727824 case-report2017
PRF0010.1177/0267659117727824PerfusionChang et al.
Case Report
Spontaneous coronary artery dissection causing acute myocardial infarction and cardiac arrest in a 25-year-old male
Perfusion 1–4 © The Author(s) 2017 Reprints and permissions: sagepub.co.uk/journalsPermissions.nav https://doi.org/10.1177/0267659117727824 DOI: 10.1177/0267659117727824 journals.sagepub.com/home/prf
Fu-Lan Chang,1 Wei-Chun Chang,2,3 Yu-Tsung Cheng,2 Tsun-Jui Liu,2,3 Wen-Lieng Lee2,3 and Chih-Hung Lai2,3
Abstract A 25-year-old previously healthy male presented to our emergency room with acute chest pain and ventricular arrhythmia-related cardiac arrest. ST elevation myocardial infarction was diagnosed and coronary angiography revealed diffuse critical narrowing from the proximal to the distal left anterior descending artery. Diffuse intramural hematoma was demonstrated on intravascular ultrasound. Two stents were placed to cover the whole dissection length and flow was successfully restored. Spontaneous coronary artery dissection can be a fatal event and could be mistaken for atherosclerotic plaque or coronary spasm rather than luminal compression on coronary angiography and intravascular imaging is helpful in this condition. Keywords spontaneous coronary artery dissection; acute myocardial infarction; ventricular arrhythmia; cardiac arrest; young age
Introduction Spontaneous coronary artery dissection (SCAD) is an infrequent, but increasingly recognized, cause of acute coronary artery syndrome. Typically, SCAD affects a younger, otherwise healthy population and, especially, females of childbearing age.1 The reported ratio of females to males is 4:1, with a mean age at occurrence of 42 years. The dissection is more frequently diagnosed in the left anterior descending coronary artery (LAD), but can involve single or multiple vessels.2 The clinical presentation of SCAD depends on the extent and severity of flow limitation of the coronary artery dissection and ranges from being asymptomatic to chest pain alone to acute coronary syndrome (ACS). The reported prevalence of SCAD is higher in ACS patients (3%-4%) compared to those with stable symptoms (0.3%).1 In addition, more than half of patients with SCAD present with ST elevation myocardial infarction (STEMI) or unstable ventricular arrhythmia. Herein, we report an extremely rare case of a 25-year-old non-smoking male who presented with potentially fatal ventricular arrhythmia and STEMI caused by SCAD of the LAD.
Case Presentation A 25-year-old male with no past medical history or any known cardiovascular risk factors presented to our
emergency room with severe chest pain and cold sweats immediately after lifting a heavy object. On arrival, the patient developed loss of consciousness and ventricular fibrillation. Defibrillation and endotracheal intubation were performed immediately and spontaneous circulation was restored after 10 minutes of resuscitation. An initial electrocardiogram (ECG) demonstrated ST elevation in the precordial leads (Figure 1) and a primary percutaneous coronary intervention (PCI) was arranged. Coronary angiography revealed diffuse narrowing of the lumen from the proximal to the distal LAD with TIMI 1 grade flow (Figure 2A). Due to cardiogenic shock with a blood pressure of 88/61 mmHg and desaturation (SpO2:88%), an intra-aortic balloon pump (IABP) was inserted and the patients was administered 1Department
of Nursing, Taichung Veterans General Hospital, Taichung, Taiwan, R.O.C 2Division of Interventional Cardiology, Cardiovascular Center, Taichung Veterans General Hospital, Taichung, Taiwan, R.O.C 3School of Medicine, National Yang-Ming University, Taipei, Taiwan, R.O.C Corresponding author: Chih-Hung Lai, Division of Interventional Cardiology, Cardiovascular Center, Taichung Veterans General Hospital, 1650 Taiwan Boulevard Sect. 4, Taichung, Taiwan 40705, ROC. Email: [email protected]
2
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Figure 1. Serial electrocardiograms (ECG). (A) At admission, ECG showed anterior wall ST elevation. (B) After intervention, ECG showed resolution of the ST segment.
