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Improved hemodynamics following endovascular treatment for acquired aortic coarctation: A case report
G Model
JCCASE-980; No. of Pages 3 Journal of Cardiology Cases xxx (2018) xxx–xxx
Contents lists available at ScienceDirect
Journal of Cardiology Cases journal homepage: www.elsevier.com/locate/jccase
Case Report
Improved hemodynamics following endovascular treatment for acquired aortic coarctation: A case report Takako Nagata (MD)a, Yuki Ikeda (MD PhD)a,*, Shunsuke Ishii (MD PhD)a, Jun Kishihara (MD PhD)a, Hirotoki Ohkubo (MD PhD)b, Toshiaki Mishima (MD PhD)b, Tadashi Kitamura (MD PhD)b, Kagami Miyaji (MD PhD)b, Junya Ako (MD PhD FJCC)a a b
Department of Cardiovascular Medicine, Kitasato University School of Medicine, Sagamihara, Kanagawa, Japan Department of Cardiovascular Surgery, Kitasato University School of Medicine, Sagamihara, Kanagawa, Japan
A R T I C L E I N F O
A B S T R A C T
Article history: Received 18 November 2017 Received in revised form 4 June 2018 Accepted 11 June 2018
A 38-year-old man underwent surgical repair of a type A aortic dissection. After aortic surgery, his left ventricular ejection fraction was progressively reduced from 65% to 15%, causing a refractory low cardiac output depending on the intravenous inotropes. There was a luminal stenosis of the descending aorta due to enlarged pseudolumen. The peak-to-peak pressure gradient at the stenosis was 25 mmHg, which was thought to contribute to the systolic dysfunction. He underwent thoracic endovascular aortic repair (TEVAR) with the use of a bare self-expanding stent. After TEVAR, the peak-to-peak pressure gradient was decreased to 9 mmHg, resulting in hemodynamic improvement. © 2018 Published by Elsevier Ltd on behalf of Japanese College of Cardiology.
Keywords: Aortic dissection Aortic coarctation Heart failure Interventional cardiology
Introduction
Case report
Aortic coarctation, in general, is a congenital heart disease that occurs as a focal stenosis of the aortic segment, particularly located in the area of the ductus arteriosus. Hypertension proximal to the stenosis accelerates cardiovascular complications [1]. Surgery or intra-aortic intervention is recommended as a primary treatment for aortic coarctation. We report a case of refractory heart failure with severe impairment of left ventricular contractility possibly aggravated by excessive left ventricular afterload due to a luminal stenosis in the descending aorta after surgical repair for type A aortic dissection. Endovascular treatment for dilation of the stenosis contributed to the improved hemodynamics.
A 38-year-old man with no history of cardiovascular disease was admitted with a diagnosis of type A aortic dissection. He had a normal left ventricular ejection fraction of 65% on transthoracic echocardiography. He underwent aortic replacement from the ascending aorta to the aortic arch using an artificial vessel. In this operation, cardiopulmonary bypass time was 252 min, and aortic cross clamping time was 136 min. After surgery, a severe luminal stenosis of the descending aorta with oppression by a residual false lumen was documented on computed tomography (Fig. 1A). After the primary surgery, there had been no event including heart failure during the first hospitalization. Two months after the aortic surgery, he was readmitted due to acute heart failure with cardiogenic shock. His left ventricular ejection fraction was reduced to 15% with diffusely impaired left ventricular contractility. He had a low cardiac output and a high pulmonary artery wedge pressure (Table 1). There was no substantial coronary stenosis or occlusion and no specific findings such as inflammatory cell infiltration on the endomyocardial biopsy. Despite the administration of intensive pharmacotherapy including intravenous diuretics, antineurohumoural agents, and
* Corresponding author at: Department of Cardiovascular Medicine, Kitasato University School of Medicine, 1-15-1 Kitasato, Minami-Ku, Sagamihara, Kanagawa 252-0374, Japan. E-mail address: [email protected] (Y. Ikeda).
https://doi.org/10.1016/j.jccase.2018.06.003 1878-5409/© 2018 Published by Elsevier Ltd on behalf of Japanese College of Cardiology.
