Characterization of the Myocardial Inflammatory Response in Acute Stress-Induced (Takotsubo) Cardiomyopathy.
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SUBMITTER: Wilson HM
PROVIDER: S-EPMC6314973 | biostudies-literature | 2018 Dec
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: Not available
| S-EPMC6301975 | 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:ECG criteria differentiating Takotsubo cardiomyopathy (TTC) from mainly anterior myocardial infarction (MI) have been suggested; however, this was in small patient populations. Twelve-lead admission ECGs of consecutive 200 TTC and 200 MI patients were compared in dichotomized groups based on the presence or absence of ST-elevation MI (STEMI versus STE-TTC and non-ST elevation MI versus non ST-elevation-TTC). When comparing STEMI and STE-TTC, ST-elevation in -aVR was characteristic of STE-TTC with a sensitivity/specificity of 43% and 95%, positive predictive value (PPV) 91%, and a negative predictive value (NPV) 62% (P<0.001); when ST-elevation in -aVR is accompanied by ST-elevation in inferior leads, sensitivity/specificity were 14% and 98% (PPV was 89% and NPV 52%) (P=0.001), and 12% and 100% when associated with ST-elevation in anteroseptal leads (PPV 100%, NPV 52%) (P<0.001). On the other hand, STEMI was characterized by ST-elevation in aVR (sensitivity/specificity of 31% and 95% P<0.001, PPV 85% and NPV 59%) and ST-depression in V2-V3-V4 (sensitivity/specificity of 24% and 100% P<0.001, PPV 100% and NPV 76%). When comparing non-ST elevation MI and non ST-elevation-TTC, T-inversion in leads I-aVL-V5-V6 had a sensitivity/specificity of 17% and 97% for non ST-elevation-TTC (PPV 83% and NPV 55%) (P<0.001), and ST-elevation in -aVR with T-inversion in any lead was also specific for non ST-elevation-TTC (sensitivity/specificity of 8% and 100%, PPV 100% and NPV 53%) (P=0.006). In non-ST elevation MI patients, the presence of ST-depression in V2-V3 was specific (sensitivity/specificity of 11% and 99%, PPV 91% and NPV 51%) (P=0.01). ECG on admission can differentiate between TTC and acute MI, with high specificity and positive predictive value. URL: https://www.clinicaltrials.gov/. Unique identifier: NCT01947621.
| S-EPMC4937281 | biostudies-literature
Project description:A healthy 66-year-old female presented to the emergency department with acute chest pain, T-wave inversion in the anterior leads, and elevated troponin-I. Coronary angiography showed a stenosis in the midportion of the left anterior descending coronary artery (LAD), which did not wrap the left ventricle (LV) apex. LV angiography demonstrated a large LV apical akinetic systolic ballooning with a 45% ejection fraction. Fractional flow reserve (FFR) of LAD lesion was 0.71. Percutaneous intervention was performed. At six months, transthoracic echocardiography was normal. Fifteen months later, the patient presented with chest pain and a small rise in troponin-I. Coronary angiogram was unchanged. Repeat FFR in distal LAD was 0.86 and left ventriculography was normal. Diagnostic criteria for Takotsubo cardiomyopathy (TTC) require the absence of obstructive coronary artery disease. In the present case, TTC was highly suspected on the basis of typical LV apex ballooning. However, significant ischemia in the same territory was demonstrated by positive FFR, which could not be falsely positive in this context. Current TTC diagnostic criteria increase specificity for diagnosing TTC. This case reminds us that it is at the price of reduced sensitivity, since there is no reason to believe that coronary lesions may protect from TTC.
