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Ascending aortic dissection in weight lifters with cystic medial degeneration
Ascending Aortic Dissection in Weight Lifters With Cystic Medial Degeneration Christian de Virgilio, MD, Ronald J. Nelson, MD, Jeffrey Milliken, Ramon Snyder, MD, Frances Chiang, MD, William D. MacDonald, MD, and John M. Robertson, MD Departments of Surgery, Pathology, and Radiology, Los Angeles County Harbor-UCLA Medical Center, Torrance, California
We report 4 cases of ascending aortic dissection in patients with long histories of weight lifting. In 2 of the patients, the initial symptoms of dissection developed while they were lifting weights. Two patients had a history of hypertension and 2 had previously used anabolic steroids. All 4 were successfully treated surgically. Histopathology showed aortic medial changes in all 4.
We believe that the hemodynamic stresses of weight lifting, namely, a rapid increase in systemic arterial blood pressure without a decrease in total peripheral vascular resistance, in combination with aortic medial degeneration may have contributed to the development of the aortic dissection. (Ann Thoruc Surg 1990;49:63842)
S
The breath sounds were clear, and cardiac examination showed a 3/6 crescendo-decrescendo systolic murmur at the left sternal border and a 4/6 decrescendo blowing diastolic murmur at the apex. Chest roentgenogram demonstrated cardiomegaly with a normal aortic knob. Electrocardiogram was normal. An emergent aortogram showed 4+ aortic insufficiency and an ascending aortic dissection that appeared to extend into the descending aorta (Fig 1). At operation, the ascending aorta was replaced with a 30-mm woven Dacron graft and the two commissures involved by the dissection were resuspended with horizontal pledgeted mattress sutures. The patient had an uneventful postoperative course and was discharged home on the ninth postoperative day. Histopathological examination of the aorta using the grading system of Klima and colleagues [6] showed grade 2 cystic medial change, grade 2 elastic fragmentation, grade 1 medial necrosis, and grade 3 periaortic fibrosis.
everal factors have been implicated in the development of aortic dissection. In patients aged more than 40 years, chronic systemic hypertension is the most common association [l]. In patients aged less than 40 years with ascending aortic dissections (Stanford type A), hypertension is less common [2, 31. Instead, congenital abnormalities such as Marfan’s syndrome, Turner’s syndrome, bicuspid aortic valve, and aortic coarctation may exist [3]. Pregnancy is also a known risk factor [2]. We report 4 cases of ascending aortic dissection seen at Harbor-UCLA Medical Center between 1985 and 1989 in previously healthy young patients who were long-term weight lifters. These patients represent 50% of all cases of ascending aortic dissection seen and operated on during this period. Symptoms of dissection developed in 2 patients while they were lifting weights. Weight lifting has previously been reported to lead to subarachnoid hemorrhage [4]and brainstem ischemia [5]. A possible contributory role of weight lifting in the pathogenesis of aortic dissection is discussed. Case Reports
Patient 2 A 22-year-old man complained in the emergency room of severe “ripping“ chest pain radiating to the neck and jaw. The patient was an avid weight lifter and 6 weeks earlier, while lifting weights, had experienced a similar “ripping” chest pain that resolved spontaneously. The patient was otherwise in excellent health with no history of hypertension or previous medical problems. Vital signs were normal except for a blood pressure (BP) of 130/30 mm Hg. Physical examination revealed a very muscular, anxious-appearing young man without a marfanoid habitus. Accepted for publication Dec 6 , 1989. Address reprint requests to Dr Robertson, Department of Surgery, HarborUCLA Medical Center, 1000 W Carson St, Bin 423, Torrance, CA 90509.
0 1990 by The Society of Thoracic Surgeons
Patient 2 A 57-year-old man examined in the emergency room had a 1-week history of epigastric and substernal discomfort, progressive weakness, and shortness of breath. The symptoms had begun 1 week earlier while he was lifting weights. He was otherwise in excellent health, with no history of hypertension or other medical problems, and lifted weights seven days a week. Vital signs were normal, including a BP of 120/48 mm Hg in both arms. Physical examination revealed an anxious-appearing, muscular male without a marfanoid habitus who was in mild distress. Bibasilar rales were present. Cardiac examination showed a grade 2/6 early systolic murmur and a grade 3/6 harsh diastolic murmur at the left lower sternal border. Chest roentgenogram showed cardiomegaly with bilateral pulmonary edema. The electrocardiogram was normal. An emergent aortogram showed severe aortic 0003-4975/90/$3.50
Ann Thorac Surg 1990;49:63%42
Fig I. Aortogram of patient 1 shows a dilated aortic root with gross regurgitation into the left ventricle. Bold arrows indicate the intimal Pap. Thin arrow shows the proximal extent of the dissection.
