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Importance of Gated Imaging in Both Phases of Myocardial Perfusion SPECT: Myocardial Stunning After Dipyridamole Infusion

Vahidreza Dabbagh Kakhki, Seyed Rasoul Zakavi, Ramin Sadeghi and Ahmad Yousefi

Department of Nuclear Medicine, Emam Reza Hospital, Mashad University of Medical Sciences, Mashad, Iran

Correspondence: For correspondence or reprints contact: Vahidreza Dabbagh Kakhki, Department of Nuclear Medicine, Emam Reza Hospital, Mashad University of Medical Sciences, Mashad, Iran. E-mail: dvdkakh@yahoo.com


    ABSTRACT
 TOP
 ABSTRACT
 INTRODUCTION
 CASE REPORT
 DISCUSSION
 References
 
We present the case report of a 72-y-old woman who underwent 99mTc-sestamibi gated myocardial perfusion SPECT with a 2-d protocol. SPECT images revealed ischemia of the apical, anteroapical, apicoseptal, and septal walls. Postdipyridamole gated SPECT revealed significant deterioration in the left ventricular ejection fraction (LVEF), wall motion, and systolic wall thickening relative to the findings obtained with rest gated SPECT. Myocardial stunning is a lingering contractile dysfunction that occurs after a brief ischemic insult. Myocardial stunning after dynamic exercise or pharmacologic stress tests has been demonstrated. Thus, the use of gated SPECT in both phases of perfusion studies may add useful information about cardiac function, as a poststress study alone probably reflects stunned myocardium in some patients undergoing ischemic stress tests. The difference between poststress LVEF and rest LVEF may have a powerful impact on prognosis, as it seems to depend on the extent and severity of induced ischemia.

Key Words: myocardial stunning; gated SPECT; dipyridamole; myocardial perfusion


    INTRODUCTION
 TOP
 ABSTRACT
 INTRODUCTION
 CASE REPORT
 DISCUSSION
 References
 
The term "stunned myocardium" has been used to describe myocardium with persistent contractile dysfunction despite the restoration of perfusion after a period of ischemia; this condition usually improves with time (1).

Electrocardiography (ECG)-gated SPECT myocardial perfusion imaging can be used for the simultaneous assessment of myocardial perfusion and left ventricular function (2,3). This integrated approach has already proved useful clinically for tissue characterization and prediction of prognosis (4).


    CASE REPORT
 TOP
 ABSTRACT
 INTRODUCTION
 CASE REPORT
 DISCUSSION
 References
 
A 72-y-old woman with a history of atypical chest pain and exertional dyspnea was referred for gated myocardial perfusion SPECT. Cardiac risk factors included hypertension, diabetes mellitus for 10 y, hypercholesterolemia, and age. The results of resting ECG were normal. The patient underwent myocardial perfusion SPECT with a 2-d protocol. On the first day, 740 MBq of 99mTc-sestamibi were injected intravenously 4 min after the infusion of dipyridamole at 0.568 mg/kg. At 90 min after the injection of 99mTc-sestamibi, gated perfusion imaging was performed in the supine position by use of a dual-head {gamma}-camera in the 90° setting (Dual-Head Variable-Angle E.CAM; Siemens) and equipped with high-resolution, low-energy collimators. After dipyridamole injection, the patient experienced no chest pain; ECG showed ST depression in the precordial leads. On the next day, at 10 min after the oral administration of a trinitroglycerin (NTG) pearl, 740 MBq of 99mTc-sestamibi were injected, and rest images were acquired with the same protocol.

The images were stored in a 64 x 64 matrix in the computer and reconstructed by filtered backprojection with a Butterworth filter (order = 5, cutoff frequency = 0.4). Gated SPECT data were analyzed with Quantitative Gated SPECT software (Cedars Cardiac Quantification; Cedars-Sinai Medical Center) for end-diastolic volume (EDV), end-systolic volume (ESV), and left ventricular ejection fraction (LVEF). Myocardial perfusion was assessed visually and semiquantitatively. A 17-segment 5-point scoring system was used for the semiquantitative assessment of myocardial perfusion.

Reversible defects (myocardial ischemia) were noted in the apical, anteroapical, apicoseptal, and anteroseptal walls (Figs. 1 and 2). The summed stress score, summed rest score, and summed difference score were 11, 5, and 6, respectively.


Figure 1
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FIGURE 1.  Abnormal 99mTc-sestamibi myocardial perfusion SPECT. Images show large reversible defect involving apical, anteroapical, apicoseptal, septal, and anteroseptal walls.

 

 

Figure 2
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FIGURE 2.  Three perfusion polar maps (from top to bottom: stress, rest, and reversibility) show extent and severity of reversible perfusion defect. ANT = anterior; INF = inferior; SEPT = septal.

 

 
The rest gated images displayed in 2-dimensional and 3-dimensional (Fig. 3) formats revealed normal left ventricular wall motion and systolic wall thickening. EDV, ESV, and LVEF calculated from the rest gated images were 53 mL, 17 mL, and 68%, respectively. The stress gated images acquired after dipyridamole injection (Fig. 3) revealed akinesia in the apicoseptal region as well as hypokinesia in the apical, anteroapical, anteroseptal, and septal walls. Calculated EDV, ESV, and LVEF were 69 mL, 46 mL, and 33%, respectively.


Figure 3
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FIGURE 3.  Three-dimensional display of ventricular wall motion in postdipyridamole and rest gated images. Poststress images reveal remarkable wall motion abnormality in apex and septum, whereas rest images reveal normal left ventricular wall motion. Wire-frame and shaded surfaces represent endocardium in end-diastolic and end-systolic phases, respectively. ANT = anterior; INF = inferior; LAT = lateral; SEPT = septal.

 

 
Dipyridamole gated 99mTc-sestamibi SPECT revealed significant deterioration in systolic myocardial function (decreased LVEF) as well as remarkable wall motion and systolic wall thickening abnormalities (myocardial stunning) in the regions of reversible defects relative to the findings obtained with rest gated SPECT.


    DISCUSSION
 TOP
 ABSTRACT
 INTRODUCTION
 CASE REPORT
 DISCUSSION
 References
 
Myocardial stunning is a lingering contractile dysfunction that occurs after a brief ischemic insult, even in the absence of necrosis, and persists for some time after the restoration of adequate blood flow (1). The histologic appearance of the stunned myocardium is normal, so there is no permanent damage and contractile function is able to recover gradually with time (5). Although in some instances full recovery may occur within a few minutes after the recovery of myocardial perfusion, in some cases it may take hours, days, or even weeks, depending on the severity of the ischemic episode (6). A variety of hypotheses have been postulated as mechanisms for myocardial stunning; these include insufficient energy production by mitochondria, impaired energy use by myofibrils, reduced myofilament responsiveness to calcium, reduced contractile protein activation, calcium overload, and generation of free radicals (6,7). Reperfusion through the restoration of the oxygen supply, which is beneficial and protective for the ischemic myocardium, induces at the same time a burst of oxygen-free radicals, complicated by intracellular Ca2+ overload, which is harmful for contractile proteins (7).

Well-documented clinical settings in which myocardial stunning can occur include percutaneous transluminal coronary angioplasty, unstable and variant angina, acute myocardial infarction with early reperfusion, cardiac surgery, and cardiac transplantation (8,

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