| S-EPMC7060413 | biostudies-literature
Project description:Takotsubo cardiomyopathy (TC) can be provoked by various triggers. It should be differentiated from acute coronary syndrome (ACS). Herein, we report a case of TC triggered by ACS. An 80-year-old woman was referred to the emergency room because of prolonged chest pain and ST-segment elevations. Echocardiography demonstrated left ventricular apical ballooning, findings suggestive of TC rather than ACS. Emergency coronary angiography revealed severe stenosis of the first diagonal branch of the left anterior descending coronary artery with distal flow delay. Recanalization of the diagonal branch was achieved by stent implantation and her chest pain was resolved. Cardiac magnetic resonance imaging showed increased signal intensities in the apex and the inner layer of the anterior wall on fat-suppressed, T2-weighted imaging. The present case highlights the importance of recognizing TC in relation to ACS not only as a differential diagnosis but also as a possibly concomitant condition unless clinical features fit one diagnosis.Learning objectiveTakotsubo cardiomyopathy can be provoked by various conditions and differentiated from acute coronary syndrome based on the presence or absence of coronary artery stenosis. Our case highlights the importance of acknowledging that takotsubo cardiomyopathy may be induced by acute coronary syndrome.
| S-EPMC10562094 | biostudies-literature
Project description:Takotsubo cardiomyopathy (TTC) shows reversible hypokinesis in the left ventricular (LV) apical-half segment and hyperkinesis in the LV basal-half segment. However, the precise pathophysiological mechanism of TTC is unclear. Therefore, this study sought to clarify the nuclear characteristics, degree of myocardial damage, and serial change of TTC and rTTC using myocardial perfusion imaging. We performed myocardial perfusion scintigraphy in 28 patients (TTC: 20, rTTC: 8) using Tc-99m sestamibi and assessed minimum percentage uptake (min-%-uptake), extent score (ES) and summed rest score (SRS) at acute and chronic phases. Min-%-uptake improved from the acute to the chronic phase (TTC: 54 [48-59]% vs 87 [81-90]%, P < 0.01; rTTC: 60 [55-64]% vs 77 [71-79]%, P < 0.01), as did the ES (TTC: 32 [26-41]% vs 0.0 [0.0-6.0]%, P < 0.01; rTTC: 16 [12-34]% vs 0.0 [0.0-0.0]%, P = 0.02) and SRS (TTC: 4.5 [3.9-5.3] vs 0.0 [0.0-0.2], P < 0.01; rTTC: 3.6 [3.3-3.8] vs 0.0 [0.0-0.0], P = 0.01). Tc-99m sestamibi uptake was reduced in hypokinetic regions in the acute phase and improved in the chronic phase. TTC and rTTC may involve a reversible disorder of the myocardial cell membrane, mitochondria, and microcirculation.
| S-EPMC9553766 | biostudies-literature
Project description:BACKGROUND:Mental stress-induced myocardial ischemia (MSIMI) is associated with increased risk of adverse cardiovascular outcomes, yet the underlying mechanisms are not well understood. We measured the inflammatory response to acute laboratory mental stress in patients with coronary artery disease (CAD) and its association with MSIMI. We hypothesized that patients with MSIMI would have a higher inflammatory response to mental stress in comparison to those without ischemia. METHODS:Patients with stable CAD underwent 99mTc sestamibi myocardial perfusion imaging during mental stress testing using a public speaking stressor. MSIMI was determined as impaired myocardial perfusion using a 17-segment model. Inflammatory markers including interleukin-6 (IL-6), monocyte chemoattractant protein-1 (MCP-1), matrix metallopeptidase 9 (MMP-9) and high-sensitivity C reactive protein (hsCRP) were measured at rest and 90?min after mental stress. Results were validated in an independent sample of 228 post-myocardial infarction patients. RESULTS:Of 607 patients analyzed in this study, (mean age 63?±?9?years, 76% male), 99 (16.3%) developed MSIMI. Mental stress resulted in a significant increase in IL-6, MCP-1, and MMP-9 (all p?<0.0001), but not hsCRP. However, the changes in these markers were similar in those with and without MSIMI. Neither resting levels of these biomarkers, nor their changes with mental stress were significantly associated with MSIMI. Results in the replication sample were similar. CONCLUSION:Mental stress is associated with acute increases in several inflammatory markers. However, neither the baseline inflammatory status nor the magnitude of the inflammatory response to mental stress over 90?min were significantly associated with MSIMI.
| S-EPMC5808921 | 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: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.
| S-EPMC5728791 | biostudies-literature