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anabolic steroids 8 years earlier for 2 years. Vital signs included a temperature of 36.7“C, a heart rate of 118 beatdmin, BP of 148/68 mm Hg, and a respiratory rate of 34/min. Physical examination showed an anxious-appearing man without a marfanoid habitus who was in mild respiratory distress. He was muscular and weighed 122.4 kg. Bilateral rales and ronchi were present. Heart examination showed a grade 3/6 systolic murmur and a grade 3/6 diastolic murmur at the left sternal border. Chest roentgenogram demonstrated a widened mediastinum and an epicardial fat pad sign consistent with a pericardial effusion. Electrocardiogram demonstrated left ventricular hypertrophy. Laboratory values included a white blood cell count of 10,6OO/pL and a hematocrit of 0.45. An aortogram showed aortic root dilatation and aortic regurgitation, but no evidence of aortic dissection. During this time, the patient’s temperature and white blood cell count increased to 38.3”C and 16,3OO/pL, respectively. He was given intravenous antibiotics. An echocardiogram showed a large pericardial effusion, and pericardiocentesis yielded 1,000 mL of bloody fluid with a hematocrit of 0.47. Because of a high index of suspicion for aortic dissection despite a negative aortogram, cardiac cineangiography was performed and showed an intimal flap in the ascending aorta that was confirmed at operation. As the aortic valve was not suitable for resuspension, the repair was performed using a 27-mm St. Jude valve graft conduit. The coronary arteries were bypassed using two reverse saphenous vein grafts because the normal
regurgitation and an intimal flap in the aortic root with a false lumen extending to the transverse aortic arch (Fig 2). At operation, a near-circumferential tear was noted in the midascending aorta. The false lumen extended to the base of the innominate artery. The aortic valve, which was judged to be nonreparable, was excised, and a preclotted 29-mm Bjork-Shiley aortic valve graft conduit was inserted. The coronary arteries were revascularized using two reverse saphenous vein grafts from the innominate artery because the normal anatomical position of the coronary ostia prevented their direct anastomosis to the graft. The patient’s postoperative course was uneventful, and he was discharged home on the tenth postoperative day. Histopathological examination of the aorta showed grade 2 cystic medial change, grade 2 elastic fragmentation, and grade l medial necrosis.
Patient 3 A 34-year-old man was examined in the emergency room after a brief syncopal episode associated with shortness of breath, diaphoresis, and intermittent burning substernal chest pain during the previous week. He had a history of mild hypertension controlled with hydrochlorthiazide. He was a national-class weight lifter and had lifted weights for many years. He admitted to having used
Fig 2 . Aortogram of patient 2 shows a markedly dilated ascending aorta. Arrows show the intimal flap extending from the valve to the transverse portion of the aortic arch.
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anatomical position of the coronary ostia precluded their direct anastomosis to the graft. Blood and pericardial fluid cultures were negative. The patient’s postoperative course was uneventful, and he was discharged home on the ninth postoperative day. Histopathology of the aortic wall showed grade 3 cystic medial change, grade 3 elastic fragmentation, grade 3 medial necrosis (Fig 3), and grade 3 periaortic fibrosis.
Patient 4 A 37-year-old man was examined at an outside hospital because of excruciating substernal chest pain that developed while he was straining at stool. He was an avid weight lifter who had lifted weights three times a week for 15 years and had just completed a rigorous weight-lifting session. The patient had a history of hypertension controlled with clonidine and had previously abused anabolic steroids, cocaine, and heroin. Cardiac catheterization at another institution showed an ascending aortic dissection. The patient refused operation, however, and left the hospital against medical advice. The patient came to our emergency room 5 months later complaining of dyspnea on exertion and mild substernal chest pain. Vital signs were normal and included a BP of
Fig 4. Histopathological section of ascending aorta (patient 4) shows complete separation of the inner and outer layers of the aortic media (clear arrow), extensive elastic fragmentation in the media, medial necrosis, and extensive periaortic fibrosis (solid arrow) (elastic stain, X l O O before 50% reduction).
