COVID-19-associated stress cardiomyopathy: Difference between revisions
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==Pathophysiology== | ==Pathophysiology== | ||
* It is thought that COVID-19-associated [[stress cardiomyopathy]] is the result of extreme [[Sympathetic nervous system|sympathetic]] stimulation due to abnormal release of [[catecholamines]] causing [[epicardial]] [[coronary vasospasm]]. | * It is thought that COVID-19-associated [[stress cardiomyopathy]] is the result of extreme [[Sympathetic nervous system|sympathetic]] stimulation due to abnormal release of [[catecholamines]] such as [[epinephrine]], [[norepinephrine]], [[dopamine]] causing [[epicardial]] [[coronary vasospasm]]. | ||
* Many mechanisms occurring in [[COVID-19]] patients may lead to [[myocardial injury]] and [[left ventricular dysfunction]].<ref name="pmid32523926">{{cite journal| author=Pasqualetto MC, Secco E, Nizzetto M, Scevola M, Altafini L, Cester A | display-authors=etal| title=Stress Cardiomyopathy in COVID-19 Disease. | journal=Eur J Case Rep Intern Med | year= 2020 | volume= 7 | issue= 6 | pages= 001718 | pmid=32523926 | doi=10.12890/2020_001718 | pmc=7279910 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=32523926 }}</ref> | * Many mechanisms occurring in [[COVID-19]] patients may lead to [[myocardial injury]] and [[left ventricular dysfunction]].<ref name="pmid32523926">{{cite journal| author=Pasqualetto MC, Secco E, Nizzetto M, Scevola M, Altafini L, Cester A | display-authors=etal| title=Stress Cardiomyopathy in COVID-19 Disease. | journal=Eur J Case Rep Intern Med | year= 2020 | volume= 7 | issue= 6 | pages= 001718 | pmid=32523926 | doi=10.12890/2020_001718 | pmc=7279910 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=32523926 }}</ref> | ||
Revision as of 07:00, 18 August 2021
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: José Eduardo Riceto Loyola Junior, M.D.[2]
Synonyms and keywords: Takotsubo syndrome, Takotsubo cardiomyopathy, broken heart syndrome, Stress cardiomyopathy
Overview
COVID-19-associated stress cardiomyopathy was first described by Elena Roca, an Italian physician, in April 2020. This disorder is the result of extreme sympathetic stimulation due to the abnormal release of catecholamines causing epicardial coronary vasospasm. The incidence of COVID-19-associated stress cardiomyopathy is approximately 7.8% of all patients presenting acute coronary syndrome.
Historical Perspective
- COVID-19-associated stress cardiomyopathy was first described by Elena Roca, an Italian physician, in April 2020.[1]
Classification
- Takotsubo cardiomyopathy is classified into two groups:[2]
- Apical takotsubo cardiomyopathy which is the most common form (80%)
- Midventricular form (20%)
Pathophysiology
- It is thought that COVID-19-associated stress cardiomyopathy is the result of extreme sympathetic stimulation due to abnormal release of catecholamines such as epinephrine, norepinephrine, dopamine causing epicardial coronary vasospasm.
- Many mechanisms occurring in COVID-19 patients may lead to myocardial injury and left ventricular dysfunction.[3]
- One of the proposed theory is that patients may experience stress-induced adrenergic discharge as consequence of fever and inflammatory response to infection. One other factor to consider is the direct SARS-CoV-2 injury causing endothelial dysfunction, which may cause microvascular vasoconstriction that can manifest in a transient left ventricular apical dysfunction, (apical ballooning).[4]
- Proposed mechanisms that have the potential to cause myocardial injury in acute coronavirus disease 2019 cardiovascular syndrome:[5]
| Stress Induced Cardiomyopathy | |||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Microvascular/Thrombotic Injury | Cytokine Storm | ||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Pre-existing cardiovascular Disease | Acute Myocardial Injury Characterized by Abnormal Troponin | Viral Myocarditis | |||||||||||||||||||||||||||||||||||||||||||||||||||||
| Hypoxemia | Hypotension +/- Shock | ||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Ventricular or Atrial Arrhythmias | |||||||||||||||||||||||||||||||||||||||||||||||||||||||
Causes
- COVID-19-associated stress cardiomyopathy may be caused by a very intense sympathetic stimulation which is theorized to be caused either due to direct viral action or the ongoing psychological, economical and social effects (physical distancing rules, lack of social interaction) of the pandemic due to the imposed quarantine.[4]
Differentiating COVID-19-associated stress cardiomyopathy from other Diseases
- For further information about the differential diagnosis, click here.
