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      Epidemiology, pathogenesis, and management of takotsubo syndrome

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          Abstract

          Takotsubo syndrome is a recently recognized acute cardiac disease entity with a clinical presentation resembling that of an acute coronary syndrome. The typical takotsubo syndrome patient has a unique circumferential left (bi-) ventricular contraction abnormality profile that extends beyond a coronary artery supply territory and appears to follow the anatomical cardiac sympathetic innervation. The syndrome predominantly affects postmenopausal women and is often preceded by emotional or physical stress. Patients with predisposing factors such as malignancy and other chronic comorbidities are more prone to suffer from takotsubo syndrome. The pathogenesis of takotsubo syndrome is elusive. Several pathophysiological mechanisms involving myocardial ischemia (multivessel coronary artery spasm, microvascular dysfunction, aborted myocardial infarction), left ventricular outlet tract obstruction, blood-borne catecholamine myocardial toxicity, epinephrine-induced switch in signal trafficking, and autonomic nervous system dysfunction have been proposed. The syndrome is usually reversible; nevertheless, during the acute stage, a substantial number of patients develop severe complications such as arrhythmias, heart failure including pulmonary edema and cardiogenic shock, thromboembolism, cardiac arrest, and rupture. Treatment of precipitating factors, predisposing diseases, and complications is fundamental during the acute stage of the disease. The epidemiology, pathogenesis, and management of takotsubo syndrome are reviewed in this paper.

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          Natural history and expansive clinical profile of stress (tako-tsubo) cardiomyopathy.

          This study was designed to define more completely the clinical spectrum and consequences of stress cardiomyopathy (SC) beyond the acute event. Stress cardiomyopathy is a recently recognized condition characterized by transient cardiac dysfunction with ventricular ballooning. Clinical profile and outcome were prospectively assessed in 136 consecutive SC patients. Patients were predominantly women (n = 130; 96%), but 6 were men (4%). Ages were 32 to 94 years (mean age 68 +/- 13 years); 13 (10%) were 2 months in 5%. Right and/or left ventricular thrombi were identified in 5 patients (predominantly by CMR imaging), including 2 with embolic events. Three patients (2%) died in-hospital and 116 (85%) have survived, including 5% with nonfatal recurrent SC events. All-cause mortality during follow-up exceeded a matched general population (p = 0.016) with most deaths occurring in the first year. In this large SC cohort, the clinical spectrum was heterogeneous with about one-third either male,
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            The brain-heart connection.

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              Mechanisms of myocardial infarction in women without angiographically obstructive coronary artery disease.

              There is no angiographically demonstrable obstructive coronary artery disease (CAD) in a significant minority of patients with myocardial infarction, particularly women. We sought to determine the mechanism(s) of myocardial infarction in this setting using multiple imaging techniques. Women with myocardial infarction were enrolled prospectively, before angiography, if possible. Women with ≥50% angiographic stenosis or use of vasospastic agents were excluded. Intravascular ultrasound was performed during angiography; cardiac magnetic resonance imaging was performed within 1 week. Fifty women (age, 57±13 years) had median peak troponin of 1.60 ng/mL; 11 had ST-segment elevation. Median diameter stenosis of the worst lesion was 20% by angiography; 15 patients (30%) had normal angiograms. Plaque disruption was observed in 16 of 42 patients (38%) undergoing intravascular ultrasound. There were abnormal myocardial cardiac magnetic resonance imaging findings in 26 of 44 patients (59%) undergoing cardiac magnetic resonance imaging, late gadolinium enhancement (LGE) in 17 patients, and T2 signal hyperintensity indicating edema in 9 additional patients. The most common LGE pattern was ischemic (transmural/subendocardial). Nonischemic LGE patterns (midmyocardial/subepicardial) were also observed. Although LGE was infrequent with plaque disruption, T2 signal hyperintensity was common with plaque disruption. Plaque rupture and ulceration are common in women with myocardial infarction without angiographically demonstrable obstructive coronary artery disease. In addition, LGE is common in this cohort of women, with an ischemic pattern of injury most evident. Vasospasm and embolism are possible mechanisms of ischemic LGE without plaque disruption. Intravascular ultrasound and cardiac magnetic resonance imaging provide complementary mechanistic insights into female myocardial infarction patients without obstructive coronary artery disease and may be useful in identifying potential causes and therapies. Clinical Trial Registration- URL: http://www.clinicaltrials.gov. Unique identifier: NCT00798122.
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                Author and article information

                Contributors
                +46 8 6161000 , per.tornvall@ki.se
                Journal
                Clin Auton Res
                Clin. Auton. Res
                Clinical Autonomic Research
                Springer Berlin Heidelberg (Berlin/Heidelberg )
                0959-9851
                1619-1560
                15 September 2017
                15 September 2017
                2018
                : 28
                : 1
                : 53-65
                Affiliations
                [1 ]Department of Cardiology, Karolinska Institutet at Karolinska University Hospital, Solna, Sweden
                [2 ]ISNI 0000 0004 1937 0626, GRID grid.4714.6, Department of Clinical Science and Education Södersjukhuset, , Karolinska Institutet, ; Sjukhusbacken 10, 118 83 Stockholm, Sweden
                Article
                465
                10.1007/s10286-017-0465-z
                5805795
                28917022
                4f9f5838-f513-4a58-90a5-ae70fe8ca038
                © The Author(s) 2017

                Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.

                History
                : 2 June 2017
                : 31 August 2017
                Categories
                Review
                Custom metadata
                © Springer-Verlag GmbH Germany, part of Springer Nature 2018

                Medicine
                takotsubo,broken heart syndrome,acute coronary syndrome,neurogenic stunned myocardium,left ventricle ballooning

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