Catheterization and Cardiovascular Diagnosis 24:182-185 (1991)
Acute Myocardial Infarction After Blunt Chest Trauma in Young People: Need for Prompt Intervention L. CalvO Orbe, MD, FSCAI, F. Garcia Gallego, MD, N. Sobrino, MD, J. Sotillo, MD, J.L. Lopez-Sendon, MD, J. Oliver, MD, 1. Coma, MD, A. Frutos, MD, J.A. Sobrino, MD, and J.M. Navarro,+ MD We describe four cases of acute myocardial infarction in young patients, secondary to blunt chest trauma. One case was treated with intracoronary thrombolysis and angict plasty, two cases received systemic thrombolysis, and the last one did not have any repertusion therapy. The coronary angiograms of the left anterior descending artery showed thrombosis in two cases, coronary dissection in one case, and no morphological lesions in the other. We encourage the early performance of angiographic studies in these patients, adjusting the therapy to their pathophysiologic mechanism. Key words: traumatic myocardial infarction, cardiac contusion, thrombolysis
INTRODUCTION
Acute myocardial infarction (AMI) is a rare complication after blunt chest trauma (BCT). Since 1980 we have found 10 published cases of post-traumatic AMI. It generally occurs in young people and is related to motor vehicle accidents and certain sports [ 1-41. Therefore its real incidence might be underestimated within the traumatic context. This study evaluates the different coronary arteriographic patterns found in four young patients with AM1 after BCT, and their response to therapeutic alternatives. CASE REPORT
Four white male patients aged between 22 and 30 yr old with no history of previous coronary disease were diagnosed as having AM1 secondary to BCT (Table I). Two of the patients suffered thoracic trauma during a soccer game, feeling oppressive chest pain within the following hour. The other two patients suffered direct precordial trauma caused by traffic accidents. All fullfilled ECG and enzymatic criteria for AMI. Localization of AM1 was inferior in one case and anterior in the rest. Only the fourth case developed cardiac failure. Coronariographic studies were performed in all patients. The first case underwent intracoronary thrombolysis with urokinase and angioplasty 4 h after clinical onset. The second and third cases were treated with systemic thrombolysis within the first 4 h with rt-PA and urokinase respectively. In the fourth case the AM1 was not initially diagnosed. The patient arrived at our hospital with acute pulmonary edema 72 h after the episode and therefore did not receive reperfusion therapy. 0 1991 Wiley-Liss, Inc.
Coronary arteriographic studies showed no evidence of atherosclerotic coronary disease in any patient. However, in case # l a thrombus located in the mid LAD was observed, associated with a 90% obstruction and distal embolization of the vessel. Left ventriculography (L.V.) showed an inferoapical akinesis, with an ejection fraction (EF) of 56%. After intracoronary thrombolysis the distal thrombi disappeared, but the mid segment thrombus persisted. It was treated with PTCA, leaving a residual stenosis of 20% (Fig. 1). In Case #2, an angiographic study performed 24 h after systemic thrombolysis (Fig. 2) showed an intracoronary thrombus in the mid LAD causing 75% obstruction. The size of the thrombus was significantly reduced in an angiographic restudy 48 h later. Initially L.V. showed anterior akinesis and apical dyskinesis, with EF 39%. At the time of restudy, the ventricular function was greatly improved, with a persistent slight antero-apical hypokinesis, and the EF 61%. In Case #3, during the study performed 24 h after thrombolytic treatment, no angiographic lesions were found except for a slow coronary flow (TIMI 2) (Fig. 3), which became normal after the administration of intracoronary NTG. Segmentary spasm could not be specifically verified. LV showed a normal global and segmentary function (Table I). The three cases remained asymptomatic at discharge. In Case #4, the angioFrom the Hospital La Paz, Madrid, Spain.
Received February 18, 1991; accepted May 30, 1991 'Deceased. Address reprint requests to Dr. Calvo Orbe, General Pardifias, 95, 28006 Madrid, Spain.
AM1 After BCT in Young People
183
TABLE 1. Clinical and TheraDeutic Data of AM1 After B C T ~~
Age (yr)
Sex
AM1 location
FC
1
26
M
Inf
I
Ball impact during soccer game
i s . TRL plus PTCA
4
2
22
M
Ant
I
Direct crash with another player during soccer game
i.v. TRL
3
3
30
M
Ant
I
Wheel impact during car accident
i.v. TRL
4
4
30
M
Ant
IV
Projection and precordial crash during bike accident
No specific treatment
Case
Chest trauma
Treatment
Delay (h)
I20
*AM], acute myocardial infarction; Ant, anterior; FC, functional class (Killip); i.c., intracoronary; i.v., intravenous; M,male; TRL, thrombolysis.
