Ann Thorac Surg 2000;69:1931-1932
© 2000 The Society of Thoracic Surgeons
Case reports
Aortic dissection in a weight lifter with nodular fasciitis of the aorta
Daniel N. Gwan-Nulla, MDa,
William R. Davidson, Jr, MDb,
Ronald T. Grenko, MDc,
Ralph J. Damiano, Jr, MDa
a Division of Surgery, Penn State Geisinger Health System, Pennsylvania State University, Hershey, Pennsylvania, USA
b Division of Medicine, Penn State Geisinger Health System, Pennsylvania State University, Hershey, Pennsylvania, USA
c Division of Pathology, Penn State Geisinger Health System, Pennsylvania State University, Hershey, Pennsylvania, USA
Address requests for reprints to Dr Damiano, Division of Cardiothoracic Surgery, Washington University School of Medicine, 1 Barnes-Jewish Hospital Plaza, Suite 3108 Queeny Tower, St. Louis, MO 63110
e-mail: rdamiano{at}msnotes.wustl.edu
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Abstract
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We report a case of spontaneous aortic dissection in a young weight lifter without aortic medial disease but with a myofibroblastic proliferation of the aortic adventitia consistent with nodular fasciitis. Successful treatment included ascending aorta replacement with Dacron graft and aortic valve resuspension. We believe that the underlying aortic pathology most likely contributed to the development of the aortic dissection.
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Introduction
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Aortic dissection is a life-threatening disorder associated with a high mortality. Although the cause is unknown, several risk factors are associated with its development. The most common factor is systemic hypertension [1]. In certain patients, particularly those less than 40 years of age, other such factors as familial predisposition, bicuspid aortic valve, coarctation of the aorta and Marfan’s syndrome have been implicated [2]. One of the more unusual associations is with weight lifting [3–5]. We report a case of type II aortic dissection in a young weight lifter with nodular fasciitis of the aortic adventitia without evidence of cystic medial degeneration.
A previously healthy, 26-year-old white male had been weight lifting approximately 8 days before presentation, when he felt a pop and a pain in his chest that radiated down his left arm and to his neck and jaw. He became acutely short of breath and diaphoretic. The symptoms resolved spontaneously. Five days later, he began having dull, aching chest pain and nausea. He was seen by his primary care physician, who heard a loud murmur on exam. An echocardiogram demonstrated an aortic dissection. He had no previous history of hypertension, and he denied using anabolic steroids or illicit drugs. He was a power lifter who bench pressed about 80 to 100 kg of weight regularly.
Physical examination revealed a fit, well-built young human without a Marfanoid habitus. There were no carotid bruits. His chest was clear to auscultation bilaterally. Cardiac examination revealed a soft-blowing holodiastolic murmur. No focal neurologic deficits were present. A chest roentgenogram demonstrated mild cardiomegaly but no mediastinal widening. His electrocardiogram was normal. A transesophageal echocardiogram revealed severe aortic insufficiency with a dissection limited to the ascending aorta (Fig 1). At the time of the operation, an aortic dissection involved a 5-cm to 6-cm area. The intimal flap was located just above the sinotubular ridge. Proximally, it extended down into the noncoronary cuff and had displaced the left coronary–noncoronary commissure. The medial wall of the ascending aorta was markedly thickened and abnormal in appearance. A significant amount of surrounding soft tissue reaction in this area was similar to an inflammatory process. There was no evidence of dissection in the distal ascending aorta. The ascending aorta was replaced with a 28-mm woven Dacron graft, and the aortic valve was resuspended with horizontal plegetted sutures.
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Fig 1. Transesophageal echo long axis view of the aortic root. Dissection flap is seen posteriorly (arrow); true and false lumens communicate freely; aortic valve is closed. No flap was seen in the aortic arch or descending aorta. (S = superior; I = inferior; P = posterior; A = anterior; F = false lumen; T = true lumen; AV = aortic valve.)
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The patient had an uneventful postoperative course and was discharged on the fifth postoperative day. Histopathologic examination of the aorta revealed acute hemorrhage along with a myofibroblastic proliferation of the adventitia. Myofibroblasts were identified by their morphology and actin staining. There was no medial degeneration. The adventitial lesion consisted of a spindle cell proliferation with a variably myxoid and fibrous stroma, scattered lymphocytes and extravasated red blood cells (Fig 2), consistent with a nodular fasciitis [9]. The resected aorta involved the entire diseased segment with a thin rim of normal aorta.
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Fig 2. Photomicrograph of the nodular fasciitis demonstrating proliferation of spindled cells in a "patternless pattern" and scattered chronic inflammatory cells. (Hemotoxylin and eosin stain; x200.)
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Comment
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The pathophysiology of aortic dissection is characterized by a separation of the media in a course parallel to the flow of blood. This is initiated by an intimal tear occurring secondary to the hemodynamic forces applied to the aorta, often in areas of underlying aortic pathology. Systemic hypertension, which is commonly associated with aortic dissection, may accentuate these forces and promote formation of atherosclerotic plaques, which may lead to intimal injury [3, 6]. Hypertension is less commonly associated with ascending aortic dissections in younger patients. In these patients, dissection is most likely to be associated with aortic medial disease and other congenital abnormalities of the aorta [2]. In spontaneous aortic dissection, the cause is often unknown, and intrinsic abnormality in the wall of the aorta is usually not identified.
Weight lifting has been implicated as an etiologic factor in ascending and descending aortic dissections in young patients [3–5]. Macdougall and colleagues showed up to a four-fold elevation in both systolic and diastolic blood pressures with heavy weight lifting. In avid weight lifters, this places critical stresses on the aorta over a prolonged period of time, which might lead to injury [7].
A nodular fasciitis-like, myofibroblastic proliferation of the aortic adventitia was associated with aortic dissection. Nodular fasciitis is an uncommon pseudoneoplastic proliferation of myofibroblasts. It typically occurs in the upper extremities or trunks of young persons [8, 9]. The relationship between aortic dissection and the myofibroblastic lesion in this case is uncertain. Nodular fasciitis is considered to be a reactive process that would imply some sort of prior insult. However, this patient had no history of trauma and no hemosiderin in the lesion to indicate prior hemorrhage, nor was there histologic evidence of cystic medial degeneration or other underlying aortic pathology to predispose to dissection. The nodular fasciitis was largely limited to the adventitia, although there was focal involvement of the outer portion of the media.
We believe the most likely explanation is that the nodular fasciitis focally weakened the aortic wall, and the increased aortic pressure associated with weight lifting resulted in dissection. However, as in previously reported cases, a direct causal relationship still remains unclear in this case. To clarify this issue, studies looking at the effects of chronic weight lifting on the aorta need to be conducted by comparing autopsy specimens of weight lifters with those who do not lift weights. These comparisons may reveal aortic wall changes in weight lifters that would suggest chronic insult, which might predispose to dissection.
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Acknowledgments
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The authors would like to acknowledge the contribution of Dr Allen Burke of the Armed Forces Institute of Pathology.
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References
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Accepted for publication October 20, 1999.
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Abstract
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