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Cardioembolism and takotsubo syndrome: A case report
Cardioembolism and takotsubo syndrome: A case report Federico Guerra, Simone Maffei, Alessandro Maolo, Daniele Contadini, Alessandro Capucci PII: DOI: Reference:
S0167-5273(16)30394-1 doi: 10.1016/j.ijcard.2016.02.153 IJCA 22122
To appear in:
International Journal of Cardiology
Received date: Accepted date:
30 January 2016 29 February 2016
Please cite this article as: Guerra Federico, Maffei Simone, Maolo Alessandro, Contadini Daniele, Capucci Alessandro, Cardioembolism and takotsubo syndrome: A case report, International Journal of Cardiology (2016), doi: 10.1016/j.ijcard.2016.02.153
This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.
ACCEPTED MANUSCRIPT Title: Cardioembolism and takotsubo syndrome: a case report.
Authors: Federico Guerra M.D.1, Simone Maffei M.D.1, Alessandro Maolo M.D.1, Daniele
IP
1
Cardiology and Arrhythmology Clinic, Ospedali Riuniti “Umberto I-Lancisi-Salesi”,
SC R
Institutions:
T
Contadini M.D.1, Alessandro Capucci M.D.1.
NU
Marche Polytechnic University, Ancona, Italy.
Corresponding author:
MA
Federico Guerra M.D., Cardiology and Arrhythmology Clinic, Marche Polytechnic University, Ospedali Riuniti “Umberto I-Lancisi-Salesi”, Via Conca 71, Ancona, Italy.
TE
D
Phone +390715966593, Fax +390715965624, E-mail: [email protected]
CE P
Financial support: This work was supported by the Marche Polytechnic University.
Keywords: Takotsubo cardiomyopathy; thromboembolism; stroke; atrial fibrillation; acute coronary
AC
syndrome; anticoagulants.
1
ACCEPTED MANUSCRIPT Case report A 79-year-old woman was referred to the emergency department for acute pain to the left arm, associated with mild chest pain and dyspnea.
T
The medical history included arterial systemic hypertension, type 2 diabetes mellitus, and
IP
dyslipidemia as cardiovascular risk factors. A previous episode of persistent atrial fibrillation
SC R
occurred 4 years earlier, when electrical cardioversion was performed.
The patient was under medical therapy with apixaban 5 mg b.i.d., olmesartan 40 mg o.d.,
NU
bisoprolol 2,5 mg o.d., amlodipine 5 mg o.d., and simvastatin 40 mg o.d. Vital signs at ED admission were stable: body temperature 36°C; heart rate 100 bpm; arterial
MA
blood pressure 120/80 mmHg; respiratory rate 20 breaths per minutes; oxygen saturation 88%. The cardiac physical examination was unremarkable. The patient showed a regular rhythm with no
D
murmurs, rubs or gallops. Pulmonary rales were present in every segment of both lungs. No
TE
peripheral edema was present. The neurological examination was normal, showing no sensory or
CE P
motor impairment. While drawing blood samples for the blood gas analysis, the absence of left arterial radial pulse was perceived.
The routine laboratory tests at ED admission were normal, with the notable exceptions of high-
AC
sensitivity troponin I: (0.24 ng/ml) and BNP (361 pg/ml). A 12-lead ECG confirmed a sinus rhythm with normal atrioventricular and interventricular conduction, biphasic T waves in V2-V3 and negative T-waves in DI, DII, aVL, aVF, and V4-V6. A long QTc (580 ms) was also recorded (Figure 1). To exclude an acute aortic dissection, which could have explained the acute left arm and chest pain, the absence of left brachial and radial pulses and the mild troponin I increase, a chest CTscan was performed, which showed no obvious signs of aortic dissection or intramural hematoma. No signs of pulmonary embolism were also reported. During the CT-scan, the patient developed a sharp increase of the chest and left arm pain, along with worsening dyspnea and spatiotemporal disorientation. Laboratory tests showed a further 2
ACCEPTED MANUSCRIPT increase of high-sensitivity troponin I (2.37 ng/ml) and a chest X-ray confirmed the pulmonary edema clinical signs. An echocardiography was performed, showing a left ventricle of normal size with a severe
T
reduction of global systolic function and a left ventricular ejection fraction of 25%. Akinesia of the
IP
medium-apical segments with hyperkinesia of the constrictors muscles was also noted, resulting in
SC R
a ballooning aspect of the left ventricle raising the suspicion of takotsubo cardiomyopathy. Right heart chambers were normal while left atrium was mildly enlarged, with no significant valvular
NU
impairment.