138/86 mm Hg. Physical examination showed a muscular man without a marfanoid habitus and in moderate distress. Breath sounds were clear, and cardiac examination showed a grade 216 systolic murmur and a grade 2l6 blowing diastolic murmur at the left sternal border. Chest roentgenogram demonstrated cardiomegaly but no mediastinal widening. Electrocardiogram was consistent with left ventricular hypertrophy. Echocardiography showed a dilated aortic root with a visible intimal flap and a large pericardial effusion. Cardiac catheterization confirmed the presence of an ascending aortic dissection and demonstrated severe aortic regurgitation as well as a large pericardial effusion. Pericardiocentesis yielded 1,800 mL of serosanguinous fluid. At operation, an intimal tear was found in the proximal ascending aorta. The prolapsing aortic valve commissure was resuspended with pledgeted horizontal mattress sutures, and the aorta was reconstructed with a 30-mm low-porosity preclotted intraluminal graft. The postoperative course was complicated by the development of a left lower lobe pneumonia, which resolved with intravenous antibiotics. The patient was discharged home on the tenth postoperative day. Histopathological examination of the aorta showed grade 1cystic medial change, grade 3 elastic fragmentation, grade 2 medial necrosis, and grade 3 periaortic fibrosis (Fig 4).
Comment
Fig 3. Histopathological section of ascending aorta (patient 3) shows medial necrosis (arrow) as well as elastic fragmentation of focal cystic 0 29% reduction). medial change (elastic stain, ~ 2 5 before
The pathogenic mechanism of aortic dissection is not entirely defined. The most likely explanation is that an intimal tear occurs secondary to the hemodynamic forces applied to the aorta. Chronic systemic hypertension accentuates these forces and promotes the formation of atheroscleroticplaques, which may be a source of intimal tears. Hypertension also weakens the media, which may lead to aneurysmal dilatation [7].Aneurysmal dilatation, by the law of Laplace, leads to a great increase in wall tension [8], further stressing the aorta. Once an intimal
Ann Thorac Surg 1990;49:63842
tear occurs, propagation of the dissection through the media is facilitated by an elevated BP, a steep pulse wave, and disease in the aortic media [9]. In one large series, hypertension was present in 406 of 614 patients (74%)[l]. Medial disease is found in most pathological specimens with aortic dissection. Klima and colleagues [6] histologically examined 339 aortic specimens from patients with ascending aortic aneurysms and devised a grading system modified from those of Carlson and Schlatmann. Histopathological abnormalities were divided into cystic medial change, elastic fragmentation, medial necrosis, atherosclerosis, periaortic fibrosis, periaortic inflammation, and thickening of the vasa vasorum. Using this grading system, Klima and colleagues [6] showed that the most common morphological change was elastic fragmentation in 94%, followed by cystic medial change and medial fibrosis. With this grading system, clinically significant medial changes were found in all 4 patients in our series. Cystic medial change and medionecrosis were once thought to be a requisite for aortic dissection. Histopathological studies on nondissected aortas indicate, however, that medial degeneration occurs as part of the aging process [lo]. In one study, cystic medial necrosis was found in only 13% of patients aged less than 40 years but was present in 50% of patients aged more than 40 years [ll]. In the same study, hypertension was more common in patients with cystic medial necrosis. These findings have led some investigators to conclude that medial degeneration is the result of aging and is accentuated in patients with hypertension [12]. In our series, all 4 patients had some degree of medial disease and 2 had a history of hypertension, but only 1was aged more than 40 years. Several reports indicate that predisposing conditions leading to dissection are different in type A (those originating in the ascending aorta) versus type B (those originating in the descending aorta distal to the left subclavian artery) aortic dissections. First, patients with type A dissections tend to be younger [13]. In one series of 108 patients, the average age of patients with type A dissections was 49 years in contrast to an average age of 60 years for type B [14]. In another series, 32 patients aged less than 40 years with aortic dissection were analyzed; 87% had type A. Second, patients with type A dissections are more likely to have congenital defects predisposing to aortic dissection. In Gore’s series [3] of patients aged less than 40 years, 44% had congenital defects known to predispose to dissection, such as bicuspid aortic valve, Marfan’s syndrome, and coarctation of the aorta. Third, type A patients are less likely to have a history of systemic hypertension [14-161. In the series of Applebaum and co-workers [14], only 30% of patients with type A dissection were hypertensive whereas 71% with type B were hypertensive, and, if the subgroup of type A patients aged less than 40 years is considered, hypertension is even less likely [2, 31. In our series, all 4 patients had a type A dissection, 3 were aged less than 40 years, 2 had a history of hypertension, and none had any congenital defects. The influence of anabolic steroids and cocaine on the development of ascending aortic dissection is unclear.
