Since its initial description by Japanese investigators 30 years ago, TakoTsubo Syndrome (TTS) has variously been regarded as a form of acute coronary syndrome and also as a form of cardiomyopathy (or more accurately, a myocarditis). There is actually good evidence that TTS embodies both of these concepts, and the main purpose of this review is to present data that they occur sequentially. The initial phase of the disorder (over perhaps the first 48 hours post onset of symptoms) represents a form of vasculitis, with associated damage to the endothelial glycocalyx and associated permeabilization of blood vessels. This is followed by a more prolonged phase of myocardial inflammation and oedema, associated with inflammatory activation and energetic impairment within the entire myocardium. Although this phase subsides after several months, it may be followed by longstanding impairment of myocardial function, reflecting residual fibrosis. Understanding of this gradual transition in TTS pathogenesis from vasculature towards myocardium remains an important limitation of patient management, especially as many patients are still told that their hearts have “recovered” within 1–2 weeks. A number of important uncertainties remain. These include development of specific early and ongoing therapeutic strategies to be used to match the sequential pathogenesis of TTS. “And so these men of Indostan Disputed loud and long, Each in his own opinion Exceeding stiff and strong, Though each was partly in the right, And all were in the wrong!” From: Six wise men of Hindustan

Chapter 24 Congenital Heart Disease Robyn Lotto, Robyn LottoSearch for more papers by this authorChristopher Nicholson, Christopher NicholsonSearch for more papers by this authorAngela M. Kucia, Angela M. KuciaSearch for more papers by this author Robyn Lotto, Robyn LottoSearch for more papers by this authorChristopher Nicholson, Christopher NicholsonSearch for more papers by this authorAngela M. Kucia, Angela M. KuciaSearch for more papers by this author Book Editor(s):Angela M. Kucia, Angela M. Kucia Adjunct Senior Lecturer Clinical Nurse Consultant UNISA Clinical and Health Sciences, University of South Australia, South Australia, Australia Acute Cardiac Assessment, Lyell McEwin Hospital, South Australia, AustraliaSearch for more papers by this authorIan D. Jones, Ian D. Jones Professor of Cardiovascular Nursing School of Nursing and Allied Health, Liverpool John Moores University, Liverpool, UKSearch for more papers by this author First published: 26 August 2022 https://doi.org/10.1002/9781119117810.ch24 AboutPDFPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShareShare a linkShare onFacebookTwitterLinked InRedditWechat Summary This chapter introduces the formation and management of congenital heart defects, valve abnormalities and genetic cardiomyopathies. Congenital heart defects (CHD) are a heterogeneous group of abnormalities, ranging in severity and associated outcome. CHD refers to a structural abnormality of the heart and great vessels present at birth that is, or could be, of functional significance. Many cases of CHD are multifactorial and result from a combination of genetic predisposition and environmental risk factors. Cyanotic heart disease can be subdivided into conditions with decreased pulmonary blood flow and conditions with mixed blood flow. An abnormal connection between the systemic and pulmonary circulations gives rise to potential excess volume of blood to flow from the systemic circulation to the pulmonary circulation resulting in the recirculation of already oxygenated pulmonary venous blood through the pulmonary vasculature. Dextrocardia refers to alignment towards the right rather than the left. CHD are the most common form of congenital anomaly. Cardiac Care: A Practical Guide for Nurses, Second Edition RelatedInformation

The pathogenesis of acute coronary syndrome (ACS) usually involves atherosclerotic plaque rupture, platelet activation and thrombus formation. Inflammatory activation and coronary artery spasm represent important components of the various ACSs. ACS generally result from atherosclerosis, which causes plaque formation in the inside lumen of medium-and large-sized coronary arteries. This chapter describes the factors related to the process of atherosclerosis. Most forms of cardiovascular disease, including hypertension, CAD, chronic heart failure, and peripheral artery disease, are associated with vascular endothelial dysfunction. Inflammation has a central role in the pathogenesis and consequences of cardiovascular disease and encompasses a broad range of processes at the site of disease, in the blood, at remote sites and as downstream sequelae of disease. The chapter describes the process of thrombogenesis and the factors related to thrombus formation at the site of a plaque rupture.