Heart & Lung 43 (2014) 41e44
Contents lists available at ScienceDirect
Heart & Lung journal homepage: www.heartandlung.org
From right to left heart failure: An unexpected transition Hassan Baydoun, MD, AACP a, *, George Khoueiry, MD b, Zahraa Ghandour, MD c, Yefim Olkovsky, MD, FACC d a
Department of Medicine, Staten Island University Hospital, 475 Seaview Avenue, Staten Island, NY 10305, USA Department of Cardiology, Dartmouth Hitchcock Medical Center, NH, USA Faculty of Medical Sciences, Lebanese University, Beirut, Lebanon d Department of Cardiology, Staten Island University Hospital, NY, USA b c
a r t i c l e i n f o
a b s t r a c t
Article history: Received 8 September 2013 Received in revised form 5 November 2013 Accepted 5 November 2013
Right and left heart failure are very common clinical syndromes with close correlation. Right-sided or right ventricular heart failure usually occurs as a result of left-sided failure. We report a very rare case of transition from right heart failure due to pulmonary embolism, followed by its resolution, to left heart failure due to Tako-tsubo syndrome within 48 h of hospitalization. Ó 2014 Elsevier Inc. All rights reserved.
Keywords: Pulmonary embolism Right ventricular failure Takotsubo syndrome Left ventricular failure
Introduction Right and left heart failure are highly prevalent clinical syndromes with close correlation but different etiologies. The 2 main causes of right ventricle (RV) failure are: chronic pulmonary arterial hypertension and pulmonary embolism (PE). Acute massive PE can lead to RV dilation and failure, primarily due to acute increase in afterload. This RV dysfunction is a well known predictor of morbidity, mortality and recurrence of PE.1 Aggressive intervention with thrombolytic therapy, vasoactive agents, or mechanical embolectomy may improve right ventricular function and clinical outcomes.2 On the other hand, Tako-tsubo cardiomyopathy, a transient and reversible left ventricular apical ballooning, is typically precipitated by an emotional stress or acute medical illness3; it mimics acute coronary syndrome in the absence of significant angiographically coronary artery stenosis. Presentation of case Ms. EG is a 58 year old woman, who presented to our emergency department (ED) for shortness of breath and palpitations of few hours duration. History goes back to one day prior to presentation when the patient went to her gastroenterologist complaining of * Corresponding author. Tel.: þ1 347 829 1980. E-mail address: [email protected] (H. Baydoun). 0147-9563/$ e see front matter Ó 2014 Elsevier Inc. All rights reserved. http://dx.doi.org/10.1016/j.hrtlng.2013.11.002
chronic constipation. She was tachycardic with irregular heart rate at the office. Thus, she was sent to the ED for further evaluation. On arrival, the patient was complaining of shortness of breath and palpitations. The onset of symptoms was associated with generalized weakness, lightheadedness and right calf pain of few days duration. Review of systems revealed 20 lbs weight loss over the past two months. Her past medical history is significant for asthma, ethanol abuse, chronic constipation, chronic low back pain, early menopause, and laxative abuse. She is allergic to penicillin. On physical examination, her blood pressure was 152/87 mm Hg, respiratory rate 22 breaths per minute, irregular pulse of 140 beats per minute and no fever (T ¼ 95.9 F). The patient appeared in mild respiratory distress. There was mild distention in the neck veins. Examination of the heart showed irregular S1 and S2 with no murmurs. Wheezes were heard throughout in both lungs. Her abdomen was soft with mild diffuse tenderness on deep palpation but no rebound tenderness. Her peripheral pulses were palpable. Right calf tenderness was noticed on palpation and on dorsal extension of the right foot. No lower extremities edema was noted. The results of other laboratory tests were within normal limits except for normocytic anemia (hemoglobin of 10.9 g/dl). The brain natriuretic peptide (BNP) was 1056 pg/ml with two sets of negative cardiac enzymes. Her electrocardiogram (ECG) showed atrial fibrillation with rapid ventricular response of 140 beats per minutes with no ischemic ST-T
42
H. Baydoun et al. / Heart & Lung 43 (2014) 41e44
Fig. 1. Electrocardiogram showing atrial fibrillation with rapid ventricular rate at 140 beats per minute.