The patient was initially stabilized with i.v. diuretics, i.v. nitrates and continuous positive airway
MA
pressure ventilation. After 60 minutes from admission, a coronary catheterization was performed, showing only a non-significant lesion in the proximal left anterior descending artery, with no
D
thrombus or signs of plaque rupture.
TE
The patient was then hospitalized with the diagnosis of “takotsubo cardiomyopathy complicated by
CE P
pulmonary edema”. During the subsequent hours, the patient's conditions improved, with the notable exception of recurrent episodes of left arm pain, even if less intense. Despite the recent chest CT-scan did not report any sign of peripheral embolization, an echocolorDoppler
AC
ultrasonography was requested. The echography showed the occlusion of left axillary artery suggestive for arterial embolism, which was treated with percutaneous revascularization. Atrial fibrillation episodes were not recorded on continuous ECG-monitoring during hospitalization. Considering the previous history of atrial fibrillation, the reported poor compliance to apixaban by the close relatives, and the high thromboembolic risk (CHA2DS2-VASc=5), a trans-esophageal echocardiogram was performed, which documented the presence of thrombotic material in the left atrial appendage. A neurologist diagnosed a mild cognitive deterioration, confirmed by a subsequent brain CT-scan that highlighted multiple previous ischemic lesions, and prescribed a low dose of acetylsalicylic
3
ACCEPTED MANUSCRIPT acid on top of apixaban, which was in turn switched to once-daily rivaroxaban in order to improve the patient’s compliance. At discharge, the patient was asymptomatic and presented a complete recovery of systolic
T
function. T-wave alterations did almost recover (Figure 3) and only QTc interval persisted
IP
moderately prolonged (480 ms).
SC R
Diagnosis at discharge was: “takotsubo cardiomyopathy triggered by axillary artery embolism and complicated by pulmonary edema in patient with a previous history of atrial fibrillation.”
NU
Discussion
In our knowledge, this is the first case report demonstrating how an acute physical trigger due to
MA
arterial peripheral embolization could start takotsubo cardiomyopathy, and beget a life-threatening complication such as pulmonary edema. In this case, the diagnosis has been complicated by the
D
peripheral embolus location at the left axillary artery level which produced symptoms similar to a
TE
typical chest pain irradiation, and by the chest CT-scan which did not report any unusual findings.
CE P
The diagnosis of acute coronary syndrome was, in fact, the first to be excluded, since, along with many characteristics mimicking an acute coronary syndrome, it has recently been shown that patients with takotsubo cardiomyopathy have a relevant prevalence of cardiovascular risk factors,
[2,3]
AC
[1] and that acute ischemic injury can in some cases directly trigger takotsubo cardiomyopathy.
Despite many clues of takotsubo were present, such as the typical echo presentation, coronary angiography is so far the only reliable tool to confirm the diagnosis and exclude an acute coronary syndrome.[4,5] The 12-lead ECG at admission, while providing some important and validated diagnostic and prognostic clues [6] such diffuse inverted T-waves and a long QTc, is not enough to safely rule out other more common causes of chest pain. Regarding the multiple cardioembolic events, the patient’s close relatives declared a poor compliance to the prescribed therapy in the past few months. This included missing many doses of apixaban which could have exposed the patient to her high thromboembolic risk (CHA2DS24
ACCEPTED MANUSCRIPT VASc=5) and further worsen cognitive impairment. In order to reduce the number of pills taken daily by geriatric patients, and thus improve their compliance, a once-daily oral anticoagulant may be preferred, as it was lately in this case. The lack of atrial fibrillation episodes during the in-
T
hospital ECG-monitoring did not rule out this hypothesis since subclinical atrial tachyarrhythmias
IP
have been demonstrated to be associated with a significantly increased risk of ischemic stroke or
AC
CE P
TE
D
MA
NU
SC R
systemic embolism.[7]
5
ACCEPTED MANUSCRIPT References [1]
Pelliccia F, Parodi G, Greco C, Antoniucci D, Brenner R, Bossone E, et al. Comorbidities Frequency in Takotsubo Syndrome: An International Collaborative Systematic Review
Nakagawa N, Fukawa N, Tsuji K, Nakano N, Kato A. Takotsubo cardiomyopathy induced by
IP
[2]
T
Including 1,109 Patients. Am J Med 2015;128:654.e11–654.e19.