Please cite this article in press as: Nagata T, et al. Improved hemodynamics following endovascular treatment for acquired aortic coarctation: A case report. J Cardiol Cases (2018), https://doi.org/10.1016/j.jccase.2018.06.003
G Model
JCCASE-980; No. of Pages 3 T. Nagata et al. / Journal of Cardiology Cases xxx (2018) xxx–xxx
2
Fig. 1.
Computed tomography and angiography before and after thoracic endovascular aortic repair (TEVAR). Severe true luminal stenosis of the descending aorta (arrow) with inward oppression by residual communicating (*) and non-communicating false lumen after surgical repair of type A aortic dissection (A). Severe true luminal stenosis of the descending aorta on angiography (B) and computed tomography (D) before TEVAR. Improved (arrowhead) and moderately remaining (**) true luminal stenosis of the descending aorta on angiography (C) and computed tomography (E) after TEVAR.
85 mmHg at the distal section), and the difference in blood pressure between the upper and lower limbs was also decreased to 3 mmHg (Figs. 1B–E and Figure 2; Table 1). Subsequently, his hemodynamic condition gradually improved, inotropic agents could be withdrawn, and he was discharged 6 months after TEVAR. His clinical parameters, including hemodynamic measurements, are presented in Table 1.
intravenous inotropes, his hemodynamic condition gradually deteriorated. We performed a transcatheter pressure measurement to assess the severity of the luminal stenosis of the descending aorta. The peak-to-peak pressure gradient at the stenosis in the true lumen was 25 mmHg (103 mmHg at the proximal section of the stenosis and 78 mmHg at the distal section). The significant step-up of pressure gradient was shown at the distal stenosis. The difference in blood pressure between the upper and lower limbs was 28 mmHg. We decided to perform thoracic endovascular aortic repair (TEVAR) using a bare self-expanding stent for dilation of the stenosis. We used Gore1 Tri-Lobe Balloon Catheter (W.L. Gore, USA) 16–34 mm–108 cm for pre-dilatation for the stenosis, then used Gore TAG1 (W.L. Gore, USA) 26–26 mm–15 cm as a stent graft. After TEVAR, the peak-to-peak pressure gradient decreased to 9 mmHg (94 mmHg at the proximal section of the stenosis and
Table 1
Discussion We report a patient with a severe true luminal stenosis of the descending aorta after surgical repair of a type A aortic dissection. We assumed that the luminal stenosis caused excessive left ventricular afterload, aggravating his heart failure and performed an intervention for dilation of this stenosis.
Clinical parameters.
Parameter
Baseline (at admission for AAD)
2 months (at readmission for HF)
4 months (before TEVAR)
5 months (after TEVAR)
10 months (at discharge)
Systolic blood pressure at upper limb (mmHg) Systolic blood pressure at lower limb (mmHg) BNP (pg/mL) Echocardiography LVEF (%) LVEDD (mm) LVESD (mm) LVPWth (mm) Cardiac catheterization CI (L/min/m2) PAWP (mmHg) Medications Dobutamine (mg/kg/min) Dopamine (mg/kg/min) Norepinephrine (mg/kg/min) Milrinone (mg/kg/min) Carvedilol (mg/day) Perindopril (mg/day) Spironolactone (mg/day) Loop diuretic (oral furosemide equivalent, mg/day)
134 N/A 18.6
99 73 810
99 71 1129
94 91 931
89 89 543
65 57 42 8
15 67 61 8
18 63 59 8
13 68 63 10
13 69 63 9
N/A N/A
1.3 39
2.0 27
2.2 21
N/A N/A
0 0 0 0 0 0 0 0
5 8 0 0 1.25 1 50 60
5 0 0.6 0.5 1.25 1 100 20
3 0 0 0.5 2.5 2 100 40
0 0 0 0 25 2 100 60
AAD, type A aortic dissection; HF, heart failure; TEVAR, thoracic endovascular aortic repair; BNP, B-type natriuretic peptide; LVEF, left ventricular ejection fraction; LVEDD, left ventricular end-diastolic dimension; LVESD, left ventricular end-systolic dimension; LVPWth, left ventricular posterior wall thickness; CI, cardiac index; PAWP, pulmonary artery wedge pressure; N/A, not available.
