Siemens system and archived in DICOM format. In those pigs having a stenosis of the circumflex artery, the minimal luminal diameter was measured using a QCA system.

All echocardiographic studies were performed using a Toshiba PowerVision 6000 (Toshiba Medical Systems, Otawara, Japan), which was equipped with an RF-interface for research purposes. The data were obtained as M-mode images using a 5 MHz phased array transducer (Toshiba, PSM- 50AT) with a pulse repetition frequency of 5 kHz. Since the area at risk was located in the posterior wall, the images were acquired from a short axis parasternal view. Recordings were done during a brief period of apnoea. The datasets were captured over 3–5 consecutive heart cycles and stored digitally. Data were transferred to a PC workstation for post-processing and analysis.

Data processing
Echocardiographic and haemodynamic data were analysed using a dedicated software package, SPEQLE (Software Package for Echocardiographic Quantification, Leuven, Belgium), as described in Ref. 4. For further processing of the data, the occurrence of global mechanical and timing events was indicated manually. Based on the ECG, end-diastole was defined at the onset of the QRS complex. The end of the electromechanical coupling period was indicated at the top of the R wave. Using the haemodynamic data, end-systole was defined to occur 20 ms before the peak negative value of dP/dt. The indication of the end of the ejection period was based on the presence of a sudden change, at the moment of aortic valve closure, in the velocity curve acquired from the septum.

Based on the RF data, grey-scale M-mode and myocardial velocity images were reconstructed. The M-mode images were used for measuring: end-diastolic wall thickness (EDWT), end-systolic wall thickness (ESWT), and maximal post-systolic wall thickness (PSWT). The relative change in the posterior wall thickness (WTindex) during occlusion and reperfusion, with regard to baseline (WTbaseline), was defined as:


Formula

WTindex was calculated, both for end-diastolic and end-systolic wall thickness, at each stage of the experiment.

Myocardial velocity images were used to calculate the natural maximal systolic radial strain rate (SR), end-systolic strain ({varepsilon}ES) and post-systolic strain ({varepsilon}PS) (calculated as the difference between maximal diastolic strain and end-systolic strain).17

Statistical analysis
Statistical analysis was performed using Statistica 6 (StatSoft, Tulsa, USA). Statistical significance was defined as p < 0. The time course of each variable, compared to its baseline, was analysed using a Wilcoxon matched pairs test. The comparisons of both groups were performed using a Mann–Whitney U test. Data are presented as mean ± standard error (SE).


   Results
Top
 Abstract
 Introduction
 Methods
 Results
Discussion
 References
 
The presence of a transmural infarct was confirmed by visual analysis of the excised hearts after TTC staining. At the onset of the occlusion–reperfusion experiment, Group I animals had an angiographically determined diameter stenosis of 30–95%.

The results of haemodynamic measurements are summarized in Table 1. The mean heart rate at baseline in the control group (Group II) was 100 ± 6 beats/min and in the stenosed group (Group I) 84 ± 6 beats/min (p = NS). During the occlusion, in Group II, the heart rate only changed significantly after 90 min, whereas in Group I, there was a gradual, significant increase in heart rate from the beginning of the occlusion.

End-systolic pressure, dP/dtmin and dP/dtmax did not alter significantly during the occlusion as well as during the reperfusion period.

Figure 2 shows typical M-mode traces of both groups at the different stages of the experiment. Table 2 summarizes the M-mode measurements.


Figure 2
View larger version (105K):
[in this window]
[in a new window]
[Download PowerPoint slide]
  		Figure 2 Typical M-mode images for both groups during the occlusion and reperfusion periods. With the occlusion, end-systolic wall thickness (ESWT) decreases to almost similar size as the end-diastolic wall thickness (EDWT) in both groups. During reperfusion, a much more pronounced increase in EDWT thickness is seen in Group II (without pre-existing stenosis) whereas ESWT returns to baseline level or slightly above.

 


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

  		Table 1 Results of the haemodynamic measurements

 


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

  		Table 2 M-mode measurements

 
During the occlusion, both groups showed a similar pattern of change. The most pronounced finding was the reduction of ESWT and PSWT compared to their baseline values. The changes were much more pronounced in the animals without a pre-existing stenosis (Group II) with both ESWT and PSWT significantly less (p < 0.03).

Additionally, the ESWTindex was significantly reduced in the control group (Group II) whereas in the animals with a pre-existing stenosis, the ESWT was not decreased as a result of the occlusion (Figure 3). However, for both groups, the EDWT, as well as the EDWTindex, remained unchanged during the occlusion (Figure 4).


