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Rare case of inferior myocardial infarction from left main coronary artery spontaneous coronary artery dissection
IHJ Cardiovascular Case Reports (CVCR) 1 (2017) 21–23
Contents lists available at ScienceDirect
IHJ Cardiovascular Case Reports (CVCR) journal homepage: www.elsevier.com/locate/ihjccr
Case Report
Rare case of inferior myocardial infarction from left main coronary artery spontaneous coronary artery dissection Giorgio A. Medranda a,∗ , Kevin Marzo b a b
Winthrop University Hospital, Department of Medicine, United States Winthrop University Hospital, Division of Cardiology, United States
a r t i c l e
i n f o
Keywords: ST elevation myocardial infarction Left main coronary artery Spontaneous coronary artery dissection
a b s t r a c t The natural history and etiology of SCAD remain unclear. This was a young female with chest pain and inferior ST elevations. Cardiac catheterization revealed type 1 angiographic SCAD of the LMCA. This case was unusual in that the injury pattern of inferior posterior MI was from a LMCA SCAD. © 2016 Cardiological Society of India. Published by Elsevier B.V. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
1. Introduction There have been more than 800 cases of SCAD reported in the literature to date.1 Recently, with increased use of cardiac catheterization and other coronary imaging modalities such as intravascular ultrasonography (IVUS) and intracoronary optical coherence tomography (IOCT), detection of SCAD in acute coronary syndrome (ACS) patients, particularly in younger patients without known cardiovascular risk factors, is increasing. Prior registries have reported SCAD in 0.07–1.1% of all coronary angiograms.2 The natural history and etiology of SCAD remain unclear. There is development of a false lumen with hematoma or blood clot, which compresses the true lumen, resulting in myocardial ischemia and infarction. This is often difficult to visualize using standard coronary angiography.3 IVUS has been shown to be a safe and effective aide in the diagnosis of SCAD.4 Several conditions have been found to be associated with SCAD including fibromuscular dysplasia (FMD), peripartum states, Marfan’s syndrome, vasculitides, cocaine abuse and intense physical activity. In one study, 30% of young women with ACS were found to have SCAD and FMD. Another study showed 72% of patients with non-atherosclerotic SCAD were found to have concomitant FMD.1 In addition, precipitating factors have been identified in most patients with SCAD, including emotional stressors, physical activity, retching, vomiting, coughing and straining.1 SCAD of the left coronary system has been found to be more common in women and SCAD of the RCA more common in men. SCAD has been found to involve the LAD in 75%, the RCA in 20%, the LCX in 4% and the LMCA in <1% of cases.5
∗ Corresponding author at: Winthrop University Hospital, 120 Mineola Boulevard, Suite 500, Mineola, NY 11501, United States. E-mail address: [email protected] (G.A. Medranda).
Currently, there are no guidelines regarding optimal management of SCAD. Current options include CABG, percutaneous coronary intervention (PCI) and medical management. Thrombolytic therapy is thought to potentially worsen existing hematomas and is felt to be relatively contraindicated in SCAD. In patients without signs of ongoing ischemia, PCI has been found to be associated with high rates of technical failure secondary to the fragility of the affected vessel and may not protect against recurrence of SCAD. Those patients managed with conservative medical management using betablockade and antiplatelet therapy have been shown to have healing of their dissection.1 Revascularization for ongoing ischemia with emergent PCI is preferred over medical management in patients without favorable anatomy for CABG. The present case of LMCA SCAD did not have a clearly defined intramural tear or spiral dissection but angiographic findings were consistent with intraluminal hematoma with clinical sequelae. Further research is needed to elucidate the etiology and optimal treatment for SCAD. Similar to takotsubo cardiomyopathy, recent increases in awareness, including national registries, could help better understand SCAD. Examples are the ongoing databases at Mayo Clinic, the virtual multicenter SCAD registry and the genetic investigations in SCAD. These registries, which have enrolled hundreds of patients to date, are opportunities to answer many questions regarding this serious condition.
2. Case report This was a 44-year-old African American female, with a medical history significant for leiomyomas and multiple spontaneous abortions, who presented from home to our institution with 1 h of midsternal chest pain. The patient did not have any significant cardiac risk factors, no history of connective tissue disease or illicit drug use. En route to the hospital, the patient received
http://dx.doi.org/10.1016/j.ihjccr.2016.09.005 2468-600X/© 2016 Cardiological Society of India. Published by Elsevier B.V. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/ licenses/by-nc-nd/4.0/).
