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Myocardial and Systemic Inflammation in Acute Stress-Induced (Takotsubo) Cardiomyopathy.

ABSTRACT: BACKGROUND:Acute 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. METHODS:In 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. RESULTS:Subjects 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. CONCLUSIONS:We 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 REGISTRATION:URL: https://www.clinicaltrials.gov . Unique identifier: NCT02897739.

SUBMITTER: Scally C

PROVIDER: S-EPMC6438459 | biostudies-literature | 2019 Mar

REPOSITORIES: biostudies-literature

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Project description:RationalTakotsubo cardiomyopathy (TCM) is a transient systolic dysfunction of the left ventricular apex without stenosis of coronary arteries and is induced by various psychological and physical factors. TCM sometimes causes lethal complications such as arrhythmia, thrombogenesis, and even cardiac rupture, and thus it should be diagnosed appropriately and managed carefully. Intensive care unit (ICU) patients are exposed to overstress during the treatment process and therefore can are at potential risk for TCM.Patient concernsThe patient was diagnosed as having pneumonia because of influenza A virus mixed with bacteria and underwent intensive care with intubation and mechanical ventilation in the ICU. His respiratory condition soon improved, and so extubation was carried out; however, redeterioration with pulmonary edema occurred at half of a day following extubation.DiagnosisThe chest x-ray revealed pulmonary edema. The electrocardiogram pattern significantly changed with time, and the echocardiogram showed weakness of wall motion around the left ventricular apex. Hence, to confirm the diagnosis, we performed cardiac catheterization immediately, with the results showing a Takotsubo-like form at the systolic phase without significant stenosis of the coronary arteries.InterventionThe patient was reintubated with administration of catecholamine for decreasing blood pressure caused by left ventricular dysfunction. Also, diuretics for pulmonary edema and anticoagulants for prevention of thrombogenesis were administered.OutcomesAs the respiratory condition improved with stabilization of cardiovascular hemodynamics, reextubation was done at ICU day 11 and was discharged from the ICU at ICU day 15. The patient was subsequently treated for pneumonia after leaving the ICU but suffered from repetitive aspiration pneumonia and was finally transferred to another hospital at hospital day 111.LessonsTCM should be considered especially under the situation of intensive care, and prompt diagnosis should be followed by appropriate management.

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Myocardial and Systemic Inflammation in Acute Stress-Induced (Takotsubo) Cardiomyopathy.

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