changes (Fig. 1). A portable chest x-ray showed small right pleural effusion and elevated left hemidiaphragm. Right deep femoral vein, right calf vein and left common femoral vein thrombosis were detected on a venous Doppler of the lower extremities. Therefore, the patient was admitted to the telemetry unit. She was started on intravenous (IV) diltiazem drip, to control her heart rate, and subcutaneous enoxaparin 1 mg/kg every 12 h. Given the high clinical suspicion of pulmonary embolism, a ventilation perfusion scan of the lung was performed and showed multiple segmental perfusion defects. Moderate dilation and systolic dysfunction of the (RV), large right atrial thrombus extending into the RV and normal left ventricle ejection fraction (LVEF) were detected on the transthoracic echocardiography (TTE) (Fig. 2). The decision was to transfer the patient to the ICU for thrombolysis with alteplase. Enoxaparin was switched later to intravenous unfractionated heparin and the patient was started on warfarin. A repeat TTE on the next day showed significant resolution of the atrial thrombus. The patient was then transferred to a regular floor. Given her clinical presentation, the presumed diagnosis was a hypercoagulable state related most probably to a colon cancer. A CT scan of the abdomen and pelvis showed large bowel obstruction with enhancing soft tissue mass lesion in the descending colon with hypodense lesions within the liver reflecting metastatic disease. A surgical consult was obtained for diverting colostomy and inferior vena cava filter (IVC) placement. All these findings and the
plan were discussed with the patient. Few hours later, she started to complain of shortness of breath. ECG showed normal sinus rhythm, frequent premature atrial beats with anterolateral ST-T changes (Fig. 3). Serial cardiac enzymes were negative and CXR showed no changes. A repeat TTE showed acute dilation of the mid and apical segments of the LV with an EF of 15e20%. The RV was within normal in size and function. There was no visualization of any thrombus in the right atrium (Fig. 4). Since the patient had no history of coronary artery disease, these findings were consistent with an acute stress-induced dilated cardiomyopathy or Tako-tsubo syndrome. Diltiazem was stopped and the patient was started on low dose carvedilol and enalapril. Few days later, and after being assessed by the cardiologist, the patient underwent an exploratory laparatomy, Hartman’s procedure and insertion of an IVC filter. A repeated TTE showed improved left ventricular systolic function with normal RV function. Discussion Acute pulmonary embolism (PE) is a common and often fatal disease. It can be classified as massive or submassive. The diagnosis of massive PE should be considered whenever there is hypotension accompanied by an elevated central venous pressure (or neck vein distension) not otherwise explained by acute myocardial infarction,
Fig. 2. Transesophageal echocardiogram showing A) Normal left ventricle size and function; B) Dilated right ventricle with large right atrial thrombus extending into the right ventricle (white arrow).
H. Baydoun et al. / Heart & Lung 43 (2014) 41e44
43
Fig. 3. Electrocardiogram showing sinus rythm with frequent supraventricular extrasystoles and non-specific ST-T changes in leads I, aVL and V1eV6.