Figure 3
View larger version (14K):
[in this window]
[in a new window]
[Download PowerPoint slide]
  		Figure 3 The evolution of the end-systolic posterior wall thickness (ESWT) index during the experiment. In Group II, with normal coronary arteries, ESWT decreases with the acute occlusion, whereas with reperfusion, it increases again to normal or even super-normal values. In Group I, with a pre-existing stenosis, changes are much less pronounced (*p < 0.05 compared to baseline (BL); {dagger}p < 0.05 comparing both groups).

 


Figure 4
View larger version (20K):
[in this window]
[in a new window]
[Download PowerPoint slide]
  		Figure 4 Changes in end-diastolic wall thickness induced by reperfusion. There is a markedly larger change with reperfusion in the group with normal coronary arteries (*p < 0.05 compared to baseline (BL); {dagger}p < 0.05 comparing both groups).

 
Starting within the first minute of reperfusion, in the control group (Group II), there was a significant increase in ESWT, EDWT, and PSWT. Soon after the onset of reperfusion, there was a similar trend in ESWT, EDWT and PSWT in the group with a pre-existing stenosis (Group I) (Figure 2).

From the onset of reperfusion, the EDWTindex suddenly increased significantly in Group II compared to either baseline or occlusion values (Figure 4). In Group I, this increase was only found to be moderate. During the reperfusion period, the increase in EDWTindex showed a logarithmic evolution with an increase of 198 ± 28% after 5 min. In comparison, in Group I, at the same timepoint, the value was only 117±9%. At 90 min of reperfusion the EDWTindex reached 202 and 130% in Group II and Group I, respectively. The comparison of both groups (using a Manne–Whitney U test), showed a significant difference (p < 0.007) in the time course of change in the values during the reperfusion period.

Additionally, in Group II, there was an immediate increase in the ESWTindex, which was significant after 5 min of reperfusion when compared to both baseline values and Group I (Figure 3). In Group I, the ESWTindex did not change and remained negative during the whole period of reperfusion (Figure 3).

Table 3 shows the results of end-systolic radial strain ({varepsilon}ES) and post-systolic strain ({varepsilon}PS). As would be expected, baseline {varepsilon}ES was significantly lower in Group I (supplied by a stenosed epicardial vessel), compared to Group II (supplied by a normal epicardial vessel) (0.43 ± 0.06 vs 0.57 ± 0.05, p < 0.05).


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

  		Table 3 Results of DMI data analysis

 
In both groups, posterior wall {varepsilon}ES showed an abrupt reduction at the onset of the total occlusion. Compared to baseline, the values remained significantly reduced during the occlusion, as well as the reperfusion period. As similar changes were present in both groups, no significant difference in {varepsilon}ES was detected between them during the experiment although in the non-stenotic Group II, there was a tendency towards a decrease in radial strain from 5 min after the onset of reperfusion.

As expected, at baseline, the group with a stenosed vessel showed clear post-systolic deformation due to the presence of the significant stenosis while the normal group had almost none at baseline. At the onset of the total occlusion, in both groups, there was a significant increase in post-systolic strain. In Group I, {varepsilon}PS dropped to the baseline value towards the end of the occlusion and remained constant during the reperfusion. In Group II, {varepsilon}PS dropped to values similar to the stenosed group towards the end of the occlusion and remained at this level during the reperfusion.

Maximal systolic strain rate SR (Figure 5) dropped markedly during the occlusion in both groups (being significantly different from baseline from the first minute of occlusion in Group I and at 90 min of occlusion in Group II). Neither in Group I nor in Group II was there a significant increase in maximal systolic SR at the onset of the reperfusion. However, after 30 min of reperfusion maximal systolic SR decreased in the control group (Group II) and became significantly lower compared to the group with a residual stenosis (Group I) (Figure 5).


Figure 5
View larger version (13K):
[in this window]
[in a new window]
[Download PowerPoint slide]
  		Figure 5 Maximal systolic strain rate (SR) in both groups (*p < 0.05 compared to baseline (BL);{dagger}p < 0.05 comparing both groups).

 

   Discussion
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
References
 
The above experimental findings (summarized in Table 4) expand the earlier observations of Turschner et al.,4 who showed that full pressure reperfusion of an acute transmural infarct is associated with an immediate increase in end-diastolic wall thickness. Their model of patent artery reperfusion of an acute infarct was planned to mimic the likely changes in the distal myocardium which would occur following a successful primary percutaneous coronary intervention. This study was designed to compare and contrast full pressure reperfusion changes with those likely to occur after low pressure reperfusion of an acute infarct following thrombolysis, where a severe residual stenosis frequently persists in the epicardial vessel.


