Abstract
A 44-year-old man had severe stenosis of the left main coronary artery. The middle portion of the left anterior descending coronary artery was in an intramyocardial location. The pericardium, ascending aorta, epicardium, and coronary arteries were encased by a metastatic, poorly differentiated papillary adenocarcinoma. The left anterior descending artery was located with the aid of a handheld epicardial ultrasonic Doppler flow detector, and grafted with the left internal thoracic artery on a beating heart. Subsequently, the patient underwent 10 cycles of chemotherapy. More than 22 months later, he was asymptomatic and in remission from neoplastic disease.
Key words: Adenocarcinoma/secondary; antineoplastic combined chemotherapy protocols; cardiopulmonary bypass/adverse effects; coronary artery bypass/methods; coronary vessel anomalies/surgery; coronary vessels/ultrasonography; heart neoplasms/secondary; human; male; pericardium/pathology; immunity, cellular; ultrasonography, Doppler
In a study of 70 patients undergoing coronary artery bypass grafting (CABG), intramyocardial coronary arteries occurred in 17.7%.1 The most common intramyocardial coronary artery (58.6%) was the proximal or middle portion of the left anterior descending coronary artery (LAD).
We present the case of a patient who had severe stenosis of the left main coronary artery and neoplastic pericarditis. The neoplasm encased the LAD.
Case Report
On 23 January 2003, a 44-year-old man presented at our institution with tiredness, exertional angina, dyspnea, and fainting spells. Over a period of 3 months, his symptoms had progressed to unstable and resting angina. Other medical history included cigarette-smoking (20 cigarettes per day since the age of 14), use of marijuana and intravenous heroine (during his teens), and hepatitis C.
During his admission to our medical center, the patient's heart rate was 92 beats/min and regular, the blood pressure was 140/60 mmHg, and, by palpation, the liver was enlarged and smooth, extending 20 cm below the right costal margin.
Electrocardiography revealed a non-Q wave myocardial infarction, and cardiac enzymes were positive for myocardial injury. Cardiac catheterization performed on the day of admission revealed a long left main coronary artery with 90% narrowing and introduced the possibility of an intramyocardial location of the middle portion of the LAD between the origin of its 1st and 2nd diagonal branches (Fig. 1). The cardiac hemodynamic function was normal. During the study, because of resting angina, an intra-aortic balloon assist device was inserted percutaneously through the right common femoral artery.

Fig. 1 Coronary angiography in the right (A) and left (B) anterior oblique projection shows a long left main coronary artery with 90% narrowing and a slight inward bending of the middle portion of the left anterior descending artery, indicating a possible intramyocardial location.
Surgical Technique
The day after his admission to the hospital, the patient was taken to the operating room. We had planned to perform CABG using a left internal thoracic artery (LITA) graft to the LAD and a saphenous vein graft to the obtuse branch of the circumflex artery, with the patient on cardiopulmonary bypass (CPB) and cardioplegic arrest.
After performing a median sternotomy, we began dissection of the LITA pedicle (diameter, 2 mm) with difficulty, because of severe dense adhesions to the underlying chest wall. The pericardium was opened longitudinally in an inverted “T” fashion, also with difficulty, due to the severely inflamed pericardium. The pericardium was 5 mm thick, covered with nodules, and firmly adherent to the epicardium of the heart, ascending aorta, and right atrium. Cannulation of the ascending aorta and the right atrium was not possible, nor was the application of an aortic cross-clamp. Biopsy of the pericardium was performed.
The left groin was readied for exposure of the left common femoral artery and vein for cannulation, if needed. We were able to dissect, with difficulty, only a part of the anterolateral surface of the left ventricle; moreover, we were unable to locate the LAD or its diagonal branches. We concentrated on the upper part of the anterior interventricular sulcus (where we expected the middle portion of the LAD to be situated), because that area seemed to be affected by the pericarditis to a lesser degree.
Then with the aid of a handheld epicardial Ultrasonic Doppler Flow Detector (model 811-BL with an 8-MHz probe; Parks Medical Electronics, Inc.; Aloha, Ore), we were able to locate and mark with a surgical marking pen the middle portion of the intramyocardial LAD, which was also encased by severely inflamed pericardium.
At this point, we were confident that we would be able to expose the middle portion of the LAD without CPB. In the event that the pericardial biopsy confirmed our suspicion of neoplastic pericarditis, the avoidance of CPB would spare the patient's cell-mediated immunity from further compromise.
On a beating heart, with use of retraction pericardial sutures and an Octopus®4 tissue stabilizer (Medtronic, Inc.; Minneapolis, Minn), we transected the thick epicardium and myocardial bridge, exposing the middle portion of the intramyocardial LAD. After a longitudinal arteriotomy and insertion of a 1.5-mm intraluminal shunt, we performed an anastomosis between the middle portion of the LAD and the LITA using a continuous double-armed 7-0 polypropylene suture.
The intra-aortic balloon pump was removed on the next day, and the patient's postoperative course was uneventful.
Results
Pathologic evaluation of the pericardial biopsy sample from the patient revealed a poorly differentiated papillary adenocarcinoma, involving vascular and lymphatic spaces. Solid tumor immunohistochemical antibody analysis was positive for all types of cytokeratin, nongastrointestinal adenocarcinomas (cytokeratin-7), endodermally derived adenocarcinomas, carcinoembryonic antigen, pancreatobiliary tumors (carbohydrate anti-gen-19.9), and pancreatobiliary thyroid (cytokeratin-19), which implied a metastatic pancreatobiliary origin for these cells.
