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Respiratory involvement from herbals
Published in Philippe Camus, Edward C Rosenow, Drug-induced and Iatrogenic Respiratory Disease, 2010
Tracey K Riley, Kahoko Taki, Christopher P Holstege
The pyrrolizidine alkaloid that has been most investigated for the development of pneumotoxicity is monocrotaline. This alkaloid is present in over 20 plants. In the published research model, it was isolated from the seeds of Crotalaria spectabilis. The occurrence of pulmonary arterial hypertension and right ventricular hypertrophy from exposure to monocrotaline, especially in rats, is very similar to the pathology that occurs in humans who develop primary pulmonary hypertension.49 The occurrence of the pathology in rats is not immediately evident. Vascular remodelling that results in the development of pulmonary hypertension takes days to weeks, long after the exposure to the alkaloid has ended.49 Also, the dose of monocrotaline administered has an effect on the pathology that develops: low doses of monocrotaline were more pulmonary toxic, while higher doses produce hepatotoxicity when given to rats.46
Systemic toxicology
Published in Chris Winder, Neill Stacey, Occupational Toxicology, 2004
W.M. Haschek, N.H. Stacey, C. Winder
Cardiovascular diseases, especially atherosclerotic vascular disease, are the major cause of death in the USA. Major risk factors for atherosclerosis include cigarette smoking, diabetes, obesity, hypertension, hyperlipidaemia, and genetic factors (Benowitz 1992). Occupational exposure has been linked to cardiovascular diseases such as arrhythmias, atherosclerosis, problems with coronary blood supply, systemic hypotension, and cor pulmonale (right ventricular hypertrophy usually due to pulmonary hypertension). Although many chemicals have been shown experimentally to be potentially cardiotoxic, the role of low-level chronic exposure to chemicals in the workplace in the aetiology of chronic cardiovascular disease in humans is still largely unknown.
Cardiac Fiber Imaging with 3D Ultrasound and MR Diffusion Tensor Imaging
Published in Ayman El-Baz, Jasjit S. Suri, Cardiovascular Imaging and Image Analysis, 2018
As cardiac fiber orientations are crucial to determine the electromechanical function of the heart, their abnormality directly relates to cardiac dysfunctions (i.e., decreased contractility or arrhythmia) that may result in heart failure or even sudden death [1, 8]. For instance, studies have shown that cardiac fiber orientations play a key role in the generation and maintenance of reentrant arrhythmia [9]. Thus the abnormal fiber orientations could directly decide the activation patterns during the electrical induction of ventricular fibrillation. More importantly, significant abnormality of cardiac fiber orientations usually occurs in ischemic heart disease, the leading cause of death worldwide. This disease causes permanent damage to the heart muscles, thus resulting in severe disarray of cardiac fibers in the infarcted myocardium. In vivo imaging showed that after injury, the death of cardiomyocytes led to increased dispersion and significant reorientation of cardiac fiber architecture in the infarct region [10, 11]. The redistribution of fiber orientations decreased the contractility of the heart and increased the risk of lethal ventricular tachycardia. Besides acute diseases, the progression of abnormal cardiac fiber orientations can also be found in chronic ventricular remodeling. In the dilated heart failure, an altered transmural fiber gradient accompanies a geometry change of local wall thinning in the septum. Hypertrophic cardiomyopathy also induces abnormal myocardial laminar orientations compared to the healthy group [12]. Specifically, right ventricular hypertrophy induced by pressure loading was found not only to increase ventricular weight and myocardium thickness but also to change intramyocardial fiber orientations [13], including decreased transmural changes of cardiac fiber orientations in the failing right ventricle [14]. Recently, considering the importance of cardiac fiber orientations, researchers have started to employ them in treatment plans to guide cardiac resynchronization therapy (CRT) [15].
Potential adverse cardiac remodelling in highly trained athletes: still unknown clinical significance
Published in European Journal of Sport Science, 2018
Luigi Gabrielli, Marta Sitges, Mario Chiong, Jorge Jalil, María Ocaranza, Silvana Llevaneras, Sebastian Herrera, Rodrigo Fernandez, Rodrigo Saavedra, Fernando Yañez, Luis Vergara, Alexis Diaz, Sergio Lavandero, Pablo Castro
Surface electrocardiogram in highly trained athletes is often a difficult element to interpret due to a large number of electrical changes that could be observed (Prakash & Sharma, 2015). These electrical changes are secondary to high vagal tone and changes in cardiac chamber size, and the majority of these variants are benign and are consequences of physiologic adaptation to exercise (Prakash & Sharma, 2015). However, some patterns may overlap with channelopathies or cardiomyopathies (Prakash & Sharma, 2016). Bradiarrhythmias are a very common finding in up to 70% of athletes, along with repolarisation changes in 60% of the cases (Papadakis et al., 2011). The early repolarisation pattern, associated with vagal tone, is seen in 25–40% of the series (Macfarlane et al., 2015). Left ventricle hypertrophy criteria are present in as many as 70% of highly trained athletes and only 12% showed criteria for right ventricular hypertrophy (Basavarajaiah et al., 2008). Partial right bundle branch block, associated with right ventricular dilatation in the context of athlete’s heart is present in up to 30% of cases (Di Paolo et al., 2012). In 2010, the European Society of Cardiology published the recommendations to interpret athletes’ electrocardiograms. They described two groups of changes: class 1 benign detected in 80% of athletes and class 2 possibly pathological in less than 5% of athletes (Corrado et al., 2010).