Journal of Geriatric Cardiology (2016) 13: 935937 ©2016 JGC All rights reserved; www.jgc301.com
Letter to the Editor
Open Access
Concomitant acute myocardial infarction and descending thoracic aorta penetrating ulcer Yong Hoon Kim, Ae-Young Her* Division of Cardiology, Department of Internal Medicine, Kangwon National University School of Medicine, Chuncheon, South Korea
J Geriatr Cardiol 2016; 13: 935937. doi:10.11909/j.issn.1671-5411.2016.11.011 Keywords: Myocardial infarction; Penetrating aortic ulcer; Stent grafts
Acute coronary syndrome (ACS) refers to a spectrum of clinical presentations ranging from unstable angina to non-ST-segment elevation myocardial infarction (NSTEMI) to ST-segment elevation myocardial infarction (STEMI).[1] Aortic dissection, intramural hematoma and penetrating atherosclerotic ulcer (PAU) are three major acute aortic syndromes (AAS).[2] ACS and AAS are different disease entities with some similar pathophysiology and rarely occur in a single scenario. Acute chest pain is most common and important symptom in these syndromes. In the emergency department, early diagnosis and detection is required as delays in treatment can result in lives lost. More commonly one disease entity is the cause of the symptom and is given focus, but two disease entities are involved and happening concomitantly. Here, we report a case of concomitant acute myocardial infarction and descending thoracic aorta penetrating ulcer. A 61-year-old female presented to the emergency room with dull, anterior chest pain of one day duration. The pain was burning and crushing in character, moderate in intensity, substernal with radiation to the back and both shoulders. She had a past history of type 2 diabetes mellitus, essential hypertension and dyslipidemia. Her blood pressure was 160/90 mmHg equal in both arms and her heart rate was 63 bpm. She had no pulse deficit or asymmetry and no cardiac murmurs. Her initial electrocardiogram (EKG) demonstrated 0.5 mm/mV ST-segment elevation in leads III, aVF and 0.5 mm/mV ST-segment depression in leads I, aVL, V4–V6 with also left ventricular hypertrophy by voltage criteria. Chest radiography was normal with no widening of the mediastinum or pleural effusion observed. Cardiac investigations including echocardiography and cardiac biomarkers returned unremarkable. A chest computed tomography (CT) scan was done to exclude acute aortic dissection and pul*Correspondence to: [email protected]
monary thromboembolism because the patient complained severe chest pain with radiating back pain. The CT scan demonstrated blood leaks through the wall but contained by the adventitia at anteromedial portion of upper descending thoracic aorta (Figure 1A & 1C). This finding was compatible with PAU. She was admitted to the intensive care unit (ICU) under close observation. Six hours later, cardiac enzymes [Troponin I: 8.767 (0–0.78 ng/mL), CK-MB: 116.87 (0–5.0 ng/mL)] were elevated but electrocardiography was unchanged. Her chest pain and both shoulders pain persisted and worsened. This complex case was discussed with attending interventional cardiologists and thoracic surgeons about the option of coronary angiography and operative intervention. The concern was that coronary angiography procedure might aggravate the PAU and cause clinical deterioration. Preparation was made for both coronary angiography and thoracic endovascular aortic repair. After local anesthesia with lidocaine, arterial puncture was made via the right radial artery instead of femoral artery to avoid direct injury to PAU. Coronary angiography revealed total occlusion of the mid-portion of the right coronary artery (Figure 2A). The left coronary artery was normal. After Across HP® 3.5 15 mm balloon dilatation (Acrostak, Inc, Switzerland), an Orsiro® (Biotronilk AG, Bulach, Switzerland) 3.5 30 mm stent was successfully deployed in the right coronary artery lesion (Figure 2B). Thereafter, the right common femoral artery was exposed using a small incision. Aortography was done. Valiant® (Medtronic Vascular; Santa Rosa, Calif) thoracic stent graft (32 117 mm) was deployed successfully. After stent graft deployment, Reliant® (Medtronic Vascular; Santa Rosa, Calif) stent graft balloon dilatation was done. Final aortography showed no visible endovascular leaks. Following the procedures, she was pain and symptom free. On one month follow-up CT angiogram, no leakage was seen at the graft site (Figure 1B & 1D).
http://www.jgc301.com; [email protected] | Journal of Geriatric Cardiology
936
Kim YH & Her AY. AMI and descending thoracic aorta penetrating ulcer
Figure 1. Contrast enhanced CT scan of the chest in patient with concomitant acute myocardial infarction and descending thoracic aorta penetrating ulcer. (A): axial section of contrast enhanced CT scan of the chest. Arrow indicates blood leaks through the wall but is contained by the adventitia or surrounding perivascular soft tissue; (B): axial section of contrast enhanced CT scan of the chest after one month follow-up; (C): three-dimensional reconstruction image of the CT angiogram demonstrating the descending thoracic aorta penetrating ulcer; and (D): follow-up CT angiogram at one month showing no endovascular leakage from the previous graft deployed site.
