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ST-Elevation Myocardial Infarction Caused by Coronary Artery Compression due to Localized Pericardial Hematoma Caused by Coronary Perforation
Coronary perforation is a rare but serious complication of percutaneous coronary intervention (PCI).1,2 The impact of a coronary perforation varies according to the device that causes the perforation, the location and the severity of the perforation.3–7 Type III coronary perforation is defined by the presence of a free jet of contrast flowing through a hole of more than 3 mm diameter and has been associated with tamponade, cardiac surgery and death.3 Patients with prior cardiac surgery are relatively protected from the severe consequences of coronary perforations due to adhesions between the parietal pericardium and the epicardium. We report a case of coronary perforation during PCI in a post cardiac surgery patient presenting with unusual ST-segment elevation.
Case Report. A 75-year-old patient was admitted to the coronary care unit with unstable angina pectoris associated with anterior ST-segment depression. He had a history of ischemic heart disease, diabetes mellitus and hypertension. Seventeen years earlier, the patient had coronary artery bypass grafting surgery (CABG), with anastomoses of left internal mammary artery (LIMA) to the left anterior descending artery (LAD), right internal mammary artery (RIMA) to the posterior descending artery (PDA) and a saphenous vein graft (SVG) to the diagonal branch (D).
Following initial stabilization, the patient underwent coronary angiography, which 
showed that the RIMA and the SVG were occluded while the LIMA graft to the LAD was patent. The LAD segment proximal to the first diagonal branch was severely stenotic and was considered the culprit lesion (Figure 1). PCI was performed by direct implantation of a bare metal stent [Prescillion, 2.5 x 13 (Johnson & Johnson)] in the aforementioned segment. Additional post-dilatation with a 3 mm diameter balloon [Durastart (Johnson & Johnson)] with inflation up to 16 atmospheres was performed. The final result was considered satisfactory and the patient was discharged the next day.
One month later, the patient was readmitted due to unstable angina. Coronary 
angiography showed findings similar to the previous angiography. However, some degree of under-expansion of the proximal end of the LAD stent was observed with a probable filling defect within the stent. Therefore, an additional intervention was planned. The stent was crossed with a hydrophilic wire (Whisper), followed by balloon pre-dilatation with a 3 mm balloon (Firestar, Johnson & Johnson) and an additional stent (3.5 mm, Driver, Medtronic) was implanted proximal to the previous one, providing a nice transition from the LAD to the diagonal branch. The final result was considered successful (Figure 2).
An hour after the completion of PCI, the patient developed severe chest pain. The 
electrocardiogram revealed marked ST-segment elevation throughout the anterior precordial leads. Acute closure with stent thrombosis was suspected. A bolus of eptifibatide was administered and the patient was urgently returned to the catheterization laboratory. Angiography demonstrated a patent stent, without any evidence of thrombus. However, three important findings were seen: 1) contrast 
leakage through the distal end of the diagonal branch, compatible with coronary perforation (Figure 3); 2) a reduction in the diameter of the distal LAD and diagonal branch; and 3) a slower TIMI flow within the LAD and diagonal branch, in comparison with the previous angiography (Figures 4 and 5). Echocardiography demonstrated a localized anterior pericardial effusion (Figure 6). At this point, the patient was hemodynamically stable, but chest pain and 
ST-egment elevation persisted.
We assumed that coronary perforation occurred, leading to localized tamponade and coronary vessel compression, causing myocardial ischemia and mimicking anterior wall STEMI. The tip of the hydrophilic wire was considered to have caused the coronary perforation during the previous intervention. Eptifibatide was discontinued and a bolus of 
protamine sulphate was administered. The patient was taken immediately to the operating room for surgical pericardial drainage. Upon chest exploration, a tense intra-pericardial mass adjacent to the anterior wall of the left ventricle was noted. After pericardial incision, a large amount of blood with considerable pressure was drained with immediate complete resolution of ST-segment elevation. A bleeding point on the anterior lateral surface of the left ventricle was identified and sutured. The postoperative course was uneventful and the patient was discharged a few days later.
Discussion. Recurrent ST elevation after PCI is a dramatic finding associated mainly with acute coronary occlusion, resulting most frequently from stent thrombosis. We present an unusual case of post-PCI ST elevation, due to a compression of an epicardial artery by a localized hematoma, secondary to coronary perforation by the guidewire.