Fig. 1. Left coronary angiogram. A: Intracoronary thrombi at proximal LAD, causing a 90% stenosis. B: Distal LAD thromboembolizatlon image. C: Dlsappearance of thrombi image after lntracoronary urokinase. D: PTCA result at proximal LAD with 20% of residual stenosis.
graphic finding 120 h after the episode was an image of intimal dissection and aneurysmal dilatation in the proximal LAD with acceptable distal flow (Fig. 4). LV showed a large antero-apical aneurysm with severe ventriculardysfunction (EF 19%). The patient was refered to another center for inclusion in a heart transplant program. DISCUSSION Acute myocardial infarction is a complication frequently unsuspected after BCT. For this reason, even though our fourth patient was admitted to a hospital after
the automobile accident, no AM1 was diagnosed during the 3 d. His chest pain was misinterpreteded and he was studied as a last resort to explain it. The etiological mechanism of post-traumatic AM1 is a controversial issue. Cardiac contusion, coronary dissection, thrombosis, and rupture or spasm after BCT have been invoked as responsible mechanisms [3,5-81. The fact that completely normal appearing coronary arteries have been found in some of these patients raises questions as whether the myocardial injury actually affects the coronary vascular system, or whether the entire process is due to severe myocardial contusion [ 1,9-121. Nevertheless, the finding of “normal” coronaries could
184
Calvo Orbe et al.
Fig. 2. Left coronary angiogram in LA1showing a lacunar contrast defect at proximal LAD suggestive of thrombi.
Fig. 3. Left coronary angiogram In RAO showing a delayed contrast filling of the LAD.
be erroneous, since it does not exclude the existence of previous coronary thrombosis and/or spasm [ 10- 141. Knowledge of the appearance and status of the coronary arteries will permit selection of the best therapeutic approach. When discrete coronary dissection is present, and the artery remains patent with adequate distal flow, the therapy may be conservative. This opinion is based on the evolution of this type of dissection after PTCA. It usually heals favorably in the subsequent 6 months [6,15-161. In this situation, short-mid term anticoagulant treatment should be considered in order to prevent further thrombotic phenomena. When thrombotic obstruction is the angiographic finding, therapy should include thrombolytic treatment, provided that there are no contraindications due to the se-
Fig. 4. Left coronary angiogram in RAO showing coronary dissection and aneurysrnatic dilatation at proximal LAD.
verity of the chest wall or other somatic trauma. In that case, the attempt to reperfuse directly with PTCA is preferred. In these four patients, AM1 after BCT appeared acutely in young patients, without prior coronary pathology, without collateral circulation, affected the proximal LAD, and therefore, resulted in the development of ventricular aneurysms and ventricular failure [ 1,121. A case of post-traumatic AM1 with severe LV dysfunction requiring heart transplant has been published previously t 171. In summary, we believe that cases such as these require that the physician: 1) Be highly suspicious of this complication after BCT, and 2) tailor the therapeutic approach to the underlying pathoanatomy and physiology. Early coronary arteriography is essential before any therapy is instituted.
REFERENCES I . Candell J, Valle V, Pay6 J, Cortadellas J, Esplugas E, Rius J: Post-traumatic coronary occlusion and early left ventricular aneurysm. Am Heart J 97:509-512, 1979. 2. Garcia Gallego F, Sotillo J, Perez Blasco P: Myocardial infarction and subtotal obstruction of the anterior descending coronary artery caused by trauma in a football player. lnt J Cardiol 12: 109-1 12, 1986. 3. Roberts WC, Maron BJ: Sudden death while playing professional football. Am Heart J 102:1061-1063, 1981. 4. O’Neill S, Walker F, O’Dwyer W F Blunt chest trauma causing myocardial infarction: an unusual football injury. Ir Med J 74: 138, 1981. 5. Vlay SC, Blumenthal DS, Shoback D, Fehir K, Bulkley BH: Delayed acute myocardial infarction after blunt chest trauma in a young woman. Am Heart J 100:907-916. 1980. 6. Kahn JK, Buda AJ: Long-term follow-up of coronary artery oc-
AM1 After BCT in Young People clusion secondary to blunt chest trauma. Am Heart J 113:207210, 1987. 7. Bjorn-Hansen LS, Thomassen AR, Nielsen 'IT: Aneurysm of the
8. 9.
