Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Coronary atherosclerosis is the most important primary etiologic factor predisposing to the development of heart failure. The mechanisms by which coronary atherosclerosis lead to heart failure likely involve the initial development of regional myocardial dysfunction, later progressing to global ventricular failure and symptomatic congestive disease. A variety of imaging strategies have been investigated for their value in identifying and characterizing markers of atherosclerosis in the effort to detect early cardiac disease. Non-invasive imaging techniques for assessing anatomic or functional manifestations of atherosclerosis include carotid ultrasonography, coronary computed tomography, cardiovascular magnetic resonance imaging, brachial artery reactivity testing, and the ankle-brachial index. Many of these imaging methods are shown to have accuracy, reliability, and the potential to add value to an office-based cardiovascular risk assessment. Further development of such imaging methods could facilitate early intervention in the development of myocardial dysfunction while enhancing our understanding of the natural course of atherosclerotic disease.
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PMID:Atherosclerosis imaging and heart failure. 1713 Oct 74

Cardiac remodeling occurs frequently in chronic kidney disease patients and affects quality of life and survival. Current treatment options are highly inadequate. As kidney function declines, numerous metabolic pathways are disturbed. Kidney and heart functions are highly connected by organ crosstalk. Among others, altered volume and pressure status, ischemia, accelerated atherosclerosis and arteriosclerosis, disturbed mineral metabolism, renal anemia, activation of the renin-angiotensin system, uremic toxins, oxidative stress and upregulation of cytokines stress the sensitive interplay between different cardiac cell types. The fatal consequences are left-ventricular hypertrophy, fibrosis and capillary rarefaction, which lead to systolic and/or diastolic left-ventricular failure. Furthermore, fibrosis triggers electric instability and sudden cardiac death. This review focuses on established and potential pathophysiological cardiorenal crosstalk mechanisms that drive uremia-induced senescence and disease progression, including potential known targets and animal models that might help us to better understand the disease and to identify novel therapeutics.
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PMID:Cardiac Remodeling in Chronic Kidney Disease. 3215 Aug 64