tension pneumothorax, pericardial tamponade, or a new arrhythmia.4 It is a very poor prognostic entity that frequently results in acute right ventricular failure and death. All acute PE not meeting the definition of massive PE are considered submassive PE.5 Few studies showed that RV dysfunction due to PE predicts increased PE-related mortality up to twofold in normotensive and hypotensive patients.6 RV dysfunction may also predict PE or DVT recurrence and PE-related death compared to patients with no RV dysfunction or RV dysfunction with regression.1 Our patient, which was admitted with submassive PE (most probably a saddle PE), had normal blood pressure on presentation but RV dysfunction on TTE. She was treated with thrombolytics and regained a normal RV function. Two days later and after the patient was told about the colon cancer found on colonoscopy, she developed acute stress-induced cardiomyopathy or Tako-tsubo syndrome. Stress-induced cardiomyopathy, also called apical ballooning syndrome, broken heart syndrome, and, in Japan, Tako-tsubo cardiomyopathy, is an increasingly reported syndrome which accounts for z1%e2% of all suspected cases of acute myocardial infarction (AMI).7 It is generally characterized by transient systolic dysfunction of the apical and/or mid segments of the left ventricle that mimics AMI but in the absence of obstructive coronary artery disease.8 About one-third of the cases involved both the right and left ventricles. It is more seen in women and accounted for 80 to 100 percent of cases with a mean age of 61e76 years.9 The onset of stress-induced cardiomyopathy is triggered most of the time by an
acute medical illness or by intense emotional or physical stress like a catastrophic medical diagnosis as in our patient case. The pathogenesis is not well understood but the possible mechanisms are coronary artery vasospasm, microvascular dysfunction or catecholamine excess.8 Previous reports on Tako-tsubo syndrome described exogenously administered catecholamine’s, those secreted by neuroendocrine tumors (e.g., pheochromocytoma) or during anaphylaxis as potential triggers.10 The most common presenting symptom is acute chest pain, but some patients present with dyspnea, syncope, shock, or electrocardiographic abnormalities.11 It is usually diagnosed by echocardiography, cardiac magnetic resonance or ventriculography. Apical ballooning (typical variant) and/or midventricular hypokinesis is usually seen on left ventriculography or echocardiography.8,11 In a minority of cases, the transient left ventricular hypokinesis is restricted to the midventricular segments (“atypical variant” or “apical sparing variant”) without involvement of the apex.7 Coronary angiography typically demonstrates either normal vessels or mild to moderate coronary atherosclerosis. Cardiac magnetic resonance (CMR) may help in the diagnosis of this syndrome especially with the Late gadolinium enhancement (LGE) which is generally absent in stress-induced cardiomyopathy unlike AMI in which intense subendocardial or transmural LGE is seen.12 CMR shows myocardial edema which is also seen in AMI and myocarditis. Despite the severity of the acute illness, stress-induced cardiomyopathy is a transient disorder which is managed conservatively and usually reverses with the resolution of the physical or
Fig. 4. Transesophageal echocardiogram done two days later showed. A, B) Mid and apical left ventricular segments dilation; B) Restoration of the right ventricular size and function with significant resolution of the atrial thrombus.
44
H. Baydoun et al. / Heart & Lung 43 (2014) 41e44
emotional stress. There is no optimal medical treatment but it is reasonable to treat these patients with standard medications for left ventricular dysfunction. These include ACE inhibitors, beta blockers and diuretics as needed for volume overload.11 Our patient was started on carvedilol and enalapril. The appropriate duration of therapy is unknown. It is usually given until there is full recovery of the systolic function which occurs in one to four weeks in most cases. The development of RV failure secondary to PE followed by complete restoration of the RV function after thrombolytics with subsequent development of Tako-tsubo syndrome has not been described in the English medical literature before. In this particular case, the stress from the acute medical condition due to PE could have lead to Tako-tsubo syndrome, but we believe that the emotional stress associated with the diagnosis of malignancy is the major culprit. Conclusion Stress-induced cardiomyopathy is an increasingly reported syndrome, as a differential diagnosis of AMI, characterized by transient regional LV dysfunction in the absence of obstructive coronary artery disease. It presents a diagnostic challenge for all the physicians. It should be suspected in postmenopausal women who present with clinical manifestations of acute coronary syndrome or ECG abnormalities after acute medical illness or intense emotional or physical stress, as our patient. The initial management of stress-induced cardiomyopathy is mainly supportive with a focus on alleviating the triggering physical or emotional stressors. In our case, the presentation and the transition from right heart failure, due to submassive PE followed by its resolution, to left heart failure due to acute stress-induced cardiomyopathy or Tako-tsubo syndrome within two days and during the same
hospitalization period are unique and were not reported elsewhere to the best of our knowledge.