Please cite this article in press as: Nagata T, et al. Improved hemodynamics following endovascular treatment for acquired aortic coarctation: A case report. J Cardiol Cases (2018), https://doi.org/10.1016/j.jccase.2018.06.003
G Model
JCCASE-980; No. of Pages 3 T. Nagata et al. / Journal of Cardiology Cases xxx (2018) xxx–xxx
Fig. 2.
3
Transcatheter pressure measurement before and after thoracic endovascular aortic repair (TEVAR). Aortic pressure at the proximal section of the stenosis (A) and at the distal section (B) before TEVAR. Aortic pressure at the proximal section of the stenosis (C) and at the distal section (D) after TEVAR.
In the current guidelines of the European Society of Cardiology, interventional treatment is recommended for adults with aortic coarctation (Class I) with a pressure difference >20 mmHg between the upper and lower limbs, those with upper limb hypertension (>140/90 mmHg), those with abnormal blood pressure response during exercise, or those with substantial left ventricular hypertrophy [2]. Patients with >50% aortic narrowing relative to aortic diameter at the diaphragm level (Class IIa) are also considered for interventional treatment [2]. The American College of Cardiology/American Heart Association guidelines recommend an interventional treatment for patients with a peak-to-peak pressure gradient at coarctation >20 mmHg, or a peak-to-peak pressure gradient <20 mmHg in the case of anatomic evidence of substantial coarctation and radiological evidence of substantial collateral flow (Class I) [3]. In a previous report, patients with peakto-peak pressure gradient >10 mmHg had a 5-year survival rate of 50%, whereas patients with a peak-to-peak pressure gradient <10 mmHg had a 5-year survival rate >90% [4]. We intervened in the present case for aortic coarctation on the basis of these guidelines [2,3]. In our patient, the peak-to-peak pressure gradient decreased from 25 to 9 mmHg after TEVAR, and his hemodynamic condition was substantially improved after withdrawal of intravenous inotropes. Considering the hemodynamic determinants between left ventricular and arterial performance, excessive left ventricular afterload has been represented as ventriculo-arterial decoupling as an elevated ratio of arterial elastance (Ea) to left ventricular elastance (Ees) [5]. In the present case, Ea decreased from 2.9 to 1.9 mmHg/mL and Ees remained unchanged at 0.5 mmHg/mL after TEVAR. Ventriculo-arterial decoupling was substantially improved, but remained moderately high, after TEVAR (Ea/Ees = 2.9/ 0.5 = 5.8 before TEVAR and 1.9/0.5 = 3.8 after TEVAR). Despite hemodynamic improvement after the interventional treatment, there were residual concerns in the present case. Left ventricular contractility remained relatively low, and cardiac output was also low. This might cause underestimation of the severity of the stenosis, as often seen in low-flow/low-gradient aortic valve stenosis [6]. Indeed, there was a residual stenosis on angiography after TEVAR (Fig. 1C). To measure the severity of stenosis accurately, other tests such as stress tests using
intravenous dobutamine should be considered for decision of additive intervention. In addition, the cause of the luminal stenosis of the descending aorta was not clear. Computed tomography after the primary surgery showed the severe true luminal stenosis of the descending aorta with inward oppression by residual communicating and non-communicating false lumen. There was a possible mechanism that aortic shrink of the distal site of the graft might be caused after the elephant trunk installation. Moreover, it is necessary to consider other perioperative