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Emergency PTCA for coronary artery occlusion after blunt chest trauma
June 1990
1408
4. 5. 6. 7.
Brief Communications
its prevalence and clinical significance in 4993 patients. Br Heart J 1985;54:392-5. Robinson FC. Aneurysms of the coronary arteries. AMHEART J 1985;109:129-35. Swaye PS, Fisher LD, Litwin P, Vignola PA, Judkins MP, Kemp HG, Mudd JG, Gosselin AJ. Aneurysmal coronary artery disease. Circulation 1983;67:134-8. Daoud AS, Pankin D, Tulgan H, Florentin RA. Aneurysms of the coronary artery: report of ten cases and review of the literature. Am J Cardiol 1963;11:228-37. Kitamura S, Kawashima Y, Miyamoto K, Kobayashi T, Matsuda H, Ohgitani N, Kodoma K, Minamino T, Manabe H. Multiple coronary aneurysms resulting in myocardial infarction in a young man: treatment by double aorta-coronary saphenous vein bypass grafting. J Thorac Cardiovasc Surg 1975;70:290-7.
Emergency PTCA for coronary artery occlusion after blunt chest trauma Martin Sigmund, MD, Silvia Nase-Htippmeier, MD, Rainer Uebis, MD, and Peter Hanrath, MD.
Aachen, West Germany
Nonpenetrating traumatic injury of the heart is one of the most serious complications of blunt chest trauma. In addition to direct contusion, the most frequent mechanism causing cardiac injury is the sudden deceleration of the victim's chest. The lesions to be discussed are pericardial disruption, hemopericardium, myocardial contusion and rupture, septal perforation and damage of valves, chordae tendineae, or papillary muscles. 1 Less common but also a factor of high risk for these patients is the injury to coronary arteries. We report on a case of acute anterior myocardial infarction occurring after blunt chest trauma. The angiographically proven occlusion of the left anterior descending artery (LAD) could be recanalized by emergency percutaneous transluminal coronary angioplasty (PTCA). At 10:00 AMon June 23,1989, a 34-year-old carpenter fell from a 4 m high ladder to a stone floor on the flat of his back. He immediately suffered from chest pain and shortness of breath, which disappeared after a few minutes; he therefore failed to consult a physician. However, during the following hours, several short episodes of nonsustained chest pain o c c u r r e d . The next day at 6:40 AM, the patient suffered from severe and sustained chest pain accompanied by a typical vagovasal reaction, which led to hospitalization. Physical examination revealed no abnormality, especially n o external signs of injury. The electrocardiogram (ECG) showed the typical pattern of an acute anterior myocardial infarction (Fig. 1, A). Chest x-ray film and creatine phosFrom the Medical Clinic I, Klinikum Rheinisch-Westf~lische Technische Hochschule. Reprint requests: Martin Sigmund, MD, Medical Clinic I, Klinikum RWTH Aachen, Pauwelsstrasse 30, 5100 Aachen, W. Germany. 4/4/19611
American Heart Journal
phokinase (CPK) enzyme levels were normal. Prior to the accident, the patient never had had any episodes of angina pectoris. Except for smoking, no atherogenic risk factors were known. A bicycle stress test 3 weeks before the accident revealed no signs of exercise-induced ischemia at a maximal work load of 175 W. After aortic dissection was ruled out by echocardiography and the patient's informed and witnessed consent was given, a diagnostic catheterization was performed by Judkins' technique. Selective coronary angiography revealed patent left main, circumflex, and right coronary arteries without any wall irregularities; however, the proximal LAD was occluded (Fig. 1, A). With respect to the preceding trauma, no thrombolytic therapy was performed; however, mechanical revascularization by means of angioplasty was done. Using a 3.0 mm balloon catheter (Type Micro Hartzler; Advanced Cardiovascular Systems, Inc., Santa Clara, Calif.), the occlusive lesion could easily be passed with the steerable guide wire. Due to the fact that afterwards only minimal perfusion could be observed, the balloon was positioned in the formerly occluded segment and was inflated four times to a maximal pressure of 7 atm. Immediate control angiography, 3 hours and 30 minutes after the onset of symptoms, revealed a sufficent perfusion of the LAD (Fig. 1, B), with a residual stenosis of 40% of the vessel diameter. Follow-up angiographies both 3 days and 3 weeks later confirmed patency of the LAD, with only minimal residual narrowing at the previous site of occlusion. However, moderate left ventricular dysfunction (ejection fraction = 40%) with anteroapical hypokinesia and apical dyskinesia with adherent thrombus was documented (Fig. 2). Four weeks after admission the patient was discharged free of symptoms. Four months later, left ventricular function had improved slightly, as judged by echocardiography. T~aumatic injury of the coronary arteries may be caused by external compression, spasm, dissective occlusion, and limited damage to the tunica intima, with secondary hemorrhage and and/or luminal thrombosis. 