an inotropic agent (dopamine), resulting in a systolic blood pressure of 110 mmHg and SpO2:98%. Initially, due to highly suspected coronary artery vasospasm, intracoronary isosorbide dinitrate and adenosine were given, but failed to achieve a response. Subsequently, thrombus suction with a manual thrombus aspirator was performed on multiple occasions, but this still failed to restore good flow. Intravascular ultrasound (IVUS) was used to investigate the cause and it revealed an intramural hematoma extending from the proximal to the distal part of the LAD, compromising the inner lumen (Figure 2B-D). Hence, under IVUS guidance, two drug-eluting stents were placed from the distal to proximal part of the LAD, sequentially, to cover the whole area of dissection. TIMI III grade flow was noted immediately after stenting (Figure 2E). After the intervention, the blood pressure was 110/82 mmHg and the ECG showed complete resolution of the ST segment elevation (Figure 1B). There was no significant findings
on a full panel of tests, including erythrocyte sedimentation rate, complement level, anti-nuclear antibody test, rheumatoid factor, thyroid function and perinuclear anti-neutrophil cytoplasmic antibody test. The inotropic agents and IABP were withdrawn on the fourth day. The patient was discharged on the tenth day and has since remained symptom free.
Discussion SCAD is defined as a non-traumatic and non-iatrogenic separation of the coronary arterial wall due to an intramural hemorrhage, creating a false lumen, with or without an intimal tear.1 Patients with SCAD are most often women (74% to 92%) and, especially, those younger than 50 years of age.1,2 SCAD is often classified, based on the associated predisposing conditions, as atherosclerotic and non-atherosclerotic.1 An atherosclerotic cause refers to rupture of plaque leading to SCAD,
Chang et al.
3
Figure 2. Before and after intervention of left anterior descending artery (LAD) and intravascular ultrasound (IVUS) image of LAD. (A) Initial coronary angiography revealed extensive spontaneous dissection over proximal to distal segment of LAD. (B) IVUS image of proximal LAD (upper arrow) revealed large dissection (asterisk). (C) IVUS image of middle LAD (middle arrow) revealed extensive dissection (asterisk). (D) IVUS image of distal LAD (lower arrow) revealed extensive dissection (asterisk). (E) After stenting, final angiography showed good patency and TIMI III flow.
whereas a non-atherosclerotic cause refers to SCAD being induced by extra-coronary vascular abnormalities, such as fibromuscular dysplasia, peripartum state, connective tissue disorders and systemic inflammatory conditions.1,3 SCAD has been reported to be due to performing activities that increase coronary shear stress and some that would be expected to greatly influence hemodynamics (severe hypertension, cocaine use, labor, weight lifting) and others that seem to be relatively benign (running, sneezing).1 In our case, the event occurred immediately after lifting a heavy object, suggesting this may have been the precipitating factor. The clinical presentation depends on the location and the severity of the coronary involvement. Coronary angiography with/without intravascular imaging is the primary tool used in the diagnosis of SCAD. In patients with an intimal tear, SCAD may appear as multiple radiolucent lines separating the true and false lumens, with or without slow contrast clearing. However, in patients with intramural hematoma with no intimal tearing, where diagnostic angiography is not definitive, intracoronary imaging techniques, such as IVUS and/ or optical coherence tomography (OCT), may be necessary, as in our case. Although dual anti-platelet therapy may reduce the burden of false lumen thrombus,
thrombolytic therapy should be avoided as it may cause extension of the dissection.1 Treatment with beta-blockers has been shown to reduce shear stress in patients with aortic dissection and, thus, it may be useful in SCAD.1 Nitroglycerin may be helpful in alleviating ischemic symptoms from underlying vasospasm. Revascularization of a dissected artery depends on the clinical status of the patient and the affected coronary segments. Although conservative therapy for SCAD usually has a favorable in-hospital outcome, revascularization, either by PCI or surgical bypass, is preferred for patients with hemodynamic instability who have ongoing ischemia or infarction and in those with a TIMI 0 to 1 coronary flow.2,4 However, PCI for SCAD patients can have a failure rate of up to 35%, which is mostly related to the passage of the coronary wire into the false lumen of the dissected vessel or loss of coronary flow through propagation of the dissection.2,4 Complications resulting from SCAD interventions are also frequently related to the placement of stents (resulting in propagation of the hematoma). The risk of stent placement should, therefore, be weighed against the expectation of a favorable clinical outcome with conservative management. Besides, adjuvant imaging guidance and a long length or multiple stents are