References 1. Sanchez O, Trinquart L, Colombet I, et al. Prognostic value of right ventricular dysfunction in patients with haemodynamically stable pulmonary embolism: a systematic review. Eur Heart J. 2008;29(12):1569e1577. 2. Lualdi JC, Goldhaber SZ. Right ventricular dysfunction after acute pulmonary embolism: pathophysiologic factors, detection, and therapeutic implications. Am Heart J. 1995;130(6):1276e1282. 3. Virani SS, Khan AN, Mendoza CE, Ferreira AC, de Marchena E. Takotsubo cardiomyopathy, or broken-heart syndrome. Tex Heart Inst J. 2007;34(1):76e79. 4. Kucher N, Goldhaber SZ. Management of massive pulmonary embolism. Circulation. 2005;112(2):e28ee32. 5. Jaff MR, McMurtry MS, Archer SL, et al. Management of massive and submassive pulmonary embolism, iliofemoral deep vein thrombosis, and chronic thromboembolic pulmonary hypertension: a scientific statement from the American Heart Association. Circulation. 2011;123(16):1788e1830. 6. ten Wolde M, Söhne M, Quak E, Mac Gillavry MR, Büller HR. Prognostic value of echocardiographically assessed right ventricular dysfunction in patients with pulmonary embolism. Arch Intern Med. 2004;164(15):1685e1689. 7. Kurowski V, Kaiser A, von Hof K, et al. Apical and midventricular transient left ventricular dysfunction syndrome (tako-tsubo cardiomyopathy): frequency, mechanisms, and prognosis. Chest. 2007;132(3):809e816. 8. Sharkey SW, Lesser JR, Zenovich AG, et al. Acute and reversible cardiomyopathy provoked by stress in women from the United States. Circulation. 2005;111(4):472e479. 9. Akashi YJ, Goldstein DS, Barbaro G, Ueyama T. Takotsubo cardiomyopathy: a new form of acute, reversible heart failure. Circulation. 2008;118(25): 2754e2762. 10. Khoueiry G, Abi Rafeh N, Azab B, et al. Reverse Takotsubo cardiomyopathy in the setting of anaphylaxis treated with high-dose intravenous epinephrine. J Emerg Med. 2013;44(1):96e99. 11. Bybee KA, Kara T, Prasad A, et al. Systematic review: transient left ventricular apical ballooning: a syndrome that mimics ST-segment elevation myocardial infarction. Ann Intern Med. 2004;141(11):858e865. 12. Eitel I, von Knobelsdorff-Brenkenhoff F, Bernhardt P, et al. Clinical characteristics and cardiovascular magnetic resonance findings in stress (takotsubo) cardiomyopathy. JAMA. 2011;306(3):277e286.
Contents lists available at ScienceDirect
Heart & Lung journal homepage: www.heartandlung.org
From right to left heart failure: An unexpected transition Hassan Baydoun, MD, AACP a, *, George Khoueiry, MD b, Zahraa Ghandour, MD c, Yefim Olkovsky, MD, FACC d a
Department of Medicine, Staten Island University Hospital, 475 Seaview Avenue, Staten Island, NY 10305, USA Department of Cardiology, Dartmouth Hitchcock Medical Center, NH, USA Faculty of Medical Sciences, Lebanese University, Beirut, Lebanon d Department of Cardiology, Staten Island University Hospital, NY, USA b c
a r t i c l e i n f o
a b s t r a c t
Article history: Received 8 September 2013 Received in revised form 5 November 2013 Accepted 5 November 2013
Right and left heart failure are very common clinical syndromes with close correlation. Right-sided or right ventricular heart failure usually occurs as a result of left-sided failure. We report a very rare case of transition from right heart failure due to pulmonary embolism, followed by its resolution, to left heart failure due to Tako-tsubo syndrome within 48 h of hospitalization. Ó 2014 Elsevier Inc. All rights reserved.