24 A direct causal relationship between trauma and myocardial ischemia frequently cannot be proven by specific morphologic criteria. In general, this relationship is at least probable if typical clinical symptoms occur shortly after a serious chest trauma; however, this relationship is very likely whenever ECG changes develop immediately or if vessel occlusion c a n be documented angiographically. 1 Even in patients with preexisting coronary artery disease, trauma can be seen as the underlying cause for myocardial infarction if the coronary obstruction is assumed to be generated by dislodging plaque material or by the induction of hemorrhage into an atheroma. 4, 5 In our reported case, myocardial infarction must be judged to be a complication of the preceding accident, considering the mechanism of the trauma and the typical immediately-occurring chest pain suggestive of an initial dissective lesion of the LAD. Similar to the findings in reported cases, 3,4 the interval to the onset of myocardial infarction, caused by secondary definite occlusion of the
Volume 1 1 9
Brief Communications
Number 6
1409
Fig. 1. Coronary angiograms (left anterior oblique projection) and corresponding ECG immediately before (A} and 1 hour after (B) mechanical revascularization of the LAD. Initially (A) the left coronary angiogram revealed a complete occlusion (arrow) of the LAD. After PTCA (B), the residual narrowing at the previous site of occlusion is only minimal (arrow). The EGG after reopening of the LAD revealed a marked reduction of initially extended ST elevation in the anterior leads.
LAD, was more than 20 hours. In general, the indication for acute catheterization in myocardial infarction after blunt chest trauma still remains a matter of discussion.2 Despite successful LAD reopening, the patient developed, due to 3I/2 hours of ischemia, a moderately extended anterior Q wave infarction. Thus in our opinion angiography should be performed as early as possible. The therapeutic approach depends on evaluation and documentation of the individual pathoanatomic situation. In addition, substantial at-
guments can be advanced to answer the important question whether there is a causal relationship between trauma and myocardial damage. 2 In keeping with the limited number of therapeutic options when thrombolytic therapy is contraindicated, in all cases reported so far patients were treated conservatively,2'6 even when coronary artery occlusion was proved by angiography. Although in principle the value of mechanical revascularization and PTCA in acute myocardial infarction remains a controversial issue, 7
June 1990
1410
Brie[ Communications
American Heart Journal
3. 4. 5. 6. 7.
of angiography--report of six cases and literature review. Cardiovasc Intervent Radiol 1983;6:20-9. De Feyter PJ, Roos JP. Traumatic myocardial infarction with subsequent normal coronary arteriogram. Eur J Cardiol 1977;6:25-31. Stephen CV, Blumenthal DS, Shoback D, Fehir K, Bulkley BH. Delayed acute myocardial infarction after blunt chest trauma in a young woman. AM HEARTJ 1980;100:90%16. Oren A, Bar-Shlomo B, Stern S. Acute coronary occlusion following blunt injury to the chest in the absence of coronary atherosclerosis. AM HEARTJ 1976;92:501-5. Pifarrb R, Grieco J, Gabibaldi A, Sullivan HJ, Montoya A, Bakhos M. Acute coronary artery occlusion secondary to blunt chest trauma. J Thorac Cardiovasc Surg 1982;83:122-5. Simoons ML, Arnold AER, Betri A, et al. Thrombolysis with tissue plasminogen activator in acute myocardial infarction: no additional benefit from immediate percutaneous coronary angioplasty. Lancet 1988;1:197-203.
Delayed rupture of tricuspid papillary muscle following blunt chest trauma Thomas Hilton, MD, Leslie Mezei, MD, and A n t h o n y C. Pearson, MD. St. Louis, Mo.