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

  		Table 4 A summary of the changes observed during the different stages of the experiment

 
In their model of full pressure reperfusion, Turschner et al. showed the acute increase in EDWT to be the result of massive extra-cellular oedema, as previously described by Reimer and Jennings.18 Prior studies, designed to look at the influence of anti-inflammatory drugs on the evolution of myocardial infarction, have suggested that this wall oedema can be reduced when these agents are administered.19,20

However, the present study shows that simply the presence of a pre-existing stenosis in a reperfused vessel after an acute coronary occlusion will influence the resulting wall dimensions of the distal transmurally infarcted myocardium. This observation would suggest that the increase in wall thickness (likely to be related to the degree of extra-cellular oedema) would appear to be strongly dependent on mechanical factors, such as elevated hydrostatic pressure, after infarct reperfusion. Does this increase in wall thickness occur after reperfusion of myocardium with either acute or chronic ischaemia with no acutely infarcted tissue? Kukulski et al. in their study on acute changes in ‘at risk’ segmental deformation, during and after percutaneous coronary angioplasty, did not observe any changes in end-diastolic wall thickness following TIMI 3 immediate reperfusion.12 This would suggest that the acutely increased wall thickness with reperfusion is only a marker of infarction and does not occur in ischaemia. Other clinical imaging studies have also related the acute increase in wall thickness in full pressure reperfusion to be, in part, due to the transmurality of the acute infarct.21–23

The usefulness of ultrasonic regional strain and strain rate, for the quantification of alterations in myocardial deformation during ischaemia has already been validated in the experimental and clinical settings.23–26 In summary, during transient acute ischaemia, a reduction of end-systolic strain, accompanied by the occurrence of post-systolic thickening (for radial deformation) or shortening (for longitudinal deformation) is observed. These changes were also observed in the early post-occlusion period in our experiment as ischaemia was induced with end-systolic strain values progressively falling to zero as ischaemia progressed to infarction.

Potential clinical implications
Rapid reperfusion is the accepted treatment strategy for acute myocardial infarction. The restoration of flow in the infarct related artery will ultimately result in improved LV performance, a better long-term outcome, and quality of life.27,28 Reperfusion can be achieved either pharmacologically or by percutaneous coronary intervention (PCI). Although clinically both strategies lead to an immediate clinical improvement in the patient, their angiographic outcome is usually different. Whereas PCI with stenting will normally result in a widely patent artery, thrombolysis will restore flow but often leaves a severe chronic stenosis in the vessel.

With regard to the findings in this study, both strategies may have a different impact on the myocardial wall dimensions and function.29 Measuring wall thickness could thus be useful to monitor reperfusion therapy. Information about the presence of a residual stenosis in the infarct related artery could be obtained. This could be useful in further decision making with regard to the therapeutic strategy.

In our animal model of myocardial infarction, we were able to observe the changes in myocardial dimensions and deformation as a consequence of reperfusion, in the setting of both a pre-existing stenosis and a completely reopened vessel. However, long-term observation is required to evaluate the influence of residual stenosis on left ventricle remodelling.

In this study we have reproduced two clinical situations of an acute coronary occlusion. The first corresponds to a patient with chronic ischaemia undergoing a myocardial infarction and treated by thrombolytic therapy, leaving a (flow limiting) stenosis after reperfusion. The second corresponds to the occurrence of an acute infarct with previously normal coronary arteries. This situation rarely occurs in daily clinical practice. In our experiments we did not consider the situation of a sudden total reopening of the vessel after an infarction in a chronically stenosed vessel, as it would occur in patients undergoing primary PCI. However, the study from Merli et al.30 shows similar results in a clinical setting, where patients undergoing primary PCI show exactly the same changes as our ‘control’ group with full pressure reperfusion, whereas the patients undergoing thrombolysis show the same changes as our group with a residual stenosis. Additionally, this study also shows that performing PCI of the residual stenosis after thrombolysis results in a further increase in EDWT, confirming that the differences we observe between both groups in our study are indeed mainly related to the residual stenosis at the time of reperfusion.

Study limitation
For the purpose of this study we used a closed-chest pig model for chronic ischaemia, mimicking the natural course of the development of a chronic stenosis in humans. However, this model has a disadvantage if used for echocardiographic assessment of the heart since the anatomy of the pig only allows adequate imaging using a parasternal short axis view.

In this study the acquired data were processed for strain/strain-rate imaging, which are known to be angle dependent. Therefore, from a parasternal view, we could only analyse the posterior wall.

In order to strengthen our suggestion that the observed changes are mainly related to differences in oedema, more detailed histological studies should be carried out.