- To view the differential diagnosis of COVID-19, click here.
Epidemiology and Demographics
- The incidence of COVID-19-associated stress cardiomyopathy is approximately 7.8% of all patients presenting acute coronary syndrome.[4]
- In comparison, the stress cardiomyopathy incidence in the pre-COVID-19 period was varying between 1.5-1.8%.[4]
Risk Factors
- There are no established risk factors for COVID-19-associated stress cardiomyopathy.
- Hypertension was, however, the most frequently comorbidity found across the groups in the COVID-19 period patients, as was hyperlipidemia.[4]
Screening
- There is insufficient evidence to recommend routine screening for COVID-19-associated stress cardiomyopathy.
Natural History, Complications, and Prognosis
- COVID-19-associated stress cardiomyopathy outcomes were similar to the stress cardiomyopathy not related to COVID-19 with regard to mortality and 30-day rehospitalization.[4]
- The same study showed that COVID-19-associated stress cardiomyopathy patients had a significantly longer hospital length of stay. in comparison to the ones not related to COVID-19.[4]
- Provided that patients survive the initial insult without any complications, most patients recover and have a normalized cardiac function within a few weeks.[6][7][8]
Diagnosis
- Diagnostic findings are largely the same in comparison to stress cardiomyopathy, and these are listed below. There is however a need to show evidence of ongoing COVID-19 infection.
Diagnostic Study of Choice
- The diagnosis of stress cardiomyopathy is made when all 4 of the following diagnostic criteria are met:
- Transient hypokinesis, akinesis, or dyskinesis of the left ventricular mid segments with or without apical involvement; the regional wall motion abnormalities extend beyond a single epicardial vascular distribution; a stressful trigger is often, but not always present.
- Absence of obstructive coronary disease or angiographic evidence of acute plaque rupture.
- New electrocardiographic abnormalities (either ST-segment elevation and/or T-wave inversion) or modest elevation in cardiac troponin.
- Absence of pheochromocytoma and myocarditis.[7][6]
- The diagnosis of COVID-19-associated stress cardiomyopathy is largely the same, but happening in the context of a SARS-CoV2 infection.
History and Symptoms
Symptoms of stress cardiomyopathy can mimic acute coronary syndrome. The most common presenting symptoms are:[6][10][7][12][17][11]
- Chest pain or chest tightness
- Shortness of breath
- Vomiting
- Loss of consciousness due to syncope or cardiac arrest in rare cases
When taking the history from a patient with suspected stress cardiomyopathy, it is important to ask about:[10][12]
- Personal history of hypertension, hyperlipidemia, paroxysmal atrial fibrillation, syncope, hypoglycemia or stroke
- Triggering event(s) to symptoms such as an unexpected death, being a victim of domestic violence or engaging in an argument or performing strenuous physical activity
Physical Examination
- The following physical examination findings may be seen in patients with stress cardiomyopathy:[18][6][9][10][8][11][12][13][19][15][20]
| Organ System | Findings | Suggestive Of |
|---|---|---|
| General appearance | Patient may be anxious, ill-appearing or diaphoretic | |
| Vital signs | Cardiogenic shock | |
| Cardiac | Murmurs, S3, gallop rhythm, displaced PMI | Heart failure |
| Respiratory | Rales, crackles | Pulmonary edema |
Laboratory Findings
- Laboratory findings consistent with the diagnosis of COVID-19-associated stress cardiomyopathy include elevated troponin and Pro-BNP.[4]
- Elevated levels of serum catecholamines may also be found in patients with stress cardiomyopathy.[6][10][12][11]
- Evidence of ongoing COVID-19 disease is required to establish the diagnosis.
