Ever since Selye's time, the belief has persisted that the outcome of stressful experience is disease. The likelihood of this eventuality is increased when the experience is damaging, unavoidable, or uncontrollable. However, in most stressful instances, these conditions do not occur. The experience either is overcome or produces disturbances in physiological functions without structural change. The prevalence of "functional" disorders are far more common in medical practice than is disease. Among the most interesting of these is the hyperventilation syndrome, which may mimic or be confused with ischemic heart disease. Its symptomatology and physiology are complex. The syndrome may produce coronary vasospasm, but it may also complicate ischemic heart disease. It is even believed that chronic hyperventilation may be a risk factor for ischemic heart disease. Stressful experience consisting of various tasks and challenges may also produce myocardial perfusion deficits in ischemic heart disease, presumably secondary to vasospasm. These deficits are in turn considerably more frequent in any one patient than ST segment changes in the electrocardiogram or the incidence of angina pectoris. Vasospasm is in turn related to cardiac arrhythmias, which may occur with ischemic heart disease during a variety of stressful experiences and during outbursts of anger. Finally, the role of stressful experience in inciting ischemic heart disease and its complications remains moot.
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J Cardiothorac Surg
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Echocardiography and Vascular Ultrasound Center, The First Affiliated Hospital, Zhejiang University School of Medicine, 79 Qingchun Road, Hangzhou, 310003, China.
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MAP Centre for Urban Health Solutions, Li Ka Shing Knowledge Institute, St. Michael's Hospital, Unity Health Toronto, 80 Bond Street, Toronto, ON, M5B 1X2, Canada.
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Key Laboratory of Cellular Physiology at Shanxi Medical University, Ministry of Education, and the Department of Physiology, School of Basic Medicine, Shanxi Medical University, Taiyuan, China.
Programmed necrosis/necroptosis greatly contributes to the pathogenesis of cardiac disorders including myocardial infarction, ischemia/reperfusion (I/R) injury and heart failure. However, the fundamental mechanism underlying myocardial necroptosis, especially the mitochondria-dependent death pathway, is poorly understood. Synaptotagmin-1 (Syt1), a Ca sensor, is originally identified in nervous system and mediates synchronous neurotransmitter release.
View Article and Find Full Text PDFZhonghua Yi Xue Za Zhi
January 2025
Ningbo Hangzhou Bay Hospital(Ningbo Branch of Renji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai),Ningbo315336, China.
To develop a predictive model for improvement of ejection fraction 1 year after heart failure with reduced ejection fraction (HFrEF) following acute ST-segment elevation myocardial infarction (STEMI). This nested case-control study included STEMI patients diagnosed with HFrEF from a prospective multicenter multimodality imaging cohort between August 2014 and March 2021. Based on the improvement of left ventricular ejection fraction (LVEF) at baseline and 1-year follow-up, the patients were classified into the heart failure with improved ejection fraction (HFimpEF) group and the persistent HFrEF group.
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