[3]
SC R
dopamine infusion after carotid artery stenting. Int J Cardiol 2016;205:62–4. Messas N, Caspar T, Jesel L, Hess S, Girardey M, Radulescu B, et al. Takotsubo
NU
cardiomyopathy triggered by ischemic injury: When lateralmyocardial infarction precipitate apical ballooning syndrome. Int J Cardiol 2016;202:858–60. Guerra F, Rrapaj E, Pongetti G, Fabbrizioli A, Pelizzoni V, Giannini I, et al. Differences and
MA
[4]
similarities of repolarization patterns during hospitalization for Takotsubo cardiomyopathy
Looi JL, Wong CW, Lee M, Khan A, Webster M, Kerr AJ. Usefulness of ECG to differentiate
TE
[5]
D
and acute coronary syndrome. Am J Cardiol 2013;112:1720–4.
[6]
CE P
Takotsubo cardiomyopathy from acute coronary syndrome. Int J Cardiol 2015;199:132–40. Guerra F, Giannini I, Pongetti G, Fabbrizioli A, Rrapaj E, Aschieri D, et al. Transient QRS amplitude attenuation is associated with clinical recovery in patients with takotsubo
[7]
AC
cardiomyopathy. Int J Cardiol 2015;187:198–205. Healey JS, Connolly SJ, Gold MR, Israel CW, Van Gelder IC, Capucci A, et al. Subclinical atrial fibrillation and the risk of stroke. N Engl J Med 2012;366:120–9.
6
ACCEPTED MANUSCRIPT Figure legends Figure 1. Twelve-lead ECG at admission.Twelve-lead ECG at admission, showing sinus rhythm (95 bpm) with normal atrioventricular and interventricular conduction, biphasic T waves in V2-V3
AC
CE P
TE
D
MA
NU
SC R
IP
T
and negative T-waves in DI, DII, aVL, aVF, and V4-V6. A long QTc (580 ms) was also recorded.
Figure 2. Four-chamber view, showing the typical ballooning aspect of left ventricle.An akinesia of the medium-apical segments with hyperkinesia of the constrictors muscles was evident, resulting in the typical ballooning aspect of the left ventricle associated with takotsubo cardiomyopathy.
7
CE P
TE
D
MA
NU
SC R
IP
T
ACCEPTED MANUSCRIPT
AC
Figure 3. Twelve-lead ECG at discharge.Twelve-lead ECG at discharge, showing sinus rhythm (80 bpm) with normal atrioventricular and interventricular conduction, flat T-waves in all limb leads and small negative T-waves in V4-V6. QTc interval persisted as moderately increased (480 ms).
8
AC
CE P
TE
D
MA
NU
SC R
IP
T
ACCEPTED MANUSCRIPT
9
S0167-5273(16)30394-1 doi: 10.1016/j.ijcard.2016.02.153 IJCA 22122
To appear in:
International Journal of Cardiology
Received date: Accepted date:
30 January 2016 29 February 2016
Please cite this article as: Guerra Federico, Maffei Simone, Maolo Alessandro, Contadini Daniele, Capucci Alessandro, Cardioembolism and takotsubo syndrome: A case report, International Journal of Cardiology (2016), doi: 10.1016/j.ijcard.2016.02.153
This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.
ACCEPTED MANUSCRIPT Title: Cardioembolism and takotsubo syndrome: a case report.
Authors: Federico Guerra M.D.1, Simone Maffei M.D.1, Alessandro Maolo M.D.1, Daniele
IP
1
Cardiology and Arrhythmology Clinic, Ospedali Riuniti “Umberto I-Lancisi-Salesi”,
SC R
Institutions:
T
Contadini M.D.1, Alessandro Capucci M.D.1.
NU
Marche Polytechnic University, Ancona, Italy.
Corresponding author:
MA
Federico Guerra M.D., Cardiology and Arrhythmology Clinic, Marche Polytechnic University, Ospedali Riuniti “Umberto I-Lancisi-Salesi”, Via Conca 71, Ancona, Italy.
TE
D
Phone +390715966593, Fax +390715965624, E-mail: [email protected]
CE P
Financial support: This work was supported by the Marche Polytechnic University.
Keywords: Takotsubo cardiomyopathy; thromboembolism; stroke; atrial fibrillation; acute coronary
AC
syndrome; anticoagulants.
1
ACCEPTED MANUSCRIPT Case report A 79-year-old woman was referred to the emergency department for acute pain to the left arm, associated with mild chest pain and dyspnea.
T
The medical history included arterial systemic hypertension, type 2 diabetes mellitus, and
IP
dyslipidemia as cardiovascular risk factors. A previous episode of persistent atrial fibrillation
SC R
occurred 4 years earlier, when electrical cardioversion was performed.