Electrocardiogram
The ECG findings are largely the same of the regular stress cardiomyopathy, and are often confused with those of an acute anterior wall myocardial infarction.[6][12] Findings on ECG include:[6][10][7][8][12][17][11]
- ST elevation in the precordial leads
- T wave inversion
- Q wave formation
- QT prolongation
- New-onset bundle branch block (BBB)
- Rarely, malignant ventricular arrhythmias may be seen
X-ray
Takotsubo in Japanese language refer to a ceramic pot, which is used to trap octopus. The typical chest x-ray findings in patients with stress cardiomyopathy include a takotsubo-shaped heart, in which there is apical ballooning and narrowing of the proximal portion near the great vessels.
Echocardiography or Ultrasound
The following echocardiographic findings may be seen in patients with stress cardiomyopathy:[10][7][8][11]
- Apical ballooning
- Apical or mid-segment dyskinesia or akinesia
- Left ventricular systolic dysfunction
- Reduced ejection fraction
CT scan
A cardiac CT scan can also help differentiate between stress cardiomyopathy and acute MI. Regional abnormalities in the wall motion of the heart, along with absence of coronary atherosclerosis support the diagnosis of stress cardiomyopathy over an acute MI.[11]
Chest CT scan may also show findings associated with COVID-19 and they can include:
- Unilateral or bilateral pneumonia[21][22][23]
- Mottling and ground-glass opacity
- Focal or multifocal opacities
- Consolidation
- Septal thickening
- Subpleural and lower lobe involvement more likely
MRI
- Cardiac magnetic resonance (CMR) is a useful imaging modality in distinguishing between stress cardiomyopathy and myocarditis or MI. In the case of myocarditis or MI, there is delayed hyper-enhancement of gadolinium. However, absence of gadolinium hyper-enhancement supports the diagnosis of stress cardiomyopathy. Also, stress cardiomyopathy results in regional wall abnormality and its extent can best be documented using cardiac magnetic resonance.[7][14][24][25][26][27][28][29][14][30][31]
- CMR in stress cardiomyopathy shows absence of irreversible damage and segmental LV dysfunction.[25]
Other findings on CMR include:[11][14]
- Hypokinetic or dyskinetic areas in the wall of the heart
- Myocardial edema
- Apical thrombi
Other Imaging Findings
Positron Emission Tomography (PET) Scan
In patients with stress cardiomyopathy, a PET scan may be done. Areas of hypokinesia or dyskinesia have reduced glucose utilization compared to normal regions.[32]
Coronary Angiography
- Stress cardiomyopathy can mimic an acute MI, mainly anterior MI, since the clinical presentation, ECG and laboratory findings are similar. Hence, coronary angiography is considered a great diagnostic modality to differentiate between the two diagnoses.
- A normal angiography or absence of substantial coronary stenosis supports the diagnosis of stress cardiomyopathy.[12][6][11]
Other Diagnostic Studies
Cardiac Catheterization
When patients with stress cardiomyopathy undergo cardiac catheterization, the following findings are usually reported:[10][12][8]
- Normal anatomy of the coronary arteries, without evidence of acute plaque rupture
- Low ejection fraction (EF)
- Minimal or no evidence of coronary vasospasm
- Minimal disturbance of microcirculation
Myocardial Biopsy
- Myocardial biopsy, although not necessary for diagnosis, can distinguish between stress cardiomyopathy and MI.
