Cardiomyopathy Takotsubo Publications (3110)
Cardiomyopathy Takotsubo Publications
Computed tomography showed a shadow-like region with a similar appearance to interstitial pneumonia. The patient was diagnosed with takotsubo cardiomyopathy induced by severe lung disease based on the results of echocardiography and coronary angiography. The patient was treated for interstitial pneumonia. However, his condition rapidly deteriorated and he died 6 hours after arrival. We were later informed of his extremely high catecholamine serum levels. We found pheochromocytoma with hemorrhage at autopsy. The patient's lungs showed acute passive congestion with edema and extravasation.
All patients were treated at Vilnius University Hospital Santariskiu Klinikos from 2001-01-01 to 2014-11-27. Data were collected on the basis of medical records and follow-up data was collected by phone.
The mean age of analyzed patients was 63.4 ± 14.6 years; the mean follow-up was 2.9 years. More than half of the patients (52%) did not have any clear stressful triggers. During admission, symptoms such as chest pain (64%) and general weakness (45%) were reported more often than other symptoms. Almost all patients (94%) had the classical TTC form; the remaining 6% of patients had "inverted" TTC. The mean left ventricular ejection fraction (LVEF) on admission was 37.7% (± 8.2%). A pseudonormal or restrictive pattern of LV filling, moderate to severe mitral regurgitation (MR), and right ventricular involvement were uncommon in the patients. The in-hospital course showed cardiogenic shock in 23% of the cases, resulting in the death of 5 (8%) patients. We discovered that only peak concentration of troponin I was a significant predictor of in-hospital mortality (HR 1.067, 95%CI 1.022-1.113, p=0.003). At the end of the follow-up period, 45 (87%) women and 8 (67%) men were alive. This makes the overall observed mortality at 3 years approximately 17.2%. Using multivariate analysis, elevation of BNP (HR for increase by 10 ng/l 1.002, 95%CI 1-1.003, p=0.022) and cardiogenic shock on admission (HR 8.696, 95%CI 1.198-63.124, p=0.032) were significant predictors of overall mortality. Other prognostic factors assessed on admission were nonsignificant predictors of overall mortality.
Our analysis shows that in-hospital mortality is influenced by the peak concentration of troponin I, and overall mortality is affected by cardiogenic shock and the elevation of BNP during admission. The assessment of troponin I and BNP can help with the prognostication of TTC patients in our daily clinical practice.
Intraoperative chest radiography revealed severe pulmonary edema and echocardiography indicated moderate left ventricular dysfunction with akinesia of the mid to apical left ventricular wall segment, which is reflective of takotsubo cardiomyopathy.
With early detection and appropriate management, the patient was stabilized in a relatively short period of time. Based on her clinical signs and symptoms, we suspect that the pulmonary edema was caused by takotsubo cardiomyopathy.
Thirty patients (29 females, 67 ± 11 years) with an apical ballooning TTC pattern 225.5 ± 27.4 days after their index event were enrolled. The control group consisted of 20 (19 females, 64 ± 9 years) age- and sex-matched volunteers without structural heart disease. Classic echocardiographic parameters, longitudinal strain and LV twist parameters were assessed and compared between the groups commencing six months after discharge for follow-up.
There were no differences in traditional LV systolic-, diastolic parameters and in global peak longitudinal strain. In comparison to controls, patients with TTC had lower mean apical rotation (14.4° ± 6.5° vs. 18.3° ± 6.7°; p = 0.048), slower mean peak early diastolic apical rotation rate (-85.1-°/s ± 40.9-°/s vs -119.4-°/s ± 41.9-°/ S: ; p = 0.006) and higher pre-stretch index in the apex (2.16, IQR 0.33-5.50 vs. 0.00, IQR 0.00-2.95, p = 0.008).
The improvement of LV function in patients with TTC as assessed by 2D STE may not always be substantial. Some residual abnormalities in LV apex function were observed in long-term recovery following TTC episodes.
