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Ann Thorac Surg 2001;71:1673-1675
© 2001 The Society of Thoracic Surgeons
a Division of Cardiac Surgery, Massachusetts General Hospital, Boston, Massachusetts, USA
b Division of Electrophysiology, Massachusetts General Hospital, Boston, Massachusetts, USA
c Department of Pathology, Massachusetts General Hospital, Boston, Massachusetts, USA
Accepted for publication July 10, 2000.
Address reprint requests to Dr Torchiana, Department of Cardiac Surgery, Massachusetts General Hospital, 55 Fruit St, Boston, MA 02114
e-mail: dtorchiana{at}partners.org
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Introduction |
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A 33-year-old man was admitted to the Emergency Department of the Massachusetts General Hospital for wide complex tachycardia. The patient, a physician, had driven himself to the hospital after experiencing an episode of shortness of breath, palpitations, and light headedness that lasted approximately 15 minutes. The symptoms had spontaneously appeared while the patient was seated, though he recalled similar symptoms occurring during past basketball games and a recent golf game. He was given lidocaine, which succeeded in terminating his tachycardia. His electrolytes were normal. The patient did not have any chest pain, and did not consume alcohol, tobacco, or caffeine, or use any illicit drugs. His only medication was Axi
, taken as needed for symptoms of dyspepsia. He also had a history of hypertension, hypertriglyceremia, and hypercholesterolemia. His family history was remarkable for a grandfather who had had a stroke, and a grandmother who had had cervical cancer.
An echocardiogram revealed a transmural homogeneous and echodense mass located near the apex of the patient’s left ventricle (Fig 1). In retrospect, the mass could also be delineated in a previous echocardiogram (done while investigating the patient’s hypertension four years earlier). The ejection fraction was 66%. Magnetic resonance imaging (MRI) confirmed the presence of a hypointense mass in the lateral free wall of the heart, from the midventricular level to near the apex. It was measured to be 4.5 x 3.1 x 4.4 cm. T2-weighted images of the mass suggested that it was encapsulated, and mostly contained in the myocardium (Fig 2). In one area, however, it appeared to reach the endocardium. After injection of gadolinium, the mass became isointense with the myocardium, indicating that it was well vascularized. A coronary angiogram found a small vascular arcade around the mass, stemming from a diagonal branch of the left anterior descending artery. The existence of the mass four years prior, its smooth contour and possible encapsulation all led to an initial diagnosis of a benign tumor.
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Pathologic examination of the tumor revealed a whorled, white mass, with small islands of browner tissue. Microscopically, these were found to be areas of mature myocytes, variably interspersed among fibroblasts and collagen. At the border of the tumor, the fibroblasts interdigitated with the surrounding myocardium, which was thought to be the reason why the tumor appeared to be encapsulated with MRI imaging. The final diagnosis was "hamartoma of mature cardiac myocytes."
The patient had an uneventful postoperative course. Intravenous lidocaine was used immediately postprocedure, and was discontinued the following morning at which point he was commenced on atenolol 50 mg daily. No ventricular tachycardia or ventricular ectopy was observed on telemetry and after 5 days observation, the patient was discharged on atenolol 100 mg bid. He was given a 30-day event recorder which he was told to activate if he had any palpitations.
Three months later, he was readmitted off atenolol for 24 hours for an electrophysiology study. Programmed ventricular stimulation was performed with 1 to 3 ventricular extrastimuli, both off and on intravenous isoprenaline at 2 right ventricular sites. No ventricular arrhythmia was inducible. This study was performed in part to exclude the possibility of a ventriculotomy related ventricular tachycardia. A follow-up MRI confirmed that the tumor had been fully excised, and that the left ventricular cavity was not significantly altered. An echocardiogram also showed no evidence of ventricular abnormalities or valve malfunction. Two years postoperatively, the patient is doing well on atenolol and Norvasc.
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Recently, Burke and associates reviewed three cases involving hamartomas of mature cardiac myocytes in a 22-year-old patient , 28-year-old patient , and 9-year-old patient [2]. The tumors were characterized by a lack of encapsulation and hypertrophy of the disarrayed myocytes. The lesions found in the first two patients were localized to the right ventricle and right atrium, respectively. The youngest patient’s heart, examined postmortem, had multiple nodules scattered throughout the heart, including papillary muscles.
Tanimura and coworkers reported a cardiac hamartoma at the apex of the heart in a 68-year-old male with retroperitoneal leiomyosarcoma [3]. This patient’s tumor contained additional mature adipose tissue. Park, Franciosi and others have also described hamartomas located in the left ventricle, but these have been classified as fibrous or vascular hamartomas [4–7]. Sturtz and colleagues [8] reported a 24-year-old human with palpitations and a hamartoma of mature cardiac myocytes in the interventricular septum which could only be partially resected.
Our patient’s hamartoma was associated with a wide complex tachycardia that originated from the left ventricle. Incessant ventricular tachycardia has been seen in a number of children with myocardial hamartomas [9]. There are a number of case reports of patients with ventricular tumors who had telemtry guided suppression of VT with antiarrhythmia drugs without surgery [10–13]. In our patient, the tachycardia appears to have been ablated by surgical excision which was undertaken for diagnosis and tumor removal as well.
In summary, we have presented a case where the diagnosis of a benign cardiac tumor was made with diagnostic imaging techniques, and surgical intervention was effective in removing a hamartoma of mature cardiac myocytes. The QRS morphology during VT, the lack of symptoms in follow-up, and the negative postoperative EP study off ß-blockade and with intravenous isoprenaline are strong evidence that the VT was tumor-related and cured by its excision.
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This article has been cited by other articles:
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  A. Galeone, P. Validire, J.-B. Gayet, and F. Laborde Hamartoma of mature cardiac myocytes of the pulmonary infundibulum Interactive CardioVascular and Thoracic Surgery, December 1, 2009; 9(6): 1029 - 1031. [Abstract] [Full Text] [PDF]
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 F. Zhang, N. Yin, B. Yin, S. Xu, and Y. Yang Giant right atrial cystic hamartoma: a case report and literature review BMJ Case Reports, June 1, 2009; 2009(jun01_2): bcr0220091587 - bcr0220091587. [Abstract] [Full Text]
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 S. C. Menon, D. V. Miller, A. K. Cabalka, and D. J. Hagler Hamartomas of mature cardiac myocytes Eur J Echocardiogr, November 1, 2008; 9(6): 835 - 839. [Abstract] [Full Text] [PDF]
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