Keywords: Pulmonary embolism Right ventricular failure Takotsubo syndrome Left ventricular failure
Introduction Right and left heart failure are highly prevalent clinical syndromes with close correlation but different etiologies. The 2 main causes of right ventricle (RV) failure are: chronic pulmonary arterial hypertension and pulmonary embolism (PE). Acute massive PE can lead to RV dilation and failure, primarily due to acute increase in afterload. This RV dysfunction is a well known predictor of morbidity, mortality and recurrence of PE.1 Aggressive intervention with thrombolytic therapy, vasoactive agents, or mechanical embolectomy may improve right ventricular function and clinical outcomes.2 On the other hand, Tako-tsubo cardiomyopathy, a transient and reversible left ventricular apical ballooning, is typically precipitated by an emotional stress or acute medical illness3; it mimics acute coronary syndrome in the absence of significant angiographically coronary artery stenosis. Presentation of case Ms. EG is a 58 year old woman, who presented to our emergency department (ED) for shortness of breath and palpitations of few hours duration. History goes back to one day prior to presentation when the patient went to her gastroenterologist complaining of * Corresponding author. Tel.: þ1 347 829 1980. E-mail address: [email protected] (H. Baydoun). 0147-9563/$ e see front matter Ó 2014 Elsevier Inc. All rights reserved. http://dx.doi.org/10.1016/j.hrtlng.2013.11.002
chronic constipation. She was tachycardic with irregular heart rate at the office. Thus, she was sent to the ED for further evaluation. On arrival, the patient was complaining of shortness of breath and palpitations. The onset of symptoms was associated with generalized weakness, lightheadedness and right calf pain of few days duration. Review of systems revealed 20 lbs weight loss over the past two months. Her past medical history is significant for asthma, ethanol abuse, chronic constipation, chronic low back pain, early menopause, and laxative abuse. She is allergic to penicillin. On physical examination, her blood pressure was 152/87 mm Hg, respiratory rate 22 breaths per minute, irregular pulse of 140 beats per minute and no fever (T ¼ 95.9 F). The patient appeared in mild respiratory distress. There was mild distention in the neck veins. Examination of the heart showed irregular S1 and S2 with no murmurs. Wheezes were heard throughout in both lungs. Her abdomen was soft with mild diffuse tenderness on deep palpation but no rebound tenderness. Her peripheral pulses were palpable. Right calf tenderness was noticed on palpation and on dorsal extension of the right foot. No lower extremities edema was noted. The results of other laboratory tests were within normal limits except for normocytic anemia (hemoglobin of 10.9 g/dl). The brain natriuretic peptide (BNP) was 1056 pg/ml with two sets of negative cardiac enzymes. Her electrocardiogram (ECG) showed atrial fibrillation with rapid ventricular response of 140 beats per minutes with no ischemic ST-T
42
H. Baydoun et al. / Heart & Lung 43 (2014) 41e44
Fig. 1. Electrocardiogram showing atrial fibrillation with rapid ventricular rate at 140 beats per minute.
changes (Fig. 1). A portable chest x-ray showed small right pleural effusion and elevated left hemidiaphragm. Right deep femoral vein, right calf vein and left common femoral vein thrombosis were detected on a venous Doppler of the lower extremities. Therefore, the patient was admitted to the telemetry unit. She was started on intravenous (IV) diltiazem drip, to control her heart rate, and subcutaneous enoxaparin 1 mg/kg every 12 h. Given the high clinical suspicion of pulmonary embolism, a ventilation perfusion scan of the lung was performed and showed multiple segmental perfusion defects. Moderate dilation and systolic dysfunction of the (RV), large right atrial thrombus extending into the RV and normal left ventricle ejection fraction (LVEF) were detected on the transthoracic echocardiography (TTE) (Fig. 2). The decision was to transfer the patient to the ICU for thrombolysis with alteplase. Enoxaparin was switched later to intravenous unfractionated heparin and the patient was started on warfarin. A repeat TTE on the next day showed significant resolution of the atrial thrombus. The patient was then transferred to a regular floor. Given her clinical presentation, the presumed diagnosis was a hypercoagulable state related most probably to a colon cancer. A CT scan of the abdomen and pelvis showed large bowel obstruction with enhancing soft tissue mass lesion in the descending colon with hypodense lesions within the liver reflecting metastatic disease. A surgical consult was obtained for diverting colostomy and inferior vena cava filter (IVC) placement. All these findings and the
plan were discussed with the patient. Few hours later, she started to complain of shortness of breath. ECG showed normal sinus rhythm, frequent premature atrial beats with anterolateral ST-T changes (Fig. 3). Serial cardiac enzymes were negative and CXR showed no changes. A repeat TTE showed acute dilation of the mid and apical segments of the LV with an EF of 15e20%. The RV was within normal in size and function. There was no visualization of any thrombus in the right atrium (Fig. 4). Since the patient had no history of coronary artery disease, these findings were consistent with an acute stress-induced dilated cardiomyopathy or Tako-tsubo syndrome. Diltiazem was stopped and the patient was started on low dose carvedilol and enalapril. Few days later, and after being assessed by the cardiologist, the patient underwent an exploratory laparatomy, Hartman’s procedure and insertion of an IVC filter. A repeated TTE showed improved left ventricular systolic function with normal RV function. Discussion Acute pulmonary embolism (PE) is a common and often fatal disease. It can be classified as massive or submassive. The diagnosis of massive PE should be considered whenever there is hypotension accompanied by an elevated central venous pressure (or neck vein distension) not otherwise explained by acute myocardial infarction,
Fig. 2. Transesophageal echocardiogram showing A) Normal left ventricle size and function; B) Dilated right ventricle with large right atrial thrombus extending into the right ventricle (white arrow).
