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Aorta thrombosis diagnosed due to acute myocardial infarct
Journal of Cardiology Cases (2010) 2, e139—e140
available at www.sciencedirect.com
journal homepage: www.elsevier.com/locate/jccase
Case Report
Aorta thrombosis diagnosed due to acute myocardial infarct Franc ¸ois Roubille (MD, PhD) a,∗, Pierre Alric (MD, PhD) b, Florence Leclercq (MD, PhD) a, Christophe Piot (MD, PhD) a a b
Cardiology Department, University Hospital Arnaud De Villeneuve, Montpellier, France Vascular Surgery Department, University Hospital Arnaud De Villeneuve, Montpellier, France
Received 25 February 2010; received in revised form 14 May 2010; accepted 24 May 2010
KEYWORDS Aorta thrombosis; Atheroma; Acute myocardial infarct (AMI); Low outflow
Summary A 54-year-old man was admitted for acute weakness in both legs. His past medical history was limited to a likely lower limb arteriopathy. His cardiovascular risk factors were heavy smoking habit and hypertension. The electrocardiogram was typical of inferior semi-recent myocardial infarct, with a Q-wave and ST-segment elevation. Transthoracic echocardiography showed an inferior hypokinesia, low left ventricular ejection fraction evaluated to 40%, normal valves, normal right cavities. An aortic computed tomography scan was then performed to rule out aortic dissection, or other aortic disorders. This scan showed an aortic thrombosis, just after the ostia of the renal arteries. Arteries were calcified, supporting the arteriopathy. This confirmed the total occlusion of the right coronary artery, without any other significant lesions. Ventricular angiography confirmed the inferior hypokinesia. The patient then suffered from an asymptomatic inferior acute myocardial infarct leading to acute aortic thrombosis, because of likely low outflow acutely worsening severe lower limb arteriopathy. The clinical presentation was surprising, as the patient had never complained of any strong pain, neither chest pain, nor lower limb pain. © 2010 Japanese College of Cardiology. Published by Elsevier Ireland Ltd. All rights reserved.
Case report A 54-year-old man was admitted for acute weakness in both legs. This was the first time. Pain had been worsening for 12 h. He had never suffered from chest pain nor dyspnea.
∗ Corresponding author at: University Hospital Arnaud De Villeneuve, Cardiology Department, 371, avenue du Doyen Gaston Giraud, 34295 Montpellier, France. E-mail address: [email protected] (F. Roubille).
His past medical history was limited to a likely lower limb arteriopathy. His cardiovascular risk factors were a heavy smoking habit and hypertension. He took only antihypertension medication (perindopril and indapamide). Physical examination revealed no heart failure. Resting blood pressure was 126/70 mm Hg. Heart rate was 62 beats/min. Peripheral pulses were abolished in both legs, but there were no cutaneous disorders. The electrocardiogram (Fig. 1A) was typical of inferior semi-recent myocardial infarct, with a Q-wave and STsegment elevation.
1878-5409/$ — see front matter © 2010 Japanese College of Cardiology. Published by Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.jccase.2010.05.007
e140
F. Roubille et al.
Figure 1 (A) Electrocardiogram. Note the inferior ST-segment elevation, and a Q-wave in II, III, AVF leads. (B) Aorta scan. Note the aorta thrombosis after the ostia of the renal arteries. Arteries are calcified. (C) Coronary angiography. Note the occlusion of the right coronary artery.
Transthoracic echocardiography showed an inferior hypokinesia, left ventricular ejection fraction evaluated to 40%, normal valves, and normal right cavities. An aortic computed tomography scan was then performed to rule out aortic dissection, or other aortic disorders. This scan (Fig. 1B) showed an aortic thrombosis, just after the ostia of the renal arteries. Arteries were calcified, supporting the arteriopathy. Three days later, the patient was admitted to the catheter laboratory in order to perform coronary angiography (Fig. 1C) (through a radial puncture). Right coronary artery occlusion was then confirmed, without any other significant lesions. Ventricular angiography confirmed the inferior hypokinesia. Biology showed normal blood cell count and renal clearance. Above all, troponin I peaked at 38 g/L and decreased after the admission. There was a biological inflammation syndrome with elevated C-reactive protein (20 mg/L, N < 0.5). The patient then suffered from an asymptomatic inferior acute myocardial infarct leading to acute aortic thrombosis, because of likely low outflow acutely worsening severe lower limb arteriopathy.
Discussion This clinical case describes a rare cause of acute aortic thrombosis, complicating an acute myocardial infarct. It is difficult to assert that acute myocardial infarct led to aortic acute thrombosis, but this hypothesis is likely, on account of the clinical description. Nevertheless, this clinical case underlines the relationship between both cardiovascular diseases. The onset of myocardial infarction and aortic thrombosis are difficult to assert. Obviously, low outflow could have led to aorta thrombosis, but this is not the only explanation. Hypercoagulable condition could have participated. Blood examinations performed later (C protein, S protein, Leiden Factor, blood cell count, C-reactive peptide) were normal, so that hypercoagulable status is not likely. Inflammatory syndrome and arterial disease are found in cases of vasculitis. Vasculitis has not been ruled out. Nevertheless, there was neither prior inflammatory syndrome, nor clinical signs in favor of vasculitis. Clinical presentation was surprising, as the patient had never complained of any strong pain, neither chest pain, nor lower limb pain. This case illustrates widespread arterial disease with two concomitant complications.