4
usually needed to seal the whole length of the dissection in order to avoid shifting the hematoma. Surgical bypass is an alternative choice of therapy, especially when revascularization with PCI fails.2 There is currently limited evidence available from randomized trials to guide our therapy of patients in cardiogenic shock complicating acute myocardial infarction.5 Early revascularization remains the gold standard for treatment of these patients.6 Mechanical circulatory support, such as IABP, Impella (AbioMed, Danvers, MA, USA), Tandem Heart (TandemLife, Pittsburgh, PA, USA), or extracorporeal membrane oxygenation (ECMO), should be considered in cardiogenic shock patients who remain unstable despite revascularization and inotropic therapy. Although there is limited evidence available from randomized trials evaluating the different percutaneous support systems in treating cardiogenic shock complicating acute myocardial infarction, except for data demonstrating the relative ineffectiveness of IABP, there is growing evidence that shows these new mechanical circulatory support devices improve hemodynamic status, organ perfusion and, even, survival, especially early initiation.5,7 Based on recent studies, the Tandem Heart or Impella systems may be better first-line mechanical support devices compared to IABP. However, at this current institution, due to the inaccessibility of other percutaneous devices, ECMO is the preferred rescue device for patients who are still unstable after IABP combined with inotropic agent administration. Although previous data showed low rates of inhospital mortality and major cardiac adverse events (MACEs) in SCAD patients (5–10%), a significant proportion of patients had recurrent SCAD or MACEs following hospital discharge (up to 15% to 37% at 5 to 7 years).1 In addition to close follow-up and recommendations to avoid precipitating factors, current recommendations suggest long-term management with aspirin, beta-blocker, angiotensin-converting ace inhibitor (ACEI) and statins. Dedicated cardiac rehabilitation programs, inclusive of exercise, psychosocial counseling and peer group support, have also been shown to be safe and beneficial for SCAD patients.1 SCAD can be a life-threatening event. We reported an unusual case of SCAD in a young man with no
Perfusion 00(0)
known cardiovascular risk factors, which was likely to be precipitated by heavy lifting before a STEMI-related cardiac arrest. This case reminds clinicians to be aware of a possible SCAD diagnosis in such situations. In addition, the use of intravascular imaging is helpful in diagnosing SCAD where the diagnosis in question. Declaration of Conflicting Interests The authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
Funding The authors received no financial support for the research, authorship, and/or publication of this article.
References 1. Saw J, Mancini GB, Humphries KH. Contemporary review on spontaneous coronary artery dissection. J Am Coll Cardiol 2016; 68: 297–312. 2. Tweet MS, Hayes SN, Pitta SR, et al. Clinical features, management, and prognosis of spontaneous coronary artery dissection. Circulation 2012; 126: 579–588. 3. Eleid MF, Guddeti RR, Tweet MS, et al. Coronary artery tortuosity in spontaneous coronary artery dissection: angiographic characteristics and clinical implications. Circ Cardiovasc Interv 2014; 7: 656–662. 4. Tweet MS, Eleid MF, Best PJ, et al. Spontaneous coronary artery dissection: revascularization versus conservative therapy. Circ Cardiovasc Interv 2014; 7: 777–786. 5. Van Herck JL, Claeys MJ, De Paep R, Van Herck PL, Vrints CJ, Jorens PG. Management of cardiogenic shock complicating acute myocardial infarction. Eur Heart J Acute Cardiovasc Care 2015; 4: 278–297. 6. Windecker S, Kolh P, Alfonso F, et al. 2014 ESC/EACTS Guidelines on myocardial revascularization: The Task Force on Myocardial Revascularization of the European Society of Cardiology (ESC) and the European Association for Cardio-Thoracic Surgery (EACTS)Developed with the special contribution of the European Association of Percutaneous Cardiovascular Interventions (EAPCI). Eur Heart J 2014; 35: 2541–2619. 7. Basir MB, Schreiber TL, Grines CL, et al. Effect of early initiation of mechanical circulatory support on survival in cardiogenic shock. Am J Cardiol 2017; 119: 845–851.