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Anabolic steroids are known to increase levels of lowdensity lipoprotein cholesterol and decrease levels of high-density lipoprotein cholesterol [171. Acute myocardial infarction was recently reported in a 22-year-old world-class weight lifter using anabolic steroids [17]. Our 2 patients who had previously used steroids had discontinued their use several years earlier and had no evidence of serious atherosclerosis in their excised aortic specimens. Cocaine increases systemic BP markedly and has been described in association with aortic dissection and aortic rupture [18, 191. Our 1patient who abused cocaine, however, was not using cocaine at the time his symptoms developed. Physical exertion or strain has previously been reported to precede aortic dissection. Hirst and associates [20] reported that of 167 patients 13% reported strenuous physical exertion before the onset of dissection. Hirst and associates [20] did not believe that the physical activity played a major role in the dissection process. Although straining or exertion cannot be implicated directly in the development of dissection, our series is remarkable in that all 4 patients had a long history of rigorous weight lifting (including 1 national-class lifter) and that symptoms developed in 2 while they were lifting weights. Several studies have analyzed the hemodynamic effects of weight lifting. MacDougall and colleagues [21] reported that lifting heavy weights resulted in an increase up to fourfold in both systolic and diastolic BP. The increase in BP resulted primarily from an increase in cardiac output, with a lesser contribution from reflex vasoconstriction in the vascular beds of the nonexercising muscles. The increased cardiac output was thought to be secondary to an increased heart rate combined with an increase in stroke volume. The Valsalva maneuver during static exercise further increases intrathoracic pressure and may further increase BP. Another study analyzed the BP response to static contraction of different size muscle groups and found that the larger the muscle group involved in the static exercise, the greater the increase in BP and heart rate [22]. Bezuchua and co-workers [23] compared the hemodynamic responses of static (quadricep in leg extension) and dynamic (two-leg cycling) exercise. Although BP increased in both exercises, the total peripheral resistance actually increased slightly during static exercise, whereas it decreased by 60% with dynamic exercise. Therefore, weight lifting may have contributed to the development of aortic dissection in our patients, particularly as these individuals lifted weights regularly for many years. Weight lifting clearly leads to a great transient increase in BP which, over a period of years, as might be anticipated in bodybuilders and powerlifters, may have placed critical hemodynamic stresses on the aorta. Because all our patients showed evidence of medial degeneration, the question that must be answered is whether the episodic hypertension created during weight lifting in these individuals led to their medial degeneration or if their preexisting medial disease predisposed them to aortic dissection. It seems reasonable to conclude, however, that once an aortic intimal tear occurs in the presence of both elevated BP and preexisting aortic medial
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disease the conditions are right for propagation of an aortic dissection. Therefore, although we cannot state unequivocally that weight lifting produces aortic dissection, we strongly believe that individuals who have evidence of cystic medial disease or family histories of this disease should avoid weight lifting. Studies investigating the long-term effects of chronic weight lifting must be performed to investigate further the possibility that chronic weight lifting and its obligatory intermittent markedly elevated BP may produce aortic wall changes resulting in acute dissection.
References 1. Crawford ES, Svensson LG, Coselli JS, Safi HJ, Hess KR. Aortic dissection and dissecting aortic aneurysms. Ann Surg 1988;208:254-72. 2. Wilson SK, Hutchins GM. Aortic dissecting aneurysms: causative factors in 204 subjects. Arch Pathol Lab Med 1982;106:175-80. 3. Gore I. Dissecting aneurysms of the aorta in persons under forty years of age. Arch Pathol 1953;55:1-13. 4. Hall Jurkowski JE, Sutton JR, Duke RJ. Subarachnoid hemorrhage in association with weightlifting [Abstract]. Can J Appl Sports Sci 1983;8:210. 5. Tuxen DV, Sutton J, Upton A, et al. Brainstem injury following maximal weight lifting attempts [Abstract]. Med Sci Sports Exerc 1983;15:184. 6. Klima T, Spjut HJ, Coelho A, et al. The morphology of ascending aortic aneurysms. Hum Pathol 1983;14810-7. 7. Roberts WC. Aortic dissection: anatomy, consequences, and causes. Am Heart J 1981;101:195-214. 8. Schlatmann TJ, Becker AE. Pathogenesis of dissecting aneurysm of aorta: comparative histopathologic study of significance of medial changes. Am J Cardiol 1977;39:214. 9. Wheat MW Jr. Acute dissecting aneurysms of the aorta: diagnosis and treatment-1979. Am Heart J 1980;99:373-87.