The patient was under medical therapy with apixaban 5 mg b.i.d., olmesartan 40 mg o.d.,
NU
bisoprolol 2,5 mg o.d., amlodipine 5 mg o.d., and simvastatin 40 mg o.d. Vital signs at ED admission were stable: body temperature 36°C; heart rate 100 bpm; arterial
MA
blood pressure 120/80 mmHg; respiratory rate 20 breaths per minutes; oxygen saturation 88%. The cardiac physical examination was unremarkable. The patient showed a regular rhythm with no
D
murmurs, rubs or gallops. Pulmonary rales were present in every segment of both lungs. No
TE
peripheral edema was present. The neurological examination was normal, showing no sensory or
CE P
motor impairment. While drawing blood samples for the blood gas analysis, the absence of left arterial radial pulse was perceived.
The routine laboratory tests at ED admission were normal, with the notable exceptions of high-
AC
sensitivity troponin I: (0.24 ng/ml) and BNP (361 pg/ml). A 12-lead ECG confirmed a sinus rhythm with normal atrioventricular and interventricular conduction, biphasic T waves in V2-V3 and negative T-waves in DI, DII, aVL, aVF, and V4-V6. A long QTc (580 ms) was also recorded (Figure 1). To exclude an acute aortic dissection, which could have explained the acute left arm and chest pain, the absence of left brachial and radial pulses and the mild troponin I increase, a chest CTscan was performed, which showed no obvious signs of aortic dissection or intramural hematoma. No signs of pulmonary embolism were also reported. During the CT-scan, the patient developed a sharp increase of the chest and left arm pain, along with worsening dyspnea and spatiotemporal disorientation. Laboratory tests showed a further 2
ACCEPTED MANUSCRIPT increase of high-sensitivity troponin I (2.37 ng/ml) and a chest X-ray confirmed the pulmonary edema clinical signs. An echocardiography was performed, showing a left ventricle of normal size with a severe
T
reduction of global systolic function and a left ventricular ejection fraction of 25%. Akinesia of the
IP
medium-apical segments with hyperkinesia of the constrictors muscles was also noted, resulting in
SC R
a ballooning aspect of the left ventricle raising the suspicion of takotsubo cardiomyopathy. Right heart chambers were normal while left atrium was mildly enlarged, with no significant valvular
NU
impairment.
The patient was initially stabilized with i.v. diuretics, i.v. nitrates and continuous positive airway
MA
pressure ventilation. After 60 minutes from admission, a coronary catheterization was performed, showing only a non-significant lesion in the proximal left anterior descending artery, with no
D
thrombus or signs of plaque rupture.
TE
The patient was then hospitalized with the diagnosis of “takotsubo cardiomyopathy complicated by
CE P
pulmonary edema”. During the subsequent hours, the patient's conditions improved, with the notable exception of recurrent episodes of left arm pain, even if less intense. Despite the recent chest CT-scan did not report any sign of peripheral embolization, an echocolorDoppler
AC
ultrasonography was requested. The echography showed the occlusion of left axillary artery suggestive for arterial embolism, which was treated with percutaneous revascularization. Atrial fibrillation episodes were not recorded on continuous ECG-monitoring during hospitalization. Considering the previous history of atrial fibrillation, the reported poor compliance to apixaban by the close relatives, and the high thromboembolic risk (CHA2DS2-VASc=5), a trans-esophageal echocardiogram was performed, which documented the presence of thrombotic material in the left atrial appendage. A neurologist diagnosed a mild cognitive deterioration, confirmed by a subsequent brain CT-scan that highlighted multiple previous ischemic lesions, and prescribed a low dose of acetylsalicylic
3
ACCEPTED MANUSCRIPT acid on top of apixaban, which was in turn switched to once-daily rivaroxaban in order to improve the patient’s compliance. At discharge, the patient was asymptomatic and presented a complete recovery of systolic
T
function. T-wave alterations did almost recover (Figure 3) and only QTc interval persisted
IP
moderately prolonged (480 ms).
SC R
Diagnosis at discharge was: “takotsubo cardiomyopathy triggered by axillary artery embolism and complicated by pulmonary edema in patient with a previous history of atrial fibrillation.”
NU
Discussion
In our knowledge, this is the first case report demonstrating how an acute physical trigger due to
MA
arterial peripheral embolization could start takotsubo cardiomyopathy, and beget a life-threatening complication such as pulmonary edema. In this case, the diagnosis has been complicated by the
D
peripheral embolus location at the left axillary artery level which produced symptoms similar to a
TE
typical chest pain irradiation, and by the chest CT-scan which did not report any unusual findings.