PRF0010.1177/0267659117727824PerfusionChang et al.
Case Report
Spontaneous coronary artery dissection causing acute myocardial infarction and cardiac arrest in a 25-year-old male
Perfusion 1–4 © The Author(s) 2017 Reprints and permissions: sagepub.co.uk/journalsPermissions.nav https://doi.org/10.1177/0267659117727824 DOI: 10.1177/0267659117727824 journals.sagepub.com/home/prf
Fu-Lan Chang,1 Wei-Chun Chang,2,3 Yu-Tsung Cheng,2 Tsun-Jui Liu,2,3 Wen-Lieng Lee2,3 and Chih-Hung Lai2,3
Abstract A 25-year-old previously healthy male presented to our emergency room with acute chest pain and ventricular arrhythmia-related cardiac arrest. ST elevation myocardial infarction was diagnosed and coronary angiography revealed diffuse critical narrowing from the proximal to the distal left anterior descending artery. Diffuse intramural hematoma was demonstrated on intravascular ultrasound. Two stents were placed to cover the whole dissection length and flow was successfully restored. Spontaneous coronary artery dissection can be a fatal event and could be mistaken for atherosclerotic plaque or coronary spasm rather than luminal compression on coronary angiography and intravascular imaging is helpful in this condition. Keywords spontaneous coronary artery dissection; acute myocardial infarction; ventricular arrhythmia; cardiac arrest; young age
Introduction Spontaneous coronary artery dissection (SCAD) is an infrequent, but increasingly recognized, cause of acute coronary artery syndrome. Typically, SCAD affects a younger, otherwise healthy population and, especially, females of childbearing age.1 The reported ratio of females to males is 4:1, with a mean age at occurrence of 42 years. The dissection is more frequently diagnosed in the left anterior descending coronary artery (LAD), but can involve single or multiple vessels.2 The clinical presentation of SCAD depends on the extent and severity of flow limitation of the coronary artery dissection and ranges from being asymptomatic to chest pain alone to acute coronary syndrome (ACS). The reported prevalence of SCAD is higher in ACS patients (3%-4%) compared to those with stable symptoms (0.3%).1 In addition, more than half of patients with SCAD present with ST elevation myocardial infarction (STEMI) or unstable ventricular arrhythmia. Herein, we report an extremely rare case of a 25-year-old non-smoking male who presented with potentially fatal ventricular arrhythmia and STEMI caused by SCAD of the LAD.
Case Presentation A 25-year-old male with no past medical history or any known cardiovascular risk factors presented to our
emergency room with severe chest pain and cold sweats immediately after lifting a heavy object. On arrival, the patient developed loss of consciousness and ventricular fibrillation. Defibrillation and endotracheal intubation were performed immediately and spontaneous circulation was restored after 10 minutes of resuscitation. An initial electrocardiogram (ECG) demonstrated ST elevation in the precordial leads (Figure 1) and a primary percutaneous coronary intervention (PCI) was arranged. Coronary angiography revealed diffuse narrowing of the lumen from the proximal to the distal LAD with TIMI 1 grade flow (Figure 2A). Due to cardiogenic shock with a blood pressure of 88/61 mmHg and desaturation (SpO2:88%), an intra-aortic balloon pump (IABP) was inserted and the patients was administered 1Department
of Nursing, Taichung Veterans General Hospital, Taichung, Taiwan, R.O.C 2Division of Interventional Cardiology, Cardiovascular Center, Taichung Veterans General Hospital, Taichung, Taiwan, R.O.C 3School of Medicine, National Yang-Ming University, Taipei, Taiwan, R.O.C Corresponding author: Chih-Hung Lai, Division of Interventional Cardiology, Cardiovascular Center, Taichung Veterans General Hospital, 1650 Taiwan Boulevard Sect. 4, Taichung, Taiwan 40705, ROC. Email: [email protected]
2
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Figure 1. Serial electrocardiograms (ECG). (A) At admission, ECG showed anterior wall ST elevation. (B) After intervention, ECG showed resolution of the ST segment.