Conclusions
Reperfusion of an acute infarction results in an immediate increase in end-diastolic wall thickness. The amount of this is related to the presence of a residual stenosis in the reopened vessel, with the biggest increase in thickness occurring when the vessel is fully reopened. The measurement of end-diastolic wall thickness is thus a simple and noninvasive tool to monitor successful reperfusion. Moreover, information about the presence of a residual stenosis, in the infarct related artery, could be obtained. Deformation of the myocardium remains impaired during early reperfusion, independently from the presence or absence of a flow limiting stenosis in the infarct related artery.


   References
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 References
 

  1. Park JL, Lucchesi BR. Mechanism of myocardial reperfusion injury. Ann Thorac Surg (1999) 68:1905–12.[Abstract/Free Full Text]
  2. L'Abbate A. Recanalization versus reperfusion for myocardial survival and prevention of ventricular geometry. Am Heart J (1999) 138:S89–95.[CrossRef][Web of Science][Medline]
  3. Verma S, Fedak PW, Weisel RD, Butany J, Rao V, Maitland A, et al. Fundamentals of reperfusion injury for the clinical cardiologist. Circulation (2002) 105:2332–6.[Free Full Text]
  4. Turschner O, D'hooge J, Dommke C, Claus P, Verbeken E, De Scheerder I, et al. The sequential changes in myocardial thickness and thickening, which occur during acute transmural infarction, infarct reperfusion and the resultant expression of reperfusion injury. Eur Heart J (2004) 25:794–803.[Abstract/Free Full Text]
  5. Pislaru C, Bruce CJ, Seward JB, Greenleaf JF. Distinctive changes in end-diastolic wall thickness and postsystolic thickening in viable and infarcted myocardium. J Am Soc Echocardiogr (2004) 17:855–6.[CrossRef][Web of Science][Medline]
  6. Granger DN. Ischemia-reperfusion: mechanism of microvascular dysfunction and the influence of risk factors for cardiovascular disease. Microcirculation (1999) 6:167–78.[CrossRef][Web of Science][Medline]
  7. Agati L. Microvascular integrity after reperfusion therapy. Am Heart J (1999) 138:S76–8.[CrossRef][Web of Science][Medline]
  8. Heyndrickx GR, Baig H, Nellens P, Leusen I, Fishbein MC, Vatner SF. Depressing of regional blood flow end wall thickening after brief coronary occlusion. Am Phys Soc (1978) H653–9.
  9. Gaasch WH, Bernhard SA. The effect of acute changes in coronary blood flow on left ventricular end-diastolic wall thickness. Circulation (1977) 56:593.[Abstract/Free Full Text]
  10. Wiesman HF, Healy B. Myocardial infarct expansion, infarct extension, reinfarction: pathophysiological concepts. Prog Cardiovasc Dis (1987) 17:1641–50.
  11. Firstenberg MS, Greenberg NL, Smedira NG, Castro P, Thomas JD, Garcia MJ. The effects of acute coronary occlusion on non-invasive echocardiographically derived systolic and diastolic myocardial strain rates. Curr Surg (2000) 57:466–72.[CrossRef][Medline]
  12. Kukulski T, Jamal F, Herbots L, D'hooge J, Bijnens B, Hatle L, et al. Identification of acutely ischemic myocardium using ultrasonic strain rate measurements. A clinical study in patients undergoing coronary angioplasty. J Am Coll Cardiol (2003) 41:810–9.[Abstract/Free Full Text]
  13. Weidemann F, Dommke C, Bijnens B, Claus P, D'hooge J, Mertens P, et al. Defining the transmurality of a chronic myocardial infarction by ultrasonic strain-rate imaging. Implications for identifying intramural viability. An experimental study. Circulation (2003) 107:883–8.[Abstract/Free Full Text]
  14. Pislaru C, Belohlavek M, Bae RY, Abraham TP, Greenleaf JF, Seward JB. Regional asynchrony during acute myocardial ischemia quantified by ultrasound strain rate imaging. J Am Coll Cardiol (2001) 37:1141–8.[Abstract/Free Full Text]
  15. Bito V, Heinzel FR, Weidemann F, Dommke C, van der Velden J, Verbeken E, et al. Cellular mechanisms of contractile dysfunction in hibernating myocardium. Circ Res (2004) 94:794–801.[Abstract/Free Full Text]
  16. Bito V, van der Velden J, Claus P, Dommke C, Van Lommel A, Mortelmans L, et al. Reduced force generating capacity in myocytes from chronically ischemic, hibernating myocardium. Circ Res (2007) 100:229–37.[Abstract/Free Full Text]
