Objectives: Heart disease is one of the chronic diseases that require adjustment and extensive changes in the patient's life. The purpose of the present study was to investigate the mediating role of difficulties in emotion regulation on the relationship between anger rumination and worry with adjustment problems to heart disease. Methods: A total of 327 patients with coronary artery disease (138 women and 189 men) participated in this study. Participants were asked to complete the Penn State Worry Questionnaire, Anger Rumination Scale, Difficulties in Emotion Regulation Scale, and Adjustment to Illness Scale. Results: Worry, anger rumination, and difficulty in emotion regulation showed a negative correlation with adjustment to heart disease. The results of path analysis indicated that the relationship between worry and anger rumination with adjustment to heart disease was mediated by difficulties in emotion regulation. Conclusion: Based on the results of the present study, management of worry and anger rumination, as well as emotion regulation strategies, should be implemented in regular medical treatments for patients with heart disease.

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Takotsubo syndrome (TTS) is a clinical syndrome characterized by transient left ventricular dysfunction, ischemic electrocardiographic changes, and minimal release of myocardial enzymes without obstructive coronary artery disease. This syndrome that mimics an acute myocardial infarction is prevalent among female patients and is regarded as a benign medical condition. The precise pathophysiological mechanism of TTS is complex and not completely understood, but specific emotional or physical events precipitate this syndrome that represents a typical condition characterized by interactions between cardiovascular and neuropsychological diseases. In addition, many different neurological disorders, such as stroke, subarachnoid bleeding, head injury, epilepsy, and bacterial meningitis, have directly or indirectly related to TTS; unfortunately, these acute neurological diseases represented the cause of death in patients nominated for organ donation and in particular for the heart donor. This article reviews the relationship between TTS and solid organ transplantation; in particular, this article highlights the possible mechanisms underlying the induction of TTS in pre- and post-transplantation phases and in heart-transplant patients.

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It is well known that bereavement can cause ominous cardiovascular events and elicit aggressive behavior in bystanders. A multidisciplinary approach in end-of-life care including communication and taking into account cultural, social, emotional, religious, spiritual preferences, and local differences needs further development and implementation in health-care systems worldwide. The direct effects of emotional stress on the cardiovascular system and cardiac diseases most frequently implicated in sudden cardiac death are discussed.

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Background: The cardiovascular system and central nervous system are known to influence each other. Accordingly, neurological changes may occur after myocardial infarction (MI), which may be mediated by neuroinflammation. We investigated tumor necrosis factor alpha (TNF-α) and microglia activation in post-MI neuroinflammation. Materials and Methods: MI or sham surgery was induced in 28 male mice. Two weeks later, we performed echocardiography and dissected the brains for the western blot on TNF-α and its receptors (n = 10) or immunohistochemical stainings for microglia, doublecortin X (DCX), and TNF-α (n = 18). Plasma was collected for the measurement of circulatory cytokines. Results: The MI mice had an average infarct size of 38% of the left ventricle, heart failure was confirmed by decreased fractional shortening and increased lung weight. Plasma cytokine levels were unaltered. In brains of MI mice, there was a higher expression of TNF-α precursor protein, with trends for higher TNF-R1 and lower TNF-R2 expression. Furthermore, MI mice had more activated microglia in the inner blade of the dentate gyrus of the hippocampus. The amount of neurogenesis measured by DCX staining was unaltered. Conclusions: Our mouse model of MI showed signs of persistent neuroinflammation as indicated by raised levels of TNF-α precursor protein and an increased number of activated microglia in the hippocampus. The extent to which these neuroinflammatory hallmarks influence central nervous system functioning remain to be determined.

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Anomalous coronary arteries are rare entities with certain categories being potentially malignant with the risk of sudden cardiac death. We present two cases of the highest risk variant consisting of an anomalous left coronary artery arising from the right sinus of Valsalva traversing between the aorta and pulmonary artery leading to recurrent syncope and chest pain in middle-aged patients.

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