H. Baydoun et al. / Heart & Lung 43 (2014) 41e44
43
Fig. 3. Electrocardiogram showing sinus rythm with frequent supraventricular extrasystoles and non-specific ST-T changes in leads I, aVL and V1eV6.
tension pneumothorax, pericardial tamponade, or a new arrhythmia.4 It is a very poor prognostic entity that frequently results in acute right ventricular failure and death. All acute PE not meeting the definition of massive PE are considered submassive PE.5 Few studies showed that RV dysfunction due to PE predicts increased PE-related mortality up to twofold in normotensive and hypotensive patients.6 RV dysfunction may also predict PE or DVT recurrence and PE-related death compared to patients with no RV dysfunction or RV dysfunction with regression.1 Our patient, which was admitted with submassive PE (most probably a saddle PE), had normal blood pressure on presentation but RV dysfunction on TTE. She was treated with thrombolytics and regained a normal RV function. Two days later and after the patient was told about the colon cancer found on colonoscopy, she developed acute stress-induced cardiomyopathy or Tako-tsubo syndrome. Stress-induced cardiomyopathy, also called apical ballooning syndrome, broken heart syndrome, and, in Japan, Tako-tsubo cardiomyopathy, is an increasingly reported syndrome which accounts for z1%e2% of all suspected cases of acute myocardial infarction (AMI).7 It is generally characterized by transient systolic dysfunction of the apical and/or mid segments of the left ventricle that mimics AMI but in the absence of obstructive coronary artery disease.8 About one-third of the cases involved both the right and left ventricles. It is more seen in women and accounted for 80 to 100 percent of cases with a mean age of 61e76 years.9 The onset of stress-induced cardiomyopathy is triggered most of the time by an
acute medical illness or by intense emotional or physical stress like a catastrophic medical diagnosis as in our patient case. The pathogenesis is not well understood but the possible mechanisms are coronary artery vasospasm, microvascular dysfunction or catecholamine excess.8 Previous reports on Tako-tsubo syndrome described exogenously administered catecholamine’s, those secreted by neuroendocrine tumors (e.g., pheochromocytoma) or during anaphylaxis as potential triggers.10 The most common presenting symptom is acute chest pain, but some patients present with dyspnea, syncope, shock, or electrocardiographic abnormalities.11 It is usually diagnosed by echocardiography, cardiac magnetic resonance or ventriculography. Apical ballooning (typical variant) and/or midventricular hypokinesis is usually seen on left ventriculography or echocardiography.8,11 In a minority of cases, the transient left ventricular hypokinesis is restricted to the midventricular segments (“atypical variant” or “apical sparing variant”) without involvement of the apex.7 Coronary angiography typically demonstrates either normal vessels or mild to moderate coronary atherosclerosis. Cardiac magnetic resonance (CMR) may help in the diagnosis of this syndrome especially with the Late gadolinium enhancement (LGE) which is generally absent in stress-induced cardiomyopathy unlike AMI in which intense subendocardial or transmural LGE is seen.12 CMR shows myocardial edema which is also seen in AMI and myocarditis. Despite the severity of the acute illness, stress-induced cardiomyopathy is a transient disorder which is managed conservatively and usually reverses with the resolution of the physical or
Fig. 4. Transesophageal echocardiogram done two days later showed. A, B) Mid and apical left ventricular segments dilation; B) Restoration of the right ventricular size and function with significant resolution of the atrial thrombus.