- The histological findings on myocardial biopsy in patients with stress cardiomyopathy include:[6][10]
- Inflammatory infiltrates, consisting of mononuclear lymphocytes, leukocytes and macrophages
- Myocardial fibrosis
- Contraction bands, which may or may not be associated with necrosis
- The combination of inflammatory changes and contraction bands distinguish stress cardiomyopathy from coagulative necrosis seen in MI.[6]
Treatment
Medical Therapy
- There is no treatment for specific treatment for stress cardiomyopathy when associated with COVID-19. The mainstay of therapy is supportive care, which is the same for the stress cardiomyopathy not related to COVID-19.
- Medical therapy in patients with stress cardiomyopathy is mostly targeted towards the treatment of complications. For stress cardiomyopathy per se, the use of heparin and aspirin are controversial. It must be noted that the use of beta blockers alone is not advised, as this will result unopposed activity of catecholamines at the alpha receptors and can cause further prolongation of the QT interval. The combined use of alpha- and beta blockers is reasonable.[9]
Treatment of Complications
The following interventions are performed if their associated complications arise:[9][10][12]
- Cardiogenic shock is treated with intraaortic balloon pump
- Pulmonary edema is treated by advising the patient to adopt an upright position, supplementation of oxygen, and administration of diuretics, morphine and sedatives
- Heart failure is managed ACE inhibitors, ARBs, diuretics and nitrates
Surgery
- Surgical intervention is not recommended for the management of COVID-19-associated stress cardiomyopathy.
Primary Prevention
- There are no established measures for the primary prevention of COVID-19-associated stress cardiomyopathy if a patient has acquired COVID-19 infection.
- Preventive measures should be taken to avoid COVID-19 infection.
Secondary Prevention
- There are no established measures for the secondary prevention of COVID-19-associated stress cardiomyopathy.
References
- ↑ Roca E, Lombardi C, Campana M, Vivaldi O, Bigni B, Bertozzi B; et al. (2020). "Takotsubo Syndrome Associated with COVID-19". Eur J Case Rep Intern Med. 7 (5): 001665. doi:10.12890/2020_001665. PMC 7213829 Check
|pmc=value (help). PMID 32399453 Check|pmid=value (help). - ↑ Templin C, Ghadri JR, Diekmann J, Napp LC, Bataiosu DR, Jaguszewski M, Cammann VL, Sarcon A, Geyer V, Neumann CA, Seifert B, Hellermann J, Schwyzer M, Eisenhardt K, Jenewein J, Franke J, Katus HA, Burgdorf C, Schunkert H, Moeller C, Thiele H, Bauersachs J, Tschöpe C, Schultheiss HP, Laney CA, Rajan L, Michels G, Pfister R, Ukena C, Böhm M, Erbel R, Cuneo A, Kuck KH, Jacobshagen C, Hasenfuss G, Karakas M, Koenig W, Rottbauer W, Said SM, Braun-Dullaeus RC, Cuculi F, Banning A, Fischer TA, Vasankari T, Airaksinen KE, Fijalkowski M, Rynkiewicz A, Pawlak M, Opolski G, Dworakowski R, MacCarthy P, Kaiser C, Osswald S, Galiuto L, Crea F, Dichtl W, Franz WM, Empen K, Felix SB, Delmas C, Lairez O, Erne P, Bax JJ, Ford I, Ruschitzka F, Prasad A, Lüscher TF (September 2015). "Clinical Features and Outcomes of Takotsubo (Stress) Cardiomyopathy". N Engl J Med. 373 (10): 929–38. doi:10.1056/NEJMoa1406761. PMID 26332547.
