Cough-Induced Takotsubo (Stress) Cardiomyopathy.
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ABSTRACT:
SUBMITTER: Lal S
PROVIDER: S-EPMC6301975 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:BackgroundAcute stress-induced (takotsubo) cardiomyopathy can result in a heart failure phenotype with a prognosis comparable with that of myocardial infarction. In this study, we hypothesized that inflammation is central to the pathophysiology and natural history of takotsubo cardiomyopathy.MethodsIn a multicenter study, we prospectively recruited 55 patients with takotsubo cardiomyopathy and 51 age-, sex-, and comorbidity-matched control subjects. During the index event and at the 5-month follow-up, patients with takotsubo cardiomyopathy underwent multiparametric cardiac magnetic resonance imaging, including ultrasmall superparamagnetic particles of iron oxide (USPIO) enhancement for detection of inflammatory macrophages in the myocardium. Blood monocyte subpopulations and serum cytokines were assessed as measures of systemic inflammation. Matched control subjects underwent investigation at a single time point.ResultsSubjects were predominantly middle-aged (64±14 years) women (90%). Compared with control subjects, patients with takotsubo cardiomyopathy had greater USPIO enhancement (expressed as the difference between pre-USPIO and post-USPIO T2*) in both ballooning (14.3±0.6 milliseconds versus 10.5±0.9 milliseconds; P<0.001) and nonballooning (12.9±0.6 milliseconds versus 10.5±0.9 milliseconds; P=0.02) left ventricular myocardial segments. Serum interleukin-6 (23.1±4.5 pg/mL versus 6.5±5.8 pg/mL; P<0.001) and chemokine (C-X-C motif) ligand 1 (1903±168 pg/mL versus 1272±177 pg/mL; P=0.01) concentrations and classic CD14++CD16- monocytes (90±0.5% versus 87±0.9%; P=0.01) were also increased whereas intermediate CD14++CD16+ (5.4±0.3% versus 6.9±0.6%; P=0.01) and nonclassic CD14+CD16++ (2.7±0.3% versus 4.2±0.5%; P=0.006) monocytes were reduced in patients with takotsubo cardiomyopathy. At 5 months, USPIO enhancement was no longer detectable in the left ventricular myocardium, although persistent elevations in serum interleukin-6 concentrations ( P=0.009) and reductions in intermediate CD14++CD16+ monocytes (5.6±0.4% versus 6.9±0.6%; P=0.01) remained.ConclusionsWe demonstrate for the first time that takotsubo cardiomyopathy is characterized by a myocardial macrophage inflammatory infiltrate, changes in the distribution of monocyte subsets, and an increase in systemic proinflammatory cytokines. Many of these changes persisted for at least 5 months, suggesting a low-grade chronic inflammatory state.Clinical trial registrationURL: https://www.clinicaltrials.gov . Unique identifier: NCT02897739.
| S-EPMC6438459 | biostudies-literature
Project description:A 48-year-old woman was scheduled by our lab to perform a standard dobutamine/atropine stress echocardiogram. During the test, the patient referred to a slight chest discomfort and developed a progressive left ventricle akinesia of all midbasal LV segments, thus mimicking a midbasal ballooning. ECG persisted without significant abnormalities and with no raise of Troponin I. Coronary angiography showed normal coronary arteries and ventriculography a severe EF reduction and apical hypercontractility. Echocardiography showed a progressive improvement with a complete recovery 48 hours later. This is a rare case of inverted takotsubo syndrome induced by dobutamine stress echocardiography that occurred with atypical presentation.
| S-EPMC4007740 | biostudies-literature
Project description:A 73-year-old patient who was admitted secondary to acute asthma exacerbation that required frequent salbutamol and adrenaline nebulization. Takotsubo cardiomyopathy (TTC) was diagnosed after the new onset of chest pain with modest troponin elevation and normal coronary angiogram. Low ejection fraction and apical akinesia were completely resolved after her symptoms got improved.
| S-EPMC9995802 | biostudies-literature
Project description:A 79-year-old woman was admitted with a left femoral neck fracture and she immediately developed circulatory shock. Echocardiography showed a markedly enlarged right ventricle (RV) with systolic ballooning of the mid-ventricular wall and preserved contractility of the apex. The left ventricular (LV) motion was normal. Multi-detector-row computed tomography showed severe congestion of the contrast media in the right atrium with no forward flow to RV, but no pulmonary embolism. She was successfully treated with percutaneous veno-arterial extracorporeal membrane oxygenation. This case presented with acute, profound, but reversible RV dysfunction triggered by acute stress in a manner similar to that seen in LV stress cardiomyopathy.