44
H. Baydoun et al. / Heart & Lung 43 (2014) 41e44
emotional stress. There is no optimal medical treatment but it is reasonable to treat these patients with standard medications for left ventricular dysfunction. These include ACE inhibitors, beta blockers and diuretics as needed for volume overload.11 Our patient was started on carvedilol and enalapril. The appropriate duration of therapy is unknown. It is usually given until there is full recovery of the systolic function which occurs in one to four weeks in most cases. The development of RV failure secondary to PE followed by complete restoration of the RV function after thrombolytics with subsequent development of Tako-tsubo syndrome has not been described in the English medical literature before. In this particular case, the stress from the acute medical condition due to PE could have lead to Tako-tsubo syndrome, but we believe that the emotional stress associated with the diagnosis of malignancy is the major culprit. Conclusion Stress-induced cardiomyopathy is an increasingly reported syndrome, as a differential diagnosis of AMI, characterized by transient regional LV dysfunction in the absence of obstructive coronary artery disease. It presents a diagnostic challenge for all the physicians. It should be suspected in postmenopausal women who present with clinical manifestations of acute coronary syndrome or ECG abnormalities after acute medical illness or intense emotional or physical stress, as our patient. The initial management of stress-induced cardiomyopathy is mainly supportive with a focus on alleviating the triggering physical or emotional stressors. In our case, the presentation and the transition from right heart failure, due to submassive PE followed by its resolution, to left heart failure due to acute stress-induced cardiomyopathy or Tako-tsubo syndrome within two days and during the same
hospitalization period are unique and were not reported elsewhere to the best of our knowledge.
References 1. Sanchez O, Trinquart L, Colombet I, et al. Prognostic value of right ventricular dysfunction in patients with haemodynamically stable pulmonary embolism: a systematic review. Eur Heart J. 2008;29(12):1569e1577. 2. Lualdi JC, Goldhaber SZ. Right ventricular dysfunction after acute pulmonary embolism: pathophysiologic factors, detection, and therapeutic implications. Am Heart J. 1995;130(6):1276e1282. 3. Virani SS, Khan AN, Mendoza CE, Ferreira AC, de Marchena E. Takotsubo cardiomyopathy, or broken-heart syndrome. Tex Heart Inst J. 2007;34(1):76e79. 4. Kucher N, Goldhaber SZ. Management of massive pulmonary embolism. Circulation. 2005;112(2):e28ee32. 5. Jaff MR, McMurtry MS, Archer SL, et al. Management of massive and submassive pulmonary embolism, iliofemoral deep vein thrombosis, and chronic thromboembolic pulmonary hypertension: a scientific statement from the American Heart Association. Circulation. 2011;123(16):1788e1830. 6. ten Wolde M, Söhne M, Quak E, Mac Gillavry MR, Büller HR. Prognostic value of echocardiographically assessed right ventricular dysfunction in patients with pulmonary embolism. Arch Intern Med. 2004;164(15):1685e1689. 7. Kurowski V, Kaiser A, von Hof K, et al. Apical and midventricular transient left ventricular dysfunction syndrome (tako-tsubo cardiomyopathy): frequency, mechanisms, and prognosis. Chest. 2007;132(3):809e816. 8. Sharkey SW, Lesser JR, Zenovich AG, et al. Acute and reversible cardiomyopathy provoked by stress in women from the United States. Circulation. 2005;111(4):472e479. 9. Akashi YJ, Goldstein DS, Barbaro G, Ueyama T. Takotsubo cardiomyopathy: a new form of acute, reversible heart failure. Circulation. 2008;118(25): 2754e2762. 10. Khoueiry G, Abi Rafeh N, Azab B, et al. Reverse Takotsubo cardiomyopathy in the setting of anaphylaxis treated with high-dose intravenous epinephrine. J Emerg Med. 2013;44(1):96e99. 11. Bybee KA, Kara T, Prasad A, et al. Systematic review: transient left ventricular apical ballooning: a syndrome that mimics ST-segment elevation myocardial infarction. Ann Intern Med. 2004;141(11):858e865. 12. Eitel I, von Knobelsdorff-Brenkenhoff F, Bernhardt P, et al. Clinical characteristics and cardiovascular magnetic resonance findings in stress (takotsubo) cardiomyopathy. JAMA. 2011;306(3):277e286.