factors that could have caused left ventricular dysfunction, including myocardial ischemia/reperfusion injury during the operation for type A aortic dissection [7]. Conflict of interest None declared. References [1] Campbell M. Natural history of coarctation of the aorta. Br Heart J 1970;32:633– 40. [2] Erbel R, Aboyans V, Boileau C, Bossone E, Bartolomeo RD, Eggebrecht H, et al. 2014 ESC guidelines on the diagnosis and treatment of aortic diseases: document covering acute and chronic aortic diseases of the thoracic and abdominal aorta of the adult. The task force for the diagnosis and treatment of aortic diseases of the European Society of Cardiology (ESC). Eur Heart J 2014;35:2873– 926. [3] Warnes CA, Williams RG, Bashore TM, Child JS, Connolly HM, Dearani JA, et al. ACC/AHA 2008 guidelines for the management of adults with congenital heart disease: a report of the American College of Cardiology/American Heart Association Task Force on practice guidelines (writing committee to develop guidelines on the management of adults with congenital heart disease). Circulation 2008;118:e714–833. [4] Zabal C, Attie F, Rosas M, Buendı´a-Herna´ndez A, Garcı´a-Montes JA. The adult patient with native coarctation of the aorta: balloon angioplasty or primary stenting? Heart 2003;89:77–83. [5] Chen CH, Fetics B, Nevo E, Rochitte CE, Chiou KR, Ding PA, et al. Noninvasive single-beat determination of left ventricular end-systolic elastance in humans. J Am Coll Cardiol 2001;38:2028–34. [6] Clavel MA, Ennezat PV, Mare´chaux S, Dumesnil JG, Capoulade R, Hachicha Z, et al. Stress echocardiography to assess stenosis severity and predict outcome in patients with paradoxical low-flow, low-gradient aortic stenosis and preserved LVEF. JACC Cardiovasc Imaging 2013;6:175–83. [7] Mangano DT. Perioperative cardiac morbidity. Anesthesiology 1990;72:153– 84.
Please cite this article in press as: Nagata T, et al. Improved hemodynamics following endovascular treatment for acquired aortic coarctation: A case report. J Cardiol Cases (2018), https://doi.org/10.1016/j.jccase.2018.06.003
JCCASE-980; No. of Pages 3 Journal of Cardiology Cases xxx (2018) xxx–xxx
Contents lists available at ScienceDirect
Journal of Cardiology Cases journal homepage: www.elsevier.com/locate/jccase
Case Report
Improved hemodynamics following endovascular treatment for acquired aortic coarctation: A case report Takako Nagata (MD)a, Yuki Ikeda (MD PhD)a,*, Shunsuke Ishii (MD PhD)a, Jun Kishihara (MD PhD)a, Hirotoki Ohkubo (MD PhD)b, Toshiaki Mishima (MD PhD)b, Tadashi Kitamura (MD PhD)b, Kagami Miyaji (MD PhD)b, Junya Ako (MD PhD FJCC)a a b
Department of Cardiovascular Medicine, Kitasato University School of Medicine, Sagamihara, Kanagawa, Japan Department of Cardiovascular Surgery, Kitasato University School of Medicine, Sagamihara, Kanagawa, Japan
A R T I C L E I N F O
A B S T R A C T
Article history: Received 18 November 2017 Received in revised form 4 June 2018 Accepted 11 June 2018
A 38-year-old man underwent surgical repair of a type A aortic dissection. After aortic surgery, his left ventricular ejection fraction was progressively reduced from 65% to 15%, causing a refractory low cardiac output depending on the intravenous inotropes. There was a luminal stenosis of the descending aorta due to enlarged pseudolumen. The peak-to-peak pressure gradient at the stenosis was 25 mmHg, which was thought to contribute to the systolic dysfunction. He underwent thoracic endovascular aortic repair (TEVAR) with the use of a bare self-expanding stent. After TEVAR, the peak-to-peak pressure gradient was decreased to 9 mmHg, resulting in hemodynamic improvement.