Fig. 2. Left ventricular angiogram 3 weeks after chest t r a u m a in the right anterior oblique projection. (A), E n d diastole; (B), end systole.
they should be considered in traumatic coronary vessel occlusion whenever revascularization appears to be achievable within the commonly accepted time window of about 6 hours after the onset of symptoms. REFERENCES
1. Liedtke AJ, De Muth WE. Nonpenetrating cardiac injuries: a collective review. AM HEARTJ 1973;86:687-97. 2. Gaspard P, Clermont A, Villard J, Amiel M. Non-iatrogenic trauma of the coronary arteries and myocardium: contribution
Tricuspid regurgitation following b l u n t chest trauma may occur by a tearing of the tricuspid valve leaflet, by disruption of the chordae tendineae, or by rupture of the papillary muscle apparatus. 1"4 It occurs rarely, with less than 40 cases reported in the literature. Previous reports have emphasized the subtle clinical manifestations, 1, 5 the value o f surface echocardiography for diagnosis, 1 the underdiagnosis of this critical condition,1 and the propensity for rightto-left s h u n t through a patent foramen ovale. 4, 6 We report a case of post-traumatic tricuspid regurgitation secondary to papillary muscle rupture in which the initial echocardiogram demonstrated normal tricuspid valve function. A 40-year-old m a n with no previous cardiac history was admitted with severe b l u n t chest t r a u m a due to a motor vehicle accident. Radiographic examination revealed evidence of sternal and bilateral rib fractures, and widening of the mediastinum. Emergency aortography revealed no evidence of aortic dissection. On initial examination, the pulse was 136 beats/rain , respirations were 28/min, and the blood pressure was 110/80 m m Hg. An electrocardiogram showed sinus tachycardia, left anterior hemiblock, and Q waves in leads V1 and V2, suggesting possible previous septa[ infarction. Creatine phosphokinase (CPK) enzymes and MB isoenzymes were elevated, suggesting myocardial conFrom the Divisionof Cardiology, Department of Internal Medicine, St. LouisUniversityHospital,St. LouisUniversitySchoolof Medicine;and St. John's MercyHospital, Departmentof Internal Medicine, Divislonof Cardiology. Reprint requests: Thomas Hilton,MD, St. LouisUniversityMedical Center, St. LouisUniversityHospital, Divisionof Cardiology,14th floor, 3635 Vista Ave. at Grand Blvd., P.O. Box 15250,St. Louis,MO 63110-0250. 4/4/19610
1408
4. 5. 6. 7.
Brief Communications
its prevalence and clinical significance in 4993 patients. Br Heart J 1985;54:392-5. Robinson FC. Aneurysms of the coronary arteries. AMHEART J 1985;109:129-35. Swaye PS, Fisher LD, Litwin P, Vignola PA, Judkins MP, Kemp HG, Mudd JG, Gosselin AJ. Aneurysmal coronary artery disease. Circulation 1983;67:134-8. Daoud AS, Pankin D, Tulgan H, Florentin RA. Aneurysms of the coronary artery: report of ten cases and review of the literature. Am J Cardiol 1963;11:228-37. Kitamura S, Kawashima Y, Miyamoto K, Kobayashi T, Matsuda H, Ohgitani N, Kodoma K, Minamino T, Manabe H. Multiple coronary aneurysms resulting in myocardial infarction in a young man: treatment by double aorta-coronary saphenous vein bypass grafting. J Thorac Cardiovasc Surg 1975;70:290-7.
Emergency PTCA for coronary artery occlusion after blunt chest trauma Martin Sigmund, MD, Silvia Nase-Htippmeier, MD, Rainer Uebis, MD, and Peter Hanrath, MD.