10.
11.
left anterior descending coronary artery after chest trauma. Eur Heart J 10:177-179, 1989. Watson JH, Bartholomae WM: Cardiac injury due to nonpenetrating chest trauma. Ann Intern Med 52:871-876, 1960. DeMuth WE, Baue AE, Odem JA: Contusions of the heart. J Trauma 7:443, 1967. Oren A, Bar-Shlomo B, Stern S: Acute coronary occlusion following blunt injury to the chest in the absence of coronary atherosclerosis. Am Heart J 92501-505, 1976. de Feyter PJ, Roos JP: Traumatic myocardial infarction with subsequent normal coronary arteriogram. Eur J Cardiol 625-31,
1977. 12. Sutherland G, Driedger A, Holliday R, Cheung H, Sibbald W:
Frequency of myocardial injury after blunt chest trauma as eval-
185
uated by radionuclide angiography. Am J Cardiol52: 1099-1003, 1983.
13. Pifarre R, Grieco J, Garibaldi A, Sullivan HJ, Montaya A, Bakhos M: Acute coronary occlusion secondary to blunt chest trauma. J Thorac Cardiovasc Surg 83:122-126, 1982. 14. Sabbah H, Mohyl J, Stein P Coronary arteriography in dogs following blunt cardiac trauma: a longitudinal assessment. Cathet Cardiovasc Diagn 15:155-163, 1988. 15. Grady AE, Cowley MJ, Vetrovec GW: Traumatic dissecting coronary arterial aneurysm with subsequent complete healing. Am J Cardiol 55: 1424-1425. 1985. 16. Kohli S, Saperia GM, Waksmonski CA, Pezella S, Singh JB: Coronary artery dissection secondary to blunt chest trauma. Cathet Cardiovasc Diagn 15:179-183, 1988. 17. Watt AH, Stephens MR: Myocardial infarction after blunt chest trauma incurred during rugby football that later required cardiac transplantation. Br Heart J 55:408-410, 1986.
Acute Myocardial Infarction After Blunt Chest Trauma in Young People: Need for Prompt Intervention L. CalvO Orbe, MD, FSCAI, F. Garcia Gallego, MD, N. Sobrino, MD, J. Sotillo, MD, J.L. Lopez-Sendon, MD, J. Oliver, MD, 1. Coma, MD, A. Frutos, MD, J.A. Sobrino, MD, and J.M. Navarro,+ MD We describe four cases of acute myocardial infarction in young patients, secondary to blunt chest trauma. One case was treated with intracoronary thrombolysis and angict plasty, two cases received systemic thrombolysis, and the last one did not have any repertusion therapy. The coronary angiograms of the left anterior descending artery showed thrombosis in two cases, coronary dissection in one case, and no morphological lesions in the other. We encourage the early performance of angiographic studies in these patients, adjusting the therapy to their pathophysiologic mechanism. Key words: traumatic myocardial infarction, cardiac contusion, thrombolysis
INTRODUCTION
Acute myocardial infarction (AMI) is a rare complication after blunt chest trauma (BCT). Since 1980 we have found 10 published cases of post-traumatic AMI. It generally occurs in young people and is related to motor vehicle accidents and certain sports [ 1-41. Therefore its real incidence might be underestimated within the traumatic context. This study evaluates the different coronary arteriographic patterns found in four young patients with AM1 after BCT, and their response to therapeutic alternatives. CASE REPORT
Four white male patients aged between 22 and 30 yr old with no history of previous coronary disease were diagnosed as having AM1 secondary to BCT (Table I). Two of the patients suffered thoracic trauma during a soccer game, feeling oppressive chest pain within the following hour. The other two patients suffered direct precordial trauma caused by traffic accidents. All fullfilled ECG and enzymatic criteria for AMI. Localization of AM1 was inferior in one case and anterior in the rest. Only the fourth case developed cardiac failure. Coronariographic studies were performed in all patients. The first case underwent intracoronary thrombolysis with urokinase and angioplasty 4 h after clinical onset. The second and third cases were treated with systemic thrombolysis within the first 4 h with rt-PA and urokinase respectively. In the fourth case the AM1 was not initially diagnosed. The patient arrived at our hospital with acute pulmonary edema 72 h after the episode and therefore did not receive reperfusion therapy. 0 1991 Wiley-Liss, Inc.