Figure 2. Coronary angiography and percutaneous coronary intervention. (A): coronary angiography revealed total occlusion of the mid portion of the right coronary artery ( arrow); (B): Orsiro® (Biotronik AG, Bulach, Switzerland) 3.5 x 30 mm stent was successfully deployed in the right coronary artery ( arrow).
The search for the existence of the other disease before reperfusion therapy was administered invariably assisted the successful outcome in patients with acute myocardial infarction. AAS also characterized similar but slightly differ-
ent clinical symptoms such as severely intense, acute, searing or tearing, throbbing and migratory chest pain compared with ACS.[3] Penetrating atherosclerotic aortic ulcer means the lesion that penetrates the elastic lamina and is associated
Journal of Geriatric Cardiology | [email protected]; http://www.jgc301.com
Kim YH & Her AY. AMI and descending thoracic aorta penetrating ulcer
with hematoma formation within the aortic wall.[3,4] The true incidence of both symptomatic and silent PAU are not known. But some author reported about 2%–7% of AAS.[5] In general PAU lesions are asymptomatic and confined to the intimal layer at an early stage but it can be progress and atherosclerotic plaque penetrates into the media, the media is exposed to pulsatile arterial flow[6] in the later and leads to several dangerous complications such as dissection, aneurysm formation or aortic rupture. Sudden onset of severe chest pain or back pain in elderly hypertensive patient it may suggest an imminent cardiovascular catastrophe.[3] Hassani, et al.[5] also reported penetrating aortic ulcer is a rare pathology, often clinically silent, but potentially fatal when manifesting as an acute aortic syndrome. He also suggested that symptomatic penetrating aortic ulcer requires coverage by thoracic endovascular stent grafting according to the recent guidelines. In our case her chest pain and back pain may be caused by acute myocardial infarction (AMI) but it also may be originated by PAU. If the origin of her chest pain was PAU we must hurry up to avoid unwanted disaster. On the other hand, a conservative medical treatment is considered also acceptable when the lesion is stable. When we consider surgical management, endovascular aortic repair (TEVAR) is alternative treatment modality to surgical repair in descending aorta and showed excellent short-term and midterm results.[7] TEVAR reduces the blood loss, procedural time, and length of hospitalization because of the minimal invasive nature of the procedure. In patients referred to emergency department with acute chest pain several important differential diagnoses should be kept in mind which include: acute coronary syndrome, aortic dissection, pneumothorax and pulmonary thromboembolism.[8] Usually these disease entities occur separately but
937
can occur simultaneously. Each diagnostic tool or treatment strategy can influence the other disease entity. In this case, if we had focused only AMI we couldn’t figure out her PAU and this may lead to unwanted result. In conclusion, it is important to exclude AAS before reperfusion therapy in patients presenting with AMI. And commonly one disease entity is the cause of the symptom and is given focus; however, as seen in this case, two different disease entities are involved and happening concomitantly.
References 1 2 3
4
5
6
7
8
Bobadilla RV. Acute coronary syndrome: focus on antiplatelet therapy. Crit Care Nurse 2016; 36: 15–27. Tsai TT, Nienaber CA, Eagle KA. Acute aortic syndromes. Circulation 2005; 112: 3802–3813. Singhal P, Lin Z. Penetrating atheromatous ulcer of ascending aorta: a case report and review of literature. Heart Lung Circ 2008; 17: 380–382. Stanson AW, Kazmier FJ, Hollier LH, et al. Penetrating atherosclerotic ulcers of the thoracic aorta: natural history and clinicopathologic correlations. Ann Vasc Surg 1986; 1: 15–23. El Hassani I, Van Damme H, Creemers E, et al. Penetrating atherosclerosis aortic ulcer: a re-appraisal. Acta Chir Belg. Published Online First: 2016 Sep 3. DOI: 10.1080/00015458. 2016.1212566. Coady MA, Rizzo JA, Hammond GL, et al. Penetrating ulcer of the thoracic aorta: what is it? How do we recognize it? How do we manage it? Vasc Surg 1998; 27: 1006–1016. D’Annoville T, Ozdemir BA, Alric P, et al. Thoracic endovascular aortic repair for penetrating aortic ulcer: literature review. Ann Thorac Surg 2016 : 101: 2272–2278 Ansari-Ramandi MM, Alemzadeh-Ansari MJ, Firoozi A. Acute type aortic dissection missed as acute coronary syndrome. J Clin Diagn Res 2016; 10: OD33–OD34.