One day after surgery, transthoracic echocardiography showed a hyperdynamic left ventricle and no evidence of metastasis to the myocardium.
Helical computed tomography (CT) of the chest, abdomen, and pelvis with intravenous contrast material 1 week after surgery revealed extensive mediastinal lymphadenopathy and complex pericardial and pleural effusion, indicating neoplastic disease. On the 8th postoperative day, a hepatic panel for hepatitis C antibody was positive, and the carcinoembryonic antigen was elevated (>100 ng/m2). The patient was discharged from the hospital on the same day without angina pectoris or dyspnea.
The patient received 5 cycles of chemotherapy. The first 2 cycles of included Gemzar (Eli Lilly and Company; Indianapolis, Ind) and Cisplatin (Baxter Health-care Corporation; New Providence, NJ). In July 2003, a whole-body positron emission tomographic (PET) scan showed increased glucose metabolism in the mediastinum and subcarinal region. Due to the patient's worsening liver function, the subsequent 3 cycles of chemotherapy were changed to Taxol and Paraplatin (Bristol-Myers Squibb Corporation; Princeton, NJ), given through December 2003. Computed tomography of the chest, abdomen, and pelvis with intravenous contrast material in November 2003, and a whole-body PET scan the next month showed no evidence of primary or metastatic neoplastic disease.
The patient has been returning for clinical follow-up imaging studies every 3 months. In June 2004, although the patient was asymptomatic, CT scanning with intravenous contrast material was performed on the chest, abdomen, and pelvis. Results showed a pericardial effusion, along with mediastinal and axillary lymphadenopathy. A whole-body PET scan showed multiple areas of increased glucose metabolism. Subsequently, the patient received an additional 5 cycles of chemotherapy with Taxol and Paraplatin. In October, results of CT scans of the chest, abdomen, and pelvis were negative except for a small right-sided pleural effusion. When last seen in November 2004, more than 22 months after surgery, the patient was asymptomatic and doing well. The small pleural effusion was being watched.
Discussion
Characteristically, on coronary angiography, the intramyocardial portion of the LAD during systole shows an inward buckling, which becomes temporarily narrowed in only 7.1% of patients.1 This localized buckling is caused by dipping of the intramyocardial portion of the LAD into the myocardium. Intramyocardial coronary arteries are free of atherosclerosis in 97.2% of the patients, and are therefore suitable for construction of an anastomosis. These vessels are usually dissected distally at the site of reemergence, and then the overlying myocardium is transected in a cephalad direction.
Metastases to the heart and pericardium are much more common than are primary cardiac tumors.2 At autopsy, metastases to the heart and pericardium have been found in 8.4% of all neoplasms, and are more common in younger than in elderly patients.3 In men, the most frequent malignancies metastasizing to the heart and pericardium are mesothelioma (100%), melanoma (50%), and lung carcinoma (31%); in women, the types and frequencies are melanoma (45%), lung tumors (26%), and renal neoplasms (20%).3 Metastases to the pericardium and heart from primary pancreatobiliary tumors, as in our patient, are unusual. Tumors may involve the heart and pericardium by retrograde lymphatic, direct contiguous, or transvenous extension, or by hematogenous spread.3
Clinical presentation of cardiac and pericardial metastases includes dyspnea, cough, chest pain, and cardiac dysfunction due to pericardial effusion.2 Any thickening or nodularity of the pericardium, myocardium, or intracardiac structures should raise suspicion of metastatic disease. Treatment includes pericardial drainage, and—depending on the type of primary tumor—radiation, chemotherapy, or both.
In 1986, Hiratzka and colleagues4 reported the use of large epicardial high-frequency ultrasonographic probes to detect coronary arteries embedded in a thick layer of epicardial fat. In 1999, Oda's group5 used an epicardial 7.5-MHz ultrasonographic color Doppler microprobe during minimally invasive CABG to detect the intramyocardial course of the LAD. In a series of 6 patients, Miwa and co-authors6 recently reported the usefulness of a 15-MHz linear transducer for detecting intramyocardial LADs and for performing anastomoses between the LITA and the LAD during off-pump CABG.
The handheld ultrasonic Doppler flow detector is useful in locating the audible arterial signal from the intramyocardial and encased coronary arteries on a beating heart (whether or not cardiac arrest is to be initiated). The method is noninvasive and fast; the equipment is easy to use, readily available, and inexpensive. In our patient, because the LAD was encased by inflamed, fibrous pericardium due to metastatic disease, and because of the intramyocardial location of the LAD, we could not see it on angiography. Therefore, we used the handheld epicardial ultrasonic Doppler flow detector to locate the middle portion of the LAD and graft it with the LITA on a beating heart.
Coronary artery bypass grafting is safer in combination with CPB when small, intramyocardial, and calcified coronary arteries are involved. However, improvement in techniques for stabilization of the segments of the coronary arteries on a beating heart has enabled us to forgo CPB under some circumstances. Cardiopulmonary bypass is known to decrease T-cell immunity.7 Therefore, in patients with neoplastic disease, it is advantageous to perform CABG on a beating heart, if possible.
In conclusion, during cardiac operations, in the presence of pericarditis, a biopsy of the pericardium should always be performed. The handheld ultrasonic Doppler flow detector can be used successfully to locate coronary arteries that are encased by inflamed pericardium or obscured by adhesions, and is useful in situations such as repeat CABG and intramyocardial coronary arteries.
Footnotes
Address for reprints: Andrew S. Olearchyk, MD, 129 Walt Whitman Blvd., Cherry Hill, NJ 08003
E-mail: asolearchyk@yahoo.com
References
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