Aachen, West Germany
Nonpenetrating traumatic injury of the heart is one of the most serious complications of blunt chest trauma. In addition to direct contusion, the most frequent mechanism causing cardiac injury is the sudden deceleration of the victim's chest. The lesions to be discussed are pericardial disruption, hemopericardium, myocardial contusion and rupture, septal perforation and damage of valves, chordae tendineae, or papillary muscles. 1 Less common but also a factor of high risk for these patients is the injury to coronary arteries. We report on a case of acute anterior myocardial infarction occurring after blunt chest trauma. The angiographically proven occlusion of the left anterior descending artery (LAD) could be recanalized by emergency percutaneous transluminal coronary angioplasty (PTCA). At 10:00 AMon June 23,1989, a 34-year-old carpenter fell from a 4 m high ladder to a stone floor on the flat of his back. He immediately suffered from chest pain and shortness of breath, which disappeared after a few minutes; he therefore failed to consult a physician. However, during the following hours, several short episodes of nonsustained chest pain o c c u r r e d . The next day at 6:40 AM, the patient suffered from severe and sustained chest pain accompanied by a typical vagovasal reaction, which led to hospitalization. Physical examination revealed no abnormality, especially n o external signs of injury. The electrocardiogram (ECG) showed the typical pattern of an acute anterior myocardial infarction (Fig. 1, A). Chest x-ray film and creatine phosFrom the Medical Clinic I, Klinikum Rheinisch-Westf~lische Technische Hochschule. Reprint requests: Martin Sigmund, MD, Medical Clinic I, Klinikum RWTH Aachen, Pauwelsstrasse 30, 5100 Aachen, W. Germany. 4/4/19611
American Heart Journal
phokinase (CPK) enzyme levels were normal. Prior to the accident, the patient never had had any episodes of angina pectoris. Except for smoking, no atherogenic risk factors were known. A bicycle stress test 3 weeks before the accident revealed no signs of exercise-induced ischemia at a maximal work load of 175 W. After aortic dissection was ruled out by echocardiography and the patient's informed and witnessed consent was given, a diagnostic catheterization was performed by Judkins' technique. Selective coronary angiography revealed patent left main, circumflex, and right coronary arteries without any wall irregularities; however, the proximal LAD was occluded (Fig. 1, A). With respect to the preceding trauma, no thrombolytic therapy was performed; however, mechanical revascularization by means of angioplasty was done. Using a 3.0 mm balloon catheter (Type Micro Hartzler; Advanced Cardiovascular Systems, Inc., Santa Clara, Calif.), the occlusive lesion could easily be passed with the steerable guide wire. Due to the fact that afterwards only minimal perfusion could be observed, the balloon was positioned in the formerly occluded segment and was inflated four times to a maximal pressure of 7 atm. Immediate control angiography, 3 hours and 30 minutes after the onset of symptoms, revealed a sufficent perfusion of the LAD (Fig. 1, B), with a residual stenosis of 40% of the vessel diameter. Follow-up angiographies both 3 days and 3 weeks later confirmed patency of the LAD, with only minimal residual narrowing at the previous site of occlusion. However, moderate left ventricular dysfunction (ejection fraction = 40%) with anteroapical hypokinesia and apical dyskinesia with adherent thrombus was documented (Fig. 2). Four weeks after admission the patient was discharged free of symptoms. Four months later, left ventricular function had improved slightly, as judged by echocardiography. T~aumatic injury of the coronary arteries may be caused by external compression, spasm, dissective occlusion, and limited damage to the tunica intima, with secondary hemorrhage and and/or luminal thrombosis. 24 A direct causal relationship between trauma and myocardial ischemia frequently cannot be proven by specific morphologic criteria. In general, this relationship is at least probable if typical clinical symptoms occur shortly after a serious chest trauma; however, this relationship is very likely whenever ECG changes develop immediately or if vessel occlusion c a n be documented angiographically. 1 Even in patients with preexisting coronary artery disease, trauma can be seen as the underlying cause for myocardial infarction if the coronary obstruction is assumed to be generated by dislodging plaque material or by the induction of hemorrhage into an atheroma. 4, 5 In our reported case, myocardial infarction must be judged to be a complication of the preceding accident, considering the mechanism of the trauma and the typical immediately-occurring chest pain suggestive of an initial dissective lesion of the LAD. Similar to the findings in reported cases, 3,4 the interval to the onset of myocardial infarction, caused by secondary definite occlusion of the
Volume 1 1 9
Brief Communications
Number 6
1409
Fig. 1. Coronary angiograms (left anterior oblique projection) and corresponding ECG immediately before (A} and 1 hour after (B) mechanical revascularization of the LAD. Initially (A) the left coronary angiogram revealed a complete occlusion (arrow) of the LAD. After PTCA (B), the residual narrowing at the previous site of occlusion is only minimal (arrow). The EGG after reopening of the LAD revealed a marked reduction of initially extended ST elevation in the anterior leads.