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10. Schlatmann TJ, Becker AE. Histologic changes in the normal aging aorta: implications for dissecting aortic aneurysm. Am J Cardiol 1977;39:1>20. 11. Carlson RG, Lillehei CW, Edwards JE. Cystic medial necrosis of the ascending aorta in relation to age and hypertension. Am J Cardiol 1970;25:411-5. 12. Hirst AE, Gore I. Is cystic medionecrosis the cause of dissecting aortic aneurysm? Circulation 1976;53:9154. 13. DeBakey ME, McCollum CH, Crawford ES, et al. Dissection and dissecting aneurysms of the aorta: twenty-year followup of five hundred twenty-seven patients treated surgically. Surgery 1982;92:1118-34. 14. Applebaum A, Karp RB, Kirklin JW. Ascending vs descending aortic dissections. Ann Surg 1976;183:296300. 15. Larson EW, Edwards WD. Risk factors for aortic dissection: a necropsy study of 161 cases. Am J Cardiol 1984;53:849-55. 16. Fradet G, Jamieson WRE, Janusz WT, et al. Aortic dissection: a six year experience with 117 patients. Am J Surg 1988; 155:697-700. 17. McNutt RA, Ferenchick GS, Kirlin PC, et al. Acute myocardial infarction in a 22-year-old world class weightlifter using anabolic steroids. Am J Cardiol 1988;62:164. 18. Grannis FW Jr, Bryant C, Caffaratti JD, et al. Acute aortic dissection associated with cocaine abuse. Clin Cardiol 1988; 11:5724. 19. Barth CW 111, Bray M, Roberts WC. Rupture of the ascending aorta during cocaine intoxication. Am J Cardiol 1986;56496. 20. Hirst AE Jr, Johns VJ Jr, Kime SW Jr. Dissecting aneurysm of the aorta: a review of 505 cases. Medicine 1958;37217-79. 21. MacDougall JD, Tuxen D, Sale DG, Moroz JR, Sutton JR. Arterial blood pressure response to heavy resistance exercise. J Appl Physiol 1985;58:785-90. 22. Seals DR, Washbum RA, Hanson PG, Painter PL, Nagle FJ. Increased cardiovascular response to static contraction of larger muscle groups. J Appl Physiol 1983;54434-7. 23. Bezucha GR, Lenser MC, Hanson PG, Nagle FJ. Comparison of hemodynamic responses to static and dynamic exercise. J Appl Physiol 1982;53:158%93.
We report 4 cases of ascending aortic dissection in patients with long histories of weight lifting. In 2 of the patients, the initial symptoms of dissection developed while they were lifting weights. Two patients had a history of hypertension and 2 had previously used anabolic steroids. All 4 were successfully treated surgically. Histopathology showed aortic medial changes in all 4.
We believe that the hemodynamic stresses of weight lifting, namely, a rapid increase in systemic arterial blood pressure without a decrease in total peripheral vascular resistance, in combination with aortic medial degeneration may have contributed to the development of the aortic dissection. (Ann Thoruc Surg 1990;49:63842)
S
The breath sounds were clear, and cardiac examination showed a 3/6 crescendo-decrescendo systolic murmur at the left sternal border and a 4/6 decrescendo blowing diastolic murmur at the apex. Chest roentgenogram demonstrated cardiomegaly with a normal aortic knob. Electrocardiogram was normal. An emergent aortogram showed 4+ aortic insufficiency and an ascending aortic dissection that appeared to extend into the descending aorta (Fig 1). At operation, the ascending aorta was replaced with a 30-mm woven Dacron graft and the two commissures involved by the dissection were resuspended with horizontal pledgeted mattress sutures. The patient had an uneventful postoperative course and was discharged home on the ninth postoperative day. Histopathological examination of the aorta using the grading system of Klima and colleagues [6] showed grade 2 cystic medial change, grade 2 elastic fragmentation, grade 1 medial necrosis, and grade 3 periaortic fibrosis.
everal factors have been implicated in the development of aortic dissection. In patients aged more than 40 years, chronic systemic hypertension is the most common association [l]. In patients aged less than 40 years with ascending aortic dissections (Stanford type A), hypertension is less common [2, 31. Instead, congenital abnormalities such as Marfan’s syndrome, Turner’s syndrome, bicuspid aortic valve, and aortic coarctation may exist [3]. Pregnancy is also a known risk factor [2]. We report 4 cases of ascending aortic dissection seen at Harbor-UCLA Medical Center between 1985 and 1989 in previously healthy young patients who were long-term weight lifters. These patients represent 50% of all cases of ascending aortic dissection seen and operated on during this period. Symptoms of dissection developed in 2 patients while they were lifting weights. Weight lifting has previously been reported to lead to subarachnoid hemorrhage [4]and brainstem ischemia [5]. A possible contributory role of weight lifting in the pathogenesis of aortic dissection is discussed. Case Reports
Patient 2 A 22-year-old man complained in the emergency room of severe “ripping“ chest pain radiating to the neck and jaw. The patient was an avid weight lifter and 6 weeks earlier, while lifting weights, had experienced a similar “ripping” chest pain that resolved spontaneously. The patient was otherwise in excellent health with no history of hypertension or previous medical problems. Vital signs were normal except for a blood pressure (BP) of 130/30 mm Hg. Physical examination revealed a very muscular, anxious-appearing young man without a marfanoid habitus. Accepted for publication Dec 6 , 1989. Address reprint requests to Dr Robertson, Department of Surgery, HarborUCLA Medical Center, 1000 W Carson St, Bin 423, Torrance, CA 90509.
