Pulmonary embolism and Takotsubo syndrome in tandem: An interplay of pathologies needing our vigilance

Pulmonary embolism and Takotsubo syndrome in tandem: An interplay of pathologies needing our vigilance

Heart & Lung 43 (2014) 168e169 Contents lists available at ScienceDirect Heart & Lung journal homepage: www.heartandlung.org Letters to the Editor ...

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Heart & Lung 43 (2014) 168e169

Contents lists available at ScienceDirect

Heart & Lung journal homepage: www.heartandlung.org

Letters to the Editor

Pulmonary embolism and Takotsubo syndrome in tandem: An interplay of pathologies needing our vigilance

Conflict of interest: None. John E. Madias, MD, FACC, FAHA* Icahn School of Medicine at Mount Sinai New York, NY, USA Division of Cardiology, Elmhurst Hospital Center Elmhurst, NY, USA

To the Editor: The interesting case report by Baydoun et al published in the JanuaryeFebruary issue of the Journal,1 of a woman with a transient right heart failure due to pulmonary embolism (PE), followed by left heart failure due to Takotsubo syndrome (TTS) within 48 h, after the patient was informed about her colon cancer, is intriguing and thought provoking. The authors appropriately ascribed the emergence of TTS to the patient’s PE and/or emotional distress upon learning about her associated metastatic to the liver colon cancer. Similarly there are currently reports of patients suffering TTS after admission with acute coronary syndromes (ACS).2 Clinicians should be vigilant to detect TTS in patients with well established afflictions, involving both the left and right ventricles, instead of only being consumed by efforts to differentiate TTS from ACS, or other morbidities. Both emotional stress related to the diagnoses of various diseases and/or the nonspecific physical disstress underlying such diseases, can conspire to result in TTS. It is conceivable that this tandem occurrence of various cardiac pathologies with TTS may be quite frequent, and currently underdiagnosed, particularly when the associated TTS is of a milder form. In addition one wonders whether in cases of PE and ACS there is a “secondary” TTS component, superimposed on the “primary” pathology. Accordingly, is it possible that some transient unexplainable left ventricular wall motion abnormalities involving the contralateral territories impacted by the “primary” pathology in patients with ACS, or a portion of right ventricular dysfunction in patients with PE, is due to TTS. We all should be evaluating our patients along this line of thought, employing frequent serial echocardiography.

References 1. Baydoun H, Khoueiry G, Ghandour Z, Olkovsky Y. From right to left heart failure: an unexpected transition. Heart Lung. 2014;43:41e44. 2. Tota F, Ruggiero M, Sassara M, et al. Subacute stent thrombosis and stressinduced cardiomyopathy: trigger or consequence? Am J Cardiovasc Dis. 2013;3: 175e179.

0147-9563/$ e see front matter Ó 2014 Elsevier Inc. All rights reserved.

* Corresponding author. Division of Cardiology, Elmhurst Hospital Center, 79-01 Broadway, Elmhurst, NY 11373, USA. Tel.: þ1 718 334 5005; fax: þ1 718 334 5990. E-mail address: [email protected] http://dx.doi.org/10.1016/j.hrtlng.2014.01.003

Reply to letter to the Editor: Cognitive impairment and medication adherence in outpatients with heart failure Dear Dr. Redeker: We thank Dr. Alkhuja and colleagues for their interest in our paper, ‘Cognitive impairment and medication adherence in outpatients with heart failure.’1 In this study of 251 outpatient veterans with heart failure (HF), 58% were found to have clinically unrecognized cognitive impairment (CI) that resulted in worsened adherence to medication. Dr. Alkhuja discussed the negative impact of sleep-disordered breathing on cognitive function in persons with HF, and suggested patients with poor adherence be screened for this diagnosis.2 We are in full agreement regarding screening HF patients for the presence of sleep-disordered breathing, and note the deleterious effects of this co-morbid disease particularly on self-care in HF.3,4 However, sleep apnea was not independently associated with the presence of CI or worsened adherence in the 68 (27.1%, n ¼ 251) patients with this diagnosis in our study sample. All of these patients had been previously identified with obstructive, central, or complex sleep apnea after full night laboratory-based polysomnography. Each patient had been supplied with the appropriate treatment modality (CPAP or adaptive servo ventilator) in consultation with a pulmonary sleep specialist. Yet, many demonstrated poor adherence to these therapies. Thus the intriguing question: does cognitive dysfunction result in poor adherence, or does poor adherence (to self-care, medication, or treatment of co-morbidities such as depression and sleep-