Keywords: Aortic dissection Aortic coarctation Heart failure Interventional cardiology
Introduction
Case report
Aortic coarctation, in general, is a congenital heart disease that occurs as a focal stenosis of the aortic segment, particularly located in the area of the ductus arteriosus. Hypertension proximal to the stenosis accelerates cardiovascular complications [1]. Surgery or intra-aortic intervention is recommended as a primary treatment for aortic coarctation. We report a case of refractory heart failure with severe impairment of left ventricular contractility possibly aggravated by excessive left ventricular afterload due to a luminal stenosis in the descending aorta after surgical repair for type A aortic dissection. Endovascular treatment for dilation of the stenosis contributed to the improved hemodynamics.
A 38-year-old man with no history of cardiovascular disease was admitted with a diagnosis of type A aortic dissection. He had a normal left ventricular ejection fraction of 65% on transthoracic echocardiography. He underwent aortic replacement from the ascending aorta to the aortic arch using an artificial vessel. In this operation, cardiopulmonary bypass time was 252 min, and aortic cross clamping time was 136 min. After surgery, a severe luminal stenosis of the descending aorta with oppression by a residual false lumen was documented on computed tomography (Fig. 1A). After the primary surgery, there had been no event including heart failure during the first hospitalization. Two months after the aortic surgery, he was readmitted due to acute heart failure with cardiogenic shock. His left ventricular ejection fraction was reduced to 15% with diffusely impaired left ventricular contractility. He had a low cardiac output and a high pulmonary artery wedge pressure (Table 1). There was no substantial coronary stenosis or occlusion and no specific findings such as inflammatory cell infiltration on the endomyocardial biopsy. Despite the administration of intensive pharmacotherapy including intravenous diuretics, antineurohumoural agents, and
* Corresponding author at: Department of Cardiovascular Medicine, Kitasato University School of Medicine, 1-15-1 Kitasato, Minami-Ku, Sagamihara, Kanagawa 252-0374, Japan. E-mail address: [email protected] (Y. Ikeda).
https://doi.org/10.1016/j.jccase.2018.06.003 1878-5409/© 2018 Published by Elsevier Ltd on behalf of Japanese College of Cardiology.
Please cite this article in press as: Nagata T, et al. Improved hemodynamics following endovascular treatment for acquired aortic coarctation: A case report. J Cardiol Cases (2018), https://doi.org/10.1016/j.jccase.2018.06.003
G Model
JCCASE-980; No. of Pages 3 T. Nagata et al. / Journal of Cardiology Cases xxx (2018) xxx–xxx
2
Fig. 1.
Computed tomography and angiography before and after thoracic endovascular aortic repair (TEVAR). Severe true luminal stenosis of the descending aorta (arrow) with inward oppression by residual communicating (*) and non-communicating false lumen after surgical repair of type A aortic dissection (A). Severe true luminal stenosis of the descending aorta on angiography (B) and computed tomography (D) before TEVAR. Improved (arrowhead) and moderately remaining (**) true luminal stenosis of the descending aorta on angiography (C) and computed tomography (E) after TEVAR.
85 mmHg at the distal section), and the difference in blood pressure between the upper and lower limbs was also decreased to 3 mmHg (Figs. 1B–E and Figure 2; Table 1). Subsequently, his hemodynamic condition gradually improved, inotropic agents could be withdrawn, and he was discharged 6 months after TEVAR. His clinical parameters, including hemodynamic measurements, are presented in Table 1.
intravenous inotropes, his hemodynamic condition gradually deteriorated. We performed a transcatheter pressure measurement to assess the severity of the luminal stenosis of the descending aorta. The peak-to-peak pressure gradient at the stenosis in the true lumen was 25 mmHg (103 mmHg at the proximal section of the stenosis and 78 mmHg at the distal section). The significant step-up of pressure gradient was shown at the distal stenosis. The difference in blood pressure between the upper and lower limbs was 28 mmHg. We decided to perform thoracic endovascular aortic repair (TEVAR) using a bare self-expanding stent for dilation of the stenosis. We used Gore1 Tri-Lobe Balloon Catheter (W.L. Gore, USA) 16–34 mm–108 cm for pre-dilatation for the stenosis, then used Gore TAG1 (W.L. Gore, USA) 26–26 mm–15 cm as a stent graft. After TEVAR, the peak-to-peak pressure gradient decreased to 9 mmHg (94 mmHg at the proximal section of the stenosis and
Table 1
Discussion We report a patient with a severe true luminal stenosis of the descending aorta after surgical repair of a type A aortic dissection. We assumed that the luminal stenosis caused excessive left ventricular afterload, aggravating his heart failure and performed an intervention for dilation of this stenosis.