an inotropic agent (dopamine), resulting in a systolic blood pressure of 110 mmHg and SpO2:98%. Initially, due to highly suspected coronary artery vasospasm, intracoronary isosorbide dinitrate and adenosine were given, but failed to achieve a response. Subsequently, thrombus suction with a manual thrombus aspirator was performed on multiple occasions, but this still failed to restore good flow. Intravascular ultrasound (IVUS) was used to investigate the cause and it revealed an intramural hematoma extending from the proximal to the distal part of the LAD, compromising the inner lumen (Figure 2B-D). Hence, under IVUS guidance, two drug-eluting stents were placed from the distal to proximal part of the LAD, sequentially, to cover the whole area of dissection. TIMI III grade flow was noted immediately after stenting (Figure 2E). After the intervention, the blood pressure was 110/82 mmHg and the ECG showed complete resolution of the ST segment elevation (Figure 1B). There was no significant findings
on a full panel of tests, including erythrocyte sedimentation rate, complement level, anti-nuclear antibody test, rheumatoid factor, thyroid function and perinuclear anti-neutrophil cytoplasmic antibody test. The inotropic agents and IABP were withdrawn on the fourth day. The patient was discharged on the tenth day and has since remained symptom free.
Discussion SCAD is defined as a non-traumatic and non-iatrogenic separation of the coronary arterial wall due to an intramural hemorrhage, creating a false lumen, with or without an intimal tear.1 Patients with SCAD are most often women (74% to 92%) and, especially, those younger than 50 years of age.1,2 SCAD is often classified, based on the associated predisposing conditions, as atherosclerotic and non-atherosclerotic.1 An atherosclerotic cause refers to rupture of plaque leading to SCAD,
Chang et al.
3
Figure 2. Before and after intervention of left anterior descending artery (LAD) and intravascular ultrasound (IVUS) image of LAD. (A) Initial coronary angiography revealed extensive spontaneous dissection over proximal to distal segment of LAD. (B) IVUS image of proximal LAD (upper arrow) revealed large dissection (asterisk). (C) IVUS image of middle LAD (middle arrow) revealed extensive dissection (asterisk). (D) IVUS image of distal LAD (lower arrow) revealed extensive dissection (asterisk). (E) After stenting, final angiography showed good patency and TIMI III flow.
whereas a non-atherosclerotic cause refers to SCAD being induced by extra-coronary vascular abnormalities, such as fibromuscular dysplasia, peripartum state, connective tissue disorders and systemic inflammatory conditions.1,3 SCAD has been reported to be due to performing activities that increase coronary shear stress and some that would be expected to greatly influence hemodynamics (severe hypertension, cocaine use, labor, weight lifting) and others that seem to be relatively benign (running, sneezing).1 In our case, the event occurred immediately after lifting a heavy object, suggesting this may have been the precipitating factor. The clinical presentation depends on the location and the severity of the coronary involvement. Coronary angiography with/without intravascular imaging is the primary tool used in the diagnosis of SCAD. In patients with an intimal tear, SCAD may appear as multiple radiolucent lines separating the true and false lumens, with or without slow contrast clearing. However, in patients with intramural hematoma with no intimal tearing, where diagnostic angiography is not definitive, intracoronary imaging techniques, such as IVUS and/ or optical coherence tomography (OCT), may be necessary, as in our case. Although dual anti-platelet therapy may reduce the burden of false lumen thrombus,
thrombolytic therapy should be avoided as it may cause extension of the dissection.1 Treatment with beta-blockers has been shown to reduce shear stress in patients with aortic dissection and, thus, it may be useful in SCAD.1 Nitroglycerin may be helpful in alleviating ischemic symptoms from underlying vasospasm. Revascularization of a dissected artery depends on the clinical status of the patient and the affected coronary segments. Although conservative therapy for SCAD usually has a favorable in-hospital outcome, revascularization, either by PCI or surgical bypass, is preferred for patients with hemodynamic instability who have ongoing ischemia or infarction and in those with a TIMI 0 to 1 coronary flow.2,4 However, PCI for SCAD patients can have a failure rate of up to 35%, which is mostly related to the passage of the coronary wire into the false lumen of the dissected vessel or loss of coronary flow through propagation of the dissection.2,4 Complications resulting from SCAD interventions are also frequently related to the placement of stents (resulting in propagation of the hematoma). The risk of stent placement should, therefore, be weighed against the expectation of a favorable clinical outcome with conservative management. Besides, adjuvant imaging guidance and a long length or multiple stents are