CE P
The diagnosis of acute coronary syndrome was, in fact, the first to be excluded, since, along with many characteristics mimicking an acute coronary syndrome, it has recently been shown that patients with takotsubo cardiomyopathy have a relevant prevalence of cardiovascular risk factors,
[2,3]
AC
[1] and that acute ischemic injury can in some cases directly trigger takotsubo cardiomyopathy.
Despite many clues of takotsubo were present, such as the typical echo presentation, coronary angiography is so far the only reliable tool to confirm the diagnosis and exclude an acute coronary syndrome.[4,5] The 12-lead ECG at admission, while providing some important and validated diagnostic and prognostic clues [6] such diffuse inverted T-waves and a long QTc, is not enough to safely rule out other more common causes of chest pain. Regarding the multiple cardioembolic events, the patient’s close relatives declared a poor compliance to the prescribed therapy in the past few months. This included missing many doses of apixaban which could have exposed the patient to her high thromboembolic risk (CHA2DS24
ACCEPTED MANUSCRIPT VASc=5) and further worsen cognitive impairment. In order to reduce the number of pills taken daily by geriatric patients, and thus improve their compliance, a once-daily oral anticoagulant may be preferred, as it was lately in this case. The lack of atrial fibrillation episodes during the in-
T
hospital ECG-monitoring did not rule out this hypothesis since subclinical atrial tachyarrhythmias
IP
have been demonstrated to be associated with a significantly increased risk of ischemic stroke or
AC
CE P
TE
D
MA
NU
SC R
systemic embolism.[7]
5
ACCEPTED MANUSCRIPT References [1]
Pelliccia F, Parodi G, Greco C, Antoniucci D, Brenner R, Bossone E, et al. Comorbidities Frequency in Takotsubo Syndrome: An International Collaborative Systematic Review
Nakagawa N, Fukawa N, Tsuji K, Nakano N, Kato A. Takotsubo cardiomyopathy induced by
IP
[2]
T
Including 1,109 Patients. Am J Med 2015;128:654.e11–654.e19.
[3]
SC R
dopamine infusion after carotid artery stenting. Int J Cardiol 2016;205:62–4. Messas N, Caspar T, Jesel L, Hess S, Girardey M, Radulescu B, et al. Takotsubo
NU
cardiomyopathy triggered by ischemic injury: When lateralmyocardial infarction precipitate apical ballooning syndrome. Int J Cardiol 2016;202:858–60. Guerra F, Rrapaj E, Pongetti G, Fabbrizioli A, Pelizzoni V, Giannini I, et al. Differences and
MA
[4]
similarities of repolarization patterns during hospitalization for Takotsubo cardiomyopathy
Looi JL, Wong CW, Lee M, Khan A, Webster M, Kerr AJ. Usefulness of ECG to differentiate
TE
[5]
D
and acute coronary syndrome. Am J Cardiol 2013;112:1720–4.
[6]
CE P
Takotsubo cardiomyopathy from acute coronary syndrome. Int J Cardiol 2015;199:132–40. Guerra F, Giannini I, Pongetti G, Fabbrizioli A, Rrapaj E, Aschieri D, et al. Transient QRS amplitude attenuation is associated with clinical recovery in patients with takotsubo
[7]
AC
cardiomyopathy. Int J Cardiol 2015;187:198–205. Healey JS, Connolly SJ, Gold MR, Israel CW, Van Gelder IC, Capucci A, et al. Subclinical atrial fibrillation and the risk of stroke. N Engl J Med 2012;366:120–9.
6
ACCEPTED MANUSCRIPT Figure legends Figure 1. Twelve-lead ECG at admission.Twelve-lead ECG at admission, showing sinus rhythm (95 bpm) with normal atrioventricular and interventricular conduction, biphasic T waves in V2-V3
AC
CE P
TE
D
MA
NU
SC R
IP
T
and negative T-waves in DI, DII, aVL, aVF, and V4-V6. A long QTc (580 ms) was also recorded.
Figure 2. Four-chamber view, showing the typical ballooning aspect of left ventricle.An akinesia of the medium-apical segments with hyperkinesia of the constrictors muscles was evident, resulting in the typical ballooning aspect of the left ventricle associated with takotsubo cardiomyopathy.
7
CE P
TE
D
MA
NU
SC R
IP
T
ACCEPTED MANUSCRIPT
AC
Figure 3. Twelve-lead ECG at discharge.Twelve-lead ECG at discharge, showing sinus rhythm (80 bpm) with normal atrioventricular and interventricular conduction, flat T-waves in all limb leads and small negative T-waves in V4-V6. QTc interval persisted as moderately increased (480 ms).
8
AC
CE P
TE
D
MA
NU
SC R
IP
T
ACCEPTED MANUSCRIPT
9