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Intramyocardial hematoma is a rare sequela of percutaneous coronary intervention after acute myocardial infarction. Clinical outcomes of intramyocardial hematoma vary from asymptomatic remission to cardiac death. Close follow-up is imperative.
Herein, we report the case of a 69-year-old man who had sustained an acute inferior myocardial infarction. During primary percutaneous coronary intervention to the occluded right coronary artery, an intramyocardial hematoma developed and immediately ruptured into the right ventricle. Because the patient remained hemodynamically stable, a conservative approach was taken. Follow-up with serial multidetector computed tomographic imaging elucidated the course and extent of the hematoma and clearly revealed the healing process. After 1 year, this method of imaging showed complete remission of the hematoma.
To the best of our knowledge, this is the 1st use of serial multidetector computed tomography to document the remission of an intramyocardial hematoma that ruptured after complicated percutaneous coronary intervention. We believe that multidetector computed tomography is useful in tracing the natural history of intramyocardial hematomas.
Intramyocardial hematoma, which usually develops along natural dissection planes between the spiral muscles of the ventricle, is an extremely rare lesion that is caused by myocardial infarction, chest trauma, or heart surgery. It can also occur spontaneously.1,2 On rare occasions, intramyocardial hematomas can form as a sequela of percutaneous coronary intervention (PCI) in patients who have sustained an acute myocardial infarction (AMI).3,4 Herein, we describe the case of a patient who developed an intramyocardial hematoma that immediately ruptured into the right ventricle (RV) during primary PCI for AMI. Multidetector computed tomography (MDCT) was used to follow the course and extent of the hematoma.
In June 2007, a 69-year-old man was admitted to our hospital with chest pain of 3 hours' duration. An electrocardiogram showed atrial fibrillation with ST-segment elevation in leads II, III, and aVF, which suggested AMI (Fig. 1). The patient immediately underwent primary PCI.
Coronary angiography showed no significant stenosis of the left coronary arteries. The right coronary artery (RCA) was totally occluded by thrombi, with faint penetration of contrast medium (Fig. 2A). A floppy guidewire was easily advanced to the distal RCA, and angioplasty was performed in the distal RCA with use of a 2 × 20-mm balloon catheter. An angiogram then revealed multiple filling defects caused by tandem thrombi along the distal RCA and the posterior descending coronary artery (PDA) (Fig. 2B). The RCA was re-entered with use of a 300-cm hydrophilic wire. An AngioJet® 3000A Rheolytic™ Thrombectomy System catheter (MEDRAD, Inc.; Warrendale, Pa) was slowly passed across the thrombi, with use of fluoroscopic guidance. Rheolytic thrombectomy was performed 5 times in the distal RCA and then 5 times in the PDA. After the wire was removed from the PDA, coronary angiography revealed a flow of contrast medium that arose from the distal PDA, drained into the RV (Fig. 2C), and then rapidly cleared into the RV outflow tract (Figs. 2C and 2D). An echocardiogram showed no pericardial effusion. An intramyocardial hematoma, passing through a dissection from the distal PDA and rupturing into the RV, was confirmed upon immediate coronary angiography. Because the patient remained hemodynamically stable, surgical intervention was considered to be unnecessary, and he was transferred to the coronary care unit for close observation. He was initially given unfractionated heparin for anticoagulation and, thereafter, oral warfarin. Five days later, the patient was prescribed aspirin (100 mg/d), warfarin (2.5 mg/d), and enalapril (5 mg/d), and he was discharged from the hospital.
One month later, MDCT was used to evaluate the exact course and extent of the intramyocardial hematoma. A large hematoma (11 × 33 mm) arose from the distal PDA, coursed into the interventricular septum, and drained into the RV (Figs. 3A and 3B). Six months after the patient's AMI, MDCT showed that the hematoma had shrunk to 8 × 28 mm (Fig. 3C) and that the 1-mm-wide rupture site between the hematoma and the RV had healed (Fig. 3C, white arrow). One year after the patient's AMI, MDCT showed complete remission of the hematoma (Fig. 3D) and continuing patency of the RCA and the PDA (Fig. 3E).
Our patient's type of intramyocardial hematoma has also been called an acquired coronary artery fistula.5-7 This entity has been described as a complication of PCI in patients who have sustained a myocardial infarction.1,2 In our patient, the hematoma probably formed during the prolonged manipulation of the hydrophilic guidewire, which could have perforated the infarct-related artery and penetrated the interventricular septum, thus creating the hematoma.8,9 The rupture may be due to either of 2 factors. First, a hematoma in an acutely infarcted area can easily rupture into the ventricle during emergent PCI. (In contrast, in elective PCI a hematoma would be surrounded by normal myocardial tissue that would tend to inhibit rupture into the ventricle.) Second, acute transmural myocardial infarction itself has been reported to destroy the coronary microvasculature and dissect the myocardium.1,5,10,11 We consider either explanation to be plausible in the case of our patient.
The clinical outcome of intramyocardial hematoma is variable. In a 1993 review of 15 cases of intramyocardial hematoma, Pliam and Sternlieb reported that only 1 of 10 medically treated patients survived, whereas all 5 surgically treated patients survived.1 Since then, spontaneous remission has been reported in a few cases.5,8,11 Accordingly, choosing an aggressive or conservative approach depends on the circumstances, and it is imperative to closely observe patients who have a relatively stable hematoma (one that does not cause hypotension or shock).
Although coronary angiography is a diagnostic tool of choice after an intramyocardial hematoma enters the cardiac chambers through a dissection, it is an invasive procedure. Furthermore, the complex 3-dimensional geometry of a serpiginous hematoma cannot be delineated precisely by use of 2-dimensional fluoroscopy.12 The noninvasive diagnosis of intramyocardial hematoma can be made by transthoracic echocardiography (TTE). However, TTE's accuracy is limited, because it cannot be used to view the entire tortuous course of the hematoma.11 Conversely, MDCT is a fast, robust, and noninvasive method for evaluating anomalous coronary vessels.7,13 The exact course and extent of our patient's ruptured hematoma were difficult to detect during emergent PCI. Because the patient was hemodynamically stable in the catheterization laboratory, we decided to take a conservative approach. One month after the patient's AMI, MDCT showed the anatomic characteristics of the hematoma (Figs. 3A and 3B). Over time, the hematoma healed and disappeared, as shown in the MDCT studies at 6 and 12 months (Figs. 3C and 3D). This outcome justifies our decision to proceed conservatively. To the best of our knowledge, this is the 1st use of serial MDCT to document the remission of an intramyocardial hematoma that ruptured after complicated PCI.
In conclusion, we suggest that a conservative yet watchful approach is feasible in patients who are clinically and hemodynamically stable when an intramyocardial hematoma is identified during PCI after AMI. Furthermore, MDCT can be very useful in determining the nature and tracing the evolution of intramyocardial hematomas.
Address for reprints: Tsu-Juey Wu, MD, PhD, Cardiovascular Center, Taichung Veterans General Hospital, 160, Sec. 3, Chung-Kang Rd., Taichung 40705, Taiwan
This study was supported in part by Yen Tjing Ling Medical Foundation (CI-97-12), Taipei, Taiwan.