- ↑ Pasqualetto MC, Secco E, Nizzetto M, Scevola M, Altafini L, Cester A; et al. (2020). "Stress Cardiomyopathy in COVID-19 Disease". Eur J Case Rep Intern Med. 7 (6): 001718. doi:10.12890/2020_001718. PMC 7279910 Check
|pmc=value (help). PMID 32523926 Check|pmid=value (help). - ↑ 4.0 4.1 4.2 4.3 4.4 4.5 4.6 4.7 Jabri A, Kalra A, Kumar A, Alameh A, Adroja S, Bashir H; et al. (2020). "Incidence of Stress Cardiomyopathy During the Coronavirus Disease 2019 Pandemic". JAMA Netw Open. 3 (7): e2014780. doi:10.1001/jamanetworkopen.2020.14780. PMC 7348683 Check
|pmc=value (help). PMID 32644140 Check|pmid=value (help). - ↑ Hendren NS, Drazner MH, Bozkurt B, Cooper LT (2020). "Description and Proposed Management of the Acute COVID-19 Cardiovascular Syndrome". Circulation. 141 (23): 1903–1914. doi:10.1161/CIRCULATIONAHA.120.047349. PMC 7314493 Check
|pmc=value (help). PMID 32297796 Check|pmid=value (help). - ↑ 6.00 6.01 6.02 6.03 6.04 6.05 6.06 6.07 6.08 6.09 6.10 Akashi YJ, Goldstein DS, Barbaro G, Ueyama T (2008). "Takotsubo cardiomyopathy: a new form of acute, reversible heart failure". Circulation. 118 (25): 2754–62. doi:10.1161/CIRCULATIONAHA.108.767012. PMC 4893309. PMID 19106400.
- ↑ 7.0 7.1 7.2 7.3 7.4 7.5 Prasad A, Lerman A, Rihal CS (2008). "Apical ballooning syndrome (Tako-Tsubo or stress cardiomyopathy): a mimic of acute myocardial infarction". Am. Heart J. 155 (3): 408–17. doi:10.1016/j.ahj.2007.11.008. PMID 18294473.
- ↑ 8.0 8.1 8.2 8.3 8.4 8.5 Tsai TT, Nallamothu BK, Prasad A, Saint S, Bates ER (2009). "Clinical problem-solving. A change of heart". N. Engl. J. Med. 361 (10): 1010–6. doi:10.1056/NEJMcps0903023. PMID 19726776.
- ↑ 9.0 9.1 9.2 9.3 Omerovic E (2011). "How to think about stress-induced cardiomyopathy?--Think "out of the box"!". Scand. Cardiovasc. J. 45 (2): 67–71. doi:10.3109/14017431.2011.565794. PMID 21401402.
- ↑ 10.0 10.1 10.2 10.3 10.4 10.5 10.6 10.7 10.8 10.9 Brenner ZR, Powers J (2008). "Takotsubo cardiomyopathy". Heart Lung. 37 (1): 1–7. doi:10.1016/j.hrtlng.2006.12.003. PMID 18206521.
- ↑ 11.0 11.1 11.2 11.3 11.4 11.5 11.6 11.7 11.8 Efferth T, Banerjee M, Paul NW (2016). "Broken heart, tako-tsubo or stress cardiomyopathy? Metaphors, meanings and their medical impact". Int. J. Cardiol. doi:10.1016/j.ijcard.2016.12.129. PMID 28041712.
- ↑ 12.0 12.1 12.2 12.3 12.4 12.5 12.6 12.7 12.8 12.9 Bybee KA, Kara T, Prasad A, Lerman A, Barsness GW, Wright RS, Rihal CS (2004). "Systematic review: transient left ventricular apical ballooning: a syndrome that mimics ST-segment elevation myocardial infarction". Ann. Intern. Med. 141 (11): 858–65. PMID 15583228.
- ↑ 13.0 13.1 Tsuchihashi K, Ueshima K, Uchida T, Oh-mura N, Kimura K, Owa M, Yoshiyama M, Miyazaki S, Haze K, Ogawa H, Honda T, Hase M, Kai R, Morii I (2001). "Transient left ventricular apical ballooning without coronary artery stenosis: a novel heart syndrome mimicking acute myocardial infarction. Angina Pectoris-Myocardial Infarction Investigations in Japan". J. Am. Coll. Cardiol. 38 (1): 11–8. PMID 11451258.