0 1990 by The Society of Thoracic Surgeons
Patient 2 A 57-year-old man examined in the emergency room had a 1-week history of epigastric and substernal discomfort, progressive weakness, and shortness of breath. The symptoms had begun 1 week earlier while he was lifting weights. He was otherwise in excellent health, with no history of hypertension or other medical problems, and lifted weights seven days a week. Vital signs were normal, including a BP of 120/48 mm Hg in both arms. Physical examination revealed an anxious-appearing, muscular male without a marfanoid habitus who was in mild distress. Bibasilar rales were present. Cardiac examination showed a grade 2/6 early systolic murmur and a grade 3/6 harsh diastolic murmur at the left lower sternal border. Chest roentgenogram showed cardiomegaly with bilateral pulmonary edema. The electrocardiogram was normal. An emergent aortogram showed severe aortic 0003-4975/90/$3.50
Ann Thorac Surg 1990;49:63%42
Fig I. Aortogram of patient 1 shows a dilated aortic root with gross regurgitation into the left ventricle. Bold arrows indicate the intimal Pap. Thin arrow shows the proximal extent of the dissection.
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anabolic steroids 8 years earlier for 2 years. Vital signs included a temperature of 36.7“C, a heart rate of 118 beatdmin, BP of 148/68 mm Hg, and a respiratory rate of 34/min. Physical examination showed an anxious-appearing man without a marfanoid habitus who was in mild respiratory distress. He was muscular and weighed 122.4 kg. Bilateral rales and ronchi were present. Heart examination showed a grade 3/6 systolic murmur and a grade 3/6 diastolic murmur at the left sternal border. Chest roentgenogram demonstrated a widened mediastinum and an epicardial fat pad sign consistent with a pericardial effusion. Electrocardiogram demonstrated left ventricular hypertrophy. Laboratory values included a white blood cell count of 10,6OO/pL and a hematocrit of 0.45. An aortogram showed aortic root dilatation and aortic regurgitation, but no evidence of aortic dissection. During this time, the patient’s temperature and white blood cell count increased to 38.3”C and 16,3OO/pL, respectively. He was given intravenous antibiotics. An echocardiogram showed a large pericardial effusion, and pericardiocentesis yielded 1,000 mL of bloody fluid with a hematocrit of 0.47. Because of a high index of suspicion for aortic dissection despite a negative aortogram, cardiac cineangiography was performed and showed an intimal flap in the ascending aorta that was confirmed at operation. As the aortic valve was not suitable for resuspension, the repair was performed using a 27-mm St. Jude valve graft conduit. The coronary arteries were bypassed using two reverse saphenous vein grafts because the normal
regurgitation and an intimal flap in the aortic root with a false lumen extending to the transverse aortic arch (Fig 2). At operation, a near-circumferential tear was noted in the midascending aorta. The false lumen extended to the base of the innominate artery. The aortic valve, which was judged to be nonreparable, was excised, and a preclotted 29-mm Bjork-Shiley aortic valve graft conduit was inserted. The coronary arteries were revascularized using two reverse saphenous vein grafts from the innominate artery because the normal anatomical position of the coronary ostia prevented their direct anastomosis to the graft. The patient’s postoperative course was uneventful, and he was discharged home on the tenth postoperative day. Histopathological examination of the aorta showed grade 2 cystic medial change, grade 2 elastic fragmentation, and grade l medial necrosis.
Patient 3 A 34-year-old man was examined in the emergency room after a brief syncopal episode associated with shortness of breath, diaphoresis, and intermittent burning substernal chest pain during the previous week. He had a history of mild hypertension controlled with hydrochlorthiazide. He was a national-class weight lifter and had lifted weights for many years. He admitted to having used
Fig 2 . Aortogram of patient 2 shows a markedly dilated ascending aorta. Arrows show the intimal flap extending from the valve to the transverse portion of the aortic arch.