Clinical parameters.
Parameter
Baseline (at admission for AAD)
2 months (at readmission for HF)
4 months (before TEVAR)
5 months (after TEVAR)
10 months (at discharge)
Systolic blood pressure at upper limb (mmHg) Systolic blood pressure at lower limb (mmHg) BNP (pg/mL) Echocardiography LVEF (%) LVEDD (mm) LVESD (mm) LVPWth (mm) Cardiac catheterization CI (L/min/m2) PAWP (mmHg) Medications Dobutamine (mg/kg/min) Dopamine (mg/kg/min) Norepinephrine (mg/kg/min) Milrinone (mg/kg/min) Carvedilol (mg/day) Perindopril (mg/day) Spironolactone (mg/day) Loop diuretic (oral furosemide equivalent, mg/day)
134 N/A 18.6
99 73 810
99 71 1129
94 91 931
89 89 543
65 57 42 8
15 67 61 8
18 63 59 8
13 68 63 10
13 69 63 9
N/A N/A
1.3 39
2.0 27
2.2 21
N/A N/A
0 0 0 0 0 0 0 0
5 8 0 0 1.25 1 50 60
5 0 0.6 0.5 1.25 1 100 20
3 0 0 0.5 2.5 2 100 40
0 0 0 0 25 2 100 60
AAD, type A aortic dissection; HF, heart failure; TEVAR, thoracic endovascular aortic repair; BNP, B-type natriuretic peptide; LVEF, left ventricular ejection fraction; LVEDD, left ventricular end-diastolic dimension; LVESD, left ventricular end-systolic dimension; LVPWth, left ventricular posterior wall thickness; CI, cardiac index; PAWP, pulmonary artery wedge pressure; N/A, not available.
Please cite this article in press as: Nagata T, et al. Improved hemodynamics following endovascular treatment for acquired aortic coarctation: A case report. J Cardiol Cases (2018), https://doi.org/10.1016/j.jccase.2018.06.003
G Model
JCCASE-980; No. of Pages 3 T. Nagata et al. / Journal of Cardiology Cases xxx (2018) xxx–xxx
Fig. 2.
3
Transcatheter pressure measurement before and after thoracic endovascular aortic repair (TEVAR). Aortic pressure at the proximal section of the stenosis (A) and at the distal section (B) before TEVAR. Aortic pressure at the proximal section of the stenosis (C) and at the distal section (D) after TEVAR.