available at www.sciencedirect.com
journal homepage: www.elsevier.com/locate/jccase
Case Report
Aorta thrombosis diagnosed due to acute myocardial infarct Franc ¸ois Roubille (MD, PhD) a,∗, Pierre Alric (MD, PhD) b, Florence Leclercq (MD, PhD) a, Christophe Piot (MD, PhD) a a b
Cardiology Department, University Hospital Arnaud De Villeneuve, Montpellier, France Vascular Surgery Department, University Hospital Arnaud De Villeneuve, Montpellier, France
Received 25 February 2010; received in revised form 14 May 2010; accepted 24 May 2010
KEYWORDS Aorta thrombosis; Atheroma; Acute myocardial infarct (AMI); Low outflow
Summary A 54-year-old man was admitted for acute weakness in both legs. His past medical history was limited to a likely lower limb arteriopathy. His cardiovascular risk factors were heavy smoking habit and hypertension. The electrocardiogram was typical of inferior semi-recent myocardial infarct, with a Q-wave and ST-segment elevation. Transthoracic echocardiography showed an inferior hypokinesia, low left ventricular ejection fraction evaluated to 40%, normal valves, normal right cavities. An aortic computed tomography scan was then performed to rule out aortic dissection, or other aortic disorders. This scan showed an aortic thrombosis, just after the ostia of the renal arteries. Arteries were calcified, supporting the arteriopathy. This confirmed the total occlusion of the right coronary artery, without any other significant lesions. Ventricular angiography confirmed the inferior hypokinesia. The patient then suffered from an asymptomatic inferior acute myocardial infarct leading to acute aortic thrombosis, because of likely low outflow acutely worsening severe lower limb arteriopathy. The clinical presentation was surprising, as the patient had never complained of any strong pain, neither chest pain, nor lower limb pain. © 2010 Japanese College of Cardiology. Published by Elsevier Ireland Ltd. All rights reserved.
Case report A 54-year-old man was admitted for acute weakness in both legs. This was the first time. Pain had been worsening for 12 h. He had never suffered from chest pain nor dyspnea.
∗ Corresponding author at: University Hospital Arnaud De Villeneuve, Cardiology Department, 371, avenue du Doyen Gaston Giraud, 34295 Montpellier, France. E-mail address: [email protected] (F. Roubille).
His past medical history was limited to a likely lower limb arteriopathy. His cardiovascular risk factors were a heavy smoking habit and hypertension. He took only antihypertension medication (perindopril and indapamide). Physical examination revealed no heart failure. Resting blood pressure was 126/70 mm Hg. Heart rate was 62 beats/min. Peripheral pulses were abolished in both legs, but there were no cutaneous disorders. The electrocardiogram (Fig. 1A) was typical of inferior semi-recent myocardial infarct, with a Q-wave and STsegment elevation.
1878-5409/$ — see front matter © 2010 Japanese College of Cardiology. Published by Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.jccase.2010.05.007
e140
F. Roubille et al.
Figure 1 (A) Electrocardiogram. Note the inferior ST-segment elevation, and a Q-wave in II, III, AVF leads. (B) Aorta scan. Note the aorta thrombosis after the ostia of the renal arteries. Arteries are calcified. (C) Coronary angiography. Note the occlusion of the right coronary artery.
Transthoracic echocardiography showed an inferior hypokinesia, left ventricular ejection fraction evaluated to 40%, normal valves, and normal right cavities. An aortic computed tomography scan was then performed to rule out aortic dissection, or other aortic disorders. This scan (Fig. 1B) showed an aortic thrombosis, just after the ostia of the renal arteries. Arteries were calcified, supporting the arteriopathy. Three days later, the patient was admitted to the catheter laboratory in order to perform coronary angiography (Fig. 1C) (through a radial puncture). Right coronary artery occlusion was then confirmed, without any other significant lesions. Ventricular angiography confirmed the inferior hypokinesia. Biology showed normal blood cell count and renal clearance. Above all, troponin I peaked at 38 g/L and decreased after the admission. There was a biological inflammation syndrome with elevated C-reactive protein (20 mg/L, N < 0.5). The patient then suffered from an asymptomatic inferior acute myocardial infarct leading to acute aortic thrombosis, because of likely low outflow acutely worsening severe lower limb arteriopathy.
Discussion This clinical case describes a rare cause of acute aortic thrombosis, complicating an acute myocardial infarct. It is difficult to assert that acute myocardial infarct led to aortic acute thrombosis, but this hypothesis is likely, on account of the clinical description. Nevertheless, this clinical case underlines the relationship between both cardiovascular diseases. The onset of myocardial infarction and aortic thrombosis are difficult to assert. Obviously, low outflow could have led to aorta thrombosis, but this is not the only explanation. Hypercoagulable condition could have participated. Blood examinations performed later (C protein, S protein, Leiden Factor, blood cell count, C-reactive peptide) were normal, so that hypercoagulable status is not likely. Inflammatory syndrome and arterial disease are found in cases of vasculitis. Vasculitis has not been ruled out. Nevertheless, there was neither prior inflammatory syndrome, nor clinical signs in favor of vasculitis. Clinical presentation was surprising, as the patient had never complained of any strong pain, neither chest pain, nor lower limb pain. This case illustrates widespread arterial disease with two concomitant complications.