- ↑ 14.0 14.1 14.2 14.3 Sharkey SW, Lesser JR, Zenovich AG, Maron MS, Lindberg J, Longe TF, Maron BJ (2005). "Acute and reversible cardiomyopathy provoked by stress in women from the United States". Circulation. 111 (4): 472–9. doi:10.1161/01.CIR.0000153801.51470.EB. PMID 15687136.
- ↑ 15.0 15.1 Desmet WJ, Adriaenssens BF, Dens JA (2003). "Apical ballooning of the left ventricle: first series in white patients". Heart. 89 (9): 1027–31. PMC 1767823. PMID 12923018.
- ↑ Krishnamoorthy P, Garg J, Sharma A, Palaniswamy C, Shah N, Lanier G, Patel NC, Lavie CJ, Ahmad H (2015). "Gender Differences and Predictors of Mortality in Takotsubo Cardiomyopathy: Analysis from the National Inpatient Sample 2009-2010 Database". Cardiology. 132 (2): 131–136. doi:10.1159/000430782. PMID 26159108.
- ↑ 17.0 17.1 Templin C, Ghadri JR, Diekmann J, Napp LC, Bataiosu DR, Jaguszewski M, Cammann VL, Sarcon A, Geyer V, Neumann CA, Seifert B, Hellermann J, Schwyzer M, Eisenhardt K, Jenewein J, Franke J, Katus HA, Burgdorf C, Schunkert H, Moeller C, Thiele H, Bauersachs J, Tschöpe C, Schultheiss HP, Laney CA, Rajan L, Michels G, Pfister R, Ukena C, Böhm M, Erbel R, Cuneo A, Kuck KH, Jacobshagen C, Hasenfuss G, Karakas M, Koenig W, Rottbauer W, Said SM, Braun-Dullaeus RC, Cuculi F, Banning A, Fischer TA, Vasankari T, Airaksinen KE, Fijalkowski M, Rynkiewicz A, Pawlak M, Opolski G, Dworakowski R, MacCarthy P, Kaiser C, Osswald S, Galiuto L, Crea F, Dichtl W, Franz WM, Empen K, Felix SB, Delmas C, Lairez O, Erne P, Bax JJ, Ford I, Ruschitzka F, Prasad A, Lüscher TF (2015). "Clinical Features and Outcomes of Takotsubo (Stress) Cardiomyopathy". N. Engl. J. Med. 373 (10): 929–38. doi:10.1056/NEJMoa1406761. PMID 26332547.
- ↑ Y-Hassan S, Yamasaki K (2013). "History of takotsubo syndrome: is the syndrome really described as a disease entity first in 1990? Some inaccuracies". Int. J. Cardiol. 166 (3): 736–7. doi:10.1016/j.ijcard.2012.09.183. PMID 23073280.
- ↑ Sharkey SW, Lesser JR, Zenovich AG, Maron MS, Lindberg J, Longe TF, Maron BJ (2005). "Acute and reversible cardiomyopathy provoked by stress in women from the United States". Circulation. 111 (4): 472–9. doi:10.1161/01.CIR.0000153801.51470.EB. PMID 15687136.
- ↑ Krishnamoorthy P, Garg J, Sharma A, Palaniswamy C, Shah N, Lanier G, Patel NC, Lavie CJ, Ahmad H (2015). "Gender Differences and Predictors of Mortality in Takotsubo Cardiomyopathy: Analysis from the National Inpatient Sample 2009-2010 Database". Cardiology. 132 (2): 131–136. doi:10.1159/000430782. PMID 26159108.
- ↑ Paul NS, Roberts H, Butany J, Chung T, Gold W, Mehta S, Konen E, Rao A, Provost Y, Hong HH, Zelovitsky L, Weisbrod GL (2004). "Radiologic pattern of disease in patients with severe acute respiratory syndrome: the Toronto experience". Radiographics. 24 (2): 553–63. doi:10.1148/rg.242035193. PMID 15026600.