Coronary arteriographic studies showed no evidence of atherosclerotic coronary disease in any patient. However, in case # l a thrombus located in the mid LAD was observed, associated with a 90% obstruction and distal embolization of the vessel. Left ventriculography (L.V.) showed an inferoapical akinesis, with an ejection fraction (EF) of 56%. After intracoronary thrombolysis the distal thrombi disappeared, but the mid segment thrombus persisted. It was treated with PTCA, leaving a residual stenosis of 20% (Fig. 1). In Case #2, an angiographic study performed 24 h after systemic thrombolysis (Fig. 2) showed an intracoronary thrombus in the mid LAD causing 75% obstruction. The size of the thrombus was significantly reduced in an angiographic restudy 48 h later. Initially L.V. showed anterior akinesis and apical dyskinesis, with EF 39%. At the time of restudy, the ventricular function was greatly improved, with a persistent slight antero-apical hypokinesis, and the EF 61%. In Case #3, during the study performed 24 h after thrombolytic treatment, no angiographic lesions were found except for a slow coronary flow (TIMI 2) (Fig. 3), which became normal after the administration of intracoronary NTG. Segmentary spasm could not be specifically verified. LV showed a normal global and segmentary function (Table I). The three cases remained asymptomatic at discharge. In Case #4, the angioFrom the Hospital La Paz, Madrid, Spain.
Received February 18, 1991; accepted May 30, 1991 'Deceased. Address reprint requests to Dr. Calvo Orbe, General Pardifias, 95, 28006 Madrid, Spain.
AM1 After BCT in Young People
183
TABLE 1. Clinical and TheraDeutic Data of AM1 After B C T ~~
Age (yr)
Sex
AM1 location
FC
1
26
M
Inf
I
Ball impact during soccer game
i s . TRL plus PTCA
4
2
22
M
Ant
I
Direct crash with another player during soccer game
i.v. TRL
3
3
30
M
Ant
I
Wheel impact during car accident
i.v. TRL
4
4
30
M
Ant
IV
Projection and precordial crash during bike accident
No specific treatment
Case
Chest trauma
Treatment
Delay (h)
I20
*AM], acute myocardial infarction; Ant, anterior; FC, functional class (Killip); i.c., intracoronary; i.v., intravenous; M,male; TRL, thrombolysis.
Fig. 1. Left coronary angiogram. A: Intracoronary thrombi at proximal LAD, causing a 90% stenosis. B: Distal LAD thromboembolizatlon image. C: Dlsappearance of thrombi image after lntracoronary urokinase. D: PTCA result at proximal LAD with 20% of residual stenosis.
graphic finding 120 h after the episode was an image of intimal dissection and aneurysmal dilatation in the proximal LAD with acceptable distal flow (Fig. 4). LV showed a large antero-apical aneurysm with severe ventriculardysfunction (EF 19%). The patient was refered to another center for inclusion in a heart transplant program. DISCUSSION Acute myocardial infarction is a complication frequently unsuspected after BCT. For this reason, even though our fourth patient was admitted to a hospital after
the automobile accident, no AM1 was diagnosed during the 3 d. His chest pain was misinterpreteded and he was studied as a last resort to explain it. The etiological mechanism of post-traumatic AM1 is a controversial issue. Cardiac contusion, coronary dissection, thrombosis, and rupture or spasm after BCT have been invoked as responsible mechanisms [3,5-81. The fact that completely normal appearing coronary arteries have been found in some of these patients raises questions as whether the myocardial injury actually affects the coronary vascular system, or whether the entire process is due to severe myocardial contusion [ 1,9-121. Nevertheless, the finding of “normal” coronaries could
184
Calvo Orbe et al.
Fig. 2. Left coronary angiogram in LA1showing a lacunar contrast defect at proximal LAD suggestive of thrombi.
