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Investigation of Sudden Cardiac Death
Published in Mary N. Sheppard, Practical Cardiovascular Pathology, 2022
Clearly, it is impossible to define the lower limit at which coronary stenosis without thrombosis or myocardial scarring or infarction is not the cause of death. All that can be said is that, if a single isolated segment of 50% diameter stenosis with a morphologically normal myocardium can cause death, the mechanism is unclear. Mechanisms such as coronary artery spasm would have to be postulated but are impossible to prove by morphological/histological studies. Many living males over 50 years in the general population will have an equivalent degree of disease without it being the cause of death. The problem becomes even more pronounced in older subjects. Cardiac hypertrophy acts both as an adjunct to coronary disease and also predisposes to ventricular arrhythmias even in the absence of coronary disease. This inevitably raises the difficult question of how much hypertrophy in the left ventricle can cause death in its own right. The probability of a causal link to death rises with increasing degrees of hypertrophy. Because of all these difficulties, many series which report the different causes of sudden death define sudden ischaemic death on the basis that at least one segment of a major coronary artery must have more than 75% diameter stenosis. The difficulties inherent in making these assessments are discussed more fully in Chapter 2.
Endothelin and Cardiac Hypertrophy
Published in Malcolm J. Lewis, Ajay M. Shah, Endothelial Modulation of Cardiac Function, 2020
Cardiac hypertrophy is a commonly observed complication of a variety of cardiovascular diseases including hypertensive and ischemic heart disease and cardiomyopathies. The nature of the hypertrophic response of the heart is a compensatory one to counter the increased afterload or disturbed function of the heart. However, when this physiological response progresses beyond a certain point, a variety of dysfunctions accompany cardiac hypertrophy (Shepherd et al., 1989). Diastolic dysfunction is one of the most common manifestations of cardiac hypertrophy, which in turn may lead to congestive heart failure due to increased filling pressure. Subsequently, disturbance of systolic function and congestive heart failure may occur late in the evolution of cardiac hypertrophy. In addition, a variety of ventricular arrhythmias may also accompany the development of cardiac hypertrophy. Thus the prevention of cardiac hypertrophy is one of the most important problems that should be targeted by both clinical and basic researchers in cardiology.
Cardiac Performance During Diabetes
Published in Grant N. Pierce, Robert E. Beamish, Naranjan S. Dhalla, Heart Dysfunction in Diabetes, 2019
Grant N. Pierce, Robert E. Beamish, Naranjan S. Dhalla
Blood pressure measurements will, of course, be dependent upon the presence of atherosclerotic complications in the arterial system during diabetes. Hypertension in the diabetic population has been reported.6 In relatively asymptomatic diabetic men, systolic blood pressure tended to be higher in those patients with autonomic neuropathy but lower in diabetics considered to have peripheral neuropathy.4 Diastolic blood pressure changes may correlate with pathological alterations in heart morphology. Shapiro and colleagues7 discovered that the posterior wall of the heart was thicker in diabetic patients if the diastolic blood pressure was between 100 to 125 mmHg than if it was less than 100 mmHg. Cardiac hypertrophy has been considered as an indicator of clinical heart disease.8
Andrographolide contributes to the attenuation of cardiac hypertrophy by suppressing endoplasmic reticulum stress
Published in Pharmaceutical Biology, 2023
Qingxin Tian, Jianlong Liu, Qin Chen, Mingxiao Zhang
Cardiac hypertrophy refers to a response of the heart to augmented workload, such as dilated cardiomyopathy, aortic stenosis and hypertension (Myers et al. 2017). Pathological cardiac hypertrophy is characterized by enlarged cardiomyocytes and obstructed contractility of the heart, accompanied by internal changes in cardiomyocytes, including apoptosis, cardiac fibrosis, metabolism and gene expression (Tham et al. 2015; Gesmundo et al. 2017). In the case of coronary artery disease, valvular heart disease and hypertension, the heart may also become hypertrophic under chronic stress or volume overload (Weeks and McMullen 2011). Moreover, cardiac hypertrophy has been reported to usually develop into heart failure (Shimizu and Minamino 2016). Several researchers have clarified that multiple signalling pathways are involved in the occurrence of cardiac hypertrophy, such as typical G protein-coupled receptor (GPCR) and calcineurin-activated T nuclear factor (NFAT) signalling pathways (Madukwe et al. 2018; Zhang et al. 2020). Nevertheless, the mortality from heart failure remains high due to the complex mechanism of the transition from hypertrophy to heart failure, as well as the difficulty of reversing cardiac hypertrophy. Therefore, it is urgent to find a new pharmacological drug that can suppress the progression of cardiac hypertrophy.
Effects of berberine hydrochloride on left ventricular structure and function in rats with myocardial hypertrophy
Published in Acta Cardiologica, 2023
Tuli Kou, Haorou Luo, Yang Shen, Ye Su, Lixue Yin
Cardiac remodelling is an essential pathological mechanism in the process of heart failure. Cardiac hypertrophy plays a vital role in cardiac remodelling. It is a critical stage in the development of cardiac structure and function from compensation to decompensation, as well as an independent risk factor for the increased prevalence and mortality of cardiovascular diseases [1]. Early detection and treatment of cardiac hypertrophy are critical. Rho/ROCK signalling pathway plays an essential role in the development of cardiovascular diseases. Overexpression of Rho and ROCK can aggravate cardiac hypertrophy; inhibition of Rho/ROCK signalling pathway-related proteins can effectively alleviate left ventricular hypertrophy and prevent cardiac remodelling from progressing to heart failure [2–4]. BBR is a natural plant alkaloid that can inhibit pathological cardiac hypertrophy by up to 50% [5–7]. However, whether berberine hydrochloride can improve cardiac hypertrophy by regulating the Rho/ROCK signalling pathway is unclear. 2D-STE is a relatively new detection technology, which is more accurate than traditional echocardiography in the early detection of abnormal changes in cardiac function [8–11]. There are few studies on applying 2 D-STE in evaluating left ventricular function in rat models of myocardial hypertrophy.
Emerging therapeutic targets for cardiac hypertrophy
Published in Expert Opinion on Therapeutic Targets, 2022
Alexander J. Winkle, Drew M. Nassal, Rebecca Shaheen, Evelyn Thomas, Shivangi Mohta, Daniel Gratz, Seth H. Weinberg, Thomas J. Hund
Cardiac hypertrophy is an important pathophysiological response to chronic changes in metabolic demand. Hypertrophy assumes different structural and functional manifestations depending on a variety of environmental, genetic factors providing the backdrop for an ongoing debate about the viability of hypertrophy as a therapeutic target to prevent heart failure. Mounting studies provide examples of molecular perturbations that yield preserved hypertrophy without cardiac dysfunction raising the question of whether hypertrophy may be ‘redirected’ rather than inhibited for therapeutic benefit in some cases. Critical gaps remain in our ability to link-specific hypertrophic stress stimuli to cell and organ-level changes. Such knowledge may clarify the role of hypertrophy in pathophysiology and point the way to improved therapies.