  17. D'hooge J, Heimdal A, Jamal F, Kukulski T, Bijnens B, Rademakers F, et al. Regional strain and strain rate measurements by cardiac ultrasound: principles, implementation and limitations. Eur J Echocardiogr (2000) 1:154–70.[Abstract/Free Full Text]
  18. Reimer KA, Jennings RB. The changing anatomic reference base of evolving myocardial infarction. Underestimation of myocardial blood flow and overestimation of experimental anatomic infarct size due to tissue edema hemorrhage and acute inflammation. Circulation (1979) 60:866–76.[Free Full Text]
  19. Hammerman H, Schoen FJ, Braunwald E, Kloner RA. Druginduced expansion of infarct: morphologic and functional correlations. Circulation (1984) 3:611–8.
  20. Brown EJ Jr, Kloner RA, Schoen FJ, Hammerman H, Hale S, Braunwald E. Scar thinning due to Ibuprofen administration after experimental myocardial infarction. Am J Cardiol (1983) 1:877–83.
  21. Biagini E, Galema TW, Schinkel AF, Vletter WB, Roelandt JR, Ten Cate FJ. Myocardial wall thickness predicts recovery of contractile function after primary coronary intervention for acute myocardial infarction. J Am Coll Cardiol (2004) 43:1489–93.[Abstract/Free Full Text]
  22. Weidemann F, Wacker C, Rauch A, Wolfgang RB, Bijnens B, Sutherland GR, et al. Ultrasonic strain rate imaging can predict the recovery of function after acute myocardial infarction and assess the transmurality of scar in chronic infarctions. Eur J Echocardiogr (2004) S143:664.
  23. Zhang Y, Chan AK, Yu CM, Yip GW, Fung JW, Lam WW, et al. Strain rate imaging differentiates transmural from nontransmural myocardial infarction: a validation study using delayed-enhancement magnetic resonance imaging. J Am Coll Cardiol (2005) 46:864–71.[Abstract/Free Full Text]
  24. Jamal F, Strotmann J, Weidemann F, Kukulski T, D'hooge J, Bijnens B, et al. Noninvasive quantification of the contractile reserve of stunned myocardium by ultrasonic strain rate and strain. Circulation (2001) 104:1059–65.[Abstract/Free Full Text]
  25. Jamal F, Szilard M, Kukulski T, Liu XS, D'hooge J, Bijnens B, et al. Changes in systolic and postsystolic wall thickening during acute coronary occlusion and reperfusion in closed-chest pigs: implications for the assessment of regional myocardial function. J Am Soc Echocardiogr (2001) 14:691–7.[CrossRef][Web of Science][Medline]
  26. Voigt JU, Lindenmeier G, Exner B, Regenfus M, Werner D, Reulbach U, et al. Incidence and characteristics of segmental postsystolic longitudinal shortening in normal, acutely ischemic, and scarred myocardium. J Am Soc Echocardiogr (2003) 16:415–23.[CrossRef][Web of Science][Medline]
  27. Miketic S, Carlsson J, Tebbe U. Improvement of global and regional left ventricular function by percutaneous transluminal coronary angioplasty after myocardial infarction. J Am Coll Cardiol (1995) 25:843–7.[Abstract]
  28. Penco M, Romano S, Agati L, Dagianti A, Vitarelli A, Fedele F, et al. Influence of reperfusion induced by thrombolytic treatment on natural history of left ventricular regional wall motion abnormality in acute myocardial infarction. Am J Cardiol (1993) 71:1015–20.[CrossRef][Web of Science][Medline]
  29. Penco M, Dagianti A Jr, Romano S, Iacoboni C, Vitarelli A, Fedele F, et al. Degree of residual stenosis of infarctrelated artery. Another variable affecting recovery of regional function after thrombolysis. Eur Heart J (1998) 19:727–36.[Abstract/Free Full Text]
  30. Merli E, Fischer A, Karu T, Baltabaeva A, Marciniak A, Bunce N, et al. Can reperfusion be predicted by acute thickening of at risk myocardium in STEMI? Full pressure vs pressure limiting reperfusion. Eur J Echocardiogr (2005) 6(Suppl. 1):S12.[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
 HeartHome page
N C Edwards, H Routledge, and R P Steeds
T2-weighted magnetic resonance imaging to assess myocardial oedema in ischaemic heart disease
Heart, August 15, 2009; 95(16): 1357 - 1361.
[Abstract] [Full Text] [PDF]

This Article
Right arrow Abstract Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow All Versions of this Article:
9/4/458    most recent
j.euje.2007.06.007v1
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 Streb, W.
Right arrow Articles by Sutherland, G. R.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Streb, W.
Right arrow Articles by Sutherland, G. R.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?