LAD, was more than 20 hours. In general, the indication for acute catheterization in myocardial infarction after blunt chest trauma still remains a matter of discussion.2 Despite successful LAD reopening, the patient developed, due to 3I/2 hours of ischemia, a moderately extended anterior Q wave infarction. Thus in our opinion angiography should be performed as early as possible. The therapeutic approach depends on evaluation and documentation of the individual pathoanatomic situation. In addition, substantial at-
guments can be advanced to answer the important question whether there is a causal relationship between trauma and myocardial damage. 2 In keeping with the limited number of therapeutic options when thrombolytic therapy is contraindicated, in all cases reported so far patients were treated conservatively,2'6 even when coronary artery occlusion was proved by angiography. Although in principle the value of mechanical revascularization and PTCA in acute myocardial infarction remains a controversial issue, 7
June 1990
1410
Brie[ Communications
American Heart Journal
3. 4. 5. 6. 7.
of angiography--report of six cases and literature review. Cardiovasc Intervent Radiol 1983;6:20-9. De Feyter PJ, Roos JP. Traumatic myocardial infarction with subsequent normal coronary arteriogram. Eur J Cardiol 1977;6:25-31. Stephen CV, Blumenthal DS, Shoback D, Fehir K, Bulkley BH. Delayed acute myocardial infarction after blunt chest trauma in a young woman. AM HEARTJ 1980;100:90%16. Oren A, Bar-Shlomo B, Stern S. Acute coronary occlusion following blunt injury to the chest in the absence of coronary atherosclerosis. AM HEARTJ 1976;92:501-5. Pifarrb R, Grieco J, Gabibaldi A, Sullivan HJ, Montoya A, Bakhos M. Acute coronary artery occlusion secondary to blunt chest trauma. J Thorac Cardiovasc Surg 1982;83:122-5. Simoons ML, Arnold AER, Betri A, et al. Thrombolysis with tissue plasminogen activator in acute myocardial infarction: no additional benefit from immediate percutaneous coronary angioplasty. Lancet 1988;1:197-203.
Delayed rupture of tricuspid papillary muscle following blunt chest trauma Thomas Hilton, MD, Leslie Mezei, MD, and A n t h o n y C. Pearson, MD. St. Louis, Mo.
Fig. 2. Left ventricular angiogram 3 weeks after chest t r a u m a in the right anterior oblique projection. (A), E n d diastole; (B), end systole.
they should be considered in traumatic coronary vessel occlusion whenever revascularization appears to be achievable within the commonly accepted time window of about 6 hours after the onset of symptoms. REFERENCES
1. Liedtke AJ, De Muth WE. Nonpenetrating cardiac injuries: a collective review. AM HEARTJ 1973;86:687-97. 2. Gaspard P, Clermont A, Villard J, Amiel M. Non-iatrogenic trauma of the coronary arteries and myocardium: contribution
Tricuspid regurgitation following b l u n t chest trauma may occur by a tearing of the tricuspid valve leaflet, by disruption of the chordae tendineae, or by rupture of the papillary muscle apparatus. 1"4 It occurs rarely, with less than 40 cases reported in the literature. Previous reports have emphasized the subtle clinical manifestations, 1, 5 the value o f surface echocardiography for diagnosis, 1 the underdiagnosis of this critical condition,1 and the propensity for rightto-left s h u n t through a patent foramen ovale. 4, 6 We report a case of post-traumatic tricuspid regurgitation secondary to papillary muscle rupture in which the initial echocardiogram demonstrated normal tricuspid valve function. A 40-year-old m a n with no previous cardiac history was admitted with severe b l u n t chest t r a u m a due to a motor vehicle accident. Radiographic examination revealed evidence of sternal and bilateral rib fractures, and widening of the mediastinum. Emergency aortography revealed no evidence of aortic dissection. On initial examination, the pulse was 136 beats/rain , respirations were 28/min, and the blood pressure was 110/80 m m Hg. An electrocardiogram showed sinus tachycardia, left anterior hemiblock, and Q waves in leads V1 and V2, suggesting possible previous septa[ infarction. Creatine phosphokinase (CPK) enzymes and MB isoenzymes were elevated, suggesting myocardial conFrom the Divisionof Cardiology, Department of Internal Medicine, St. LouisUniversityHospital,St. LouisUniversitySchoolof Medicine;and St. John's MercyHospital, Departmentof Internal Medicine, Divislonof Cardiology. Reprint requests: Thomas Hilton,MD, St. LouisUniversityMedical Center, St. LouisUniversityHospital, Divisionof Cardiology,14th floor, 3635 Vista Ave. at Grand Blvd., P.O. Box 15250,St. Louis,MO 63110-0250. 4/4/19610