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G.A. Medranda, K. Marzo / IHJ Cardiovascular Case Reports (CVCR) 1 (2017) 21–23
Fig. 1. ECG on presentation demonstrating an acute inferior MI with posterior wall involvement.
325 mg of aspirin by mouth and 0.4 mg of nitroglycerine sublingually, which provided minimal relief. On initial presentation, the patient’s supine blood pressure was 155/106 mm Hg with a heart rate of 91 beats per minute. There were no murmurs, gallops or rubs, her lungs were clear to auscultation with no peripheral edema. Electrocardiogram (ECG) on presentation showed normal sinus rhythm, ST segment elevations in leads II, III, aVF, V5 and V6, and ST segment depressions in leads I, aVL, V2, V3 and V4 (Fig. 1). The right-sided ECG showed normal ST segments and upright T waves in V4 R. Initial cardiac enzymes were negative. The patient was treated with full dose aspirin, unfractionated heparin and clopidogrel. She was taken for emergent cardiac catheterization, which revealed type 1 angiographic spontaneous coronary artery dissection (SCAD) of the left main coronary artery (LMCA) (Fig. 2). There was no angiographic evidence of atherosclerotic disease and there was thrombolysis in myocardial infarction (TIMI) flow grade 3 in the left anterior descending (LAD) artery, left circumflex (LCX) artery and right coronary artery (RCA) despite persistent ST elevations. Left
ventriculogram showed apical inferior and lateral wall hypokinesis with minimally decreased ejection fraction. Given the persistence of symptoms and urgency of the situation, IVUS was not an option. The patient was taken for emergent coronary artery bypass grafting (CABG) saphenous vein graft (SVG) to her LAD artery and first obtuse marginal (OM1). Venous grafts were chosen over internal mammary artery grafting given its shorter time to revascularization in the setting of persistent ischemia. Postoperative ECG (Fig. 3) showed resolution of ST elevations, with Q waves inferiorly and laterally. 3. Discussion The present case was unusual in terms of the ECG injury pattern of inferior posterior MI from a LMCA SCAD. 100% occlusion of the LMCA is often fatal and associated with hemodynamic collapse. Left main disease associated with narrowing >50% causing ischemia characteristically causes diffuse ST depressions and ST
Fig. 2. Coronary angiography in the right anterior oblique position showing irregularity of the LMCA with radiolucent line representing intimal flap delineating both lumens, the true lumen of the LMCA, LAD, LCX and RCA with TIMI flow grade 3.
G.A. Medranda, K. Marzo / IHJ Cardiovascular Case Reports (CVCR) 1 (2017) 21–23
23
Fig. 3. Postoperative ECG showing resolution of ST elevations, with Q waves inferiorly and laterally.
elevation in aVR. In this patient, the ECG injury pattern localized to the LCX artery distribution and there appeared to be no obvious LAD ischemic changes in V4-V6 and no ST elevation in aVR. Theoretically, an inferior STEMI can present from occlusion of either the LCX, RCA or Type III LAD. In this patient the ECG findings could be a combination of LCX and Type III LAD occlusion given the involvement of the LMCA. With ongoing ischemic pain, and persistent ST elevations, the patient was hemodynamically stable with wall motion abnormalities localized to the LCX artery. CABG was emergently performed without complication. Conflicts of interest The authors have none to declare.
References 1. Saw J, Aymong E, Sedlak T, et al. Spontaneous coronary artery dissection: association with predisposing arteriopathies and precipitating stressors and cardiovascular outcomes. Circ Cardiovasc Interv. 2014;7:645–655. 2. Vanzetto G, Berger-Coz E, Barone-Rochette G, et al. Prevalence, therapeutic management and medium-term prognosis of spontaneous coronary artery dissection: results from a database of 11,605 patients. Eur J Cardiothorac Surg. 2009;35:250–254. 3. Adlam D, Cuculi F, Lim C, Banning A. Management of spontaneous coronary artery dissection in the primary percutaneous coronary intervention era. J Invasive Cardiol. 2010;22:549–553. 4. Klein AJ, Hudson PA, Kim MS, Cleveland Jr JC, Messenger JC. Spontaneous left main coronary artery dissection and the role of intravascular ultrasonography. J Ultrasound Med. 2010;29:981–988. 5. Almeda FQ, Barkatullah S, Kavinsky CJ. Spontaneous coronary artery dissection. Clin Cardiol. 2004;27:377–380.