http://www.jgc301.com; [email protected] | Journal of Geriatric Cardiology
Letter to the Editor
Open Access
Concomitant acute myocardial infarction and descending thoracic aorta penetrating ulcer Yong Hoon Kim, Ae-Young Her* Division of Cardiology, Department of Internal Medicine, Kangwon National University School of Medicine, Chuncheon, South Korea
J Geriatr Cardiol 2016; 13: 935937. doi:10.11909/j.issn.1671-5411.2016.11.011 Keywords: Myocardial infarction; Penetrating aortic ulcer; Stent grafts
Acute coronary syndrome (ACS) refers to a spectrum of clinical presentations ranging from unstable angina to non-ST-segment elevation myocardial infarction (NSTEMI) to ST-segment elevation myocardial infarction (STEMI).[1] Aortic dissection, intramural hematoma and penetrating atherosclerotic ulcer (PAU) are three major acute aortic syndromes (AAS).[2] ACS and AAS are different disease entities with some similar pathophysiology and rarely occur in a single scenario. Acute chest pain is most common and important symptom in these syndromes. In the emergency department, early diagnosis and detection is required as delays in treatment can result in lives lost. More commonly one disease entity is the cause of the symptom and is given focus, but two disease entities are involved and happening concomitantly. Here, we report a case of concomitant acute myocardial infarction and descending thoracic aorta penetrating ulcer. A 61-year-old female presented to the emergency room with dull, anterior chest pain of one day duration. The pain was burning and crushing in character, moderate in intensity, substernal with radiation to the back and both shoulders. She had a past history of type 2 diabetes mellitus, essential hypertension and dyslipidemia. Her blood pressure was 160/90 mmHg equal in both arms and her heart rate was 63 bpm. She had no pulse deficit or asymmetry and no cardiac murmurs. Her initial electrocardiogram (EKG) demonstrated 0.5 mm/mV ST-segment elevation in leads III, aVF and 0.5 mm/mV ST-segment depression in leads I, aVL, V4–V6 with also left ventricular hypertrophy by voltage criteria. Chest radiography was normal with no widening of the mediastinum or pleural effusion observed. Cardiac investigations including echocardiography and cardiac biomarkers returned unremarkable. A chest computed tomography (CT) scan was done to exclude acute aortic dissection and pul*Correspondence to: [email protected]
monary thromboembolism because the patient complained severe chest pain with radiating back pain. The CT scan demonstrated blood leaks through the wall but contained by the adventitia at anteromedial portion of upper descending thoracic aorta (Figure 1A & 1C). This finding was compatible with PAU. She was admitted to the intensive care unit (ICU) under close observation. Six hours later, cardiac enzymes [Troponin I: 8.767 (0–0.78 ng/mL), CK-MB: 116.87 (0–5.0 ng/mL)] were elevated but electrocardiography was unchanged. Her chest pain and both shoulders pain persisted and worsened. This complex case was discussed with attending interventional cardiologists and thoracic surgeons about the option of coronary angiography and operative intervention. The concern was that coronary angiography procedure might aggravate the PAU and cause clinical deterioration. Preparation was made for both coronary angiography and thoracic endovascular aortic repair. After local anesthesia with lidocaine, arterial puncture was made via the right radial artery instead of femoral artery to avoid direct injury to PAU. Coronary angiography revealed total occlusion of the mid-portion of the right coronary artery (Figure 2A). The left coronary artery was normal. After Across HP® 3.5 15 mm balloon dilatation (Acrostak, Inc, Switzerland), an Orsiro® (Biotronilk AG, Bulach, Switzerland) 3.5 30 mm stent was successfully deployed in the right coronary artery lesion (Figure 2B). Thereafter, the right common femoral artery was exposed using a small incision. Aortography was done. Valiant® (Medtronic Vascular; Santa Rosa, Calif) thoracic stent graft (32 117 mm) was deployed successfully. After stent graft deployment, Reliant® (Medtronic Vascular; Santa Rosa, Calif) stent graft balloon dilatation was done. Final aortography showed no visible endovascular leaks. Following the procedures, she was pain and symptom free. On one month follow-up CT angiogram, no leakage was seen at the graft site (Figure 1B & 1D).
http://www.jgc301.com; [email protected] | Journal of Geriatric Cardiology
936
Kim YH & Her AY. AMI and descending thoracic aorta penetrating ulcer
Figure 1. Contrast enhanced CT scan of the chest in patient with concomitant acute myocardial infarction and descending thoracic aorta penetrating ulcer. (A): axial section of contrast enhanced CT scan of the chest. Arrow indicates blood leaks through the wall but is contained by the adventitia or surrounding perivascular soft tissue; (B): axial section of contrast enhanced CT scan of the chest after one month follow-up; (C): three-dimensional reconstruction image of the CT angiogram demonstrating the descending thoracic aorta penetrating ulcer; and (D): follow-up CT angiogram at one month showing no endovascular leakage from the previous graft deployed site.