In the current guidelines of the European Society of Cardiology, interventional treatment is recommended for adults with aortic coarctation (Class I) with a pressure difference >20 mmHg between the upper and lower limbs, those with upper limb hypertension (>140/90 mmHg), those with abnormal blood pressure response during exercise, or those with substantial left ventricular hypertrophy [2]. Patients with >50% aortic narrowing relative to aortic diameter at the diaphragm level (Class IIa) are also considered for interventional treatment [2]. The American College of Cardiology/American Heart Association guidelines recommend an interventional treatment for patients with a peak-to-peak pressure gradient at coarctation >20 mmHg, or a peak-to-peak pressure gradient <20 mmHg in the case of anatomic evidence of substantial coarctation and radiological evidence of substantial collateral flow (Class I) [3]. In a previous report, patients with peakto-peak pressure gradient >10 mmHg had a 5-year survival rate of 50%, whereas patients with a peak-to-peak pressure gradient <10 mmHg had a 5-year survival rate >90% [4]. We intervened in the present case for aortic coarctation on the basis of these guidelines [2,3]. In our patient, the peak-to-peak pressure gradient decreased from 25 to 9 mmHg after TEVAR, and his hemodynamic condition was substantially improved after withdrawal of intravenous inotropes. Considering the hemodynamic determinants between left ventricular and arterial performance, excessive left ventricular afterload has been represented as ventriculo-arterial decoupling as an elevated ratio of arterial elastance (Ea) to left ventricular elastance (Ees) [5]. In the present case, Ea decreased from 2.9 to 1.9 mmHg/mL and Ees remained unchanged at 0.5 mmHg/mL after TEVAR. Ventriculo-arterial decoupling was substantially improved, but remained moderately high, after TEVAR (Ea/Ees = 2.9/ 0.5 = 5.8 before TEVAR and 1.9/0.5 = 3.8 after TEVAR). Despite hemodynamic improvement after the interventional treatment, there were residual concerns in the present case. Left ventricular contractility remained relatively low, and cardiac output was also low. This might cause underestimation of the severity of the stenosis, as often seen in low-flow/low-gradient aortic valve stenosis [6]. Indeed, there was a residual stenosis on angiography after TEVAR (Fig. 1C). To measure the severity of stenosis accurately, other tests such as stress tests using
intravenous dobutamine should be considered for decision of additive intervention. In addition, the cause of the luminal stenosis of the descending aorta was not clear. Computed tomography after the primary surgery showed the severe true luminal stenosis of the descending aorta with inward oppression by residual communicating and non-communicating false lumen. There was a possible mechanism that aortic shrink of the distal site of the graft might be caused after the elephant trunk installation. Moreover, it is necessary to consider other perioperative factors that could have caused left ventricular dysfunction, including myocardial ischemia/reperfusion injury during the operation for type A aortic dissection [7]. Conflict of interest None declared. References [1] Campbell M. Natural history of coarctation of the aorta. Br Heart J 1970;32:633– 40. [2] Erbel R, Aboyans V, Boileau C, Bossone E, Bartolomeo RD, Eggebrecht H, et al. 2014 ESC guidelines on the diagnosis and treatment of aortic diseases: document covering acute and chronic aortic diseases of the thoracic and abdominal aorta of the adult. The task force for the diagnosis and treatment of aortic diseases of the European Society of Cardiology (ESC). Eur Heart J 2014;35:2873– 926. [3] Warnes CA, Williams RG, Bashore TM, Child JS, Connolly HM, Dearani JA, et al. ACC/AHA 2008 guidelines for the management of adults with congenital heart disease: a report of the American College of Cardiology/American Heart Association Task Force on practice guidelines (writing committee to develop guidelines on the management of adults with congenital heart disease). Circulation 2008;118:e714–833. [4] Zabal C, Attie F, Rosas M, Buendı´a-Herna´ndez A, Garcı´a-Montes JA. The adult patient with native coarctation of the aorta: balloon angioplasty or primary stenting? Heart 2003;89:77–83. [5] Chen CH, Fetics B, Nevo E, Rochitte CE, Chiou KR, Ding PA, et al. Noninvasive single-beat determination of left ventricular end-systolic elastance in humans. J Am Coll Cardiol 2001;38:2028–34. [6] Clavel MA, Ennezat PV, Mare´chaux S, Dumesnil JG, Capoulade R, Hachicha Z, et al. Stress echocardiography to assess stenosis severity and predict outcome in patients with paradoxical low-flow, low-gradient aortic stenosis and preserved LVEF. JACC Cardiovasc Imaging 2013;6:175–83. [7] Mangano DT. Perioperative cardiac morbidity. Anesthesiology 1990;72:153– 84.
Please cite this article in press as: Nagata T, et al. Improved hemodynamics following endovascular treatment for acquired aortic coarctation: A case report. J Cardiol Cases (2018), https://doi.org/10.1016/j.jccase.2018.06.003