- ↑ Ajlan AM, Ahyad RA, Jamjoom LG, Alharthy A, Madani TA (October 2014). "Middle East respiratory syndrome coronavirus (MERS-CoV) infection: chest CT findings". AJR Am J Roentgenol. 203 (4): 782–7. doi:10.2214/AJR.14.13021. PMID 24918624.
- ↑ Chen, Nanshan; Zhou, Min; Dong, Xuan; Qu, Jieming; Gong, Fengyun; Han, Yang; Qiu, Yang; Wang, Jingli; Liu, Ying; Wei, Yuan; Xia, Jia'an; Yu, Ting; Zhang, Xinxin; Zhang, Li (2020). "Epidemiological and clinical characteristics of 99 cases of 2019 novel coronavirus pneumonia in Wuhan, China: a descriptive study". The Lancet. doi:10.1016/S0140-6736(20)30211-7. ISSN 0140-6736.
- ↑ Haghi D, Fluechter S, Suselbeck T, Kaden JJ, Borggrefe M, Papavassiliu T (2007). "Cardiovascular magnetic resonance findings in typical versus atypical forms of the acute apical ballooning syndrome (Takotsubo cardiomyopathy)". Int. J. Cardiol. 120 (2): 205–11. doi:10.1016/j.ijcard.2006.09.019. PMID 17175045.
- ↑ 25.0 25.1 Mitchell JH, Hadden TB, Wilson JM, Achari A, Muthupillai R, Flamm SD (2007). "Clinical features and usefulness of cardiac magnetic resonance imaging in assessing myocardial viability and prognosis in Takotsubo cardiomyopathy (transient left ventricular apical ballooning syndrome)". Am. J. Cardiol. 100 (2): 296–301. doi:10.1016/j.amjcard.2007.02.091. PMID 17631086.
- ↑ Deetjen AG, Conradi G, Mollmann S, Rad A, Hamm CW, Dill T (2006). "Value of gadolinium-enhanced magnetic resonance imaging in patients with Tako-Tsubo-like left ventricular dysfunction". J Cardiovasc Magn Reson. 8 (2): 367–72. PMID 16669180.
- ↑ Abe Y, Kondo M, Matsuoka R, Araki M, Dohyama K, Tanio H (2003). "Assessment of clinical features in transient left ventricular apical ballooning". J. Am. Coll. Cardiol. 41 (5): 737–42. PMID 12628715.
- ↑ Dec GW (2005). "Recognition of the apical ballooning syndrome in the United States". Circulation. 111 (4): 388–90. doi:10.1161/01.CIR.0000155234.69439.E4. PMID 15687123.
- ↑ Handy AD, Prasad A, Olson TM (2009). "Investigating genetic variation of adrenergic receptors in familial stress cardiomyopathy (apical ballooning syndrome)". J Cardiol. 54 (3): 516–7. doi:10.1016/j.jjcc.2009.08.008. PMID 19944334.
- ↑ Eitel I, von Knobelsdorff-Brenkenhoff F, Bernhardt P, Carbone I, Muellerleile K, Aldrovandi A, Francone M, Desch S, Gutberlet M, Strohm O, Schuler G, Schulz-Menger J, Thiele H, Friedrich MG (2011). "Clinical characteristics and cardiovascular magnetic resonance findings in stress (takotsubo) cardiomyopathy". JAMA. 306 (3): 277–86. doi:10.1001/jama.2011.992. PMID 21771988.
- ↑ Eitel I, Behrendt F, Schindler K, Kivelitz D, Gutberlet M, Schuler G, Thiele H (2008). "Differential diagnosis of suspected apical ballooning syndrome using contrast-enhanced magnetic resonance imaging". Eur. Heart J. 29 (21): 2651–9. doi:10.1093/eurheartj/ehn433. PMID 18820322.
- ↑ Testa M, Feola M (2014). "Usefulness of myocardial positron emission tomography/nuclear imaging in Takotsubo cardiomyopathy". World J Radiol. 6 (7): 502–6. doi:10.4329/wjr.v6.i7.502. PMC 4109102. PMID 25071891.