Figure 2. Coronary angiography and percutaneous coronary intervention. (A): coronary angiography revealed total occlusion of the mid portion of the right coronary artery ( arrow); (B): Orsiro® (Biotronik AG, Bulach, Switzerland) 3.5 x 30 mm stent was successfully deployed in the right coronary artery ( arrow).
The search for the existence of the other disease before reperfusion therapy was administered invariably assisted the successful outcome in patients with acute myocardial infarction. AAS also characterized similar but slightly differ-
ent clinical symptoms such as severely intense, acute, searing or tearing, throbbing and migratory chest pain compared with ACS.[3] Penetrating atherosclerotic aortic ulcer means the lesion that penetrates the elastic lamina and is associated
Journal of Geriatric Cardiology | [email protected]; http://www.jgc301.com
Kim YH & Her AY. AMI and descending thoracic aorta penetrating ulcer
with hematoma formation within the aortic wall.[3,4] The true incidence of both symptomatic and silent PAU are not known. But some author reported about 2%–7% of AAS.[5] In general PAU lesions are asymptomatic and confined to the intimal layer at an early stage but it can be progress and atherosclerotic plaque penetrates into the media, the media is exposed to pulsatile arterial flow[6] in the later and leads to several dangerous complications such as dissection, aneurysm formation or aortic rupture. Sudden onset of severe chest pain or back pain in elderly hypertensive patient it may suggest an imminent cardiovascular catastrophe.[3] Hassani, et al.[5] also reported penetrating aortic ulcer is a rare pathology, often clinically silent, but potentially fatal when manifesting as an acute aortic syndrome. He also suggested that symptomatic penetrating aortic ulcer requires coverage by thoracic endovascular stent grafting according to the recent guidelines. In our case her chest pain and back pain may be caused by acute myocardial infarction (AMI) but it also may be originated by PAU. If the origin of her chest pain was PAU we must hurry up to avoid unwanted disaster. On the other hand, a conservative medical treatment is considered also acceptable when the lesion is stable. When we consider surgical management, endovascular aortic repair (TEVAR) is alternative treatment modality to surgical repair in descending aorta and showed excellent short-term and midterm results.[7] TEVAR reduces the blood loss, procedural time, and length of hospitalization because of the minimal invasive nature of the procedure. In patients referred to emergency department with acute chest pain several important differential diagnoses should be kept in mind which include: acute coronary syndrome, aortic dissection, pneumothorax and pulmonary thromboembolism.[8] Usually these disease entities occur separately but
937
can occur simultaneously. Each diagnostic tool or treatment strategy can influence the other disease entity. In this case, if we had focused only AMI we couldn’t figure out her PAU and this may lead to unwanted result. In conclusion, it is important to exclude AAS before reperfusion therapy in patients presenting with AMI. And commonly one disease entity is the cause of the symptom and is given focus; however, as seen in this case, two different disease entities are involved and happening concomitantly.
References 1 2 3
4
5
6
7
8
Bobadilla RV. Acute coronary syndrome: focus on antiplatelet therapy. Crit Care Nurse 2016; 36: 15–27. Tsai TT, Nienaber CA, Eagle KA. Acute aortic syndromes. Circulation 2005; 112: 3802–3813. Singhal P, Lin Z. Penetrating atheromatous ulcer of ascending aorta: a case report and review of literature. Heart Lung Circ 2008; 17: 380–382. Stanson AW, Kazmier FJ, Hollier LH, et al. Penetrating atherosclerotic ulcers of the thoracic aorta: natural history and clinicopathologic correlations. Ann Vasc Surg 1986; 1: 15–23. El Hassani I, Van Damme H, Creemers E, et al. Penetrating atherosclerosis aortic ulcer: a re-appraisal. Acta Chir Belg. Published Online First: 2016 Sep 3. DOI: 10.1080/00015458. 2016.1212566. Coady MA, Rizzo JA, Hammond GL, et al. Penetrating ulcer of the thoracic aorta: what is it? How do we recognize it? How do we manage it? Vasc Surg 1998; 27: 1006–1016. D’Annoville T, Ozdemir BA, Alric P, et al. Thoracic endovascular aortic repair for penetrating aortic ulcer: literature review. Ann Thorac Surg 2016 : 101: 2272–2278 Ansari-Ramandi MM, Alemzadeh-Ansari MJ, Firoozi A. Acute type aortic dissection missed as acute coronary syndrome. J Clin Diagn Res 2016; 10: OD33–OD34.
http://www.jgc301.com; [email protected] | Journal of Geriatric Cardiology