Contents lists available at ScienceDirect
IHJ Cardiovascular Case Reports (CVCR) journal homepage: www.elsevier.com/locate/ihjccr
Case Report
Rare case of inferior myocardial infarction from left main coronary artery spontaneous coronary artery dissection Giorgio A. Medranda a,∗ , Kevin Marzo b a b
Winthrop University Hospital, Department of Medicine, United States Winthrop University Hospital, Division of Cardiology, United States
a r t i c l e
i n f o
Keywords: ST elevation myocardial infarction Left main coronary artery Spontaneous coronary artery dissection
a b s t r a c t The natural history and etiology of SCAD remain unclear. This was a young female with chest pain and inferior ST elevations. Cardiac catheterization revealed type 1 angiographic SCAD of the LMCA. This case was unusual in that the injury pattern of inferior posterior MI was from a LMCA SCAD. © 2016 Cardiological Society of India. Published by Elsevier B.V. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
1. Introduction There have been more than 800 cases of SCAD reported in the literature to date.1 Recently, with increased use of cardiac catheterization and other coronary imaging modalities such as intravascular ultrasonography (IVUS) and intracoronary optical coherence tomography (IOCT), detection of SCAD in acute coronary syndrome (ACS) patients, particularly in younger patients without known cardiovascular risk factors, is increasing. Prior registries have reported SCAD in 0.07–1.1% of all coronary angiograms.2 The natural history and etiology of SCAD remain unclear. There is development of a false lumen with hematoma or blood clot, which compresses the true lumen, resulting in myocardial ischemia and infarction. This is often difficult to visualize using standard coronary angiography.3 IVUS has been shown to be a safe and effective aide in the diagnosis of SCAD.4 Several conditions have been found to be associated with SCAD including fibromuscular dysplasia (FMD), peripartum states, Marfan’s syndrome, vasculitides, cocaine abuse and intense physical activity. In one study, 30% of young women with ACS were found to have SCAD and FMD. Another study showed 72% of patients with non-atherosclerotic SCAD were found to have concomitant FMD.1 In addition, precipitating factors have been identified in most patients with SCAD, including emotional stressors, physical activity, retching, vomiting, coughing and straining.1 SCAD of the left coronary system has been found to be more common in women and SCAD of the RCA more common in men. SCAD has been found to involve the LAD in 75%, the RCA in 20%, the LCX in 4% and the LMCA in <1% of cases.5
∗ Corresponding author at: Winthrop University Hospital, 120 Mineola Boulevard, Suite 500, Mineola, NY 11501, United States. E-mail address: [email protected] (G.A. Medranda).
Currently, there are no guidelines regarding optimal management of SCAD. Current options include CABG, percutaneous coronary intervention (PCI) and medical management. Thrombolytic therapy is thought to potentially worsen existing hematomas and is felt to be relatively contraindicated in SCAD. In patients without signs of ongoing ischemia, PCI has been found to be associated with high rates of technical failure secondary to the fragility of the affected vessel and may not protect against recurrence of SCAD. Those patients managed with conservative medical management using betablockade and antiplatelet therapy have been shown to have healing of their dissection.1 Revascularization for ongoing ischemia with emergent PCI is preferred over medical management in patients without favorable anatomy for CABG. The present case of LMCA SCAD did not have a clearly defined intramural tear or spiral dissection but angiographic findings were consistent with intraluminal hematoma with clinical sequelae. Further research is needed to elucidate the etiology and optimal treatment for SCAD. Similar to takotsubo cardiomyopathy, recent increases in awareness, including national registries, could help better understand SCAD. Examples are the ongoing databases at Mayo Clinic, the virtual multicenter SCAD registry and the genetic investigations in SCAD. These registries, which have enrolled hundreds of patients to date, are opportunities to answer many questions regarding this serious condition.
2. Case report This was a 44-year-old African American female, with a medical history significant for leiomyomas and multiple spontaneous abortions, who presented from home to our institution with 1 h of midsternal chest pain. The patient did not have any significant cardiac risk factors, no history of connective tissue disease or illicit drug use. En route to the hospital, the patient received
http://dx.doi.org/10.1016/j.ihjccr.2016.09.005 2468-600X/© 2016 Cardiological Society of India. Published by Elsevier B.V. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/ licenses/by-nc-nd/4.0/).
