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CASE REPORT
Year : 2006  |  Volume : 21  |  Issue : 1  |  Page : 23-24 Table of Contents   

Tc99m-Pyrophosphate Scanning for Traumatic Myocardial Infarction


Department of Nuclear Medicine, All India Institute of Medical Sciences, New Delhi, India

Correspondence Address:
Rakesh Kumar
E-62, Ansari Nagar (East), AIIMS Campus,New Delhi 110029
India
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Source of Support: None, Conflict of Interest: None


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   Abstract 

We present a 40-year-old male who had myocardial infarction (MI), 48 hours following a road traffic accident. EKG showed anterior wall MI and complete heart block. Tc99m-Pyrophosphate scan and angiography confirmed the diagnosis. The possibility of traumatic MI should be considered in cases of chest trauma and the patient should be observed for 48 hours. Pyrophosphate scintigraphy can be useful in these patients.

Keywords: Traumatic Myocardial Infarction, Tc99m- Pyrophosphate scan, Chest injury.


How to cite this article:
Chawla M, Kumar R, Malhotra A. Tc99m-Pyrophosphate Scanning for Traumatic Myocardial Infarction. Indian J Nucl Med 2006;21:23-4

How to cite this URL:
Chawla M, Kumar R, Malhotra A. Tc99m-Pyrophosphate Scanning for Traumatic Myocardial Infarction. Indian J Nucl Med [serial online] 2006 [cited 2019 Aug 23];21:23-4. Available from: http://www.ijnm.in/text.asp?2006/21/1/23/43436


   Introduction Top


Acute myocardial infarction (MI) most commonly results from thrombus formation at the site of a previously stenosed vessel. Other less common causes of acute MI include embolus, coronary vasospasm, systemic inflammatory disorders and trauma. Blunt trauma generally produces mechanical damage to coronary artery endothelium, which in turn encourages thrombus formation, resulting in MI. In management of patients with suspected or known MI, the important clinical steps are not only to confirm the diagnosis, but also to assess the site and size of infarct. The EKG is the most commonly used diagnostic tool and has an accuracy of around 80 %. But there are certain limitations in the interpretation of EKG, which include previous infarcts, conduction defects, acute pericarditis, electrolyte abnormalities and use of cardio-active drugs [1],[2],[3] . Moreover, EKG cannot accurately define the size and specific location of the infarct. Elevated serum enzyme levels provide a sensitive means of diagnosing acute MI, but these peak during first 24 hours following MI, hence have a limited role in patients with late presentation [4] . Radionuclide infarct imaging with Tc-99m­pyrophosphate (PYP) and In-111- labelled Antimyosin antibody provides a sensitive and reasonably specific means of diagnosing acute MI and estimating the size of infarct 3-10 days after the myocardial infarction. We present the case of a young male who suffered an acute MI after a road traffic accident, which was later confirmed by Tc-99m-PYP scan.


   Case Report Top


A 40-year-old male complained of generalised body aches and chest pain, following a road traffic accident. There were no visceral or bony injuries. The X-Ray chest was normal. On day 2, he had a syncopal attack lasting for nearly 30 minutes with chest pain but no breathlessness. On examination BP was 110/ 70 mm/Hg and pulse 50/min. S1, S2 were found to be normal. The EKG showed ST elevation and QS pattern in V1 lead with PR interval of 0.20s and QRS interval of 0.16s. The CPK level was 268 IU/L (Normal 25-90 1U/ L) and LDH level was 819 IU/L (Normal 88- 230 IU/ L). The patient was hospitalised with the presumptive diagnosis of an acute ante­rior wall MI with AV Block. The patient was given aspirin, morphine and isosorbide-dinitrate. On day 3, the patient had another episode of syncopal attack, which was diagnosed as Stroke-Adams Syndrome. An EKG done soon after the syn­copal attack showed acute anterior wall MI with complete heart block. The patient was put on a temporary pace maker as the heart block did not respond to intravenous atropine. On day 4, echocardiography was done which revealed left ven­tricular ejection fraction (LVEF) of 35 % with akinesia in distal 1/3 of septum, apex and anterior wall. On day 5, the patient was referred for Tc99m- Pyrophosphate (PYP) myocardial scan for confirmation of diagnosis and for the delineation of the extent of the MI. The PYP scan demonstrated abnormally in­creased radiotracer uptake in anterior wall, septum and apex [Left Anterior Descending (LAD) artery territory] [Figure 2]. On day 15, after the patient stabilised angiography was done to see the status of coronaries, which showed 100 % block of LAD with the thrombus