Coronary perforation is an infrequent complication of PCI with potentially lethal consequences.1–7 The perforation observed in this case can be classified as type III according to the classification proposed by Ellis,3 with contrast dye emerging through a frank perforation. This type of perforation is considered ominous for it is highly associated with tamponade (40–63%), need for surgical intervention (28–63%) and mortality (2–44%).3,4,6,7 The most common type of perforation is caused by the guidewire (21–68%),6–8 as in this case. The combination of a hydrophilic wire and a small-caliber vessel might have contributed to this complication. Perforation at the distal segment of the vessel, as happened in our patient, occurs in 35% of perforations.8 Management of distal segment perforation is difficult, because covered stents can not be applied in this type of perforation. Previous reports of various intervention methods (glue, coils, foam pledges) showed benefit. However, these techniques are not widely available. In our case, distal injection of beads or placement of distal coils were not valid, since the perforation was diagnosed only later and in the presence of a tense pericardial hematoma that required immediate evacuation.
Pericardial hematoma evacuation can be performed either by placement of a percutaneous pericardial drain in the cath lab or by emergent surgical pericardial drainage in the operating room, an approach that was undertaken in this case.
Early detection of distal wire perforation is essential to prevent hemodynamic complications. A careful and constant observation of the location and contour of the tip of the wire relative to the course of the vessel is needed. The existence of a loop at the tip of the wire in a small-sized artery, as was observed in our case, is alarming. Performing longer fluoroscopy runs at the end of a coronary intervention could detect contrast dye leakage. In our case, a revision of the last run revealed contrast leaking, a finding that was not originally noted. Finally, performing routine echocardiography for detection of pericardial effusion in any patient with unexplained symptoms after PCI is mandatory.
Localized hematoma or tamponade is a rare complication of coronary perforation. A localized hematoma might develop in the absence of a free pericardial space (due to fibrosis or adhesions between the two pericardial layers and the epicardium). This phenomenon is mostly encountered in patients after cardiac surgery, but may also occur after chest trauma, radiation or pericarditis.10 Tamponade can be associated to localized hematoma secondary to coronary perforation and the clinical presentation depends on the cardiac structure being compressed by the hematoma. The compressed cavity is usually the one with the lowest pressure, such as the right ventricle, the atria or the coronary sinus.9 As in our patient, hemodynamic status might be preserved, without clinical signs of tamponade.9,11,12
Patients after cardiac surgery are considered relatively protected from serious consequences of coronary perforation due to the obliteration of the pericardial cavity which frequently occurs after surgery. However, as shown by our case, a localized hematoma may still develop. Therefore, a coronary perforation should be highly suspected in patients presenting with atypical symptoms or signs soon after PCI.
The most intriguing finding is the unexpected ST-segment elevation due to localized hematoma compressing the epicardial vessel, a phenomenon that to the best of our knowledge has never been described before.
ST elevation developing soon after PCI is a well known and serious complication associated with acute coronary occlusion, mostly due to stent thrombosis. Prompt intervention is required, frequently including administration of IIb/IIIa receptor antagonists, urgent coronary angiography and reintervention. ST elevation due to other causes is rare and has not been described as a consequence of a localized pericardial hematoma due to coronary perforation. Epicardial hematoma secondary to coronary perforation has been previously associated with ST elevation due to compression of the epicardial artery or to the presence of the hematoma by itself.14,15 In another patient, an association between the existence of localized pericardial hematoma and obstruction of a saphenous vein graft has been described; however, no ST elevation was observed in that case.11
The prompt resolution of ST elevation after evacuation of the pericardial hematoma proves that external compression of the LAD by the hematoma caused this patient’s ST elevation. A few mechanisms to explain this rare phenomenon might be postulated. The first is an elevated intra-pericardial pressure exceeding the intra-coronary pressure, and facilitating compression of an epicardial artery. The attenuated coronary flow observed in the diagonal branch and the distal segment of the LAD support this possibility. Another mechanism could be referred to compression of the epicardial microcirculation by the intra-pericardial pressure, with secondary epicardial ischemia of the anterior wall of the left ventricle and subsequent ST elevation.
We conclude that in the context of coronary perforation ST-elevation myocardial infarction may rarely be a manifestation of a pericardial hematoma causing external compression of an epicardial coronary vessel. Anti thrombotic agents should therefore be used with great caution (if at all) in these patients until the anatomy is clearly demonstrated.
References
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