Fig. 3. Left coronary angiogram In RAO showing a delayed contrast filling of the LAD.
be erroneous, since it does not exclude the existence of previous coronary thrombosis and/or spasm [ 10- 141. Knowledge of the appearance and status of the coronary arteries will permit selection of the best therapeutic approach. When discrete coronary dissection is present, and the artery remains patent with adequate distal flow, the therapy may be conservative. This opinion is based on the evolution of this type of dissection after PTCA. It usually heals favorably in the subsequent 6 months [6,15-161. In this situation, short-mid term anticoagulant treatment should be considered in order to prevent further thrombotic phenomena. When thrombotic obstruction is the angiographic finding, therapy should include thrombolytic treatment, provided that there are no contraindications due to the se-
Fig. 4. Left coronary angiogram in RAO showing coronary dissection and aneurysrnatic dilatation at proximal LAD.
verity of the chest wall or other somatic trauma. In that case, the attempt to reperfuse directly with PTCA is preferred. In these four patients, AM1 after BCT appeared acutely in young patients, without prior coronary pathology, without collateral circulation, affected the proximal LAD, and therefore, resulted in the development of ventricular aneurysms and ventricular failure [ 1,121. A case of post-traumatic AM1 with severe LV dysfunction requiring heart transplant has been published previously t 171. In summary, we believe that cases such as these require that the physician: 1) Be highly suspicious of this complication after BCT, and 2) tailor the therapeutic approach to the underlying pathoanatomy and physiology. Early coronary arteriography is essential before any therapy is instituted.
REFERENCES I . Candell J, Valle V, Pay6 J, Cortadellas J, Esplugas E, Rius J: Post-traumatic coronary occlusion and early left ventricular aneurysm. Am Heart J 97:509-512, 1979. 2. Garcia Gallego F, Sotillo J, Perez Blasco P: Myocardial infarction and subtotal obstruction of the anterior descending coronary artery caused by trauma in a football player. lnt J Cardiol 12: 109-1 12, 1986. 3. Roberts WC, Maron BJ: Sudden death while playing professional football. Am Heart J 102:1061-1063, 1981. 4. O’Neill S, Walker F, O’Dwyer W F Blunt chest trauma causing myocardial infarction: an unusual football injury. Ir Med J 74: 138, 1981. 5. Vlay SC, Blumenthal DS, Shoback D, Fehir K, Bulkley BH: Delayed acute myocardial infarction after blunt chest trauma in a young woman. Am Heart J 100:907-916. 1980. 6. Kahn JK, Buda AJ: Long-term follow-up of coronary artery oc-
AM1 After BCT in Young People clusion secondary to blunt chest trauma. Am Heart J 113:207210, 1987. 7. Bjorn-Hansen LS, Thomassen AR, Nielsen 'IT: Aneurysm of the
8. 9.
10.
11.
left anterior descending coronary artery after chest trauma. Eur Heart J 10:177-179, 1989. Watson JH, Bartholomae WM: Cardiac injury due to nonpenetrating chest trauma. Ann Intern Med 52:871-876, 1960. DeMuth WE, Baue AE, Odem JA: Contusions of the heart. J Trauma 7:443, 1967. Oren A, Bar-Shlomo B, Stern S: Acute coronary occlusion following blunt injury to the chest in the absence of coronary atherosclerosis. Am Heart J 92501-505, 1976. de Feyter PJ, Roos JP: Traumatic myocardial infarction with subsequent normal coronary arteriogram. Eur J Cardiol 625-31,
1977. 12. Sutherland G, Driedger A, Holliday R, Cheung H, Sibbald W:
Frequency of myocardial injury after blunt chest trauma as eval-
185
uated by radionuclide angiography. Am J Cardiol52: 1099-1003, 1983.
13. Pifarre R, Grieco J, Garibaldi A, Sullivan HJ, Montaya A, Bakhos M: Acute coronary occlusion secondary to blunt chest trauma. J Thorac Cardiovasc Surg 83:122-126, 1982. 14. Sabbah H, Mohyl J, Stein P Coronary arteriography in dogs following blunt cardiac trauma: a longitudinal assessment. Cathet Cardiovasc Diagn 15:155-163, 1988. 15. Grady AE, Cowley MJ, Vetrovec GW: Traumatic dissecting coronary arterial aneurysm with subsequent complete healing. Am J Cardiol 55: 1424-1425. 1985. 16. Kohli S, Saperia GM, Waksmonski CA, Pezella S, Singh JB: Coronary artery dissection secondary to blunt chest trauma. Cathet Cardiovasc Diagn 15:179-183, 1988. 17. Watt AH, Stephens MR: Myocardial infarction after blunt chest trauma incurred during rugby football that later required cardiac transplantation. Br Heart J 55:408-410, 1986.