   Discussion Top


Traumatic MI, though rare, is a serious complication following chest trauma, which produces coronary endothelial damage leading to subsequent thrombus formation and consequent MI. It is more often missed than diagnosed because its possibility is not suspected and the observed clinical manifestations are attributed to commonly associated lung trauma. Nearly 20% of chest trauma involves the heart and can lead to potential complications, including MI. LAD artery being the anterior most is most vulnerable to injury. Generally a patient with trauma is treated on an out patient basis if skeletal fracture or visceral trauma is excluded. But excluding these injuries does not preclude the possibility of a traumatic MI. If a coronary artery is severed it may produce MI instantly, but if the injury is of a lesser degree it may produce MI as late as 48 hours, as seen in this case. So it is advisable to keep the patient under observation for 48 hours even if there is a slightest suspicion of cardiac injury. It is also advisable to undergo radionuclide infarct imaging if enzyme profile and EKG findings are equivocal.[Figure 1]

Thrombotic occlusion of an artery produces hypoxia, which triggers massive production of free radicals resulting in damage to the cell membrane. Decreased production of ATP and damage to the cell membrane results in calcium influx into the cell. The influxed calcium is avidly taken up by mitochondria and causes membrane and cytoskeletal damage. Damage to cell membrane ultimately causes cell death and exposes Actin and Myosin filaments. Increased influxed calcium and exposed Actin and Myosin filaments are the basis of radionuclide infarct imaging. PYP is a calcium-seeking agent, which accumulates at the site of increased calcium deposition. This usually occurs in irreversibly damaged myocardium. Poliner LR et al studied 52 patients with acute Q wave MI and reported a sensitivity of 90 % with planar imaging [5] . Turi et al studied 726 patients with acute non-Q MI and reported a sensitivity of 89% [6] . Radiolabelled anti-myosin Fab is a viable alternative to PYP scanning with a similar sensitivity and specificity for infarct detection.

In this case, the patient was stable on the first day after the road traffic accident and deteriorated on the second day. This pattern is characteristic in patients with traumatic MI, as the thrombus formation generally takes place some time after the endothelial damage of the coronary artery. In conclusion, the possibility of traumatic MI should be considered in cases of chest trauma. The suspected cases of cardiac injury should at least be observed for 48 hours since the clinical manifestation of traumatic MI may not develop soon after the traumatic event. PYP scintigraphy can be a useful diagnostic modality in patients with late or atypical presentation to confirm the diagnosis and to determine the extent of myocardial injury.

 
   References Top

1.Levine H D, Phillips E. Apprasial of the newer electrocardiography correlation in 150 consecutive cases. N Engl J Med 1951:245:83343.  Back to cited text no. 1    
2.Savage R M, Wagener G S, Ideker R E, et al. Correlation of post­mortem anatomic findings with electrocardiographic changes in patient with myocardial infarction. Retrospective study of patients with typical anterior and posterior infarcts. Circulation 1977; 55: 279-85  Back to cited text no. 2    
3.Cooksey J D, Dunn M, Massie E. Clinical vectocardiography and electrocardiography. 2nd edn Chicago: Yearbook Medical Publishers 1977; 361.  Back to cited text no. 3    
4.Lee T H, Weisberg M, Cook E F, et al. Clinical impact of creatinine kinase - MB for diagnosis of myocardial infarction in the emergency room. Arch Inter Med 1987; 147: 115-21.  Back to cited text no. 4    
5.Poliner LR, Buja L M, Parkey RW, et al. Clinicopathologic findings in 52 patient s studied by technetium- 99m stannous pyrophosphate myocardial scintigraphy. Circulation 1979; 59: 257-67.  Back to cited text no. 5    
6.Turi ZG, Rutherford JD, Roberts R, et al. Electrocardiographic enzymatic and scinitigraphic criteria of acute myocardial infarction as determined from study of 726 patients (a MILIS study) Am J Cardiol 1985;56:252-56.  Back to cited text no. 6    


    Figures

  [Figure 1], [Figure 2]



 

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