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anatomical position of the coronary ostia precluded their direct anastomosis to the graft. Blood and pericardial fluid cultures were negative. The patient’s postoperative course was uneventful, and he was discharged home on the ninth postoperative day. Histopathology of the aortic wall showed grade 3 cystic medial change, grade 3 elastic fragmentation, grade 3 medial necrosis (Fig 3), and grade 3 periaortic fibrosis.
Patient 4 A 37-year-old man was examined at an outside hospital because of excruciating substernal chest pain that developed while he was straining at stool. He was an avid weight lifter who had lifted weights three times a week for 15 years and had just completed a rigorous weight-lifting session. The patient had a history of hypertension controlled with clonidine and had previously abused anabolic steroids, cocaine, and heroin. Cardiac catheterization at another institution showed an ascending aortic dissection. The patient refused operation, however, and left the hospital against medical advice. The patient came to our emergency room 5 months later complaining of dyspnea on exertion and mild substernal chest pain. Vital signs were normal and included a BP of
Fig 4. Histopathological section of ascending aorta (patient 4) shows complete separation of the inner and outer layers of the aortic media (clear arrow), extensive elastic fragmentation in the media, medial necrosis, and extensive periaortic fibrosis (solid arrow) (elastic stain, X l O O before 50% reduction).
138/86 mm Hg. Physical examination showed a muscular man without a marfanoid habitus and in moderate distress. Breath sounds were clear, and cardiac examination showed a grade 216 systolic murmur and a grade 2l6 blowing diastolic murmur at the left sternal border. Chest roentgenogram demonstrated cardiomegaly but no mediastinal widening. Electrocardiogram was consistent with left ventricular hypertrophy. Echocardiography showed a dilated aortic root with a visible intimal flap and a large pericardial effusion. Cardiac catheterization confirmed the presence of an ascending aortic dissection and demonstrated severe aortic regurgitation as well as a large pericardial effusion. Pericardiocentesis yielded 1,800 mL of serosanguinous fluid. At operation, an intimal tear was found in the proximal ascending aorta. The prolapsing aortic valve commissure was resuspended with pledgeted horizontal mattress sutures, and the aorta was reconstructed with a 30-mm low-porosity preclotted intraluminal graft. The postoperative course was complicated by the development of a left lower lobe pneumonia, which resolved with intravenous antibiotics. The patient was discharged home on the tenth postoperative day. Histopathological examination of the aorta showed grade 1cystic medial change, grade 3 elastic fragmentation, grade 2 medial necrosis, and grade 3 periaortic fibrosis (Fig 4).
Comment
Fig 3. Histopathological section of ascending aorta (patient 3) shows medial necrosis (arrow) as well as elastic fragmentation of focal cystic 0 29% reduction). medial change (elastic stain, ~ 2 5 before
The pathogenic mechanism of aortic dissection is not entirely defined. The most likely explanation is that an intimal tear occurs secondary to the hemodynamic forces applied to the aorta. Chronic systemic hypertension accentuates these forces and promotes the formation of atheroscleroticplaques, which may be a source of intimal tears. Hypertension also weakens the media, which may lead to aneurysmal dilatation [7].Aneurysmal dilatation, by the law of Laplace, leads to a great increase in wall tension [8], further stressing the aorta. Once an intimal
Ann Thorac Surg 1990;49:63842
tear occurs, propagation of the dissection through the media is facilitated by an elevated BP, a steep pulse wave, and disease in the aortic media [9]. In one large series, hypertension was present in 406 of 614 patients (74%)[l]. Medial disease is found in most pathological specimens with aortic dissection. Klima and colleagues [6] histologically examined 339 aortic specimens from patients with ascending aortic aneurysms and devised a grading system modified from those of Carlson and Schlatmann. Histopathological abnormalities were divided into cystic medial change, elastic fragmentation, medial necrosis, atherosclerosis, periaortic fibrosis, periaortic inflammation, and thickening of the vasa vasorum. Using this grading system, Klima and colleagues [6] showed that the most common morphological change was elastic fragmentation in 94%, followed by cystic medial change and medial fibrosis. With this grading system, clinically significant medial changes were found in all 4 patients in our series. Cystic medial change and medionecrosis were once thought to be a requisite for aortic dissection. Histopathological studies on nondissected aortas indicate, however, that medial degeneration occurs as part of the aging process [lo]. In one study, cystic medial necrosis was found in only 13% of patients aged less than 40 years but was present in 50% of patients aged more than 40 years [ll]. In the same study, hypertension was more common in patients with cystic medial necrosis. These findings have led some investigators to conclude that medial degeneration is the result of aging and is accentuated in patients with hypertension [12]. In our series, all 4 patients had some degree of medial disease and 2 had a history of hypertension, but only 1was aged more than 40 years. Several reports indicate that predisposing