4
usually needed to seal the whole length of the dissection in order to avoid shifting the hematoma. Surgical bypass is an alternative choice of therapy, especially when revascularization with PCI fails.2 There is currently limited evidence available from randomized trials to guide our therapy of patients in cardiogenic shock complicating acute myocardial infarction.5 Early revascularization remains the gold standard for treatment of these patients.6 Mechanical circulatory support, such as IABP, Impella (AbioMed, Danvers, MA, USA), Tandem Heart (TandemLife, Pittsburgh, PA, USA), or extracorporeal membrane oxygenation (ECMO), should be considered in cardiogenic shock patients who remain unstable despite revascularization and inotropic therapy. Although there is limited evidence available from randomized trials evaluating the different percutaneous support systems in treating cardiogenic shock complicating acute myocardial infarction, except for data demonstrating the relative ineffectiveness of IABP, there is growing evidence that shows these new mechanical circulatory support devices improve hemodynamic status, organ perfusion and, even, survival, especially early initiation.5,7 Based on recent studies, the Tandem Heart or Impella systems may be better first-line mechanical support devices compared to IABP. However, at this current institution, due to the inaccessibility of other percutaneous devices, ECMO is the preferred rescue device for patients who are still unstable after IABP combined with inotropic agent administration. Although previous data showed low rates of inhospital mortality and major cardiac adverse events (MACEs) in SCAD patients (5–10%), a significant proportion of patients had recurrent SCAD or MACEs following hospital discharge (up to 15% to 37% at 5 to 7 years).1 In addition to close follow-up and recommendations to avoid precipitating factors, current recommendations suggest long-term management with aspirin, beta-blocker, angiotensin-converting ace inhibitor (ACEI) and statins. Dedicated cardiac rehabilitation programs, inclusive of exercise, psychosocial counseling and peer group support, have also been shown to be safe and beneficial for SCAD patients.1 SCAD can be a life-threatening event. We reported an unusual case of SCAD in a young man with no
Perfusion 00(0)
known cardiovascular risk factors, which was likely to be precipitated by heavy lifting before a STEMI-related cardiac arrest. This case reminds clinicians to be aware of a possible SCAD diagnosis in such situations. In addition, the use of intravascular imaging is helpful in diagnosing SCAD where the diagnosis in question. Declaration of Conflicting Interests The authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
Funding The authors received no financial support for the research, authorship, and/or publication of this article.
References 1. Saw J, Mancini GB, Humphries KH. Contemporary review on spontaneous coronary artery dissection. J Am Coll Cardiol 2016; 68: 297–312. 2. Tweet MS, Hayes SN, Pitta SR, et al. Clinical features, management, and prognosis of spontaneous coronary artery dissection. Circulation 2012; 126: 579–588. 3. Eleid MF, Guddeti RR, Tweet MS, et al. Coronary artery tortuosity in spontaneous coronary artery dissection: angiographic characteristics and clinical implications. Circ Cardiovasc Interv 2014; 7: 656–662. 4. Tweet MS, Eleid MF, Best PJ, et al. Spontaneous coronary artery dissection: revascularization versus conservative therapy. Circ Cardiovasc Interv 2014; 7: 777–786. 5. Van Herck JL, Claeys MJ, De Paep R, Van Herck PL, Vrints CJ, Jorens PG. Management of cardiogenic shock complicating acute myocardial infarction. Eur Heart J Acute Cardiovasc Care 2015; 4: 278–297. 6. Windecker S, Kolh P, Alfonso F, et al. 2014 ESC/EACTS Guidelines on myocardial revascularization: The Task Force on Myocardial Revascularization of the European Society of Cardiology (ESC) and the European Association for Cardio-Thoracic Surgery (EACTS)Developed with the special contribution of the European Association of Percutaneous Cardiovascular Interventions (EAPCI). Eur Heart J 2014; 35: 2541–2619. 7. Basir MB, Schreiber TL, Grines CL, et al. Effect of early initiation of mechanical circulatory support on survival in cardiogenic shock. Am J Cardiol 2017; 119: 845–851.