| S-EPMC5596277 | biostudies-literature
Project description: Not available
| S-EPMC7398589 | biostudies-literature
Project description:BACKGROUND: Takotsubo cardiomyopathy is a novel, yet well-described, reversible cardiomyopathy triggered by profound psychological or physical stress with a female predominance. OBJECTIVE: This review is designed to increase general clinician awareness about the diagnosis, incidence, pathogenesis, and therapies of this entity. DATA SOURCES: A complete search of multiple electronic databases (Pubmed, EMBASE, Science Citation Index) was carried out to identify all full-text, English-language articles published from 1980 to the present date and relevant to this review. REVIEW METHODS: The following search terms were used: takotsubo cardiomyopathy, stress-induced cardiomyopathy, and left ventricular apical ballooning syndrome. Citation lists from identified articles were subsequently reviewed and pertinent articles were further identified. RESULTS: Takotsubo cardiomyopathy is typically characterized by the following: 1) acute onset of ischemic-like chest pain or dyspnea, 2) transient apical and mid-ventricular regional wall-motion abnormality, 3) minor elevation of cardiac biomarkers, 4) dynamic electrocardiographic changes, and 5) the absence of epicardial coronary artery disease. The pathogenesis of the syndrome is unknown but has mostly been associated with acute emotional or physiologic stressors. Dote, Sato, Tateishi, Uchida, Ishihara (J Cardiol. 21(2):203-214, 1991); Desmet, Adriaenssens, Dens (Heart. 89(9):1027-1031, Sep., 2003); Bybee, Kara, Prasad, et al. (Ann Intern Med. 141(11):858-865, Dec 7, 2004); Sharkey, Lesser, Zenovich, et al. (Circulation. 111(4):472-479, Feb 1, 2005) The short and long-term prognosis of these patients is overwhelmingly favorable and often only requires supportive therapy. CONCLUSION: Whether an emotional or physical event precedes one's symptoms, it is apparent that takotsubo cardiomyopathy case presentations mimic ST-segment elevation myocardial infarction, and thus is an important entity to be recognized by the medical community.
| S-EPMC2585677 | biostudies-other
Project description:Takotsubo cardiomyopathy is an acute stress-induced heart failure syndrome for which the exact pathogenic mechanisms are unclear, and consequently, no specific treatment exists. In an experimental model of stress-induced takotsubo-like cardiomyopathy, the authors describe the temporal course of a chronic inflammatory response post-induction, with an initial early influx of neutrophils into myocardial tissue followed by macrophages that are typical of a proinflammatory M1 phenotype, and a nonsignificant increase in systemic inflammatory cytokines. Post-mortem myocardium from the more complex clinical takotsubo patients share features of the study's experimental model. These findings suggest modulators of inflammation could be a potential therapeutic option.
| S-EPMC6314973 | biostudies-literature
Project description:Takotsubo cardiomyopathy is associated with a constellation of cardiac findings including reversible left ventricular dysfunction and an acute triggering stressor. Epicardial coronary vasospasm is a rarely reported etiology for takotsubo cardiomyopathy, and its pathophysiologic mechanisms still remain incompletely understood. We present the case of a 54-year-old female with chest pain and ST-elevation myocardial infarction who was found to have takotsubo cardiomyopathy due to diffuse multivessel coronary artery vasospasm in the absence of obstructive coronary artery disease. To our knowledge, this is the first angiographically confirmed case of this rare phenomenon to be reported, as most literature involves focal, segmental, or single coronary artery involvement. Moreover, we review current literature and develop a discussion on the targeted treatment of vasospastic disease as part of the multimodal approach to the management of takotsubo syndrome.
| S-EPMC8786520 | biostudies-literature
Project description:Takotsubo syndrome (TTS) is an acute, stress-induced cardiomyopathy that occurs predominantly in women after extreme physical and/or emotional stress. To date, our understanding of the molecular basis for TTS remains unknown and, consequently, specific therapies are lacking. Myocardial infiltration of monocytes and macrophages in TTS has been documented in clinical studies. However, the functional importance of these findings remains poorly understood. Here, we show that a single high dose of isoproterenol (ISO) in mice induced a TTS-like cardiomyopathy phenotype characterized by female predominance, severe cardiac dysfunction, and robust myocardial infiltration of macrophages. Single-cell RNA-Seq studies of myocardial immune cells revealed that TTS-like cardiomyopathy is associated with complex activation of innate and adaptive immune cells in the heart, and macrophages were identified as the dominant immune cells. Global macrophage depletion (via clodronate liposome administration) or blockade of macrophage infiltration (via a CCR2 antagonist or in CCR2-KO mice) resulted in recovery of cardiac dysfunction in ISO-challenged mice. In addition, damping myeloid cell activation by HIF1α deficiency or exposure to the immunomodulatory agent bortezomib ameliorated ISO-induced cardiac dysfunction. Collectively, our findings identify macrophages as a critical regulator of TTS pathogenesis that can be targeted for therapeutic gain.
| S-EPMC8855841 | biostudies-literature
Project description: Not available
| S-EPMC7932813 | biostudies-literature