conditions leading to dissection are different in type A (those originating in the ascending aorta) versus type B (those originating in the descending aorta distal to the left subclavian artery) aortic dissections. First, patients with type A dissections tend to be younger [13]. In one series of 108 patients, the average age of patients with type A dissections was 49 years in contrast to an average age of 60 years for type B [14]. In another series, 32 patients aged less than 40 years with aortic dissection were analyzed; 87% had type A. Second, patients with type A dissections are more likely to have congenital defects predisposing to aortic dissection. In Gore’s series [3] of patients aged less than 40 years, 44% had congenital defects known to predispose to dissection, such as bicuspid aortic valve, Marfan’s syndrome, and coarctation of the aorta. Third, type A patients are less likely to have a history of systemic hypertension [14-161. In the series of Applebaum and co-workers [14], only 30% of patients with type A dissection were hypertensive whereas 71% with type B were hypertensive, and, if the subgroup of type A patients aged less than 40 years is considered, hypertension is even less likely [2, 31. In our series, all 4 patients had a type A dissection, 3 were aged less than 40 years, 2 had a history of hypertension, and none had any congenital defects. The influence of anabolic steroids and cocaine on the development of ascending aortic dissection is unclear.
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Anabolic steroids are known to increase levels of lowdensity lipoprotein cholesterol and decrease levels of high-density lipoprotein cholesterol [171. Acute myocardial infarction was recently reported in a 22-year-old world-class weight lifter using anabolic steroids [17]. Our 2 patients who had previously used steroids had discontinued their use several years earlier and had no evidence of serious atherosclerosis in their excised aortic specimens. Cocaine increases systemic BP markedly and has been described in association with aortic dissection and aortic rupture [18, 191. Our 1patient who abused cocaine, however, was not using cocaine at the time his symptoms developed. Physical exertion or strain has previously been reported to precede aortic dissection. Hirst and associates [20] reported that of 167 patients 13% reported strenuous physical exertion before the onset of dissection. Hirst and associates [20] did not believe that the physical activity played a major role in the dissection process. Although straining or exertion cannot be implicated directly in the development of dissection, our series is remarkable in that all 4 patients had a long history of rigorous weight lifting (including 1 national-class lifter) and that symptoms developed in 2 while they were lifting weights. Several studies have analyzed the hemodynamic effects of weight lifting. MacDougall and colleagues [21] reported that lifting heavy weights resulted in an increase up to fourfold in both systolic and diastolic BP. The increase in BP resulted primarily from an increase in cardiac output, with a lesser contribution from reflex vasoconstriction in the vascular beds of the nonexercising muscles. The increased cardiac output was thought to be secondary to an increased heart rate combined with an increase in stroke volume. The Valsalva maneuver during static exercise further increases intrathoracic pressure and may further increase BP. Another study analyzed the BP response to static contraction of different size muscle groups and found that the larger the muscle group involved in the static exercise, the greater the increase in BP and heart rate [22]. Bezuchua and co-workers [23] compared the hemodynamic responses of static (quadricep in leg extension) and dynamic (two-leg cycling) exercise. Although BP increased in both exercises, the total peripheral resistance actually increased slightly during static exercise, whereas it decreased by 60% with dynamic exercise. Therefore, weight lifting may have contributed to the development of aortic dissection in our patients, particularly as these individuals lifted weights regularly for many years. Weight lifting clearly leads to a great transient increase in BP which, over a period of years, as might be anticipated in bodybuilders and powerlifters, may have placed critical hemodynamic stresses on the aorta. Because all our patients showed evidence of medial degeneration, the question that must be answered is whether the episodic hypertension created during weight lifting in these individuals led to their medial degeneration or if their preexisting medial disease predisposed them to aortic dissection. It seems reasonable to conclude, however, that once an aortic intimal tear occurs in the presence of both elevated BP and preexisting aortic medial
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disease the conditions are right for propagation of an aortic dissection. Therefore, although we cannot state unequivocally that weight lifting produces aortic dissection, we strongly believe that individuals who have evidence of cystic medial disease or family histories of this disease should avoid weight lifting. Studies investigating the long-term effects of chronic weight lifting must be performed to investigate further the possibility that chronic weight lifting and its obligatory intermittent markedly elevated BP may produce aortic wall changes resulting in acute dissection.
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