In this review, we have summarized the data from studies investigating the implications of cardiac troponin concentrations in various acute and chronic conditions beyond ACS, i.e., heart failure, myocarditis, Takotsubo cardiomyopathy, aortic dissection, supraventricular arrhythmias, valve disease, pulmonary arterial hypertension, stroke, and in the perioperative setting.
Cardiac troponin concentrations are often detectable and frankly increased in non-ACS conditions, in particular when measured with high-sensitivity (hs) assays. With the exception of myocarditis and Takotsubo cardiomyopathy, cardiac troponin concentrations carry strong prognostic information, mainly with respect to mortality, or incipient and/or worsening heart failure. Studies investigating the prognostic benefit associated with cardiac troponin-guided treatments however, are almost lacking and the potential role of cardiac troponin in the management of non-ACS conditions is not defined.
Increased cardiac troponin indicates increased risk for adverse outcome in patients with various cardiovascular conditions beyond ACS. Routine measurement of cardiac troponin concentrations can however, not be generally recommended unless there is a suspicion of ACS. Nonetheless, any finding of an increased cardiac troponin concentration in a patient without ACS should at least prompt the search for possible underlying conditions and these should be managed meticulously according to current guidelines to improve outcome.
Recognizing apical ballooning syndrome is challenging in patients with a history of respiratory disease because the symptoms of the last entity may complicate the diagnostic approach. It is difficult to distinguish clinically apical ballooning syndrome from the acute airway exacerbation itself. Both asthma and takotsubo cardiomyopathy share the same clinical presentation with dyspnea and chest tightness. In our patient, the electrocardiographic abnormalities, the rapidly reversible distinctive characteristics of echocardiography and the modest elevation of serum cardiac biomarkers levels, in combination with the presence of a stress trigger (severe asthma attack), strongly supported the diagnosis of broken heart syndrome.
Clinicians should re-evaluate asthma management and be aware of the complications associated with asthma attacks such as stress-induced cardiomyopathy.
An assessment of myocardial perfusion (99mTc-MIBI) and glucose metabolism (18F-FDG) was performed within 18 days.
SPECT showed no regional perfusion abnormalities in 10/18 patients, and a mild perfusion defect was found in 8/18 patients. Perfusion abnormalities were limited to apical and para-apical regions. In 8/18 cases, there was an increased selective apical 18F-FDG accumulation. In 10/18 cases, in spite of the fastened 18F-FDG protocol, slightly inhomogeneous 18F-FDG uptake was present in the entire myocardium: with relatively reduced uptake of 18F-FDG in the apical region and LV mid-segments.
This study demonstrated the heterogeneous nature of myocardial 18F-FDG accumulation in patients with TTC. Selective, preferential apical 18F-FDG uptake in almost half of the patients confirms an existing disorder of glucose metabolism, similar to that observed in stunned or hibernated myocardium.
41ng/mL which peaked at 0.66ng/mL. Echocardiogram showed a depressed left ventricular ejection fraction to 35% with severely hypokinetic anterior wall and left ventricular apex was severely hypokinetic. EMG nerve conduction study showed severely decreased conduction velocity and prolonged distal latency in all nerves consistent with demyelinating disease. She was treated with 5days of intravenous immunoglobulin therapy to which she showed significant improvement in strength in her lower extremities. Echocardiogram repeated 4days later showing an improved left ventricular ejection fraction of 55% and no left ventricular wall motion abnormalities. Takotsubo cardiomyopathy is a rare complication of Miller-Fisher syndrome and literature review did not reveal any cases. Miller-Fisher syndrome is an autoimmune process that affects the peripheral nervous system causing autonomic dysfunction which may involve the heart. Due to significant autonomic dysfunction in Miller-Fisher syndrome, it could lead to arrhythmias, blood pressure changes, acute coronary syndrome and myocarditis, Takotsubo cardiomyopathy can be difficult to distinguish. The treatment of Takotsubo cardiomyopathy is supportive with beta-blockers and angiotensin-converting enzyme inhibitors are recommended until left ventricle ejection fraction improvement. Takotsubo cardiomyopathy is a rare complication during the acute phase of Miller-Fisher syndrome and must be distinguished from autonomic dysfunction as both diagnoses have different approaches to treatment.