22
G.A. Medranda, K. Marzo / IHJ Cardiovascular Case Reports (CVCR) 1 (2017) 21–23
Fig. 1. ECG on presentation demonstrating an acute inferior MI with posterior wall involvement.
325 mg of aspirin by mouth and 0.4 mg of nitroglycerine sublingually, which provided minimal relief. On initial presentation, the patient’s supine blood pressure was 155/106 mm Hg with a heart rate of 91 beats per minute. There were no murmurs, gallops or rubs, her lungs were clear to auscultation with no peripheral edema. Electrocardiogram (ECG) on presentation showed normal sinus rhythm, ST segment elevations in leads II, III, aVF, V5 and V6, and ST segment depressions in leads I, aVL, V2, V3 and V4 (Fig. 1). The right-sided ECG showed normal ST segments and upright T waves in V4 R. Initial cardiac enzymes were negative. The patient was treated with full dose aspirin, unfractionated heparin and clopidogrel. She was taken for emergent cardiac catheterization, which revealed type 1 angiographic spontaneous coronary artery dissection (SCAD) of the left main coronary artery (LMCA) (Fig. 2). There was no angiographic evidence of atherosclerotic disease and there was thrombolysis in myocardial infarction (TIMI) flow grade 3 in the left anterior descending (LAD) artery, left circumflex (LCX) artery and right coronary artery (RCA) despite persistent ST elevations. Left
ventriculogram showed apical inferior and lateral wall hypokinesis with minimally decreased ejection fraction. Given the persistence of symptoms and urgency of the situation, IVUS was not an option. The patient was taken for emergent coronary artery bypass grafting (CABG) saphenous vein graft (SVG) to her LAD artery and first obtuse marginal (OM1). Venous grafts were chosen over internal mammary artery grafting given its shorter time to revascularization in the setting of persistent ischemia. Postoperative ECG (Fig. 3) showed resolution of ST elevations, with Q waves inferiorly and laterally. 3. Discussion The present case was unusual in terms of the ECG injury pattern of inferior posterior MI from a LMCA SCAD. 100% occlusion of the LMCA is often fatal and associated with hemodynamic collapse. Left main disease associated with narrowing >50% causing ischemia characteristically causes diffuse ST depressions and ST
Fig. 2. Coronary angiography in the right anterior oblique position showing irregularity of the LMCA with radiolucent line representing intimal flap delineating both lumens, the true lumen of the LMCA, LAD, LCX and RCA with TIMI flow grade 3.
G.A. Medranda, K. Marzo / IHJ Cardiovascular Case Reports (CVCR) 1 (2017) 21–23
23
Fig. 3. Postoperative ECG showing resolution of ST elevations, with Q waves inferiorly and laterally.
elevation in aVR. In this patient, the ECG injury pattern localized to the LCX artery distribution and there appeared to be no obvious LAD ischemic changes in V4-V6 and no ST elevation in aVR. Theoretically, an inferior STEMI can present from occlusion of either the LCX, RCA or Type III LAD. In this patient the ECG findings could be a combination of LCX and Type III LAD occlusion given the involvement of the LMCA. With ongoing ischemic pain, and persistent ST elevations, the patient was hemodynamically stable with wall motion abnormalities localized to the LCX artery. CABG was emergently performed without complication. Conflicts of interest The authors have none to declare.
References 1. Saw J, Aymong E, Sedlak T, et al. Spontaneous coronary artery dissection: association with predisposing arteriopathies and precipitating stressors and cardiovascular outcomes. Circ Cardiovasc Interv. 2014;7:645–655. 2. Vanzetto G, Berger-Coz E, Barone-Rochette G, et al. Prevalence, therapeutic management and medium-term prognosis of spontaneous coronary artery dissection: results from a database of 11,605 patients. Eur J Cardiothorac Surg. 2009;35:250–254. 3. Adlam D, Cuculi F, Lim C, Banning A. Management of spontaneous coronary artery dissection in the primary percutaneous coronary intervention era. J Invasive Cardiol. 2010;22:549–553. 4. Klein AJ, Hudson PA, Kim MS, Cleveland Jr JC, Messenger JC. Spontaneous left main coronary artery dissection and the role of intravascular ultrasonography. J Ultrasound Med. 2010;29:981–988. 5. Almeda FQ, Barkatullah S, Kavinsky CJ. Spontaneous coronary artery dissection. Clin Cardiol. 2004;27:377–380.