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      Stress-induced cardiomyopathy (Takotsubo) – broken heart and mind?

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          Abstract

          Stress-induced cardiomyopathy (SIC), also known as Takotsubo cardiomyopathy, is characterized by severe but potentially reversible regional left ventricular wall motion abnormalities, ie, akinesia, in the absence of explanatory angiographic evidence of a coronary occlusion. The typical pattern is that of an akinetic apex with preserved contractions in the base, but other variants are also common, including basal or midmyocardial akinesia with preserved apical function. The pathophysiology of SIC remains largely unknown but catecholamines are believed to play a pivotal role. The diverse array of triggering events that have been linked to SIC are arbitrarily categorized as either emotional or somatic stressors. These categories can be considered as different elements of a continuous spectrum, linked through the interface of neurology and psychiatry. This paper reviews our current knowledge of SIC, with focus on the intimate relationship between the brain and the heart.

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          Most cited references35

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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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            Stress cardiomyopathy after intravenous administration of catecholamines and beta-receptor agonists.

            The aim of this study was to report a series of patients with stress cardiomyopathy precipitated by the intravenous administration of catecholamines and beta-receptor agonists. Stress cardiomyopathy is a syndrome of transient cardiac dysfunction precipitated by intense emotional or physical stress. Excessive sympathetic stimulation is believed to be central to the pathogenesis of this disorder, but a causal link has not been convincingly demonstrated. We observed 9 cases of stress cardiomyopathy precipitated immediately by the intravenous administration of epinephrine (n = 6) or dobutamine (n = 3). Patients were evaluated with coronary angiography and with serial echocardiography, electrocardiography, and cardiac enzymes. The median age was 44 years (interquartile range [IQR]: 30 to 48 years), and 7 (78%) were woman. Troponin-I was mildly elevated (median 4.07 ng/ml, IQR: 0.47 to 5.63 ng/ml), but none of the patients undergoing angiography had obstructive coronary disease. All patients developed corrected QT interval (QTc interval) prolongation (median QTc interval 504 ms, IQR: 477 to 568 ms) within 24 h of receiving drug. All 3 previously described variants of left ventricular "ballooning" (apical, midventricular, and basal) were observed. The median ejection fraction on admission was 35% (IQR: 35% to 40%). During follow-up (median 7 days, IQR: 4 to 13 days) there was recovery of left ventricular systolic function in all patients (median ejection fraction 55%, IQR: 40% to 60%, p < 0.001 vs. admission). Exposure to catecholamines and beta-receptor agonists used routinely during procedures and diagnostic tests can precipitate all the features of stress cardiomyopathy, including cardiac isoenzyme elevation, QTc interval prolongation, and rapidly reversible cardiac dysfunction. These observations strongly implicate excessive sympathetic stimulation as central to the pathogenesis of this unique syndrome.
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              Prospective reports of chronic life stress predict decreased grey matter volume in the hippocampus.

              Chronic stress in non-human animals decreases the volume of the hippocampus, a brain region that supports learning and memory and that regulates neuroendocrine activity. In humans with stress-related psychiatric syndromes characterized by impaired learning and memory and dysregulated neuroendocrine activity, surrogate and retrospective indicators of chronic stress are also associated with decreased hippocampal volume. However, it is unknown whether chronic stress is associated with decreased hippocampal volume in those without a clinical syndrome. We tested whether reports of life stress obtained prospectively over an approximate 20-year period predicted later hippocampal grey matter volume in 48 healthy postmenopausal women. Women completed the Perceived Stress Scale repeatedly from 1985 to 2004; in 2005 and 2006, their hippocampal grey matter volume was quantified by voxel-based morphometry. Higher Perceived Stress Scale scores from 1985 to 2004 - an indicator of more chronic life stress - predicted decreased grey matter volume in the right orbitofrontal cortex and right hippocampus. These relationships persisted after accounting for age, total grey matter volume, time since menopause, use of hormone therapy, subclinical depressive symptoms, and other potentially confounding behavioral and age-related cerebrovascular risk factors. The relationship between chronic life stress and regional grey matter volume - particularly in the hippocampus and orbitofrontal cortex - appears to span a continuum that extends to otherwise healthy individuals. Consistent with animal and human clinical evidence, we speculate that chronic-stress-related variations in brain morphology are reciprocally and functionally related to adaptive and maladaptive changes in cognition, neuroendocrine activity, and psychiatric vulnerability.
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                Author and article information

                Journal
                Vasc Health Risk Manag
                Vasc Health Risk Manag
                Vascular Health and Risk Management
                Vascular Health and Risk Management
                Dove Medical Press
                1176-6344
                1178-2048
                2013
                2013
                17 April 2013
                : 9
                : 149-154
                Affiliations
                Department of Molecular and Clinical Medicine, Sahlgrenska Academy at University of Gothenburg, Gothenburg, Sweden
                Author notes
                Correspondence: Björn Redfors, The Wallenberg Laboratory at Sahlgrenska Academy, Bruna Stråket 16, 413 45 Göteborg, Sweden Tel +46-31 342 7560 Fax +46 31 82 6732 Email bjoern.redfors@ 123456wlab.gu.se
                Article
                vhrm-9-149
                10.2147/VHRM.S40163
                3632585
                23626469
                3d1186a0-3626-4906-9324-fb141b93472b
                © 2013 Redfors et al, publisher and licensee Dove Medical Press Ltd

                This is an Open Access article which permits unrestricted noncommercial use, provided the original work is properly cited.

                History
                Categories
                Review

                Cardiovascular Medicine
                stress-induced cardiomyopathy,takotsubo cardiomyopathy,catecholamine,cerebral injury,emotional stress,somatic stress

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